The purpose of my web site is to report what I have found concerning the PARANORMAL phenomenon and to make it easy to down load or save to your disk. I have compiled a collection of reports on the UFO scene including documents on the BLACK government projects as well as Chemtrails, FBI freedom of information on UFO's, William Cooper documents, Montauk events at the USAF base there. Also I have some ghost info. I have lots of data but only a fraction of it is here. If you need more data contact me at pauldharris@hotmail.com
MILKY WAY GALAXY
Do you know where you live? Your street addresses how about your town or neighborhood or state. What country are you from? What planet are we from? What galaxy? DO you know what neighborhood of the Milky Way are we from? Do you know the stars in the night sky? Have you heard of Sagittarius? Is it just a constellation? Or is it the area or arm of the Milky Way Galaxy that we are from and live in? A large S constellation in the brightest part of the Milky Way, beyond which lies the center of our galaxy. Take a look at the gif it is a composite photo of our home the glorious Milky Way galaxy and we live in the Sagittarius arm of the galaxy.
What it all means is that if a people have a free mind then their nation will also be of a free people.
FBI FREEDOM OF INFORMATION on Majestic 12
If the Majestic 12 organization is bogus and the documents are bogus, why investigate a bogus document about a bogus organization? Because the document had a top-secret heading so the FBI investigates all secret documents that are leaked. So if Majestic 12 organization is real then the FBI will investigate the leak of top-secret documents. If Majestic 12 is phony then why investigate a document on a bogus organization. The FBI does not say if Majestic 12 organization is real or false. You don't investigate a bogus or make believe organization so why investigate a document on an organization that does not exist unless it does then you have to check out all leaks. Why waste resources on something that does not exist. So that makes me think that Majestic 12 is a real organization if not why investigate a document about it.
SO DO ENTER IF YOU DARE!
UFO VIDEO This video is of a UFO in South America
UFO SPACE VIDEO This video was taken by the Space Shuttle
Message From: james_wolff1@yahoo.com(James
Wolff)
Date: Fri,Aug 20, 1999, 7:09am (EDT-3)
To: mailto:PaulDHarris@hotmail.com
Subject: Knowledge, UNCENSORED NEWS, Movies, NEGS., etc.~~
A few years ago I rented a house. There were two female NEGS.: "ghosts" hiding there. They followed me on jets, buses, etc. They have tried to kill, me, etc. They want me to throw out the documentation from a Remote Viewing Lab, RE-AN, etc.
Know any bounty hunters that get rid of "ghosts" that kill. The two female NEGS.: ghosts here have killed children and adults.
Hello, Matrix (sort of like the true White Light but fake, info about the real Matrices, Haarp, etc)see the sites at http://www.greatdreams.com/ for more Life force(Psychic Vampires, etc.), Phantasm: (Ophanin Angels,Silver Spheres, entities coming through mirrors, etc.),
Independence Day: (look at the alien entities with an entity inside of them...sort of like the new "soul-mates" some have talked about),
The Boys From Brazil: (Cloning,Nazis, and South America) Web
sites: Light Technology:
http://www.sacredspaces.org/
800-637-5222(catalog), Holoform CD(s), Harmonizers, Acu-Vac
Coils, Feedback Loops.
http://members.aol.com/BDelphin/Bi04000.htm
(LINK NO LONGER ACTIVE)
Light Tool Pictures:
http://geobiology.technology.webjump.com/default.htm
(LINK NO LONGER ACTIVE)
Suppressed Knowledge:
http://www.isleofavalon.co.uk/edu/g-bank/a3-scien.html
(LINK NO LONGER ACTIVE)
Dolphin and Whale People's Light Technology, etc.
Knowledge:
http://hometown.aol.com/BDelphin/Bi05000.htm
(LINK NO LONGER ACTIVE)
(Note the article about the Ozone Layer problem and the real(?)cause of it)
Environment, Dolphins, Whales, etc.:
http://earthisland.org/
http://hometown.aol.com/BDelphin/Bi08000.htm
(LINK NO LONGER ACTIVE)
http://www.igc.apc.org/videoproject/index.html
(LINK NO LONGER ACTIVE)
http://www.earthtransitions.com/
http://www.earthjustice.org/
http://www.enn.com/
Sick people/ Bad Weather:
http://www.greatdreams.com/
http://www.greatdreams.com/radar.htm
http://www.prolognet.qc.ca/clyde/
http://www.home.earthlink.net/~ravenlmr/
(LINK NO LONGER ACTIVE)
Astral/Etheric/etc., Knowledge:
http://www.concentric.net/~asciiexp/
(LINK NO LONGER ACTIVE)
http://www.concentric.net/~asciiexp/ghb/
(LINK NO LONGER ACTIVE)
http://www.egroups.com/list/unexplainedworld/
Discussion, knowledge about Lizards, Greys, NEGS.,etc.:
http://art@trionica.com/
(LINK NO LONGER ACTIVE)
Lizards, Greys, NEGS.:
http://www.reptoids.com/
You decide if these Entities are NEG. or POS.
Entities; they have been around for awhile:
http://www.paoweb.com/gfmember.htm
UFO EXPOSURE:
http://www.caus.org/maillist.html
(LINK NO LONGER ACTIVE)
News:
http://www.truthinmedia.org/
http://www.foundingspirit.com/
(LINK NO LONGER ACTIVE)
http://members.aol.com/bufocalvin
(LINK NO LONGER ACTIVE)
Catalogs:
http://www.pyramidcollection.com/
Note: no http yet; Videos about Nazis and UFO(s), Dreamland
(Area 51), etc. Catalog called Things You Never Knew Existed,
Johnson Smith Company,
Catalog: 941-747-2356,
Fax: 941-746-7896,
Questions, etc.: 941-747-5566
TELL YOUR FRIENDS/TV/NEWS SOURCES...THE GIFT OF KNOWLEDGE!
Have a good week! Best,
James W. Magus/Magician (Tarot / Numerology)
Self Existing White Dog(Mayan)
316-235-1345 (in the phone book, Pittsburg,KS)
316-232-2400 (work...Politron Co., Pittsburg,Kansas)
=== James W. (Wolff)
(Magus/Magician -Numerology/Tarot) Pittsburg, Kansas, 66762
316-235-1345
("unusual" phone problems, house - in the phone book)
316-232-2400
(work - Politron Co., Pittsburg, Kansas)
Two MURDERING NEG. entities (spirits - dead humans): one brunette and one blonde female hiding here. Remote Viewing Report, etc. available. The two NEGS. are whining for KNOWLEDGE they aren't going to get! Any PEACE KEEPERS available to take care of business? Want a copy of THE LIGHT TECHNOLOGY LETTER: Light Harmonizers, Holoform Music, etc.? Send me an E-Mail! James_Wolff1@yahoo.com
Dear friends...
As most of you know, I have been an "amateur" ufologist for some years now. I have collected a substantial library of mostly-out-of-print publications on the subject, written and published articles on UFO's, and created and contributed exhibits to the International UFO Museum & Research Center in Roswell, New Mexico, including: Authoring and producing the recorded tour of the Museum (in three languages.) Writing, producing, and performing (on numerous occasions) the stage play "Mac Brazel Speaks," the story of Mac Brazel's discovery of the strange metallic debris that was responsible for spawning the famous Roswell Incident back in 1947. Designing, building and installing at the museum a diorama depicting KGFL radio's involvement in the 1947 Roswell Incident. Contribution of poster-size prints (from the original negatives) of the original J. Bond Johnson photographs taken in General Roger Ramey's office in 1947 which are now on display at the museum. You may also know that I've had an in-depth interest in fellow Hoosier Dr. Morris K. Jessup and his involvement in what has become known as "The Philadelphia Experiment." Some 20 years ago, I acquired a copy of what has now become known as "The Varo Edition" of Dr. Jessup's 1955 book, The Case For The UFO. (This publication is also known as "The Annotated Version" since it contains the notations made by three mysterious characters, one of which is presumed to be Carlos Allende, a merchant seaman who alleged that he witnessed The Philadelphia Experiment in 1943 which resulted rendering a navel destroyer and it's crew invisible for some period of time.) Now, I wonder if I could enlist your help. My copy of this "Varo Edition" (re-published in very limited numbers in 1973 by Gray Barker, now deceased) contains a blank page. I'm seeking to find others who may also have a copy of this book and would be willing to provide me a photocopy of page #128 so that I might complete my copy for research & display purposes. Could you help me spread the word either by 1) forwarding this email to any parties you think might be able to help me, 2) by forwarding me the email addresses of any such parties, or 3) by putting such parties in touch with me at the email address below?
I would appreciate any help you could provide.
Thanking you for your time and consideration (not to mention your years of service to ufology), I remain...
Cordially yours,
Bob Barnes
bbarnes@fwi.com
Bob Barnes
262 E. Taylor St.
Huntington, IN 46750-3723
bbarnes@fwi.com
A genuine photo of a red orb at my cousins funeral
From: Bernie Harris BernieHarris@excite.com
To: PaulDHarris@Hotmail.com
Subject: Moore Family Cemetery
Date: Sat, 12 Aug 2000 19:26:43 -0700 (PDT)
I was taking pictures of the thick fog in the hollow on the
morning of Buck's funeral and took this one of the Moore Family
Cemetery. Thought you might be interested in it.
Bernard
moore_family_cementary.jpg 240x320
"A Red Orb In Fog" taken at The Moore Family Cemetery at
Spanishburg West Virginia.
Hi,
Here's a photo of me for those who care. I believe it was taken in June of this year. The purple/pink light around me was emanating from the back of my head on that day. I can't figure it out.
After that last conspiracy based election email that I sent out, I only lost one list member. That's not bad. Just so everybody knows, I will always consider a theory and pass it on to you if I think you might find it interesting. It doesn't mean I buy into the theory - but I might.
I have the next couple of days off so I will be able to send out some good stuff. There's a great (I hope) UFO program that will be airing on the internet next week. This one is different because the host is a respected, national journalist. His brother is known around the world. More tomorrow...
If you would like to blow up my photo and through darts at it, feel free. I wave all of my copyright protection.
And yes, I really am 35 1/2 years old.
In the next email, I will update you on some major life changes that may potentially happen with me.
Take care,
Joe Ladd
Ufojoe1@aol.com
joe_photo_1.jpg 480x640
"UFO Joe and Ghost Photo"
Hi Paul
Thanks for all your help on my web page SHAPES of th UK and here is a photo of the Brown Lady ghost. Again many thanks
Bye Tom Turner tom@on-edie.net
MISSION STATEMENT
SHAPES U.K is a non profit making society, formed for like
minded people to investigate paranormal activity.
SHAPES U.K will endeavor to help all those that wish help to the
best ability of the society.
SHAPES U.K cannot take any responsibility for what happens during
an investigation, but would not leave untill client is happy.
SHAPES U.K will not publish any finding without prior
consent.
brown_lady.jpg 470x408
"Brown Lady on Stairs Ghost"
WARNING INCREASED ALERT
CHEMTRAILS CONTRAILS
I've followed the UFO situation for more than twenty years and its hard to explain but, I have a feeling something is very wrong, but it is not much more than a hunch. Consequently, I need help from anyone reading this report to use your resources to collect data about this new turn in events. My strong premonition is based on some reliable information that started a couple years back when Chuck Warren, told me he was photographing low level contrails made by large four engine white jet aircraft flying over the Philadelphia area. I have some 5,000 flying hours and have often seen contrails being formed by our aircraft, but never at these lower levels. We generally flew at 30,000 feet or higher in our C-141 Starlifter and often I observed four contrails developing well behind the engines, these would combine into on long contrail that would soon dissipate. Jet aircraft engines emit tiny particles that serve as condensation nuclei. At high altitudes water vapor collects on these particles and crystallizes, and in turn creating streaks of frozen water vapor otherwise known as contrails.
Chuck and his friends assured me these were not normal
contrails, that the aircraft were flying much too low to form the
standard contrails. He showed me some film of what appeared to be
a white 707 or KC-135 aircraft flying at a few thousand feet
leaving two contrails. The spray was coming from the tail area
and not from the engines. According to hundreds of reports this
spray called chemtrails falls to the ground and often makes some
people sick with flu like symptoms and skin rashes. The planes
are often seen flying in a crisscross checkerboard pattern and
soon the whole sky is clouded over. Weather satellite photos also
show the operation from space. These photos can be seen at
several web sites such as http://www.contrail
connection.com/
(LINK NO LONGER ACTIVE).
I first thought the government was spraying perhaps due to the Nile Fever scare. I checked with some old tanker Air Force and National Guard people all of whom denied any knowledge of the spraying. Samples of the chemtrails have been collected and are alleged to contain various toxins and reportedly red and white blood cells, and other unidentified cell types. Using a sub micron fiber sample these appear to be cells of a desicate freeze dried nature. These samples were sent to the EPA who thus far have given unsatisfactory answers. Their response has been that aircraft normally form contrails and spread toxins similar to cars exhaust. There is nothing to worry about.
On July 9, 2000, I was at Long Beach Island, New Jersey over looking at the Atlantic Ocean when I noticed a white four engine jet making a long contrail. It was a very thick heavy contrail in a beautiful blue sky. I looked left towards New York and the contrail was at least fifty miles long. Within a few seconds I looked back to the front of the contrail to get a closer look at the aircraft and it had disappeared. I searched the sky with binoculars, but it was gone. The contrail had suddenly stopped where I last saw the aircraft. I thought that was very strange, but perhaps I just lost it in the clear blue sky?
At the recent MUFON Conference Louisiana State Director Greg Avery explained his video camera was picking up UFOs inside the chemtrails and showed us some videos to that effect. Greg is a private trail lawyer whose philosophy concerning UFOs is: "that more often than not the evidence of the existence of flying saucers would have been judged a "proven fact" a long time ago if the question and the evidence had been put before an American jury using the same standards of proof used in civil trials for more than two hundred years." Driving home from the MUFON conference the Georgia State MUFON director who is a retired Chief of Police and others saw aircraft spraying. All those in the car noticed the contrails. While they were watching the spraying from the aircraft it disappeared. These are high quality witnesses, they are not mistaken. I've learned from other contrail experts this has happened before. To my knowledge humans do not possess aircraft that can disappear. The spraying is real, therefore I suspect that UFOs are involved. I want to know what they are spraying and why. The UFO and the chemtrial phenomena may have moved to a new level of seriousness.
My inquiries lead me to believe no one in government is noticing or analyzing the data? If anyone happens to see an aircraft at low level making contrails I urge you to videotape and get other witnesses watching. The more important the witness you can notify the better. Attempt to collect the spray. For example, large plates, plastic or your car's hub caps could be used to collect the liquid. Once the spray lands use Q tips to collect the spray and put into clean glass or plastic containers. Keep a record of what's happening. Let me know and I will give you an address to send the samples and videotapes. There is an urgent need for airborne sample collection flying behind the airborne chemtrails. This could be dangerous, but airborne samples would be much more valuable if properly collected and recorded.
I also suggest you put your name and address on this letter and send it to the most powerful person you know. We are attempting to get the news media and politicians aware of this potential problem. I will be on the Jeff Rense show Tuesday night to talk more about it. The EPA wrote David Peterson at the Chemtrail Research Fund on February 22, 2000. "We are not aware of any program to disperse fibrous material on the US population. My experience is that the government authorities are not engaged in quiet research to determine the problem, but tend to scoff at our efforts.
I wish to caution the reader that our data is not proven, the results of this spraying could be either helpful or hurtful to mankind. We are attempting to collect data and sort this out. We have obtained reports from almost every state in the US and numerous foreign countries such as Australia, England, France, Holland, Italy, New Zealand, Scotland, and Sweden.
The following are Essential Elements of Information that we need collected: Describe the craft and how it seems to disappear? Report location, date, time, speed, angle above the horizon, distance, size, etc. We can estimate altitude of the craft based on the angle and distance. For example, if the aircraft was 800 feet away at 30 degrees above the horizon its altitude would be 762 feet. Caution concerning your reports. High flying aircraft with contrails are a normal situation. Generally an aircraft smaller than your thumb nail at arm's length is at altitudes where normal contrails form. If the aircraft is larger than your thumb at arm's length it is unlikely contrails will naturally form and these should be especially videotaped. Attempt to get an overall wide angle view of the scene before and after zooming in on the object.
The obvious possibility is that the chemtrails are being spread by white unidentified flying objects that appear fairly normal until they suddenly disappear. It is much too early to come to conclusions, but it is important to collect data on this phenomenon. I certainly suspect a control system is operating. The phenomenon may be forcing us through a learning curve. The chemtrails and recent reports of threatening UFOs indicate a potentially more serious situation is developing. The following Kentucky report and those from Sweden and Australia help confirm this data.
THE NEXT ISSUE OF PLANET X MAGAZINE IS NOW AVAILABLE! http://www.planetxmagazine.com/ (LINK NO LONGER ACTIVE) EMAIL US FOR INFO! smoon@calweb.com UFOs Information Site Links Welcome to Planet X Magazine. If you're into Sci-Fi and Pop Culture from the 50's, 60's and 70's, you've come the the right place. The Outer Space issue, with Vitina Marcus, Richard O'Brien, The Angry Red Planet, and The Spotnicks, is still available. You can even use PayPal to purchase it online. And while the Underwater Issue is sold out, we have on-line excerpts with Diver Dan, Cap'n Mitch, and the man who invented Sea-Monkeys and X-Ray Spex, Harold Von Braunhut. Planet X also hosts the official website for legendary Creature Feature host Bob Wilkins. If you grew up watching late night monster movies with Bob, you can relive your favorite Creature Feature memories!
http://www.primenet.com/~thelab/autopsy.html (LINK NO LONGER ACTIVE)- Hello, and thank you for visiting. On this page, I won't tell you that the 'ALIEN AUTOPSY' really happened, was really filmed, was really swapped with a fake, and then really shown, but I'll show you why I think that that's what happened...
http://www.anomalous-images.com/ "UFO images, UFO, UFOs, extraterrestrial, Greys, Grays, reptilian, Draco, contrail, chemtrails, weather anomalies, MP3, midi, anomalous images, anomalies, lunar anomalies, moon anomalies, Mars, Mars anomalies, UFO files, news, anomalous news, Stonehenge, Stonehenge on Mars, Mars Stonehenge, Montauk, Phil Schneider, deep underground Bases, Reptilian, New Denver Airport, Masonic, disappearing children, New World Order, George Bush, Area 51, Dulce, CIA"
http://www.ghostweb.com/pictures.html See Your Photograph Showcase on the Largest Ghost Hunting Web Site in the World!
http://www.clantongang.com/oldwest/ghost.htm Scary, Unexplained ghost photos you MIGHT NOT want to see!
http://www.sjgr.org/ Welcome to the Official South Jersey Ghost Research web site. We are a professional research and investigation group with years of experience dealing with ghosts and haunting. We conduct ghost "hunts", discreet investigations and promote the learning and understanding of ghosts and other psychic phenomenon. Our group consists of experienced investigators some of which have been investigating ghosts and the super natural for over 40 years. We also welcome and train amateur investigators. We come from all walks of life, from law enforcement to grandmothers. Our ages range from eighteen to the sixties. We are all serious about the pursuit of knowledge, the assisting of those in need and we invite all open minded individuals to join us in our quest to understand ghosts better. We offer all our services for free.
http://www.angelfire.com/ma/NightWatch/ (LINK IS ACTIVE BUT SITE IS DEAD)NightWatch was founded on the principle that people should be able to discuss and debate ideas relating to UFO, Science, Technology, Modern Global Issues, and Paranormal phenomena without being belittled or harassed. Through safe open global communication, we believe that truth can be discovered. Area_51 Majestic:_MJ-12 Faked_Moon_Landings? Disaster_Control_&_UFOs Alien_Types "Reptilian" & Reptiles in History Krill_Report Recommended Links: UFO Roundup: Latest Sightings / Archive Roswell Rods Live CHAT NightWatch Online Chat: Port 1 NIGHTWATCH: BRIEF
http://www.cosmicsociety.com/Ghost Photographs - Spirit Pictures - Paranormal Photos Fake or Real??? Cosmic Society of Paranormal Investigation Home Page, paranormal,meta... - *Welcome to the internet's LARGEST *FREE* SPIRIT ENERGY PHOTOGRAPH Web site! *See note near bottom GHOST PHOTO OF THE MONTH ©1998 Susan Hubbell Full Details under Children 3 on Photos Page.
http://www.ufochronicles.com/home.htm (SIGHT NO LONGER THERE BUT LINK IS ACTIVE)- MJ12 The secret alien agenda. MOONGATE Is there a Moon Conspiracy? Paul Castardo Former Top Secret Military Speaks. Secret Underground facilities exposed. MJ12 The secret alien agenda. MOONGATE Is there a Moon Conspiracy? Paul Castardo Former Top Secret Military Speaks. Secret Underground facilities exposed. North Bay UFO Sightings& NASA. Starchild Alien Skull Discovered (photos) . Revealing information about Alien Implants. The Matrix Information from deep within Enemy Lines.Alien Anatomy The anatomy of the "Grey" Alien. Alien Meta Super natural Alien Occurrences or Technology. The Genetic Language of Crop Circles . Near Death Experience. OPUS: Support for paranormal experiences. Index of Ghost Stories. Uncovered technology to contact the dead. Haunted Hotel has guests up in arms. Exo & Astrobiology - DNA is continually Raining in. SETI should be Searching the Inferred not Microwave. Patrick Flanagan takes hearing to a new level. Robert Moringsky Aliens Battle over Earth.Infinite Reality: Universal Instincts. Biomagnetic Synergy: Enlightening Metaphysics. Alien Types: ALFs, EBEs & ETs.
http://www.eprf.tzo.com/(LINK NO LONGER ACTIVE) Sightings Hundreds of paranormal events are chronicled here. Updated bi-monthly. The most current sightings can be found in our newsletter . Photographs Our on-line archives of over 300 photos of various paranormal phenomenon: UFOs, ghosts, crop circles and more. Encounters Stories of close contact with alien beings. These encounters can be a very close, personal, and sometimes traumatic experience
http://www.ufocasebook.com/091905.htmlUFO CASEBOOK Free Downloads, UFO Video Club, online Magazine, Best Ever, UFO Documents, Paranormal, UFO, UFO Sightings, Roswell pictures, Crop Circles, UFO Video Downloads, REAL MEDIA, Alien photographs, Free Alien Pictures, UFO Video Club, Best UFO Pictures, Writer B J Booth, UFO Photographs, UFO Videos, Alien Abductions, UFO ART, Shag Harbor, Lonnie Zamora, Alien Abductions, Extraterrestrial, Roswell Crash, Close Encounters, Betty and Barney Hill, Travis Walton, Project Bluebook, Dr. J Allen Hynek, Rendelsham, Bentwaters, Flying Saucers, Photographs, Pictures, Images, Stanford, Kentucky, Pascagoula, New Guinea, Father Gill, Mike Rogers, Area 51, Falcon Lake, Wales Crash, Roswell, Kecksburg UFO, Loring Air Force Base, Alien Pictures, Alien Graphics
http://ufos.about.com/ABOUT UFO's UFO ufos ufo UFOs alien aliens abductions area 51 groom lake roswell aztec philadelphia experiment photos video sightings bermuda triangle montauk flying saucers axtraterrestrials seti spook lights ghost lights anomalies charles fort flight 19 carlos allende airships mysterious disappearances et visitors ancient astronauts aliens bermuda triangle area 51 flying triangles black aircraft top secret disclosure sightings sighting.
http://www.ghostweb.com/ [IGHS] Newsletter is a good ghost e zine check out there web site for pictures.
_NightWatch_@yahoogroups.com NightWatch was founded on the principle of the free exchange of ideas, however, flames, rudeness, antagonism and immaturity will not be tolerated.
http://www.paranormalnews.com/ Your source for ufo and paranormal related information. Search thousands of paranormal images, or browse our large new and used book collection at http://www.paranormalphernalia.com/ (THIS LINK IS ACTIVE BUT SITE IS DOWN FOR RELOCATING)
ScaryScreaming@yahoogroups.com This is an email newsletter about ghost related topics
WeeklyFiles@filersfiles.com This is an email newsletter about UFO related topics
Patrick OConnell tapa-chemtrails@yahoogroups.com This is an email newsletter about chemtrails and other conspiracy theroies
Alien_Mothership_Mailing_List@yahoogroups.com (Weird World)This is an email newsletter about paranormal topics but mainly news related to space
The X-Project ParaWire is a regular E-Mail companion to the popular X-Project Paranormal Magazine. - http://www.xprojectmagazine.com/
http://www.ufomind.com/ Paranormal Phenomena Ufomind Paranormal Index & BookStore YTINAMUH SEIL ECNEICS FO LIEV EHT DNIHEB
http://whatsonthe.net/paranormalmks.htm Paranormal On the Net 400 paranormal, sites, paranormal links Included Page: Paranormal : On the Net 400 paranormal, sites, paranormal links
Paranormal Parlor Free for All Links This site will let you add a link to theirs. It is almost 100k(LINK IS ACTIVE BUT DOWN FOR RENOVATIONS)
http://www.angelfire.com/ri/paralinks/main.html Welcome!! ParaLinks was created to give people links to all sorts of paranormal activities, mysteries, folklore, psychic phenomenon, and much more.
http://www.abcfield.force9.co.uk/WELCOME to B.U.F.O.D. Space, Above and Beyond, this is a web site that contains information mainly about UFOs and related subjects. UFOs are still a mystery to many people and only the people who witness such an event can really believe what is out there. This web site will help you understand the UFO phenomenon and provide evidence to help the truth be known
| SETI, Or The Search For Extraterrestrial Intelligence | SETI@HOME | SETI@HOME: SIGNAL CRUNCHING YIELDS LITTLE SO FAR |
SETI, or the Search for Extraterrestrial Intelligence, is a scientific effort aiming to determine if there is intelligent life out in the universe. There are many methods that SETI scientific teams use to search for extraterrestrial intelligence. Many of these search billions of radio frequencies that flood the universe, looking for another civilization that might be transmitting a radio signal. Other SETI teams search by looking for signals in pulses of light emanating from the stars.
For more information about SETI and the various SETI projects that exist, take a look at the links below:
SETI@home is one of the SETI projects that searches for extraterrestrial life. SETI@home allows anyone with a computer and an Internet connection to take part in the search. By using the computer while the owner is away, the SETI@home screensaver is able to search for extraterrestrial signals.
For more information about SETI@home and the SETI@home client
program, take a look at the links below:
Section 6 subsection 2
pauldharris@yahoo.com
| Your credit: | |
| Name (and URL) |  |
| Results Received | 1551 |
| Total CPU Time | 3.169 years |
| Average CPU Time per work unit | 17 hr 53 min 53.0 sec |
| Average results received per day | 0.84 |
| Last result returned: | Sun Dec 19 21:00:44 2004 UTC |
| Registered on: | Wed Dec 1 07:36:39 1999 UTC |
| Registration Class | |
| SETI@home user for: | 5.057 years |
| View User Profile | |
| Your group info: | |
| You do not currently belong to a group. | |
| You are not currently the founder of any teams. | |
| Your rank: (based on current workunits
received) |
|
| Your rank out of 5289305 total users is: | 191453rd place. |
| The number of users who have this rank: | 92 |
| You have completed more work units than | 96.379% of our users. |
| User Certificates | |
| Download 1,000 Workunit Certificate | |
| Download 750 Workunit Certificate | |
| Download 500 Workunit Certificate | |
| Download 250 Workunit Certificate | |
| Download 100 Workunit Certificate | |
http://setiathome.ssl.berkeley.edu/ Copyright 2002 SETI@home |
MOUNTAIN VIEW, CALIFORNIA -- More than a dozen candidate signals have been snagged by a global network of volunteers in a search for extraterrestrial intelligence called SETI@home. But one by one, the prospective SETI hits have been downgraded to misses and tagged as radio interference.
The SETI@home project has been under way since May 1999. Using data collected by the world’s largest radio telescope in Arecibo, Puerto Rico, some 3 million volunteers around the globe have attempted to tease out from the telescope’s star sweeping any signs of radio chatter eking from distant, inhabited worlds.
SETI@home is separate from the SETI Institute, which is engaged in several scientific and educational projects designed to search for extraterrestrial intelligence in the Universe. SPACE.com has a partnership with the SETI Institute.
Information crunching
SETI@home is based on the use of small personal computers, all working simultaneously to form the world’s largest supercomputer, said Dan Werthimer, chief scientist for the effort at the University of California, Berkeley. "It’s better than any supercomputer at any of our laboratories on the planet," he told SPACE.com.
Volunteers donate time on their computers, making use of special software to analyze data received over the Internet, and then report back the fruits of information crunching to the UC Berkeley SETI@home team.
"The volunteers donate a thousand years of computing time every day. So far, they’ve donated 700 thousand years," Werthimer said.
Candidate signals
In combing through the data, analysts eliminate signals that are caused by radio frequency interference, computer errors, and to keep an eye out for signals that repeat.
The result of that weeding through of data produced 17 extraterrestrial candidate signals -- those that show a pattern indicative of intelligence in the natural buzz and crackle of deep space.
"The most interesting signals are things that we’ve seen two or more times. We actually have a human being looking at the data, trying to figure our what are these repeating signals and why do we see them again," Werthimer said.
So far, however, all the candidate signals have turned out to be radio frequency interference. The patterns were found to be associated with the same radio frequency.
"We know they are radio pollution because when the telescope is pointed to other places, we see them as well," Werthimer said. "The pollution is coming in from the side of the telescope."
Next page: radio corruption
Corruption
Werthimer said that radio pollution is the "big bugaboo" in SETI. "It’s getting harder and harder to do SETI as more of the radio bands are corrupted by satellites, television transmitters and cell phones. Some radio bands are just so polluted we can’t search through those bands anymore."
At the moment, while SETI@home has been highly successful in attracting public involvement, none of the data crunching has yielded evidence for any extraterrestrial civilization.
"Nothing is popping out at us. But we’re going to keep digging. And the further you dig down, the better chance you have of finding a signal ... if it’s there," Werthimer said.
Despite the Universe still holding tight the true whereabouts of any ET, there is some good news. The technology for surveying all possible radio frequency bands of interest is getting better and better.
"Right now, I would say that Earthlings are just getting into the game," Werthimer said. "We need another factor of a million or a billion in capabilities before we can do a thorough search. But at the rate that technology is growing, we don’t have to wait long. It’s only 20 or 30 years away."
Deaf ear to the Universe?
Given the response to SETI@home, officials running the project are now scoping out SETI@home II.
The upgrade program means that radio band coverage at Arecibo may be increased by adding another recorder system. An additional recording system might also be utilized at a radio telescope in the southern hemisphere, opening up an entirely different part of the sky to SETI scientists.
Even with these augmentations, the search could still be putting a deaf ear to the Universe.
"Maybe we’re barking up the wrong tree ... and there’s some better technology that we don’t know about. Or, perhaps, we’ve got to wait 500 years for the next revolution in physics," Werthimer said.
"But that’s like telling Christopher Columbus: Don’t bother sailing the seas ... you’ll have airplanes and that’ll make your job much easier, Werthimer said. "The point is, you’ve got to start somewhere."
Visit SPACE.com for more space-related news including videos, launch coverage and interactive experiences. Check out our huge collection of Image Galleries and Satellite Views from Space. Follow the latest developments in the search for life in our universe in our SETI: Search for Life section. Sign up for our free daily email newsletter today!
MERCK MANUAL 13th ed. 1977 Ch. 6 pp. 1203-1209 DISTURBANCES IN ACID-BASE METABOLISM
The pH of ECE in health is maintained at about 7.40 (range, 7.35 to 7.45). Acute changes in pH due to acid or alkali loads (or deficits) are immediately damped by interaction with extracellular and intracellular buffer systems. In the absence of pulmonary disease, respiratory compensation further diminishes pH aberrations. Ultimately, however, the kidneys maintain pH homeostasis by excretion or retention of hydrogen ions and regeneration of lost buffers.
The bicarbonate (HCO3-) buffer system, one of several body buffers, is of singular importance. The Henderson-Hasselbaich equation, expressed in terms of the HCO3- systems, reads:
pH -6.1+ log HCO3-
a(Paco2)
where a = .03 mM/L/mm Hg at 38 C
At a pH of 7.4, the ratio of HCO3- to a (Paco2) is 20:1. Their ratio, rather than their concentrations, determines blood pH. The physiologic importance of this buffer system derives from the fact that two mechanisms (renal and respiratory) exist for adjusting the ratio of this major ECF buffer pair, and thus the pH of the ECF. The denominator a (Paco2) can be modified rapidly by changes in respiratory minute ventilation, while the numerator (HCO3- is subject to renal regulation.
Renal regulation of the HCO3- concentration of ECF is accomplished in servral ways. Hydrogen ion may be secreted into the renal tubular lumen in exchange for Na; for each hydrogen ion secreted, a HCO3- ion is added to the ECF. Thus, net reabsorption of filtered HCO3- occurs. Since the pH of the fluid leaving the proximal tubule is about 6.5, most filtered HCO3- is reabsorbed in the proximal tubules. In the distal tubule, hydrogen ion secretion is partially dependent, upon aldosterone-mediated Na reabsorption and can lower the pH to as low as 4.5 to 5. Throughout the nephron, secreted hydrogen ion is buffered by urinary buffers such as phosphate (titratable acid) and ammonia. In this manner, filtered HCO3 operationally is reabsorbed, and also new HCO3- can be generate4 to replace that lost in body buffer reactions. Since filtered Na is reabsorbed either in association with an anion (i.e., chloride) or by cationic exchange (i.e., with hydrogen ion and, to a lesser extent, potassium), the total Na reabsorbed approximates the sum of the chloride reabsorbed and hydrogen ion secreted. Thus, there is an inverse relationship between chloride reabsorption and hydrogen ion secretion. This relationship is highly dependent upon the existing level of Na reabsorption.
The renal HCO3- threshold also is influenced by body potassium stores. There is a general reciprocal relationship between intracellular potassium content and hydrogen ion secretion. Thus, potassium depletion is associated with increased hydrogen ion secretion and attendant HCO3- generation, leading to a HCO3-increase in ECF and metabolic alkalosis. Finally, the renal HCO3- threshold is influenced by the Paco2 and the state of ECF volume. An increased Paco2 leads to increased HCO3- reabsorption, and a decreased ECF volume leads to increased Na reabsorption and HCO3- generation; e.g., in the proximal tubule.
Clinical disturbances of acid-base metabolism classically are defined in terms of the HCO3- buffer system (see Henderson-Hasselbalch equation, above). Rises or falls of the numerator (HCO3-) are teritted, respectively, metabolic alkalosis or acidosis; rises or falls in the denominator (aPaco2) define, respectively, respiratory acidosis and alkalosis. Simple disturbances, include both the primary alteration and the expected compensation (e.g., in metabolic acidosis there is a primary fall in the HCO3- concentration of the ECF and a secondary fall in the Paco2 due to compensatory hyperventilation). Compensation may be classified as uncompensated, partial, or complete. Mixed disturbances are more complex disorder in which two or more primary alterations coexist (e.g., respiratory acidosis with superimposed diuretic-induced metabolic alkalosis).
It may be necessary to refer to a nomogram in order to distinguish simple from mixed disorders. However, measurement of the pH of arterial (or arterialized venous) blood, the Paco2, and the CO2 combining power (CO2 CP) of venous blood (or calculation of HCO3-) along with recognition of a disease entity known to produce an acid-base derangement and knowledge of the expected responses of the blood gases and buffers, including compensatory changes, are usually sufficient to correctly identify most clinical acid-base problems (see Table 11-36).
| Disturbance | pH | Paco2 | co2 Combing Power |
|---|---|---|---|
| Normal | 7.34-7.38 (venous) 7.38-7.42 (arterial) | 43mm Hg (venous) 40mm Hg (arterial) | 21-28 mEq/L |
| Metabolic alkalouis | up | up** | up* |
| Metabolic acldosis | down | down** | down* |
| Respiratory alkalosis | up | down** | down* |
| Respiratory acidosis | down | up* | up** |
| Mixed metabolic and respiratory acidosis | down | up | down |
| Mixed metabolic and respiratory alkalosls | up | down | up |
| Mixed metabolic acidosis and respiratory alkalosis | up down | down | down |
| Mixed metabolic alkalosis and respiratory acidosis | up down | up | up |
METABOLIC ACIDOSIS
A primary fall in extracellular fluid bicarbonate concentration pH and carbon dioxide combining power are reduced
Etiology and Pathogenesls
The principal causes of metabolic acidosis are shown in TABLE 11-37.
Excessive acid production or Ingestion: A common form is diabetic ketoacidosis with increased production of acetoacetic and B-hydroxybutyric acid. Occasionally, diabetic acidosis maybe associated with an altered NADH/NAD ratio leading to lactic aciddsis and elevated levels of B hydroxybutyric acid. The plasma ketone level is not increased when measured by the usual methods which detect only acetoacetic acid. Lactic acidiosis may develop in any state of diminished tissue oxygenation (e.g., vascular shock), with phenformin administration, or ethanol ingestion. Rarely it occurs idiopathically. In salicylate, methanol, or ethylene glycol poisoning, interference with normal intermediary metabolism or accumulation of exogenous organic anions may cause metabolic acidosis.
PRINCIPAL CAUSES OF METABOLIC ACIDOSIS AND METABOLIC ALKALOSIS
- Metabolic Acidosis
- With elevated "anion gap"
- Renal failure
- Diabetic ketoacidosis
- Lactic acidosis
- Exogenous poisons (ethylene glycol, salicylates, methanol, peraldehyde)
- With normal "anion gap"
- GI alkali loss (diarrhea, ileostomy, colostomy)
- Renal tubular acidosis
- Interstitial renal disease (e.g.,"selective hypoaldosteronism")
- Ureterosigmoid loop
- Ingestion of acetazolamide or ammonium chloride
- Metabolic Alkalosis
- Diuretic therapy (thiazides, ethacrynic acid, furosemide)
- Vomiting or gastric drainage
- Hyperadrenocorticism (CushIng’s syndrome, aldosteronism, exogenous corticosterold administration)
Impaired renal excretion of acid occurs in acute or advanced chronic renal failure due to reduced hydrogen ion excretion. In chronic renal failure, the major defect is insufficient ammonia production (and thus decreased ammonium ion excretion) as the result of progressive diminution in functioning renal mass. In renal tubular acidosis (RTA) with a relatively normal filtration rate, the defect is either proximal tubular HCO3- wasting (proximal RTA) or an inability to generate an acid urine (gradient-limited or distal RTA).
Symptoms, Signs, and Diagnosis
The major symptoms and signs of acidosis are often obscured by or difficult to separate from those of the underlying disease. Mild acidosis may be asymptomatic or may be accompanied by vague lassitude, nausea, and vomiting. The most characteristic finding in severe metabolic acidosis (e.g., pH <7.2 and CO2 CP<10 mEq/L) is hyperpnea, manifested by an early increase in depth and, later, frequency of respiration (Kussmaul breathing). Signs of ECF volume depletion may also be present, especially in patients with diabetic acidosis or gastrointestinal alkali loss. Severe acidosis may cause circulatory shock, due to impaired myocardial contractility and peripheral vascular response to catecholamines, and progressive obtundation.
Laboratory Findings
The urine pH is < 5.5 when the plasma HCO3- concentration falls to low levels with severe acidosis. The blood pH is < 7.35 and CO2 CP < 21 mEq/L. In the absence of pulmonary disease, the Paco2 is <40 mm Hg. Many forms of metabolic acidosis are characterized by an abnormal anion gap (Table 11-37). The anion gap (representing undetermined plasma anions) is estimated by subtracting the sum of the chloride concentration and CO2 CP from the plasma Na concentration (normal up to 15 mEq/L). Diabetic acidosis usually is characterized by the presence of hyperglycemia and ketonemia. In diabetic patients with hyperglycemia and nonketotic acidosis, blood lactic acid and B-hydroxybutyric acid levels are elevated. Ethylene glycol poisoning should be suspected in individuals having unexplained acidosis and oxate crystals in the urine. Sailcylate poisoning is characterized early by respiratory alkalosis with metabolic acidosis developing later; blood levels of salicylate are usually > 30 to 40 mg/ 100 ml; boiled urine gives a positive test (violet color) with ferric chloride.
Since volume depletion often accompanies acidosis, mild azotemia (BUN 30 to 60 mg/ 100 ml) is common. Greater elevations of the BUN, especially in conjunction with hypocalcemia and hyperphosphatemia, suggest renal failure as the cause of the acidosis. Changes in the serum potassium during acidosis were discussed earlier in this chapter.
Treatment
Therapy of chronic renal acidosis is discussed under ANOMALIES IN KIDNEY AND GASTROINTESTINAL TRANSPORT in §11, Ch. 7. The treatment of metabolic acidosis consists of therapy of the underlying disease (e.g., insulin in diabetic acidosis) and IV administration of sodium bicarbonate when acidosis is severe (pH <7.2). This can be given by adding varying amounts of sodium bicarbonate (44 to 88 mEq) to either D/W or hypotonic saline (one fourth or one half isotonic saline), or by using 5% sodium bicarbonate solutions, depending on the clinical setting and attendant water and volume disturbances. The goal of HCO3-therapy is to raise the CO2 CP to about 10 to 12 mEq/L. The amount of sodium bicarbonate necessary can be approximated by the formula:
mEq of NaHCO3 required =(CO2 CP desired - CO2 CP observed) x 25%TBW
The apparent distribution space of HCO3- is> 25% of TBW, due to continuing transfer of intracellularly buffered hydrogen ion out of cells into the ECF. However, it is best to raise the pH of the ECF only to a safe level, such as 7.2, while other measures are instituted to correct the cause of the acidosis, thereby averting some of the cqmplicatlons of alkali treatment. These include volume overload in patients with cardiac and renal disease and the precipitation of acute tetany in patients with renal failure. Too rapid correction of acidosis may also result in a rise in the Paco2 at a time when CSF bicarbonate levels are still low, thus inducing a "relative CSF acidosis". Occasionally, this may be associated with obtundation, coma, or death. In patients with marked overproduction of hydrogen ions (e.g., lactic acidosis), it may be necessary to give very large quantities of sodium bicarbonate IV in conjunction with dialysis to minimize ECF volume expansion.
RESPIRATORY ACIDOSIS
A primary increase in arterial carbon dioxide pressure; pH as low and carbon dioxide combining power increases renal function is intact.
Etiology and Pathogenesis
Respiratory acidosis is the result of alveolar hypoventilation leading to pulmonary CO2 retention.
It occurs with
- depression of the central respiratory center caused by drugs, anesthesia, neurologic disease, abnormal sensitivity to CO2 (e.g., cardiopulmonary obesity syndrome);
- abnormalities of the chest bellows (e.g., poliomyelitis, myasthenia gravis, Guillain-Barr6 syndrome, crush injuries of the thorax);
- severe reduction of alveolar surface area for gas exchange (conditions characterized by ventilation/perfusion imbalance; e.g., chronic obstructive pulmonary disease [emphysema, chronic bronchitis], severe pneumonia, pulmonary edema, asthma, or pneumothorax); and
- laryiigeal or tracheal obstruction. Neurologic changes with CO2 retention may depend upon the development of CSF acidosis or intracellular acidosis in the brain. Hypoxemia and metabolic alkalosis frequently accompany respiratory acidosis and may contribute to tho neurologic abnormalities.
Symptoms, Signs, and Diagnosis
The most characteristic change is metabolic encephalopathy with headache and drowsiness progressing to stupor and coma. It usually develops slowly with advancing respiratory failure, but abrupt, full-blown encephalopathy may be precipitated by sedatives or pulmonary infection in patients with advanced respiratory insufficiency. Asterixis and multifocal myoclonus are generally present; in some patients, dilation of retinal venules and papilledema result from increased intracranial pressure. The encephalopathy may be reversible if hypoxic brain damage has not occurred.
Laboratory Findings
In acute respiratory acidosis, the low pH is due to the acute elevation in Paco2. The CO2 CP may be normal or slightly increased. When renal compensation is fully developed, as in chronic respiratory acidosis, the fall in pH is blunted due to renal HCO3- retention and elevation of the CO2 CP. If diuretic therapy (e.g., for chronic cor pulmonale) causes superimposed metabolic alkalosis, the high Paco2 may be associated with a high CO2 CP, hypochloremia, and a normal or alkaline blood pH.
Treatment
The treatment must improve the underlying pulmonary disturbance. Severe respiratory failure with marked hypoxemia often requires mechanically assisted ventilation. Sedative drugs (narcotics, hypnotics) should be avoided except as necessary to facilitate mechanical ventilation. Although most patients with chronic CO2 retention and hypoxia tolerate modest O2 enrichment of inspired air, some patients respond with a significant fall in respiratory minute volume and further acute elevation of the Paco2. Presumably, such patients have adapted to chronic hypercapnia so that their major respiratory stimulus is hypoxemia. Therefore the lowest O2 concentration required to elevate the Paco2 to acceptable levels (>50mm Hg) should be given. This can be accomplished with O2 administration by a Ventimask, beginning with a 24% concentration. The Paco2 should be carefully monitored and, if it rises to dangerous levels (>50 to 55mm Hg), mechanical ventilation must be considered.
If mechanical ventilation is used in patients with chronic respiratory failure, the Paco2 should be lowered slowly, especially if concomitant metabolic alkalosis (high CO2 CP and normal or alkaline pH) is present. Rapid lowering of the Paco2 will cause severe metabolic alkalosis (pH >7.5).The resultant leftward shift of the oxyhemogiobin dissociation curve and cerebral vasoconstriction may lead to seizures and death. Providing adequate inspired 02, lowering the Paco2 more slowly, and repairing potassium or chloride deficits will prevent such neurologic consequences.
METABOLIC ALKALOSIS
A primary increase in blood bicarbonate; pH and carbon dioxide combining power are elevated.
Etiology and Pathogenesis
Metabolic alkalosis develops as the consequence of loss of acid from the ECF; e.g., loss of acid-containing gastric juice, loss of acid via the urine or stool, transfer of hydrogen ions into cells, excessive loads of HCO3- (e.g., alkali administration to patients with renal failure), or rapid contraction of the extracellular space (e.g., with potent diuretics). Whatever the cause, the kidney tends to correct the alkalosis rapidly by excreting excess HCO3-, unless other factors, such as volume contraction, result in both a Na-acquisitive state and an increased HCO3- threshold. Thus, a diminished effective arterial volume, potassium deficiency, and persistent adrenal steroid excess are common clinical settings for chronic metabolic alkalosis (TABLE 11-37, p. 1205). Perhaps the most frequent and important of these settings is ECF volume contraction and avid renal sodium reabsorption.
Diuretics cause metabolic alkalosis by several mechanisms, including
- acute contraction of the ECF volume (sodium chloride excretion without HCO3-), thereby increasing the concentration of HCO3- in the ECF;
- diuretic-induced potassium and chloride depletion, and
- secondaiy aldosteronism. Continued use of the diuretic or either of the latter two factors may maintain the alkalosis.
The loss of gastric hydrochloric acid by suction or vomiting produces metabolic alkalosis which is perpetuated by concomitant ECF volume contraction (sodium chloride loss in gastric juice) and development of potassium deficiency, due to secondary aldosteronism and potassium loss in gastric juice.
In states of persistent adrenal steroid excess, alkalosis results from steroid-mediated reabsorption of Na in the distal tubule in exchange for hydrogen ion. Sodium chloride reabsorption in the distal tubule leads to ECF volume expansion and decreased proximal Na reabsorption. Thus, a continuing supply of Na is delivered distally for exchange with hydrogen and potassium ions. Potassium depletion then leads to persistence of the alkalosia.
Symptoms. Signs, and Diagnosis
Metabolic alkalosis should be suspected in the above clinical settings. The most common clinical manifestations are irritability and neuromuscular hyperexcitability, perhaps due to hypoxia from a transient leftward shift of the oxyhemoglobin dissociation curve. When severe, the ionized calcium fraction may fall low enough to provoke tetany, although total serum calcium is unchanged (see HYPOCALCEMIA, above). Muscular weakness, impaired gastrointestinal motility (e.g., gastric retention, ileus), and polyuria should suggest potassium depletion.
Laboratory Findings
The blood pH and CO2 CP are elevated. Striking increases in the Paco3 to levels as high as 50 to 60 mm Hg may occur with compensatory hypoventilation, especially in patients with mild renal insufficiency. The urine is alkaline except in the presence of severe potassium depletion, in which case it may be acid ("paradoxic acidurla"). Hypochloremia and hypokalemia are usual.
Treatment
Correction of the underlying disturbance is desirable when possible. Metabolic alkalosis usually resolves when ECF volume deficits are replaced with oral or IV sodium chloride. However, when potassium deficiency is severe, or in patients with adrenal steroid excess, the alkalosis cannot be corrected until the potassium deficit is repaired (saline-resistant alkalosis). In the post-hypercapnic state, persistent metabolic alkalosis responds to chloride, given as potassium chloride, sodium chloride (if volume depletion is present), ammonium chloride, or arginine hydrochloride. When mild, metabolic alkalosis usually requires no specific therapy. It should be corrected promptly, however, in patients with myocardial irritability and those with neuromuscular hyperexcitability. In such instances, ammonium chloride administration may be desirable along with other measures (e.g., correction of hypokalemia).
RESPIRATORY ALKALOSIS
A primary decrease in carbon dioxide pressure; blood pH is increased and carbon dioxide combining power is reduce.
Etiology and Pathogenesis
Hyperventilation, leading to excessive loss of CO2 in expired air, results in respiratory alkalosis. The Paco2 and cerebral tissue Paco2 fail, and both plasma and cerebral tissue pH rise. Cerebral vasoconstriction results and, along with the Bohr effect, may produce cerebral hypoxia and the characteristic symptom complex.
This develops following stimulation of the respiratory system
- directly, as in salicylism, fever, hepatic coma, CNS lesions, overventilated patients on assisted ventilation, and psychogenic hyperventilation;
- by reflex stimulation of peripheral chemoreceptors as in hypoxemia, mountain sickness, and respiratory disease; or
- by unknown mechamsms, as in intra-abdominal space-occupying lesions (especially cirrhosis), congestive heart failure, and intrapulmonary lesions, includang pneumomtis.
Symptoms, Signs, and Diagnosis
Obvious hyperventilation may be present although the breathing pattern in the anxiety-induced syndrome is variable. Tetany, circumoral paresthesias, acroparesthesias, giddiness or lightheadedness, and syncope may occur. In such patients, the symptoms often can be reproduced by voluntary overventilation. Blood lactate and pyruvate levels increase and ionized calcium falls. In all situations, the diagnosis of hyperventilation is confirmed by finding a low Paco2.
Treatment
Respiratory alkalosis due to anxiety resolves on rebreathing expired CO2 from a paper bag (plastic bags may cause accidental suffocation). Other measures aimed at amelioration of chronic anxiety may be helpful (e.g., sedative or tranquilizing drugs). Overventilation with mechanical respirators can be corrected by diminishing minute ventilation, when excessive, or by adding dead space. When hyperventilation is due to hypoxemia, O2 enrichment of inspired air and treatment aimed at correction of abnormal pulmonary gas exchange is appropriate. Correction of respiratory alkalosis by increasing the inspired CO2 concentration may be dangerous in patients with CNS disturbances (which may be associated with a low CSF pH). The treatment of salicylism is given in §lO, Ch.4
http://science.nasa.gov/headlines/y2002/01feb_anthrax.htm?list103823
NASA- and industry-sponsored research aimed at growing plants in space has led to a device that attacks and destroys airborne pathogens -- like Anthrax.
February 1, 2002: Unseen and odorless, a cloud of Anthrax spores wafts through an office. People inside are talking, laughing ... breathing. They have no idea something is in the air. One yawn, one gasp, one happy guffaw could be deadly.
That's how bioterrorism works.
But this office has a defense: Bolted to the ceiling is a curious flat box. It's made of metal, about the size of a table-top, and it's humming softly -- the sound of fans drawing airborne spores toward it and away from the people. The breeze is gentle but insistent. Eight cubic feet of air per minute flow into the box.
What lies inside is bad news for Anthrax. Swirling air forces spores through a bewildering maze of thin tubes bristling with hydroxyl (OH-) ions that attack and destroy pathogens. Some spores are buffeted against the OH--lined walls of the labyrinth. Others are caught in windy eddies where they linger, exposed to high-energy (254 nm) ultraviolet photons. Every second, one hundred billion such photons bathe the chamber -- and just one is enough to destroy a spore.
"Spores that pass through the box aren't filtered, they're fried," says John Hayman, whose company, KES Science & Technology, Inc., builds and sells the device called AiroCide TiO2. "That's appealing," he notes, "for people who don't want to change an Anthrax-laden air filter." Tests show that as many as 93% of Anthrax spores that enter AiroCide TiO2 are destroyed. Survivors circulate out of the chamber where they are likely to be sucked back in again for another pass.
This extraordinary Anthrax killer is a result of NASA- and industry-sponsored research aimed at building better greenhouses in space. "Greenhouses may seem to have little to do with the war against terror," says Mark Nall, the director of NASA's Space Product Development (SPD) program. "But this shows how space research, along with its direct benefits, also helps people on Earth in indirect and unexpected ways."
Hayman explains: "[Space faring] astronauts will eventually need to grow some of their own food in greenhouses. But there's a problem: the leaves of growing plants release ethylene (C2H4) -- a gas that causes fruits and vegetables to mature." In the close quarters of a spacecraft (or inside an enclosed plant growth chamber), ethylene would build up and ripen greenhouse plants prematurely.
Space greenhouses needed a new technology to remove that ethylene.
Marc Anderson, a professor and chemist at the University of Wisconsin-Madison, led the team that made a crucial discovery in the mid-1990's. They found that ultra-thin layers of titanium dioxide (TiO2) exposed to ultraviolet light would efficiently convert ethylene into carbon dioxide (CO2) and water (H2O) -- substances that are good for plants. Titanium dioxide itself is a harmless, non-toxic coloring agent used in many consumer products. It is a catalyst for the ethylene-destroying reaction; no TiO2 is consumed.
TiO2-based ethylene removers have since flown to space inside a pair of plant growth chambers: ASTROCULTURE™ on board NASA's space shuttle and ADVANCED ASTROCULTURE™ on the International Space Station (ISS). Both were designed and built by the Wisconsin Center for Space Automation and Robotics (WCSAR) in collaboration with Marc Anderson. (WCSAR is a NASA Commercial Space Center at the University of Wisconsin -- one of 17 such centers around the country sponsored by NASA's Space Product Development program to encourage the commercialization of space by industry.)
The technology worked so well that the University of Wisconsin then joined forces with KES Science and Technology, Inc., to develop an ethylene scrubber for Earth. The device, called Bio-KES, works wonders in supermarkets where ethylene in the air of produce aisles reduces the shelf life of vegetables. Bio-KES was nominated as Discover Magazine's Product of the Year in 1998, and it's since been shipped across the globe for use by grocers and florists.
Moreover, Bio-KES is the parent of AiroCide TiO2.
"It was a serendipitous discovery," recalls Hayman. Tests showed that Bio-KES not only removed ethylene, but also killed airborne dust mites. Marc Anderson quickly realized why: When ultraviolet (UV) photons strike something coated by TiO2 -- like the tubes inside Bio-KES -- positive and negative charges appear on its surface. Those charges tear apart nearby water molecules. The OH- ion, a by-product of the reaction, disrupts organic molecules. It's deadly to dust mites, Anthrax and many other pathogens.
Technicians modified Bio-KES -- adding higher-power UV lamps, for example, to give it "an extra kick," says Hayman -- and AiroCide TiO2 was born.
Dean Tompkins, a colleague of Anderson's at the University of Wisconsin, is in charge of testing AiroCide TiO2. "We don't use real Anthrax," he notes. "That would be too dangerous. Instead, we experiment with one of its non-virulent cousins: Bacillus thurengiensis." During a typical experiment, Tompkins propels a cloud of approximately 1000 spores through the AiroCide chamber. Only 100 or so emerge intact.
Spores that enter AiroCide TiO2 spend at least 5 to 10 seconds in transit through the device. "That's important," adds Hayman, "because pathogens that remain inside longer are more likely to die." To slow the spores, TiO2-coated tubes within the unit are randomly arranged -- there's no direct path through the machine. When air moves across the jumbled tubes, the flow becomes turbulent -- forcing spores to linger where they can be attacked by OH- and illuminated by germ-killing ultraviolet light.
Such powerful tools against bio-terror indeed seem a far cry from star-trekking greenhouses, but that's how many discoveries are made: You never know what new invention might emerge -- like AiroCide TiO2 -- or what might be annihilated in the process -- like Anthrax!
http://www.global-elite.org/
Aigina, Greece: 16th July 2003, Meeting against aerosol spraying over Aigina
Following the vote on 4th June by Aigina Council to take legal action against those responsible for what press reports have characterized as dangerous aerial spraying over Aigina and the successful public meeting of 16th July on the same subject organized by the magazine “Schedia sta Anoichta tis Aiginas”, news came at the beginning of August of another city council, or at least city councillor, this time in the United States, taking a public stance against chemtrails. Al Snow, a member of the city council of LaVerkin, a town of 3,500 residents in the state of Utah, has just published a book entitled “Chemtrails: Death in the Sky”, which alleges that military aircraft are spraying urban areas of the United States with aerosols containing barium.
Snow first became aware of the trails in the spring of 2001 when his wife, Laura, asked him if he had noticed the white trails in the sky that day. While working outside for several weeks, she had apparently been watching numerous jet trails that «spread out and made one big cloud».
“Since then I’ve been taking pictures on a daily basis and I keep a daily chemtrail tracking report with direction of the flights, number of jets and more.” Holder of a doctorate in nutrition, Snow then went on to write his present book.
His initial investigations began with the Utah Dept of Air Quality. He telephoned their office in Salt Lake City and requested to speak with someone on the subject of chemtrails. According to Snow, the astonished woman on the other end of the line muffled the phone and asked the assistance of a man nearby. Snow says he overheard the man’s response: “You tell him there’s nothing you can do about it.”
From there Snow pursued answers from other government agencies in Denver and Washington D.C. Their responses were: “We don’t get involved with those kinds of things.”
The lack of action from the government officials and agencies did not deter Snow from his quest. He started researching and found correlating medical studies, equipment patents, military operations, laws and regulations, chemical compounds, and press articles.
Snow is a conservative American, who is more inclined to blame the United Nations than his own goverment for everything bad, including chemtrails. The La Verkin city council made history in 2001 when it became the first municipality in the United States to become a “United-Nations-free-zone”. Asked by a journalist from Utah’s KSL television if he thinks it is the United Nations that is doing the spraying, Snow replied: “I think they are, yeah. But I want people to think about it and make up their own minds.”
Whatever one thinks about Al Snow’s view of the United Nations, the UN, while denouncing the United States’ failure to support the Treaty of Kyoto, has said not a single word about the United States alternative “dynamic” approach to global warming, as embodied in the at least one of the ongoing programmes of chemtrail spraying. Moreover, it is worth remembering that Gore Vidal, one of the strongest opponents of the Bush regime and an equally strong supporter of the United Nations, has said he thinks it would be a good idea for the United States to leave the United Nations for a period.
James F. Balch, M.d. · Phyllis A. Balch, C.N.C.
Avery Publishing Group
Garden City Park, New York
Antioxidants
Part One Elements Of Health Antioxidants pp43-46
There is a group of vitamins, minerals, and enzymes called antioxidants that help to protect the body from the formation of free radicals. Free radicals are atoms or groups of atoms that can cause damage to cells, impairing the immune system and leading to infections and various degenerative diseases such as heart disease and cancer. Free radical damage is thought by scientists to be the basis for the aging process as well. (See Free Radicals on page 44.)
There are a number of known free radicals that occur in the body, including superoxide, hydroxy radicals, hydrogen peroxide, various lipid peroxides, hypochlorite radicals, nitric oxide, and singlet oxygen. They may be formed by exposure to radiation and toxic chemicals such as those found in cigarette smoke, over exposure to the sun’s rays, or various metabolic processes, such as the process of breaking down stored fat molecules for use as an energy source.
Free radicals are normally kept in check by the action of free radical scavengers that occur naturally in the body. These scavengers neutralize the free radicals. Certain enzymes serve this vital function. Four important enzymes that neutralize free radicals are superoxide dismutase (SOD), methionine reductase, catalase, and glufathione peroxidase. The body makes these as a matter of course. There are also a number of nutrients that act as antioxidants, including vitamin A, beta-carotene, vitamins C and E, and the mineral selenium.
Another antioxidant is the hormone melatonin, which is a powerful free radical neutralizer. Certain herbs have antioxidant properties as well.
Although many antioxidants can be obtained from food sources such as sprouted grains and fresh fruits and vegetables, it is difficult to get enough of them from these sources to hold back the free radicals constantly being generated in our polluted environment. We can minimize free radical damage by taking supplements of key nutrients. A high intake of antioxidant nutrients appears to be especially protective against cancer.
A free radical is an atom or group of atoms that contains at least one unpaired electron. Electrons are negatively charged particles that usually occur in pairs, forming a chemically stable arrangement. If an electron is unpaired, another atom or molecule can easily bond with it, causing a chemical reaction. Because they join so readily with other compounds, free radicals can effect dramatic changes in the body, and they can cause a lot of damage. Each free radical may exist for only a tiny fraction of a second, but the damage it leaves behind can be irreversible.
Free radicals are normally present in the body in small numbers. Biochemical processes naturally lead to the formation of free radicals, and under normal circumstances the body can keep them in check. Indeed, not all free radicals are bad. Free radicals produced by the immune system destroy viruses and bacteria. Other free radicals are involved in producing vital hormones and activating enzymes that are needed for life. We need free radicals to produce energy and various substances that the body requires. If there is excessive free radical formation, however, damage to cells and tissues can occur. The formation of a large number of free radicals stimulates the formation of more free radicals, leading to even more damage.
The presence of a dangerous number of free radicals can alter the way in which the cells code genetic material. Changes in protein structure can occur as a result of errors in protein synthesis. The body’s immune system may then see this altered protein as a foreign substance and try to destroy it. The formation of mutated proteins can eventually damage the immune system and lead to leukemia and other types of cancer, as well as a host of other diseases.
In addition to damaging genetic material, free radicals can destroy the protective cell membranes. The formation of free radicals can also lead to retention of fluid in the cells, which is involved in the aging process. Calcium levels in the body may be upset as well.
Many different factors can lead to the production of free radicals. Exposure to radiation, whether from the sun or from medical x-rays, activates the formation of free radicals, as does exposure to environmental pollutants such as tobacco smoke and automobile exhaust. Diet also can contribute to the formation of free radicals. When the body obtains nutrients through the diet, it utilizes oxygen and these nutrients to create energy. In this oxidation process, oxygen molecules containing unpaired electrons are released.
These oxygen free radicals can cause damage to the body if produced in extremely large amounts. A diet that is high in fat can increase free radical activity because oxidation occurs more readily in fat molecules than it does in carbohydrate or protein molecules. Cooking fats at high temperatures, particularly frying foods in oil, can produce large numbers of free radicals.
Substances known as antioxidants neutralize free radicals by binding to their free electrons. Antioxidants available in supplement form include the enzymes superoxide dismutase and glutathione peroxidase; vitamin A, beta-carotene, and vitamins C and E; the trace mineral selenium; and the hormone melatonin. By destroying free radicals, antioxidants help to detoxify and protect the body.
Alpha-lipoic acid helps to neutralize the effects of free radicals on the body by enhancing the antioxidant functions of vitamin C, vitamin E, and glutathione. An additional benefit of this nutrient is that it assures the proper functioning of two key enzymes that convert food into energy.
The herb bilberry is a strong antioxidant that keeps capillary walls strong and flexible. It also helps to maintain the flexibility of the walls of red blood cells and allows them to pass through the capillaries better. In addition, this herb supports and strengthens collagen structures, inhibits the growth of bacteria, acts as an anti-inflammatory, and has anti-aging and anticarcinogenic effects.
Coenzyme Q10 is an antioxidant similar to vitamin E. It also plays a crucial role in the generation of cellular energy, is a significant immunologic stimulant, increases_circulation, has anti-aging effects, and is beneficial for the cardiovascular system.
This sulfur-containing amino acid is needed to produce the free radical fighter glutathione. It is used by the liver and the lymphocytes to detoxify chemicals and other poisons. Cysteine is a powerful detoxifier of alcohol, tobacco smoke, and environmental pollutants, all of which are immune suppressors. Taking supplemental L-cysteine can boost the levels of protective enzymes in the body, thus slowing some of the cellular damage that is characteristic of aging.
Ginkgo biloba is a powerful antioxidant herb that is best known for its ability to enhance circulation. It has the ability to squeeze through even the narrowest of blood vessels to increase the supply of oxygen to the heart, brain, and all other body parts. This aids in mental functioning (ginkgo biloba is known as the “smart herb”) and helps to relieve muscle pain. Ginkgo biloba also lowers blood pressure, inhibits blood clotting, and has anti-aging properties.
Glutathione is a protein that is produced in the liver from the amino acids cysteine, glutamic acid, and glycine. It is a powerful antioxidant that inhibits the formation of, and protects against cellular damage from, free radicals. It helps to defend the body against damage from cigarette smoking, exposure to radiation, cancer chemotherapy, and toxins such as alcohol. As a detoxifier of heavy metals and drugs, it aids in the treatment of blood and liver disorders.
Glutathione protects cells in several ways. It neutralizes oxygen molecules before they can harm cells. Together with selenium, it forms the enzyme glutathione peroxidase, which neutralizes hydrogen peroxide. It is also a component of another antioxidant enzyme, glutathione-S-transferase, which is a broad-spectrum liver-detoxifying enzyme.
Glutathione protects not only individual cells but also the tissues of the arteries, brain, heart, immune cells, kidneys, lenses of the eyes, liver, lungs, and skin against oxidant damage. It plays a role in preventing cancer, especially liver cancer, and may also have an anti-aging effect. Glutathione can be taken in supplement form. The production of glutathione by the body can be boosted by taking supplemental N-acetylcysteine or L-cysteine plus L-methionine. Studies suggest that this may be a better way or raising glutathione levels than taking glutathione itself.
See under Oligomeric Proanthocyanidins in this section.
Green tea contains numerous compounds, including the flavonoid catechin, that have antioxidant and health-enhancing properties. It protects against cancer, lowers cho1esterol levels, and reduces the clotting tendency of the blood. It also shows promise as a weight-loss aid that can promote the burning of fat and help to regulate blood sugar and insulin levels. Black tea is not effective for these purposes because valuable compounds are destroyed in processing.
Among the newest antioxidants to be discovered, the hormone melatonin may also be the most efficient free radical scavenger that has thus far been identified. While most antioxidants work only in certain parts of certain cells, melatonin can permeate any cell in any part of the body. In animal experiments, it has been shown to protect tissues from an amazing array of assaults. Within the cell, melatonin provides special protection for the nucleus— the central structure that contains the DNA. Thus, it protects the structure that enables a damaged cell to repair~self. Melatonin also stimulates the enzyme glutathione peroxidase, another antioxidant.
Oligomeric proanthocyanidins (OPCs) are naturally occurring substances present in a variety of food and botanical sources. They are unique flavonols that have powerful antioxidant capabilities and excellent bioavailability. Clinical tests suggest that OPCs may be as much as fifty times more potent than vitamin E and twenty times more potent than vitamin C in terms of bioavailable antioxidant activity. In addition to their antioxidant activity, they strengthen and repair connective tissue, including that of the cardiovascular system, and they moderate allergic and inflammatory responses by reducing histamine production.
OPCs are found throughout plant life, however, the two main sources are pine bark extract (Pycnogenol) and grape seed extract. Pycnogenol was the first source of OPC's discovered, and the process for extracting it was patented in the 1950s. As a result, even though Pycnogenol a trademarked name for pine bark extract, the term is often used informally to refer to other OPC sources as well, most notably grape seed extract.
See under Oligomeric Proanthocyanidins in this section.
A partner and synergist with vitamin E, selenium is also an essential component of the antioxidant enzyme glutathione peroxidase (each molecule of this enzyme contains four atoms of selenium). This enzyme targets harmful hydrogen peroxide in the body and converts it into water. It is a particularly important guardian of blood cells and of the heart, liver, and lungs. Selenium also stimulates increased antibody response to infection.
Superoxide dismutase (SOD) is an enzyme. SOD revitalizes cells and reduces the rate of cell destruction. It neutralizes the most common, and possibly the most dangerous, free radical—superoxide. It also aids in the body’s utilization of zinc, copper, and manganese. SOD levels tend to decline with age, while free radical production increases. Its potential as an anti-aging treatment is currently being explored.
There are two types of SOD: copper/zinc SOD (Cu/Zn SOD) and manganese SOD (Mn SOD). Each of these enzymes works to protect a particular part of the cell. Cu/Zn SOD protects the cytoplasm, where free radicals are produced as a result of various metabolic activities. Mn SOD is active in protecting the mitochondria of the cells, which Antioxidants contain the cells’ genetic information and act as the site of cellular energy production.
SOD occurs naturally in barley grass, broccoli, Brussels sprouts, cabbage, wheatgrass, and most green plants. It is also available in supplement form. SOD supplements in pill form must be enteric coated—that is, coated with a protective substance that allows the pill to pass intact through the stomach acid into the small intestines to be absorbed. Cell Guard from Biotec Food Corporation is a good source of SOD.
Vitamin A and its precursor, beta-carotene, are powerful free radical scavengers. Vitamin A also is necessary for healthy skin and mucous membranes, the body’s first line of defense against invading microorganisms and toxins, and promotes the immune response. Beta-carotene and vitamin A destroy carcinogens (cancer-causing substances), guard against heart disease and stroke, and lower cholesterol levels.
Vitamin C is a very powerful antioxidant that also protects other antioxidants, such as vitamin E. The cells of the brain and spinal cord, which frequently incur free radical damage, can be protected by significant amounts of vitamin C. Vitamin C acts as a more potent free radical scavenger in the presence of a bioflavonoid called hesperidin.
In addition to its role as an antioxidant, vitamin C detoxifies many harmful substances and plays a key role in immunity. It increases the synthesis of interferon, a natural antiviral substance produced by the body, and stimulates the activity of certain key immune cells.
Vitamin E is a powerful antioxidant that prevents the oxidation of lipids. Since cell membranes are composed of lipids, it effectively prevents the cells’ protective coatings from becoming rancid as a result of the assault of free radicals. Vitamin E also improves oxygen utilization, enhances immune response, plays a role in the prevention of cataracts caused by free radical damage, and may reduce the risk of coronary artery disease. New evidence suggests that zinc is needed to maintain normal blood concentrations of vitamin E.
Selenium enhances vitamin E uptake. These two nutrients should be taken together.
In addition to having antioxidant properties on its own, zinc is a constituent of the antioxidant enzyme superoxide dismutase (SOD). It is also needed for proper maintenance of vitamin E levels in the blood and aids in the absorption of vitamin A. Other important functions of this mineral include the promotion of glandular and reproductive health and proper functioning of the immune system.
There are also products available that combine two or more of these vital nutrients. It is now easy to find formulas that give you a balance of multiple antioxidants. Some recommended antioxidant combination products include the following:
· ACES + Zinc and ACES + Selenium from Carlson Laboratories.
· Advanced Carotenoid Complex from Solgar.
· Body Language Super Antioxidant from OxyFresh USA.
· Cell Guard from Biotec Food Corporation.
· Juice Plus from Kelco.
· Life Guard from Thompson Nutritional Products.
· Oxy-5000 Forte from American Biologics
Using a combination supplement is often more convenient than taking many different products separately.
http://www.whale.to/v/mazlen.html
Role of bioengineering in CFS, GWS & AIDS CFS Radio
Program
Dec. 19th, 1999 Roger G. Mazlen, M.D. Host with Donald W.
Scott
http://www.carolsweb.net/ccf/
http://member.aol.com/rgm1/private/transcr.htm
Dr. Mazlen
Our guest is waiting from Canada and be with us shortly. We're
going to be talking with Don W. Scott, the author of the
Brucellosis Triangle. Interestingly enough, Donald Scott was our
guest on the year end show in 1998. He was here on the show the
20th of December and we're here again at the year end show and
we're going to follow up and it's going to be a really exciting
and interesting follow-up. We're going about basically,
infectious diseases for which our Chronic Fatigue Syndrome
audience are particularly susceptible, most of them being
significantly immunosuppressed and vulnerable to just about
anything that's contagious that comes along. So they should be
listening carefully. Now, we're going to talk about the West Nile
Virus, which was present with us here in New York during the late
summer. The West Nile Virus appeared in New York and then was
found in Connecticut and New Jersey. It's mosquito-borne. It
killed 7 people in those three states before the summer was over
and it's been predicted, and I'm quoting from the New York Times
in an article published on December 15th, they said "The virus
would likely re-emerge next spring when mosquitoes come out of
hibernation." This quote is from health experts testifying before
the United States Senate. So, with that, we're going to kick off
and talk to Donald W. Scott because he has some news for our
listening audience about where this West Nile Virus may actually
have come from. We're not saying we know it for sure, and we're
not documenting it but we want to present you with some facts. Hi
Donald, welcome to the show.
Don Scott
Good morning, it's nice to be here.
Dr. Mazlen And I'd like you to tell our audience something about the information that you have from the Riegle Committee with regard to this West Nile Virus.
Don Scott
As you and many of your listeners will recall, when the West Nile
Virus was first identified, official government sources said,
"well this is very strange because there has never been any West
Nile virus in continental United States that we ever knew of."
However, if one turns to the Riegle Report which was authored and
supervised in its compilation by Donald Riegle who was a senator
from Michigan, one will find that on May 21st, 1985, the United
States had a supply of West Nile virus in the United States and
that they shipped a quantity of that to Suddam Hussein. And that
was in 1985 so that Suddam could use it against Iran with whom
Iraq, at that point, was at war. So, there was West Nile virus in
the United States well before 1985. It was shipped in 1985. There
are still stocks of such a virus in the United States and the
possibilities are two as to where the current outbreak came from.
1. Either accidentally from local facilities such as Plum Island
there was an inadvertent escape of the virus on the mosquitoes or
other insects or, there is always the possibility that one of
Suddam Hussein's agents returned to the United States and was
able to release a quantity of West Nile virus.
Dr. Mazlen
Well, I hope everybody's listening because you all have
Congressman and Senators and public officials that you might know
and you might be able to ask them about this and ask them to
inquire about where this West Nile virus went when it got to
Iraq. One thing I want to point out, and Donald, you can listen
to this because this was also recently in the newspaper in New
York, it was in the New York Times on the 5th of December and
it's a quote. It says, "The scientists at the Centers for Disease
Control and Prevention in Atlanta using scientific techniques,"
I'm paraphrasing that, "have also independently determined that
the West Nile virus found in New York is very close to one
isolated in 1998 from a stork in Israel" which is not far from
Iraq. So, we have another way that it could have come around and
rejoined us here in the United States because for all we know
Iraq found a way to get it into Israel with whom they have no
friendly relations. In fact, they're still at war with
Israel.
Don Scott
Yes, people who know the migrating patterns of birds can infect
that particular type of bird and release it in such an area that
they know its migratory pattern would be over a selected country
and if your congressman or your senator says, "well, give us some
proof" tell them to get out the Riegle Report, published by the
Congressional Printing Office and turn to page 47 and check the
date, May 21st, 1985 and they will see that lo and behold, West
Nile virus was shipped from the United States to Iraq on that
date.
Dr. Mazlen
And, of course, we don't even know whether or not is was possibly
even used in the Gulf War which is another subject we'll be
turning to shortly. I want to also point out, that you're the
author of the book, the Brucellosis Triangle and so we're going
to stop next at another agent, that was shipped to Iraq and you
have evidence of that, also, which was the agent, brucella
melitensis, and tell us about that, because we also sent that
over there.
Don Scott
Yes, they did. Brucellosis was a disease known for thousands of
years actually, but in 1942 Canada, the United States and Great
Britain entered into a secret agreement to take the brucellosis
bacteria and make it more contagious and more virulent and to
weaponize it, make it such that it would do serious damage to an
enemy and they came up with a variant which they had tested in a
number of places in Canada, the United States and Britain as well
as other countries and they had indeed weaponized brucellosis.
And when Iraq was at war with Iran, and Iraq wanted biological
weapons to use against Iran who was winning that war, the United
States shipped a supply of brucella melitensis bio type I and bio
type III from the American type culture collection in Rockville,
Maryland. They shipped that to Iraq and said, here you go, let
this stuff out over Iran, it won't kill all the civilians that
you're targeting, but it will produce a disease known as chronic
fatigue as well as several other serious symptoms. So, in the
Riegle report, lo and behold, that our research was confirmed.
Brucella melitensis was shipped to Iraq from the United States
and that evidence is found on page 41 of the Riegle report.
Dr. Mazlen
Now, just a quick aside. It's labeled as a class 3 pathogen. I
presume that means it's fairly detrimental.
Don Scott
Yes, that means it's disabling but not deadly.
Dr. Mazlen
OK, for the audience so that they get an idea of how they
classify these things.
Don Scott
Yes, well Donald Riegle spelled it out on page 38 of his report
when he said, brucella melitensis is bacteria which can cause
chronic fatigue, loss of appetite, profuse sweating when at rest,
pain in joints and muscles, insomnia, nausea and damage to major
organs which includes the heart, the liver and so on. Now, not
only are you describing Chronic Fatigue Syndrome with that
description, you're also describing Gulf War Illness. In other
words, Suddam Hussein used the brucella melitensis that had been
shipped to him against the Desert Storm forces in the Desert
Storm attack of 1991.
Dr. Mazlen
I just want to ask Donald, where do you want people to contact
you about this topic or about your book, the Brucellosis
Triangle?
Don Scott
They can reach me at Box 133, Station B, Sudbury, Canada, P3E
4N5. And for this particular show's listening audience, I would
like to indicate that if they want a copy of the Brucellosis
Triangle which details the development of the weaponized
Brucellosis bacteria, they can send a $20 check to me, Don Scott,
at the address given and that $20 check will get them the
Brucellosis Triangle which is regularly $21.95, but I will put
in, in addition, a copy of our new Journal of Degenerative
Diseases which covers all of the neurodegenerative diseases and
especially in a series on Chronic Fatigue Syndrome, and I will
also put in 10 pages of documents on history from congressional
records including the June 9th, 1969 congressional meeting that
may get to speak about, NSSM 200 (National Security Study
Memorandum 200) by Henry Kissinger and pages from the Riegle
report, so they can see for themselves why this disease that has
existed for thousands of years suddenly erupted in two forms, one
disabling, Chronic Fatigue Syndrome, and one lethal as AIDS. $20
will get you that whole package because we want people to see
this for themselves.
Dr. Mazlen
And I can understand your willingness to do this to get it out
and it's appreciated. I want to stop you there because I want to
talk to you about the reason why, as you had said to me, why the
Desert Storm attack was halted after 100 hours of amazing
progress against Iraqi forces. What happened there?
Don Scott
Well, when the Desert Storm attack was launched, they were, of
course, going great guns. They would have been in Baghdad in
another 12 hours, as everybody knows. However, there were a
series of scud explosions, somewhere close to 24 scud explosions,
which did not shower shrapnel down upon the Desert Storm forces,
but instead seemed to emit nothing but kind of a blue haze. Well,
those scud missiles, plain and simply were armed with brucella
melitensis as well as some other toxic agents. Now the other
toxic agents included mustard gas, for example. They weren't
trying to kill anybody with the mustard gas, they just wanted to
make sure that the people being attacked knew they were being
attacked. The people in the intelligence branch knew immediately
from the 14,000 biological alarms that went off all up and down
the front that they were being hit by brucella melitensis and
they knew that thousands of veterans in the Desert Storm would
become ill with Gulf War Illness. However, they also knew
something else. They knew that back in 1985 and on other dates,
the United States had not only provided brucella melitensis to
the Iraqis, they had also provided anthrax. There were several
shipments of anthrax to Iraq for use against Iran and the allied
intelligence forces knew that when this melitensis attack
occurred, the next volley of scuds would be armed with anthrax
unless Desert Storm stopped dead in it's tracks, and George Bush
new this. He phoned Schwartzkof in the middle of the night and he
said "stop where you are," and Schwartzkof--we've got this in
news accounts from the period--said "why is that Bob, things are
going great," and George Bush said "I can't talk to you about it
now, but stop where you are, don't move another foot," and Desert
Storm stopped short of Baghdad, left Suddam Hussein in power
because if they didn't stop, the next volley of scud missiles
would be armed with anthrax and at 10% fatality rate there would
be 70,000 dead allied troops on the desert within the next week.
They stopped Desert Storm dead in its tracks, they began to
withdraw two weeks later, Suddam Hussein is still in power and
the leaders of most of the allied countries are out of power.
Dr. Mazlen
Well, that's a certainly striking story and we'd love to hear
more about the documents or the information as to the phone call,
as to what information Bush had gotten from national or military
security sources. We just have a few minutes here but we need to
cover a couple of quick important topics because mycoplasma are
found in between 40 to 60% of Chronic Fatigue Syndrome patients
and Gulf War patients as well have a huge prevalence of it.
Where's the connection here and how does it relate to cancer,
Don?
Don Scott
The mycoplasma is, as you know, a fragment of bacterial DNA and
this particular fragment varies with the bacteria from which it
was derived. The National Academy of Science, in 1995 in
Washington, D.C. received a presentation from a group of top line
microbiologists who had by experiment determined that there is a
linkage between the mycoplasma fermentans incognitus strain and
cancer. Now, we did not know of this, even though it was back in
1995, the report was made at that time, but for some reason or
other mainstream medicine and the National Institutes of Health
and so on do not seem to have done very much to make it common
knowledge. Now, we have secured, as anybody can secure, and we
will provide a copy if you want to write to us--they'd have to
pay the cost of copying--but we have secured a copy of the report
that clearly links or suggest very strongly that there's a
linkage between the mycoplasma fermentans incognitus and cancer.
That was the National Academy of Science, Washington, D.C.,
1995.
Dr. Mazlen
That's startling and very important. Just quickly, what is the
story in terms of the AIDS virus as you see it?
Don Scott
Well on June, 9th, 1969 Dr. Donald McArthur of Pentagon
Biological Warfare research branch spoke to several congressmen
in a top secret meeting and he told those congressmen if they
voted him an additional 10 million dollars, the Pentagon would
have within a 10 year period a new microorganism, one which does
not naturally exist and for which, these are his words "no
immunity could have been acquired." In other words, he promised
the congressmen that if you give us 10 million dollars and 10
years we will give you the AIDS virus and you will be able to use
that AIDS virus in strategic warfare, which means such things as
reducing the population of certain target countries and that is
in the hearings of June 9th, 1969 and that page is one of the
pages that I will provide to anybody that wants to send me the
$20 for the Brucellosis Triangle. I'll send them that page and
I'll send them other relevant pages so they can see for
themselves that AIDS and Chronic Fatigue Syndrome were both
diseases that were engineered in biological warfare research
laboratories. There's no doubt when you read these documents,
which are government documents, achieved under freedom of
information.
Dr. Mazlen
OK, now one quick thing. On our last show we mentioned about the
mosquitoes that were raised and infected. Just very quickly how
many mosquitoes were raised back when this happened and infected
with these biological agents?
Don Scott
Yes, the Canadian government agreed to cooperate with the
American government, and in Belleville, Ontario, the dominion
parasite laboratory back in the 1950's and 1960's and into the
80's the dominion parasite laboratory raised 100 million
mosquitoes a month which were transferred to certain universities
to be contaminated with certain disease agents such as the
disease agent that causes Chronic Fatigue Syndrome and these were
then let out in a controlled way in certain communities so the
the community could be studied to see how effective the mosquito
was as a vector.
Transcribed by
Carolyn Viviani
carolynv@inx.net
Permission is given to repost, copy and distribute this transcript as long as my name is not removed from it.
© 1999 Roger G. Mazlen, M.D.
http://www.whale.to/m/scott8.html
Journal of Degenerative Diseases - Vol 1; Number 1
Biological Warfare Weapons Development and Testing: A Chronology by Donald C. Scott
1942: Canada enters into a secret agreement with Britain and the United States to participate in a program to develop biological weapons. The principal diseases used as starting points included anthrax and brucellosis.
1945: At the end of the war the Agreement was continued into peacetime due to a perceived Communist threat. U.S. hires principal German and Japanese biowar researchers, including Dr. Ishii Shiro who had used allied prisoners to test anthrax and had conducted tests of a 'mystery' disease agent in the heartland of New Guinea.
1946: Dr. George Merck, head of the biological research in the U.S. reported in a secret memo that his researchers had learned how to extract the disease toxin from bacteria in a crystalline form suitable for aerosol diffusion.
1949: Several bio-weapons were tested at Dugway Proving Grounds in Utah. There were two principal classes of weapon: one class to disable and one class to kill.
1952-53: Several bio-weapons were emplopyed by the U.S. in Korea, including brucellosis. Evidence also suggests that a pathogen causing hemorrhagic fever was deployed along the Hantaan River, but it 'blew back' over American troops, killing several hundred. D. Carleton Gajdusek (see article by Ms. Heslin this issue) sent by Pentagon to help contain the damage.
1950: Canada agreed to breed one hundred million mosquitoes a month in the Dominion Parasite Laboratory in Belleville, Ontario, The mosquitoes were to be contaminated with certain crystalline bacterial toxins and tested on unwitting U.S. and Canadian public. Queens University in Kingston involved.
1957: Carleton Gajdusek turned up in remote New Guinea highlands where hundreds of Fore tribe were suffering from Creutzfeldt-Jakob disease (kuru).
1969: The Pentagon's chief researcher asked Congress in a secret meeting for ten million dollars to develop a new weapon which would be 'refractory' to the human immune system and for which ..."No natural immunity could have been acquired." In other words, the victims would have a DEFICIENCY of ACQUIRED IMMUNITY. At the same Meeting Dr. MacArthur stated that his researchers were going to try to 'mutate bacteria and viruses' to create new microorganisms Which 'did not naturally exist'. (See Dr. Martin's "Viteria" this issue).
He again emphasized two classes of weapon: one to and one to kill. Both would have to be on unwitting victims and the tests would be by the U.S. Public Health Agencies (ie The CDC and the National Institutes of Health).
1974:Henry Kissinger wrote National Security Memorandum 200 in which he advised Ford that the world's population would have be limited as far as its growth was concerned. Such limits would require an increased death rate or birth rate.
1976: U.S. Centers for Disease Control visited most the countries identified by Kissinger as population threats and offered the populace a free vaccination against small pox. Millions received the vaccine and within five years close to sixty percent had a new disease: AIDS. A disease which, Dr. MacArthur had promised the Congressmen, refractory to the human immune system. The population who received the free vaccine had no acquired immunity to the new disease.
1976: A new hepatitis vaccine was also offered in this year to gay men in New York. Over 1000 accepted the vaccination and in five years sixty percent of these had developed AIDS.
1980's: Tests of new disabling disease pathogens somewhere in the U.S. and Canada.
At the same time mystery diseases were breaking out as far away as Incline Village, Nevada St. Lawrence Seaway in Canada. The CDC and NIH were not interested in studying these mystery outbreaks whose symptoms greatly resembled symptoms of brucellosis mutated by the visna virus.
1985-1989: U.S. sells several hundred units of bio-weapons to Iraq for use against Iran. Included in shipments were deadly anthrax plus disabling brucella agents: melitensis, suis and abortis. The latter caused "chronic fatigue" as well as disabling damage to major organs.
1991: Desert Storm Forces attacked by SCUDS. Several hundred thousand U.S., British and Canadian troops become ill with symptoms of mutated brucellosis. (See story on Lt. Richard and Gulf War Protest Oct. 13 in this issue). Allied attack halted immediately after attack by SCUDS. Possibly to prevent a second attack with anthrax armed SCUDS.
1992 to present: U.S., British and Canadian Military tell sick Gulf War Veterans that their illnesses were all in their imagination. NIH agrees !
1999: Veterans told "Pay for your own treatment".
© 1999 Journal of Degenerative Diseases http://www.carolsweb.net/ccf/biowarfare.htm
http://www.cdc.gov/ncidod/dbmd/diseaseinfo/brucellosis_t.htm
For comprehensive CDC information about bioterrorism and related issues, please visit http://www.bt.cdc.gov/
Clinical Features
In the acute form (<8 weeks from illness onset), nonspecific
and "flu-like" symptoms including fever, sweats, malaise,
anorexia, headache, myalgia, and back pain. In the undulant form
(<1 year from illness onset), symptoms include undulant
fevers, arthritis, and epididymo-orchitis in males. Neurologic
symptoms may occur acutely in up to 5% of cases. In the chronic
form (>1 year from onset), symptoms may include chronic
fatigue syndrome, depression, and arthritis.
Etiologic Agent
Brucella species, usually B. abortus (cattle), B. melitensis,
B.ovis (sheep, and goats), B. suis (pigs), and rarely B. canis
(dogs).
Incidence
In the United States, < 0.5 cases per 100,000 population,
primarily B. melitensis. . Most cases are reported from
California, Florida, Texas, and Virginia.
Sequelae
Variable, including granulomatous hepatitis, peripheral
arthritis, spondylitis, anemia, leukopenia, thrombocytopenia,
meningitis, uveitis, optic neuritis, papilledema, and
endocarditis.
Transmission
Zoonotic. Commonly transmitted through abrasions of the skin from
handling infected mammals. In the United States, occurs more
frequently by ingesting unpasteurized milk or dairy products.
Highly infectious in the laboratory via aerosolization; handling
cultures warrants biosafety level-3 precautions.
Risk Groups
Abattoir workers, meat inspectors, animal handlers,
veterinarians, and laboratorians.
Surveillance
Brucellosis is a nationally notifiable disease and reportable to
the local health authority.
Trends
For previous 10 years, approximately 100 cases per year have been
reported.
Challenges
Elimination of domestic and feral animal reservoirs. In 2001, the
National Brucellosis Eradication Program reported only 3 newly
affected cattle herds, compared to 14 herds identified in 2000.
Establish and validate methods for isolation and detection of
Brucella spp. in foods.
Opportunities
Validation of rapid diagnostic technologies developed for
identification of Brucella spp. in natural or
bioterrorism-associated outbreaks.
Family with Lupus, Arthritis and Pulmonary Pneumonia.
By Anita Sands astrology@earthlink.net
Like many cat lovers, I became an involuntary cat breeder after taking in a pregnant Queen back in the 70's. She and her babies multiplied in intervening decades, until I had as many as thirty cats in the back yard of my rented house, a jungle which looked like a Rousseau painting with these green eyes staring out at you from under every leaf.
It wasn't all so picturesque, however. Cat Plagues ping-pong among my flock, among them a smelly lung disease. Having holistic interests, I nursed cats who had it with New Age herbs. While dosing them with astragalus and echinecea from an eye dropper, my face close up, I noted the odd, fetid aroma to the lung phlegm.
One day, a sick cat I was holding sneezed! I felt mucus enter my eye. SPLAT. An hour later I had a massive sore throat, HIGH FEVER, followed by chills, aches in my joints, that same, odd, fetid phlegm in my lungs and a 103 degree fever that didn't break for two weeks.
I tended myself with orange and carrot juices, echinecea, astragalus, zinc, Vit C but neither herbs nor my immune system recognized the bug. The disease ran over me like a train, progressing into a pneumonia type bronchitis with bad chest/lung phlegm (in spite of my Hollywood tofu & green salad lifestyle, "mucus-free" California root and nut diet, very small amounts of dairy and meat,) the bug JUST PLOWED ME UNDER. I lay flat on my back in bed. In this period, I had time to think about the cat that did this to me.
The sprayer had chronic respiratory problems from a kitten disease which she'd survived. MOST of my kittens died of whatever it was. The survivor's Virus or Bacteria had abated in her, but somehow became resident . When the disease peaked, once a year, she'd get the bad odor and wheeze and sneeze and shoot green phlegm like a Martian out of Men in Black. The smell would announce it was time to try to keep her away from other cats and their dishes but several adult cats caught it from her and strong though they were, they died of it.
Was I dying? MY phlegm had same fetid, cheesy odor, reinforcing the feeling that I caught a CAT disease which, by the way, was having the time of its BUG life in a non whiskered life form. This bug was unlike any flu I'd known in my first half century of life. The fever lasted so LONG and was so violent, I knew it was NO microbe that I'd ever had before. THIS WAS truly from Mars.
Slowly, I began to recover, and when I did, I noticed that I had joint aches. I assumed that the first arthritis of my age group has struck. I accepted old age and just kept on swigging carrot juice and eating my tofu. Grateful to be well, I thought nothing of it. Except that once a year I seem to get a running start on the same sore throat glands and fever, but now my immune system beats it much faster. I don't get all-the-way ill. For years, it goes on that way. I 'come down with it' occasionally. Spontaneously, on my own, as I no longer get within sneezing distance of the sick cat or her dish.
Then I get this PC. First week on the Net, I go surfing around, looking for vets who have web sites, find plenty of these. I click on "lung diseases" and find the names of all cat lung diseases. I look at a lot of web sites. ONE of the lung diseases is mycoplasma, so I go elsewhere looking that one up.
Holistic writers and magazine publishers have plenty on mycoplasma as it's tied into chronic fatigue syndrome and immune system failure. Many web sites in cyber space have researches on this new, wide-spread plague of auto immune diseases and on one, The Townsend Letter for Physicians and Doctors, in an article on Lupus and chronic fatigue syndrome, I read that both can be caused by mycoplasma bacteria which basically is a barnyard bacteria. When found in humans (usually in the blood of Gulf War Veterans, victims of intentionally applied bio-toxins) it causes immune system failure similar to AIDS.
The Iraqi took the only thing they had plenty OF --- Barnyard bacteria --- and put it in their bombs. There were other ways for humans to get it, direct close contact with animals who carried it, and as pigs and lambs were part of the barnyard carriers, humans sometimes became ill from eating rare-cooked flesh.
Internet researchers called mycoplasma something between a bacteria and a virus. It had features of both. Like many pneumococcus organisms, this single celled creature can become bloodstream resident meaning you don't need people to give it to you again once you've got it-- like flu and colds, measles or chicken pox get 'given' which explained why I was able to get relapses annually when I am a hermit. I live far from people, I am not exposed to anyone's water glass, or hand on my towels. No kids sneeze in my face. My cats are happy in the yard or garage. They don't give it to me, anymore. However, WHENEVER I get tired or worn out, I get the sore throat glands and fever and fight it for a month at a time (I am currently in third or fourth week of it). My immune system fights and I always win. I mean, I'm still here. No segue into lung phlegm any more. The fever and sore glands whip my body into a heat which seems to bake it out but it's a bother as it's a month of CHILLS and feverish feelings, and fatigue feelings but my antibodies recognize that bacteria. NO LONGER do I go into that massive high fever, (103), totally painful, ached joints, laid out in bed-lung infection and smelly lung phlegm.
When I'm in good health, I beat it in ten days. If I'm having a hard life, not sleeping, not eating well, the FIGHTING it stage lasts a month. THIS TIME it is lasting almost a month due to a slightly bad tooth root also contributing some contamination to the throat lymph area.
Anyway, I'm up studying the thing again and here's what I learned on the web, and I'll quote from my notes: "Examination of the joints of Lupus, Scleroderma and Rheumatoid Arthritis sufferers have turned up the very common, feline, mycoplasma bacteria. There are 20 known species of Mycoplasma found in sheep, pigs, goats and calves, animals that we generally don't live with but do consume."
I had read that sputum could transfer the disease, but here was information saying that ingestion of rare meat also cause this disease to transfer to meat eaters' bodies. There was another possibility mentioned, breathing near cat litter boxes. "Mycoplasma bacterium is a single cell life form that mimics mushrooms and ferns in that it spreads by air born spores, hence the name, 'myco' or 'like a mushroom.' The spores are in cat feces and float in the air when feces is dry. " This made me uneasy. Living with an infected cat, or next door to one may possibly transfer this disease to humans. My cats could be spreading it even from the yard. If this were so and as cats are the most frequently owned pet in America, we could be talking about an airborne disaster and perhaps the source of all chronic fatigue syndrome in the USA.
The question for any pet owner is ---does your cat have it? This week, I have one less cat as the last of them who had the lung problem for her brief, three years, or since weaning, when they get it, just died of her worst outbreak. Her current companions never caught it. I believe this is because I began adding freshly grown greens to home-cooked turkey burger and sprinkling the finished stew with garlic powder. ( Back in the old days when I used canned Whiskas meat, every cat caught the disease from a sick one. Nobody had an immune system. )
Today I note that the several wild tomcats that visit our house daily for turkey and greens stay healthy, so I feel increasing an animal's immune system through good diet works. (Secrets of cooking Super kittie cuisine easily are at http://home.earthlink.net/~astrology/holistic.html if you want to take a peek. )
Now while I don't fully trust Vets who don't know from good diet and still recommend canned meat-by-products I believe them when they say --- as they do in the Merck Veterinary Manual (pps 760-761) that 40-45% of chronic, feline upper respiratory diseases are caused by Rhino virus, Herpes virus, Calcivirus, Chlamydia or Mycoplasma. There are diverse causes of cat-lung problems. Some cats die of this lung affliction, I read but most will live for years with the bacteria, exhibiting only a light lung mucus, hence becoming carriers. As sneezing or air born spores can spread Mycoplasma, I deduced that arthritis and Lupus can be given to humans from cats. Of course, the research I read indicated there were other causes of the disease in humans. Eating Rare cooked meat could do it so it's possible that under cooked veal, lamb or pork chops could transfer Mycoplsma to humans as pigs and lamb communities frequently have Mycoplasma. Cats don't get arthritis from mycoplasma but Sheep and pigs do!
If one has the head to be a medical detective, ponder another part of the Mycoplasma puzzle: Mycoplasma is the bacteria found in joints affected by both rheumatoid arthritis and Lupus. Is it possible that the Lupus and Arthritis are mistaken for one another? The more frequently diagnosed rheumatoid syndrome might really be undiagnosed Lupus or the other way around. Only a blood test for antibodies or a culture of the joint fluid could tell you for certain but if your bones ache, one might invest in a complete panel of tests.
I however, trusted my Sherlock Holmes work, knew that my joints had begun to ache after a cat had snorted in my eye so I deduced that she and I had mycoplasma and continued to research along those lines and lo and behold, found that the good news was: this mushroom-like (hence called myco) plasma bacteria that causes my sore throat and Lupus and Arthritis can easily be attacked with anti-biotics.
The very harmless Minocycline is the anti-biotic of choice and has worked well in placebo trials. There seem to be very little side effects from it use although it's always good to take a good, multi-flora Acidophillis strain for a few weeks after treatment to replenish friendly bacteria in the digestive tract.
Can the average cat owner tell if he has Mycoplasma in his body? The cat owner might not know if he'd ever been exposed. He might have a painfully swollen joint somewhere, a thumb, ankle, foot or wrist but the lung congestion caused by the bacteria would long ago have been confused with a cold that came and went and would now be forgotten and he'd assume as I did for years that my joints were simply aging.
Or, you might have a very developed case of the disease and lots of medical coverage and be able to afford tests and you might know what you have is diagnosed Lupus which occurs when the immune system seems to go wild, attacking many of the patient's joints at once. Well, I'm here to tell you that my research indicates you might try Minocyline and say goodbye LUPUS!
The latest researches with Lupus indicate that the disease can be alleviated (AMA has the patent on the word 'cure' or 'heal') with some other holistic methods that make use of youth hormones which in turn, tone the body's immune system, giving it the ability to fight Mycoplasma naturally, from the inside, with our own antibodies.
Researchers have used DHEA, a natural body hormone, and precursor stimulant of the body's abilities to make other hormones, hence a "Master" hormone. Deepak Chopra calls DHEA "the single most significant medical breakthrough in the field of anti-aging/longevity research."
DHEA is found in Mexican Yam Extract and Raw Adrenal Concentrate which will supplement and stimulate the body's own natural DHEA production. Such production naturally ceases with old age. (A loss of hair on the legs, lower body is a symptom of a need for DHEA.) Mexican Squaw vine, Yam and adrenal concentrate are sold in all health food stores. They are not toxic, and don't cause cancer the way estrogen can. DHEA is very safe and there appeared to be no downside to its use. In fact, there appeared to be a significant upside: Rats live twice as long with a little in their diets! But recently it was found that 25 to 50 milligrams a day caused fast or arrthymic heart beats to some humans, but it would be easy to lower the dosage if that occurred, as the benefits of DHEA are hefty.
Researchers have also used Progesterone hormone which the young body produces, and the aging body doesn't, along with Pregnenolone, a DHEA precursor hormone. By rejuvenating the body's immune system and making it more like that of a young person, Dr. Davis Lamson, a private practitioner and researcher in Kent, Washington, has had success in backing off arthritis with none of the side effects that the doctors' favorite rheumatism drug, cortisone causes, i.e. osteoporosis.
Some researchers have used another natural substance, DMSO, to transport topically applied hormones into the bones. DMSO is a sulfur oxide that penetrates the skin very easily, as all sulfur will; (you'll recall the ancients soaking their aching bones in sulfur and mineral-rich hot springs?) Well, the sulfur carried the other minerals RIGHT into the bones, fixing the arthritis! DMSO is the Vet's favorite shin rub for race horses and is easy to get from equine doctors but in our case we will have to add something TO the DMSO to get carried IN.
I remember doing Ann Miller's horoscope, visiting her at her house. She complained that the American run of BABES had been hard on her legs, and she was not going to do the London run. She had only one hope. She thought she might get a jar of shin rub from her vet. (She must have done so because she went on to open in London to great reviews. )
Those of us who suspect Lupus, Arthritis or Mycoplasma bacteria to reside in our bones, might might mix DMSO shin rub with Minocycline, pregnenolone and a liberal dose of fresh squeezed garlic, (a bacteriacide) apply this germ-killing mush to our aches. It is literally transported into the joints.
Holistic doctors warn you to be careful that hands are 100% clean as cosmetics, chemicals, --- anything that is on your hands will also be carried in through the skin! Sterile bandages wrap the garlic joint and one goes off to dream land, smelling like a pizza!
There is much one can read on the subject of aging, aching bones, and youth hormones. The Number #1 Researcher in the field is Dr. Ray Peat, PHD, a nutrition scientist who specializes in Auto Immune diseases. Dr. Peat is a regular contributor to America's best holistic bulletin for doctors, The Townsend Newsletter for Physicians & Doctors and one of America's most respected medical researchers. He's written many books, thousands of articles for medical journals and has his own newsletter. His book on Progesterone treatment of LUPUS and rheumatoid arthritis is seminal.
To contact researchers: holistic writer, Dr. Julian Whitaker, c/o his publishers, Dr. Eugene Roberts, City of Hope Medical Ctr, Duarte CA, Dr William Regelson, Virginia Commonwealth Univ. Medical College; Elizabeth Barret Connor, M.D. Dept Community Med, UCSD; Dr. Kenneth Bonnet, Dept of Psych NYU. Send SASE and all will send you research.
I know one should show this material to a doctor and get his OK to do the treatment. Dr. Peat says diagnosed Lupus sufferers should take DHEA, Progesterone, Pregnenolone and DMSO. The hormones are fairly easy to get through holistic pharmaceutic channels.* For dosage, call Dr. Ray Peat, and when you do, get on his mailing list. DMSO is available through an equine vet or through Arizona Healthfoods. +
The criteria for diagnosis of Lupus is by its most common symptoms: photo sensitivity, low leukocytes in blood, anti-DNA antibodies in blood, renal disorder, oral ulcers, body rashes, skin lesions and aching bones and joints. It's easy to see why Lupus in early stages can be mistaken for rheumatoid arthritis. All aching joints are the same in the dark! "Tout les chats son le meme en la nuit."
According to another Lupus researcher, Dr. Stanley Jacob, MD Oregon Health Sciences University, (the author of 8 textbooks, 140 Medical Journal articles,) one should take DMSO with the anti-biotic Minocycline worked into the gel.
As DMSO is a harmless mineral, sulfur, we can use it orally, in venous transfusion or topically. Always dilute with distilled water. As DMSO is a carrying agent that moves toward the bones, it acts to transport the antibiotic into the affected areas, just as it will transport hormones applied topically.
Dr. Stanley Jacob points out that Mycoplasma is a cell wall-deficient bacteria, hence your usual, activated antibiotics don't work. Luckily Doxycycline, Tetracycline and "Minocin" or Minocycline work well on it, especially, if you add human or vet grade DMSO to the medication.
If anyone suspects his cat has Mycoplasma lung bacteria, he might have the vet outline a cure for FLUFFY using Minocycline antibiotic. Maybe the Vet could win himself a Nobel Prize or something.
The link between cats and arthritis has been known for a long time but ignored. In NATURE JOURNAL in 1939, (56 years ago), Dr. Thomas McPherson Brown recounted how he isolated the Mycoplasma Bacterium that cats have in human, rheumatoid joints. It is tragic that the medical community is so slow to listen to holistic researchers and that for more than a half century, millions of people have been crippled by a disease that one of the least injurious anti-biotics could have cured.
As some readers may already know they are diagnosed with Lupus and would be interested, --- here's a piece of info on ALTERNATE THERAPY FOR ARTHRITIS OR LUPUS: Another tack for Lupus is based on research done by the famed Mexican Cancer clinic, and is called "The GERSON therapy". It works on cleansing the liver, and involves a wheat grass juice fast. Dr. Max Gerson says fasting works well on Lupus. (If that's true, this would indicate that many of our livers are very toxic and many of our immune systems are deficient these days. Yeah, No DUH!)
To mimic Gerson's clinical approach at home, go on a good 14 day raw juice fast, (no food at all) with 6 mini meals a day of mixed juices (carrot, celery, wheat grass and beet). The trick is to stir in a few tbsps of psyllium seed (unflavored metamucil), and drink immediately, before it 'clots.' First time fast should go on a high-bulk, vegetarian diet for a week beforehand to get the colon whisked clean enough to tolerate the highly cleansing, liquid diet. Wheat grass is easy to grow in flats at home. Try your neighborhood farm or poultry feed store to find wheat seed, sow it thickly on rich loam in a horticulturist's flat, shear when blades are 3 inches long. Get a wheat grass extractor at your health food store as the usual juicer will have no effect on these 'blades of steel.' If you are hypoglycemic, have avocado, bean sprouts and peeled, blanched almonds FRESHLY SOAKED AT HOME to loosen skins .. when you get hungry and there'll be no problem. It'll be a " SORT OF" Fast.
NOTES: For more background facts, read Townsend Letter for Doctors, Issue # 145 Pg 111, Issue #141 P 132, Issue #143 Pg 104, Issue # 148 Pg 18 and Issue 149, P 99. Read the January 95 article by Dr. Tilly B.C. Volume 122 Pg 81-89, in the Annals of Internal Medicine.
For more info on Minocycline for Lupus, send SASE with 55c to The Road Back Foundation 4985 N. Lakehill Rd. Delaware OH 43015.
Contact Dr. Peat at PO BOX 5764 Eugene OR 97405, (503) 345-9855 in Eugene Or.
*You can get Pregnenolone and DHEA hormones from "Lifelink" 445 Lierly Ln Arroyo Grande CA 93420. (805) 473-1389. 180 capsules 40$ but there are other dosage at other prices. Shipping 4.50 UPS. TRY: HOME LINK 800-272-4767. Maybe cheapest of all suppliers: LIFE ENHANCEMENT PROD. PO Box 751390, Petaluma CA 94975. Get pregnenalone hormone from BEYOND A CENTURY 800-777-1324, 150 caps of 30m $59.50 It is a precursor of body's own supply of DHEA.
+ARIZONA HEALTH FOODS in PHOENIX has DMSO; try 800-INFO for #. Get DMSO more cheaply from your VET. Veterinarian grade is just as pure as human grade. Just tell vet "my horse limps, I want shin rub."
For INFO on DMSO protocols send SASE to Dr. Stanley Jacob L225, Oregon Health Sciences Univ. Portland OR 97201. For more about DMSO, call American Academy Metabolic Medicine 800-982-2101 ext 123. Treatment protocols will be provided.
Get DHEA RESEARCH bulletin #463 from American Society of Nutritional Research, 12416 N. 28th, Suite 18, PO Box 241 Phoenix AZ 85029.
Get NUTRITION NEWS "DHEA WILD YAM" PO Box 55279 Riverside CA 92517.
Contact Dr. Arthur Schwartz, Fels Institute, Temple University, Philadelphia, PA. a longtime researcher in DHEA.
DOSAGE: DHEA can be given in doses of from 3 mg to 30mg daily but as high as 1,600 mg a day for 28 days was found not to be injurious, subsiding later to a low daily maintenance level, 3x a week. If arrthymia's result, retreat to 25 mg. If Deepak Chopra who is a DR, calls it the true Fountain of Youth and Doctors tell us there is no downside, maybe you can believe it. All it does is juice up the natural hormone-making ability of the body, which we lose in old age.
APPENDIX I. DOCUMENT BY CENTER FOR DISEASE CONTROL ON MYCOPLASMA PNEUMONIA: Investigation into community-acquired pneumonia bad enough to require hospitalisation, & Results of a population- based active surveillance Study in Ohio, "The Community-Based Pneumonia Incidence Study Group" written by some doctors at Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC, Atlanta, Ga 30303, USA where THEY SAID:
"Pneumonia seems to be the leading cause of death due to infectious diseases in the United States; however, the incidence of most infections causing community-acquired pneumonia in adults is not well defined. METHODS: We reviewed all adults, residing in 2 counties in Ohio, who were hospitalized in 1991 because of community-acquired pneumonia. Information about risk factors, symptoms, and outcome was collected through interview and medical chart review. Serum samples were collected from consenting individuals during the acute and convalescent phases, and specific etiologic diagnoses were assigned based on results of bacteriologic and immunologic tests.
RESULTS: The incidence of community-acquired pneumonia requiring hospitalisation in the study counties in 1991 was 266.8 per 100,000 population; the overall case-fatality rate was 8.8%. Pneumonia incidence was higher among blacks than whites (337.7/100,000 vs 253.9/ 100,000; P < .001), was higher among males than females (291.4 vs 244.8; P < .001), and increased with age (91.6/100,000 for persons aged < 45 years, 277.2/ 100,000 for persons aged 45-64 years, and 1012.3/ 100,000 for persons aged > or = 65 years; P < .001). Extrapolation from study incidence data showed the projected annual number of cases of community-acquired pneumonia requiring hospitalisation in the United States to be 485,000. These data provide previously unavailable estimates of the annual number of cases that are due to Legionella species (8000-18,000), Mycoplasma pneumoniae (18,700-108,000), and Chlamydia pneumoniae (5890-49,700).
CONCLUSIONS: These data provide information about the importance of community-acquired pneumonia and the relative and overall impact of specific causes of pneumonia. The study provides a basis for choosing optimal empiric pneumonia therapy, and allows interventions for prevention of pneumonia to be targeted at groups at greatest risk for serious illness and death.
http://www.medicineau.net.au/clinical/medicine/CFS.html
|
Executive Summary Introduction Terminology Evaluation of postulated aetiological factors Epidemiology Investigations Differential diagnosis Treatment Course and prognosis Conclusions Bibliography |
The cause of chronic fatigue syndrome remains unknown at this point in time. A number of research teams throughout the world have investigated possible links to a number of virus infections (including Epstein-Barr virus, enteroviruses and poliomyelitis as well as and fungal agents (in particular, Candida albicans). Despite extensive studies, the evidence that CFS is caused by any particular infective agent is equivocal. Nor has it been shown that physical or mental stress cause chronic fatigue syndrome.
Chronic fatigue syndrome occurs more commonly in women with a peak incidence in those in the third and fourth decades. Despite media references to the condition being more common in those in middle income and groups, evaluation of social status of cases indicate that CFS occurs with about equal frequency in all social classes. In general, no forms of treatment are shown to alter the course of the condition. Recovery is reported in a number of studies to be facilitated by rest complemented by a supervised program of gentle exercise. In general, no forms of medication have been shown to alter the course of the disease although treatment of specific symptoms is recommended when present. The prognosis varies greatly across the spectrum of cases reported to date, with the majority of sufferers eventually recovering after a period of one to ten years.
Wallace (1991:943) divides the various synonyms into two groups: epidemic and endemic. Synonyms in the former group include: epidemic neuromyaesthenia, Adelaide epidemic, Royal Free disease, Iceland disease and Lake Tahoe disease, whilst synonyms in the latter group include: myalgic encephalomyelitis, fibrositis myalgia, "Yuppie" flu, idiopathic chronic fatigue syndrome, Epstein Barr disease and chronic infectious mononucleosis. The eponyms in the former group derive from areas of the world where epidemics have been documented. These epidemics give some support to the hypothesis that, in some circumstances at least, the condition is transmissible. The synonyms for the endemic form of CFS appear to be based largely on the unproven assumption that infective agents have a role to play in the causation of the condition. Despite this expectation, plausible studies have yet to corroborate such a view.
Definitions The range of synonyms reflect the diversity of opinion that exists within the medical community as to whether or not chronic fatigue syndrome is a disease and, if so, what the disease complex entails. Some writers point to the general scepticism of many practitioners in the past as to the validity of the diagnosis. They hold that many practitioners consider the diagnosis is a misnomer in that patients with features of CFS are instead suffering from some form of psychiatric illness (with chronic depression being the most common) or are suffering a delayed convalescence to an infective process (such as infectious mononucleosis).
More recent research generally fails to support either of these viewpoints. Firstly, several working groups have recently recommended that co-existing psychiatric illness should not exclude consideration of the diagnosis of chronic fatigue syndrome when a number of the other minor criteria are present in addition to chronic fatigue (infra vide). In addition, some psychometric studies indicate that the response times of those with CFS are often significantly reduced whilst response times in those with depression and other psychiatric ailments are not significantly altered. Moreover, Kirmayer et al. (1989:940-948) hold that the profound muscle ache after exercise seen in CFS is not a feature of depression.
The situation is further compounded by inconsistencies in working definitions. A major source of confusion in this regard arises from the original definition promulgated by the Centres for Disease Control, Atlanta. Holmes et al (1988:387-388) of the CDC confirm that their original definition was intentionally restrictive to maximise the chances that research would identify associations if they exist. In more recent times, other working groups have recommended that the pre-existence or co-existence of psychiatric disease of itself is no longer sufficient reason to exclude considering a diagnosis of CFS.
The criteria of Holmes et al. (1988:387-9) are:-
Table 1. Diagnostic criteria for chronic fatigue syndrome For diagnosis, both major criteria must be present, plus the following minor criteria: (1) at least 6 of 11 symptoms and at least 2 of 3 physical signs or (2) at least 8 of 11 symptoms.
| Major criteria |
|---|
| 1. New-onset fatigue lasting longer than 6 months with a 50% reduction in activity. |
| 2. No other medical or psychiatric conditions that could cause symptoms. |
| Minor criteria |
| Symptoms (must begin at or after the onset of fatigue) |
| 1. Low-grade fever (ie. 37.5C to 38.6C) |
| 2. Sore throat |
| 3. Painful cervical or axillary lymphadenopathy |
| 4. Generalised muscle weakness |
| 5. Myalgias (muscle pains) |
| 6. Fatigue lasting 24 hours or more after moderate exercise |
| 7.Headaches |
| 8. Migratory arthralgia |
| 9. Sleep disturbance (hypersomnia or insomnia) |
| 10. Neuropsychological complaints (one or more of the following: photophobia, visual scotomas, forgetfulness, irritability, confusion, difficulty concentrating, depression). |
| 11. Acute onset (over a few hours to a few days) |
| Physical signs (documented by a medical practitioner twice at least 1 month apart) |
| 1. Low-grade fever |
| 2. Pharyngitis (non-exudative) |
| 3. Cervical or axillary lymphadenopathy |
The British perspective as expressed at the Green College Working Group meeting in 1990 is slightly different in that the general term recommended for all cases of chronic fatigue is "post viral fatigue syndrome".
California: The first recorded epidemic occurred in doctors and nurses in several hospitals in Los Angeles in 1934. Reported symptoms included muscle weakness, involuntary muscle contractions and twitching, clonic movements and cramps in affected muscles and muscle inco-ordination. Pain was extreme in the back and extremities and lasted for a number of months. Sensory changes were also a common feature, including hyperaesthesia, paraesthesia and areas of anaesthesia - sometimes following the distribution of a nerve trunk and sometimes a whole extremity. Vasomotor and trophic changes , excessive sweating or abnormal dryness of skin, coldness, cyanosis and brittle nails were also commonly reported. Inflammation of the joints occurred in one-third of adult cases, with a third of these being transitory and the remaining two-thirds developing permanent arthritic changes in the joints involved.
Iceland: In early winter in 1948 to 1949, an extensive epidemic broke out in the town of Akureyri in Iceland. Women were affected more than men, although the sex ratio was equal less than 20 years of age. The illness spread rapidly but was confined to the town. It did not appear to be spread by water, milk, food or sewerage but instead by close contact with those affected. In 1955, 39 patients of the 1948 epidemic were re-examined. Of those more severely affected, only 25% had completely recovered, 52% had residual muscle tenderness and 65% had objective neurological signs. Of those only mildly affected in 1948, only 44% had recovered fully with 50% having muscle tenderness and 19% having residual objective neurological signs.
Adelaide: A few months after the 1948 Akureyri epidemic, an epidemic of poliomyelitis occurred in Adelaide. By 1951, 800 patients had been admitted to hospital with a condition called "epidemic neuromyasthenia" with symptoms indistinguishable from poliomyelitis but without microbiological evidence of poliomyelitis. Recovery was delayed for many patients for up to 2 years.
New York State: Similar to Adelaide, a widespread epidemic of poliomyelitis in New York State in 1950 occurred with a number of patients having features distinct from those of polio in the absence of any microbiological evidence of poliomyelitis. Muscle aching and weakness were predominant symptoms in this subgroup who lacked the classical muscle wasting characteristic of poliomyelitis.
Cumbria: A GP in Cumbria reported an outbreak of a disease similar to that described in Iceland in 1948 wherein 233 cases were recorded in a practice population of 1675 people, an incidence of 14%. The illness was thought to be spread by contact. Recovery for many patients was delayed for many months and, in some cases, several years. The features were similar to those described by Holmes et al. (1988) listed above. No virological evidence of either Coxsackie or echo virus infection was found although the clinical picture was suggestive of either of these infections.
Great Ormond Street: A further outbreak of 'epidemic neuromyasthenia' occurred at this hospital for children in 1970 and 1971, with 145 of the 1900 total staff being affected (mostly nurses). Interestingly, a number of children had been referred to the hospital in the preceding years with unexplained symptoms similar to those that the affected staff members developed and similar to those described by Holmes et al.
Comment: Jenkins (1991) raises the question of whether these epidemics represent an epidemic form of post viral fatigue syndrome transmissible by an unidentified agent but does not give any firm answers. He argues that the recognition of such epidemics is more likely to occur in an institutional setting, especially health institutions, for obvious reasons and suggests that the recognition of low-grade epidemics in the community would be more difficult when only two or three cases a year occur in each general practice. The failure to recognise epidemics in the community in the past is also held to be a product of the lack of recognition given to the condition disease surveillance agencies (such as the Centres for Disease Control in the USA and the Surveillance Centre for Communicable Diseases in the UK) until recently. Jenkins also notes that no institutional epidemics of chronic fatigue have been reported since 1970.
Recommendation: These case reports suggest a condition which is transmissible in the community resulting in epidemics of illness with symptoms indistinguishable from those described for CFS. Given the uncertainties expressed by Jenkins as to exactly what that agent was, it is recommended that the epidemic form of disease be treated as a clinical entity distinct from the endemic form of the disease.B. Traditional models of infections as a cause of endemic chronic fatigue syndrome There has been extensive research undertaken to determine whether or not one or more biological agents cause CFS of either epidemic or endemic type. To date, no agent has been shown to satisfy the required criteria proposed by Koch so as to be held to have a causal role in this regard. For the reasons given below, the majority view of the research community is that such associations are at best to be treated as having temporal significance for some patients without it being possible to infer an aetiological link. The evidence on which this assertion is based in presented below in summarising the findings to date for the more common agents under consideration.
The search for a biological agent appears to be a product of the frequency with which CFS patients report symptoms interpreted as being consistent with an acute "viral" illness preceding the onset of chronic fatigue syndrome. Lloyd et al. (1990:527) for example report that 75% of the patients they interviewed gave such a history, with the majority having a healthy premorbid status. Manu et al. (1993) found that 70% of CFS patients (versus 30% of controls) attribute their illness to a viral cause. Despite this perception, studies which have looked at the frequency of infection with a range of viruses have, in general, failed to substantiate that a particular virus is more common in those with CFS (see Shafran 1991:730-9 and Kroenke 1991:44-55) compared to the natural rate of asymptomatic infection in the general community. Winters and Quinet (1992: 260-270) state that the evidence supports persistent viral infection in only a small percentage of CFS patients.
Epstein Barr Virus (EBV): This agent (a type of herpes virus) is generally accepted as causing infectious mononucleosis (or glandular fever); a condition seen most commonly in adolescents and younger adults. Kroenke (1991:49) states that "EBV was incriminated as a cause of chronic fatigue syndrome in the mid-1980s but that a critical appraisal of the evidence casts strong doubt on this hypothesis". One of the difficulties in attributing a role of EBV as a cause of CFS is that EBV is ubiquitous in the community, with 95% of healthy persons over the age of 30 have serologic evidence of past infection with EBV. Moreover, whilst it is well known that a number of acute cases of infectious mononucleosis have a protracted recovery (termed "chronic mononucleosis") with many having high levels of IgG-VCA (1:320 or higher) and elevated anti-ECA (1:40 or higher), this profile is also seen in 50% of the healthy community. Furthermore, antibody titres to cytomegalovirus, measles virus and various herpesviruses are also often elevated in patients with CFS.
These elevations are now generally viewed as an epiphenomenon of the mild immunologic abnormalities found in some patients with CFS (see Holmes 1991:S53-55). In other words, the presence of antibodies to a range of viruses in some patients with CFS may equally likely have occurred after the onset of CFS and are due to decreased resistance of the body's immune system to a range of viruses normally present in the community.
Enteroviruses: Approximately 70 serotypes are described for this group of viruses which are members of the family Picornaviridae. Three types have been suggested at various times as having played a role in the onset of PVFS, namely: polio, coxsackie and echo. A possible role for polio virus is suggested by the experiences of the Akureyri epidemic in Iceland in 1948 (described above). Interestingly, not only was no isolate of polio made in the Akureyri group but also no outbreak of poliomyelitis occurred in the Akureyri area in 1956 (at a time when it was rampant in the remainder of Iceland). In addition, Akureyri children were found not to produce antibodies to polio 1 in 1956 but developed unusually high titres when given its vaccine, suggesting previous exposure to polio virus 1.
Kennedy (1991:809-814) alludes to a number of studies that suggest a role for the Coxsackie viruses in the causation of post viral fatigue syndrome (PVFS) and gives his support to the possibility that this virus is responsible for a number of cases of PVFS. In saying this, however, Kennedy accepts that the immunological evidence of preceding Coxsackie infection in these cases is inconsistent.
He also states that high levels of antibodies to Coxsackie B virus are widespread throughout the general community in the absence of PVFS, making the data difficult to interpret. Furthermore, Kennedy states that no plausible biological mechanism has been formulated to explain how Coxsackie viruses cause PVFS to date. The conclusion drawn by this author is that Kennedy's study provides some indirect support for Coxsackie virus infection as a possible precipitant of some cases of PVFS but does not provide support for a role for Coxsackie viruses as a causal agent for CFS.
Gow and Behan (1991:874) report an extensive study of Coxsackie antibody titres in Scotland in the 1980s which failed to confirm initial suspicions of a role for Coxsackie based on early findings of raised IgM titres for Coxsackie in a number of cases. The larger well-controlled study failed to show any significant difference in antibody titres between cases and controls. Gow and Behan's own findings in relation to Coxsackie revealed that 20% of PVFS cases had enteroviral genome for Coxsackie virus in their muscles. A similar incidence is reported by Cunningham et al (1991:858). These finding, however, are entirely consistent with the hypothesis discussed above that CFS affects the immune system and allows infection with one or more of a range of viruses ubiquitous in the community to occur, since the rate of sero-conversion in the general community approximates these levels.
Other viruses : Elevated titres of various types are reported to be more frequent in CFS patients than in the general population with the authors of the reports suggesting that these agents play a role in the causation of CFS or its variant PVFS. For example, Yamanishi (1992:2612-6) reports elevated titres of human T-lymphotropic virus (HTLV) and HTLV type II. He cites a number of studies that report an increased incidence of human herpesvirus type 6 in CFS patients as well. Lloyd et al.'s Australian study (1990:526) describes three cases where sero-conversion to Ross River virus occurred, as well as sero-conversion to EBV in two cases, mumps virus in one patient and Coxsackie B virus in another. Dowsett et al. (1990:528) report sero-conversion to a range of viruses [apart from EBV (33%) and enteroviruses (31%)] such as hepatitis A (2 cases), respiratory syncytial virus (2 cases), parvovirus (2 cases), influenza B (1 case), varicella (1 case) and rubella (1 case) within the 420 patients with PVFS in their study group.
Conclusions The existence of a wealth of studies reporting sero-conversion to a large number of agents should not be taken to mean that any of these agents have a causal role to play in the development of CFS (or even PIFS for that matter). All of the studies identified to date rely on retrospective serologic evaluation of CFS patients and extrapolate the findings to suggest that the presence of serological marker for a particular virus should be taken to mean that the agent has caused the CFS. There are obvious flaws in this type of logic that greatly weaken the conclusions drawn. Firstly, no prospective studies appear to have been conducted to date to show that infection with a particular type of virus is followed by the development of CFS. Secondly, many retrospective studies fail to recognise the possibility that CFS is the primary condition which in turn predisposes to secondary infection with any one of a range of viruses. Thirdly, most studies fail to publish regional statistics to indicate the frequency with which sero-conversion to the type of virus under consideration occurs in the healthy general population.
C. Psychiatric diseases and chronic fatigue syndrome The question of what is the exact nature of the relationship between psychiatric disease and chronic fatigue syndrome remains one of the most controversial aetiological issues concerning CFS. Despite this controversy, it is worthwhile comparing and contrasting the views of a number of authorities on different aspects of this issue.
The first aspect is whether the pre-existence or co-existence of a psychiatric illness should preclude the diagnosis. As discussed above, the support given by the CDC to excluding those with any form of psychiatric illness originally was intentionally artificial in order to establish guidelines for initial investigation. In more recent times, a number of other authorities have adopted the view that pre-existing or co-existing psychiatric disease should not exclude a person from inclusion in the CFS diagnostic group if the other criteria are met (see Holmes et al. 1988).
The second aspect is whether any form of psychiatric disease has a causal role in the development of CFS. A number of earlier papers from the United Kingdom (Wessely and Powell 1989:940-948), Canada (Taerk et al. 1987:49-56) and the United States (Kruesi et al. 1989:53-56) suggested that patients were likely to have psychological disorders before the onset of CFS, raising the possibility that CFS may occur in "psychologically vulnerable" individuals. A more recent study by Hickie et al. (1990:534-540) found that the premorbid incidence of major depression was 12.5% in those with CFS; a rate similar to estimates of major depression in the general community. Hickie et al. also found that the premorbid incidence of psychiatric disease in his control group with major depression was in the order of 62%. One other point made by Hickie et al. was that 50% of the CFS group subsequently developed a psychiatric illness, most often depression, during the course of their CFS.
The findings of Woods and Goldberg (1991:908-918) are similar to those of Hickie's group in relation to the sub-group considered to have post-viral fatigue syndrome. The classification posited by Holmes et al (1988) also supports the notion of psychiatric disease being most likely an outcome rather than a precedent for CFS. Sharpe (1991:989-1005) adds to this by recommending that in deciding whether or not a person has chronic fatigue syndrome, only those with major psychiatric illnesses such as schizophrenia, other major psychoses and manic depression should be excluded from consideration in the CFS group.
The third aspect concerns consistent differences reported in those with CFS versus those with primary psychiatric disease in relation to cognitive, psychological and psychomotor functioning. Whilst Jamal and Miller (1991:815-825) were unable to detect any consistent abnormalities for a range of neurophysiological parameters in those with CFS compared to normal controls, Behan and Bakheit (1991:793-808) describe pronounced difficulties in dealing with mental tasks requiring intense concentration and an inability to initiate and carry out any complex sequences of thought compared to those with depression. They also point out that those with CFS are not troubled by the inability to experience pleasure, including sexual libido and ability, that mark those with primary psychiatric illnesses with a component of depression.
Other features of CFS include marked sleep disturbance, irritability, lack of guilt feelings, definite forgetfulness despite normal memory function on formal testing and, in some cases, hypersensitivity to light and noise and frightening hypnogognic nightmares. One other common symptom related to sleep is pronounced nocturnal sweating.
Lloyd (1990:530-533) makes reference to a number of studies that have shown that CFS patients have unique patterns of psychological impairment not seen in patients with depression or in normal controls. For example, studies by Sandman at the University of California found that CFS patients demonstrated a unique pattern of impairment of memory recall tests, made worse by brief disruption of the test by showing a video clip. Likewise, Prasher et al.'s (1990:247-253) neurophysiological study of CFS sufferers showed prolonged latency in cognitive event-related potentials not present in patients with depression. A number of other authors also make reference to notable reductions in a range of cognitive functions in CFS patients.
The postulate that CFS leads to a reduction in psychomotor and other cognitive abilities has not been universally endorsed however. David (1991:966-988) questions the validity of the conclusions drawn by Prasher et al. and opines that similar cognitive deficits have been documented in primary depression, schizophrenia and borderline personality disorders. He cites the findings of Millon et al. (1989:131-141) and Atlay et al. 1990:141-149) that the PVFS patients they studied did not perform suboptimally on psychometric testing. David considers that further studies might serve to clarify this issue better. In light of this, it would appear to be premature at this point to recommend the use of psychometric testing as an adjunct to the diagnosis of chronic fatigue syndrome.
D. Misconceptions of the role of physical and mental stress in the development of CFS Whilst there is a common perception in the lay community that the title of Chronic Fatigue Syndrome infers a role for either mental or physical stress or both in the development of the condition, there is little evidence in the literature to support such a view. Whilst a number of authors have investigated the role of stress in relation to a number of other conditions characterised by chronic fatigue, none of these conditions appear to satisfy the criteria for CFS promulgated by the major authorities cited in this work. Several authors (Makowska et al. 1992:323-333; David et al. 1990:1199-1202) in reporting a possible role for stress make mention of self-reported domestic and family stressors as the primary source rather than work-related stress. Stricklin, Sewell and Austad (1990:31-34) in a relatively small study of 25 women identify a statistically significant difference (p less than 0.001) in the self-reported incidence of stress in those with "epidemic neuromyasthenia" (a synonym for CFS) compared to an equal number of healthy women. The study group, however, were also found to have statistically significant differences in their psychological profiles compared to the healthy group.
Cathebras et al (1993:168) suggest that people with pre-existing psychiatric conditions are more likely to report increased levels of stress. Melamed et al. (1993:469-474) define a distinctly different condition they term the "burnout syndrome" as a consequence of increased physical or mental stress or both. Ng (1992:294-295) and Waylonis (1992:343-348) note an increased level of self-reported stress in patients with fibromyalgia., a condition they hold to be distinct from other conditions causing chronic fatigue. None of the major authorities cited in this work make mention of mental or physical stress or both as having a role to play in the onset of chronic fatigue syndrome.
The popular perception of the media that the condition is more prevalent in the middle and upper social classes is not substantiated by objective analysis. Lloyd et al. (1990:522) found an equal distribution across all social classes. Wallace (1991:947) likewise has found the prevalence of CFS to be about equally distributed across the social classes, with a slight over-representation in Classes 4 and 5 (ie. lower socio-economic groups). He was unable to identify any particular sub-groups more likely to develop the disease. These findings serve to dismiss the media perjorative of "Yuppie flu" as a misnomer. As well, the findings fail to show that endemic CFS is more common in particular occupations, unlike the situation for epidemic CFS (supra vide).
There is a wide variation in the incidence of the disease with near universal acceptance that the prevalence of the condition is probably higher than reported. This is particularly so for epidemiological studies conducted using the original CDC criteria which exclude inclusion of suspected cases with psychiatric disease. Hence, Price's figure of prevalence of less than 1 in 10,000 people as reported by Kroenke (1991:44) is a gross under estimate of the true prevalence.
Lloyd et al (1991:522) suggest that the prevalence of 3.71 in 10,000 (95% confidence interval: 26.8-50.2) obtained from their Australian study is conservative. Ho-Yen and McNamara (1991:324-6) suggest a rate of 13 in 10,000 in a UK study. To date, there have been no major studies reported to suggest an increased or decreased prevalence according to region or climate.
Kroenke (1991:50) recommends the following investigations be performed routinely: complete blood count, determination of erythrocyte sedimentation rate, biochemistry profile (including electrolytes, serum creatinine and serum transaminases) and thyroid function tests.
He suggests that more elaborate investigations such as sleep studies, radiological imaging and endoscopy should be limited to only those with the appropriate clinical symptoms. Whilst Kroenke does not recommend serologic testing for Epstein Barr virus, cytomegalovirus or other viruses as a routine, it is to be expected that many patients will already have such tests done by their primary practitioner where an infectious cause is suspected (e.g. those who fulfil Wallace's criteria of "post-infectious fatigue syndrome"). Serological investigations need not be exhaustive. When patients present early in the stage of the disease (within the first two months), it may prove useful to repeat the serologic tests after six weeks to allow for more accurate interpretation of the results.
As well, there would appear to be little justification for performing highly technical imaging tests such as computerised axial tomography (CAT scanning), magnetic resonance imaging (MRI), positron emission tomography (PET), single-photon emission computed tomography (SPECT) or BEAM (a brain scan that incorporates measurements of electrical brain activity). Nor does Kroenke recommend the use of sophisticated immunologic testing or detailed neurophysiologic testing as neither have been shown to produce useful results in the ordinary clinical setting. The same can be said for psychometric assessment in light of what has been said above.
In some cases, the differential diagnosis needs to be expanded to take account of unusual presenting symptoms in addition to profound fatigue. This is especially so when a patient reports symptoms such as (1) balance disturbances, (2) claudication, (3) gastrointestinal symptoms or (4) fluid retention. The differential diagnosis in the first category should include recurrent, acute and chronic labyrinthitis. In the second category, ischaemia of the cauda equina and occult spinal multiple sclerosis bear consideration.
In the third group, occult gastro-intestinal malignancies need to be excluded. In the fourth category, fluid retention and fatigue are prominent symptoms of the fluid retention syndrome whilst fluid retention is also reported in PVFS (Behan and Bakheit (1991:801). Finally, exclusion of a range of psychiatric ailments is indicated when a patient presents with one or more psychiatric symptoms.
Kroenke (1991:53) gives some useful guidelines in this regard. He recommends that depression be treated selective by the use of anti-depressants which are non-sedating such as desipramine hydrochloride or fluotexine hydrochloride (Prozac). In severe cases, referral to a psychiatrist in the early stages is recommended. When myalgias are a major problem, non-steroidal anti-inflammatory drugs may be prescribed in the absence of contraindications.
Rest combined with a program of gentle exercise is also held to be appropriate in the majority of cases. This may necessitate a prolonged absence from work when the work duties require moderate or strenuous exertion. For those with less demanding positions, exclusion from the work place is not mandatory although long-term placement on lighter duties (for periods of six to twelve months with regular review) should be seriously considered, depending on the requirements of the work environment.
Any decision to maintain a patient in the work environment represents a balance between the severity and likely chronicity of the condition and the likely socio-economic effects of being displaced from the work force for a protracted period of time. Both Kroenke et al. (1988:929-34) and Straus et al. (1988:855-862) report lower recovery rates and a greater likelihood of clinical relapse can be anticipated in those with chronic fatigue for several years or longer.
A number of therapies have been trialed and shown to have little, if any benefit. Several other treatments are currently under investigation as to their benefits. In the former category should be included antibiotics of any type (including long-term antibiotic therapy), transfer factor (a low molecular weight protein extracted from donor leucocytes), interferons, interleukin-2, acyclovir, immunovir (inosine pranobex), immunosuppressives (such as cyclophosphamide, azathioprine and corticosteroids), vitamins, most 'special diets', treatments aimed to eliminate candida and other fungal infections (such as nystatin, ketaconazole and amphotericin B), herbal remedies, homeopathy, acupuncture, aromatherapy, reflexology, colonic irrigations and a number of other pseudo-medical therapies (McBride and McCluskey 1991:904).
In the second category, the evidence that they alter the course of the disease is either minimal or has yet to be substantiated in properly designed and controlled studies. Therapies that fall in to this category include supervised diets aimed to eliminate salicylates, amines and glutamate (Loblay and Swain 1986:169-177), ampligen (mis-matched double-stranded RNA), intravenous therapy with pooled immunoglobulin, calcium blocking agents to counter exercise-induced fatigue and amantadine (McBride and McCluskey 1991:897-880). In the absence of solid evidence that any of these therapies significantly alter the course of the disease, none are recommended for the treatment of CFS at this point in time.
The course of CFS is highly variable, depending on the severity of the condition and the premorbid state of the patient. Convalescence is widely accepted as being aided by ensuring adequate rest in conjunction with a supervised regimen of gentle exercises. Lloyd et al. (1990:522) found that 43% of CFS patients in their study group were unable to attend to work, housework or school during the course of their illness. Aggravating factors of established CFS as reported by Dowsett et al (1990:527) include physical and mental stress (100%), intercurrent infection (42%), climactic changes or hot baths (12%), surgery, immunisation and hormonal disturbances (9%) and psychoactive, anti-arthritic or steroid drugs (5%).
Gold et al. (1990:48-53), and Kroenke and Mangeldorff (1989:262-266) found that 40 to 50% of patients show improvement within 12 months but do not indicate if this meant complete recovery. Kroenke et al. (1988:929-934) and Straus et al. (1988:1692-1698) indicate that lower recovery rates and a higher rate of clinical relapse can be anticipated for those who have fatigue for several years or longer.
The Green College working group indicate a similar prognosis. Behan and Bakheit (1991:801) agree with Kroenke that whilst it is difficult to give general guidelines for all PVFS patients, their experience has been that when the illness has been present for a year or more than the prospects of a full recovery are generally poor. The numbers who enter this state are reported to be but a small group of all PVFS patients. A larger number are reported as undergoing complete remission whilst the majority of patients are reported as being able to lead a life wherein they are able to modify their lifestyle and work environment so as to avoid stresses likely to make their illness worse. Interestingly, they report a number of female patients who entered a remission during pregnancy with relapse during the puerperium.
Similar figures are given by Dowsett et al (1990:527) in reporting the outcomes for a group of 420 CFS patients. They found that the duration of the illness was less than 12 months in 9% of cases, 1 to 2 years in 32% of cases, 3 to 10 years in 47% of cases, 11 to 20 years in 8% of cases and 21 to 60 years in 4% of cases. The illness was reported as improving in 31%, fluctuating in 20%, a steady level of disability in 25% and no remission or worse in 24%. No indication is given as to whether or not any of the 420 patients were beneficiaries of disability income support.
There appear to be two main forms of chronic fatigue syndrome, epidemic and endemic. The history of the former group has been reviewed at length in this paper. For a number of reasons, it is not clear whether epidemic CFS is the same disease as endemic CFS; for the purpose of this work the two groups are held to be distinctly different. Accordingly, this author is of the view that the conclusions drawn here are relevant to endemic CFS but may not hold true for the epidemic form of the disease. A key distinction between the two groups is that, whilst there is a body of evidence that epidemic CFS is caused by a transmissible agent (as evidenced by the numbers of hospital staff affected in a number of epidemics), there is no good evidence to suggest that the endemic CFS is transmissible.
Using the Green College working group recommendations, endemic CFS (which they term "post viral fatigue syndrome" or PVFS) is held to encompass two sub-groups, namely one comprised of patients with disease of spontaneous onset (which they term "chronic fatigue syndrome" or "CFS") and another consisting of patients proven to have an infection associated with the onset of chronic fatigue (which they term "post infectius fatigue syndrome" or "PIFS"). For the purpose of this paper, the British term "PVFS" is held to be entirely synonymous with the term CFS used in other countries in the world. A number of authorities suggest that a range of viruses and other infections may be responsible for the onset of CFS. The viruses considered by proponents of this hypothesis are ubiquitous in the community and in almost every case cannot be said to relate to exposure to a particular environment or particular type of occupation.
There is also a contrary body of medical opinion which suggests that any infective agents found to be present have not caused CFS but rather are secondary or coincidental to its manifestation. An plausible, alternative explanation is that CFS is a condition of spontaneous onset which manifests in a way similar to viral infections.
Under such a model, the identification of a particular viral strain is held either to be coincidental to the condition or is a secondary event which follows changes in the patient's immune system as a result of CFS. Recent research findings are consistent with this counter view.
In light of this, any claims that the onset of CFS was as a result of an infection acquired in the work place should be treated as speculative unless (a) the claimant has serological evidence to indicate recent infection with a particular viral agent and (b) there is unequivocal evidence of an epidemic infection within the work place with the type of viral agent infecting the claimant. It is recommended that claims based on alleged infections acquired traveling to and from work should generally fail. Likewise, it is recommended that claims in which it is alleged that an infection is unique to a region to which the claimant has been posted or were acquired during the course of work-related travel should be treated with scepticism unless the conditions of (a) and (b) above are both satisified.
There is no evidence that heredity, genetic or developmental factors play a part in the onset of CFS. Nor is there any consistent evidence that the condition is associated with particular types of occupation, lifestyle, mental or physical stress or pre-existing psychiatric illness. All of the studies of patient characteristics fail to report an increased incidence in any one occupational group, social class or region. The evidence that stress has a contributing role is considered to be equivocal. In particular, there are no studies to show a role for work-related stress in the development of CFS. None of the authorities reviewed here make mention of either physical or mental stress as a cause of CFS. The findings of Dowsett et al. that those with existing CFS report aggravation of their symptoms when exposed to strenuous exercise, other physical stresses and mental stresses is expected, given the nature of CFS and its widespread effects on physical and psychological function.
The onset of psychiatric illness in CFS is shown to be secondary to the impairment of body function in general and the chronic pain that is part of the condition. There is little, if any, evidence to support a role for any form of psychiatric illness or personality type in the onset of chronic fatigue syndrome.
Investigation of CFS patients is aimed mainly at excluding other illnesses as the cause of fatigue. There are no tests which can be considered to be diagnostic of the condition. Accordingly, there would appear to be no justification for undertaking sophisticated serological investigations nor highly technical radiological investigations in the ordinary course of investigation of the disease unless there are good reasons to suspect a serious occult disease (such as malignancy) as the cause of fatigue.
Treatment of the condition is aimed at ensuring an adequate degree of rest in conjunction with a supervised course of gentle graded exercises throughout the course of the illness. Treatment of specific symptoms such as muscle pains and depression are recommended as being appropriate but the use of narcotic and other addictive forms of medication would appear to be inappropriate in all cases. A range of other therapies have been trialed at various times but none have yet to be shown to offer any particular benefit.
Whilst it is not possible to provide specific guidelines to assist in determining the prognosis of individual patients, there is reasonable uniformity of opinion that an improved prognosis is associated with early treatment (including work and lifestyle modifications). Conversely, when the illness is severe or has been present for more than one year or both, the prognosis is generally held to be poorer. Accordingly, early identification of CFS patients is important. In many cases, temporary removal from the work place is recommended (especially those with severe disease) until there is good evidence of a sustained recovery. For the remainder, it is recommended that placement on lighter duties and/or reduced working hours be initiated early in the course of the illness. Unless the patient has severe disease however, there would appear to be little justification for recommending mandatory removal from the work place if the person is not required to undertake moderate or strenuous duties and if suitable changes to the work environment can be made.
Dr Peter Grant pgrant@gil.com.au
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From: Jef Vde nvdeynde@xxxxxxxxx.xxx
Date: Sat Jan 8, 2000 9:16am
Subject: Fw: San Diego Union-Tribune: Antibiotic May Defeat Gulf
War Syndrome-4 articles, 4/14/99
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Datum: zaterdag 8 januari 2000 16:10
Onderwerp: San Diego Union-Tribune: Antibiotic May Defeat Gulf
War Syndrome-4 articles, 4/14/99 Mycoplasma Registry for gulf war
illness & chronic fatigue syndrome
Sean & Leslee Dudley
303 47th Street, J-10
San Diego, CA 92102-5961
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FRONT PAGE OF THE SAN DIEGO UNION-TRIBUNE APRIL 14, 1999
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VETERANS SET TO BEGIN TRIALS OF MEDICATION HERE, ACROSS
U.S.
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- Eight years after the Persian Gulf War, the government is about to start testing a simple antibiotic as a possible cure for the mysterious health problems plaguing many veterans of that conflict. Ailing veterans in San Diego and across the country will receive the antibiotic in a major scientific trial, based on the theory that bacterial infection may cause at least some cases of the so-called Gulf War syndrome. Specifically, the researchers will be looking for strains of a very small, little-understood type of bacteria, called mycoplasma.
A MYSTERIOUS MALADY WITH BAFFLING ORIGINS
Finally, the military is focusing on a likely cause of Gulf War syndrome. If mycoplasma is the culprit, that's good news: It's treatable. And it's bad news because it means the debilitating illness is probably contagious -- as some military families already are convinced -- and may well be spreading among nonmilitary communities. "We're not dealing with a black plague," said Dr. Charles Engel, director of the Gulf War health center at Walter Reed Army Medical Center in Washington D.C. "Most people feel relatively comfortable it is not infectious in the way that would result in some sort of catastrophic epidemic. "But it may well be that we'll find out micro-organisms are responsible for a lot of these multisymptom illnesses." Beginning this month, Gulf War veterans can sign up -- at 30 military and veterans' health centers, including one in San Diego -- for the antibiotic study or another study testing exercise and behavior-change counseling. They are the first potential treatments to be tested for the complex of symptoms afflicting an estimated 100,000 of the 700,000 troops who were deployed in the war against Iraq. The condition is marked by extreme fatigue, joint and muscle pain, concentration and memory problems, rashes, fever, diarrhea and other symptoms that last six months or more. For years, Gulf War veterans complained that their health problems were not taken seriously or were considered psychological. Now, the Defense Department and the Veterans Affairs Department have about 120 projects under way trying to pin down the cause, characteristics and prevalence of the illness. The two departments are spending a combined $20 million to investigate treatments -- $8 million for the antibiotic trial and $12 million to buy exercise equipment and pay therapists for the second study. The idea that Gulf War illness is infectious still faces skepticism five years after it was first proposed by a maverick biochemist, Garth Nicolson, now based in Huntington Beach. Instead, some scientists suspect veterans are experiencing reactions to chemical exposures, stress or a mixture of wartime conditions. But Nicolson reports finding Mycoplasma fermentans, a species of the smallest type of bacteria, in the blood of almost half of the 600 sick Gulf War veterans he has tested. He also finds the bacterium in almost all family members of infected veterans who share the symptoms, he said. And, most significantly, he reports that getting rid of the mycoplasma usually makes the veterans feel much better. In 1995, Nicolson began publishing his discovery in a variety of scientific journals that the common antibiotic doxycycline helped Desert Storm veterans recover and cleared M. fermentans from their blood. Of those he has monitored, 75 percent have fully recovered, he said. "The hypothesis is plausible. It could be true," said Engel, one of the leaders of the Pentagon and VA study. "But most of the evidence Mr. Nicolson has presented is in a very preliminary state. Usually a trial like this, that involves treatment of people, wouldn't go forward based on this level of evidence."MOVING FAST
In this case, the researchers say, political and public pressure has speeded up science, so that a potential treatment and cause are being tested at the same time. "We want this study done quickly," said Dr. Sam Donta, an infectious disease specialist at the Boston Veterans Affairs Medical Center who is heading the study. "If it works, it will spawn additional studies." And if it doesn't work, that won't necessarily eliminate mycoplasmas as the cause, Donta said. "We may not have the right drug or the right dose. You've got to start someplace." Nicolson said the official study of his methods is long overdue and may not be designed well enough to find accurate answers. "As a first step, it's OK," he said. "I'm not entirely satisfied with it. I have concerns about the statistical analysis." A former department chairman at a renowned cancer research center in Texas, Nicolson has a role in the government's study. He taught the researchers the technique he developed for finding mycoplasma in blood, and he will recheck their results on 10 percent of the blood samples tested. Only veterans who test positive for mycoplasma can participate in the antibiotic study. Others who are sick probably are suffering from other infections or toxic exposures, Nicolson said. He believes those same factors, along with the multiple vaccines given before deployment, could have weakened some troops' immunity enough to let mycoplasma infection take hold. The organism may have been present in the gulf either as a biological weapon or as a normal part of the bacterial stew carried in some people's respiratory tracts. It can ride there harmlessly unless impaired immunity allows it to infect the blood system, one theory goes. Nicolson believes M. fermentans is an airborne bug and "moderately contagious," striking mostly at people with weakened immune systems. Some species of mycoplasma are known to be transmitted in saliva or through coughing and sneezing, and there's some evidence that fermentans may be spread in similar ways, said Joseph Tully, chief of mycoplasma research for the National Institute of Allergy and Infectious Disease in Bethesda, Md. However, he said the evidence is not yet strong enough to warrant concern about an epidemic. "At this point, I don't think that's a real risk," Tully said. "But I tell people, I just don't know."
VETERAN'S VIEWS
Among many veterans' families and advocacy groups, there is no doubt the illness is contagious. Joyce Riley, an Air Force Reserve nurse from Missouri, tracks more than 10,000 sick Gulf War veterans through the American Gulf War Veterans Association she founded five years ago. She said at least 80 percent of them have family members who also are sick enough to seek medical treatment. "We know it's communicable," Riley said. "We're very concerned about the spread of this disease." But Engel said relatively few family members have sought care at VA and military medical clinics. The family members who are sick could have chronic fatigue syndrome, or fibromyalgia syndrome, two other disorders with very similar symptoms, he said. The VA now is trying to determine whether those families have more such disease than the general population. One major VA study is exploring whether the illness has spread to veterans' spouses and children, but results are not expected for another two years, said Timothy Gerrity, the VA's chief research and development officer. The antibiotic study starting this month will include 450 Gulf War veterans who test positive for M. fermentans. Half of them will take doxycycline daily for a year, while the other half will take a phony pill, or placebo. No one will know who is taking which until the study is over. All participants will be retested for mycoplasma infection after six months, again after taking the drug for a year and once again six months after they finish the drug. Donta said he also hopes to give doxycycline to a smaller group of veterans who are sick, but don't have mycoplasma infection. If they get better, the problem could be one of the many other micro-organisms vulnerable to the antibiotic. Doxycycline, a member of the tetracycline family, is among the most commonly used antibiotics, said Dr. Gregory Gray, of the Naval Health Research Center on Point Loma, who is leading the study locally. He said many people take it for years at a time to treat acne. It may be difficult to get veterans to sign up for the study, the researchers admitted, because many can get doctors to prescribe doxycycline for them and they may not want to risk the 50 percent chance of wasting a year on a placebo. "We'd like to appeal to veterans on behalf of the larger veteran community," Engel said. "This is a unique opportunity for them to provide scientific information regarding a treatment that is potentially helpful to other veterans."
ANOTHER APPROACH
The second study starting this month will test whether exercise and "cognitive behavioral therapy" -- either separately or in combination -- can ease the veterans' symptoms and improve their physical functioning. The study will involve 1,360 veterans, including an expected 68 in San Diego. Some will undertake an aerobic exercise program, some the cognitive therapy, some will get both and some neither. Engel, a psychiatrist and epidemiologist, said he has been using both types of therapy at the Walter Reed center for four years. He said the patients generally have "a very slight reduction" in physical symptoms and a greater reduction in their distress. "Most Gulf War veterans come here very actively concerned about many health issues," Engel said. "The concern they have . . . is becoming one of the more debilitating aspects of their illness." Cognitive behavioral therapy uses relaxation techniques, guided imagery to relax muscles and patients are gradually encouraged to resume activities they believe they can't do, Engel said. "We're not trying to tell them this is in their head," he said. "Rather than reassuring them, you help them design their life." In the next few weeks, notices are expected to be mailed to many veterans and veteran organizations, seeking volunteers for both studies. The local Naval Health Research Center has set up a special phone line for interested veterans to call, (619) 524-0069. Eligible veterans can choose which study they want to take part in, Gray said.
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For more information:
Gulf War veterans who wish to volunteer for the studies using antibiotics, exercise or cognitive therapy can contact the Naval Health Research Center after April 19 at: (619) 524-0069 Military research about Gulf War syndrome: http://www.nhrc.navy.mil/. U.S. Centers for Disease Control and Prevention: http://www.cdc.gov/. Garth Nicolson's research: http://www.immed.org/.------------------------------------------------------------------------- ------------------------------------
© Copyright 1999 Union-Tribune Publishing Co.
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GERM OF AN IDEA FINALLY, THE MILITARY IS FOCUSING ON A LIKELY CAUSE OF GULF WAR SYNDROME
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- Lean, mean and evasive as a stealth fighter, a stripped-down, parasitic mini-bacterium has emerged as a prime suspect in the disabling illnesses that continue to dog veterans of the Persian Gulf War. Prodded relentlessly by one very determined biochemist, the military and the Department of Veterans Affairs are spending $8 million to test whether Gulf War illness can be cured with antibiotics and whether it may be, at least in part, caused by a barely known species of an exceedingly tiny bug, Mycoplasma fermentans. If the treatment works and the mycoplasma disappears from treated veterans' blood, the study may solve a highly controversial medical mystery that has dragged on for eight years. The results also may have profound implications for a number of other infectious diseases. Mycoplasmas, a large family of the smallest and simplest bacteria, have been known for decades to cause some plant and animal diseases. Some strains have been implicated in a variety of human disorders -- including AIDS, rheumatoid arthritis and infertility -- but the bug is so tricky to find that proof is scarce. In the last five years, Garth Nicolson, a biochemist based in Huntington Beach, has brought the species Mycoplasma fermentans to the forefront of the search for what ails more than 100,000 Gulf War veterans. Since his stepdaughter returned ill from service in the gulf -- and he then became sick himself -- Nicolson has tested the blood of hundreds of sick Gulf War veterans and their families. He reports finding M. fermentans in 45 percent of the veterans tested, compared with fewer than 10 percent of healthy people. Among family members who share the veterans' symptoms, almost all have the microorganism in their blood, he says. The sick veterans who aren't infected with mycoplasma probably are suffering from chemical exposures or other infections, Nicolson believes. In many cases, he said, multiple infections and toxic exposures work along with mycoplasma to overburden the immune system and produce the collection of symptoms known as Gulf War syndrome. Those symptoms -- joint and muscle pain, extreme fatigue, memory loss, rashes and many other problems -- are shared, in differing proportions, with chronic fatigue syndrome and fibromyalgia, two illnesses of unknown cause. Nicolson said he finds M. fermentans in 60 percent or 70 percent of people with those diagnoses who come to him for testing. "There's no such thing as Gulf War syndrome -- there's no distinct syndrome," he said. "We have millions of civilians with similar symptoms." If his theory is right, how did so many Gulf War veterans become infected with mycoplasma at once? That's where Nicolson makes other scientists nervous: He believes that the organism was used as a biological weapon and may also have been contained in vaccines given to soldiers, either through accidental contamination or inept experimentation by the U.S. military. Military scientists say there is no evidence that biological weapons were used or that vaccines were unsafe. Another possibility, more plausible to bacterial experts, is that the toxic exposures and other stresses of warfare lowered soldiers' immune resistance enough that mycoplasma, normally dormant in some people's respiratory tracks, became actively infectious and then spread among the troops. "We think that there were multiple sources of Mycoplasma fermentans," Nicolson said. "It doesn't matter; they've got it. Let's treat it." And Nicolson believes he has found an effective treatment, the antibiotic doxycycline. He said three-quarters of veterans with M. fermentans infection recover fully after lengthy treatment with doxycycline or other antibiotics. And, with treatment, the mycoplasma vanishes from their blood. Other scientists are suspicious because most of Nicolson's results have not been duplicated in other researchers' tests and have not been published in the most reputable scientific journals. But they are intrigued enough -- as are members of Congress who pushed through funding for the study -- to not only test his theory but immediately begin testing his treatment. "I think you'd have to believe it's probably more real than not," Dr. Sam Donta said of the mycoplasma theory of Gulf War illness. "We can't just keep waiting for more and more evidence while people continue to suffer." Donta, an infectious diseases specialist at the Boston Veterans Affairs medical center, is leading the $8 million national antibiotic treatment study for the VA and the Department of Defense. The Naval Health Research Center in San Diego is one of 30 centers that hope to each sign up 15 veterans for the study. The participants' blood samples will go to Joel Baseman, chief of microbiology at the University of Texas Health Sciences Center in San Antonio, for mycoplasma testing before and after they take antibiotics for a year. "This theory is without enough substantiated proof and, on the other hand, it's very provocative," Baseman said. "This is certainly a leading theory . . . a hypothesis that really needs to be clarified. I'm excited about it." However, there is some evidence discrediting the theory. Dr. Shyh-Ching Lo, chief of molecular pathology at the Armed Forces Institute of Pathology in Washington, D.C., tested veterans' blood when Nicolson first proposed the idea in 1994, and found M. fermentans in only 1 percent, the same rate he found in non-veterans. Nicolson argues that Lo's testing technique is not sufficient to find the organism inside cells. The VA study will use Nicolson's method. Lo has been arguing for 10 years that M. fermentans plays a role in AIDS, but he does not believe that the microbe causes Gulf War illness. The culprit, he said, might be an as-yet-undetected species of mycoplasma. "Mycoplasma infection potentially can cause all different kinds of mysterious symptoms . . . often chronic, debilitating illness," Lo said. "It sounds like a good candidate, but we have to see some evidence."
THE VAST UNKNOWNS
The idea that a bacterium could cause the chronic illnesses of Gulf War veterans fits with what Baseman calls "an infectious disease rebirth" now under way. In recent years, bacteria increasingly have been accused of causing diseases previously considered non-infectious; one bacterium is now known to cause ulcers and another looks guilty of promoting atherosclerosis, the clogging of arteries in heart disease. Mycoplasmas are among the most streamlined of bacteria, nearly as small as viruses. The tiny organisms don't even have a cell wall, just a thin outer membrane. They burrow inside cells, where they are tough to find and tougher still to fight. Previously considered primitive and not very dangerous, they now are thought to be all the more sinister because of their simplicity; they lack many of the ingredients needed for replication and must scavenge them from inside cells. "It forces them to be very sophisticated pathogens, because they need the host cell completely in order to survive," Baseman said. In addition, mycoplasmas' simplicity helps them to evade antibiotics. The drugs normally kill bacteria by targeting certain molecular processes -- such as cell wall development -- that most bacteria have, but that mycoplasmas do not. Mycoplasmas simply use the apparatus of the cells they invade rather than carrying around their own, making them very slim targets. For that reason, antibiotics can only slow the parasitic organisms, leaving it up to the immune system to finish them off, said Joseph Tully, chief of the mycoplasma lab at the National Institute of Allergy and Infectious Diseases, a part of the National Institutes of Health. That makes mycoplasma infection particularly dangerous for anyone whose immune system is weakened by disease or, as in transplant cases, must be held in check with drugs, Tully said. Exactly how mycoplasmas damage cells once they are inside -- whether they excrete toxins, steal the cell's nutrients, trigger autoimmune reactions by mimicking the cell wall or all of the above -- isn't well understood. Scientists who have spent much of their careers studying mycoplasmas believe that they are just beginning to discover what harm the organisms can do. Those discoveries have been easier in recent years because of the development of a diagnostic technique called polymerase chain reaction (PCR). It is used to find and amplify genetic traces of the organism, which is very difficult to culture and grow to measurable amounts. The evidence to date is sketchy but sobering: In 1989, Lo and colleagues at the Armed Forces Institute of Pathology fingered M. fermentans in the mysterious deaths of six previously healthy adults from different geographic regions who had developed flulike symptoms and died within a few weeks. The pathologists found the microorganism in many of the victims' internal organs and could not find signs of any other type of infection or disorder. Some prominent AIDS researchers believe that M. fermentans paves the way for the human immunodeficiency virus to cause AIDS, and may even be a necessary accomplice. A decade ago, Dr. Luc Montagnier, a French scientist who first identified the human immunodeficiency virus, announced that theory and fought for several years to have it tested. Lo reached the same conclusion as Montagnier when he found M. fermentans in the brain, blood and other tissues of AIDS patients but not in healthy people. He believes that attacking the mycoplasma with antibiotics could protect many HIV-infected people from developing AIDS. But no one has been able to get funding to study that theory, Lo said, because of stiff resistance from the many AIDS experts who believe that HIV is the sole cause and mycoplasma just a secondary, opportunistic infection. "We treat AIDS patients when they have (other) opportunistic infections," Lo said. "We believe the mycoplasma is pathological. . . . it needs to be diagnosed and treated. The HIV proponents say, 'It's just mycoplasma.' It's very absurd." Other researchers, since 1993, have found a new species, Mycoplasma penetrans, almost exclusively in the urine of HIV-infected patients, raising the possibility that it also may contribute to AIDS. In new research published last summer, Lo and a group of New Jersey doctors showed that the presence in the genital tract of another species, Mycoplasma genitalium, makes transmission of HIV from one person to another much more likely. The researchers compared 302 heterosexual couples in which at least one partner was infected with HIV. They found Mycoplasma genitalium more than twice as often among couples who shared the infection as among those in which one partner resisted infection over several years. Many other potential variables were tested; herpes infection was the only other difference that seemed to increase the risk of transmitting HIV. Again, Lo believes that antibiotic treatment for people infected with HIV could be a relatively easy way to control the spread of the virus. In 1996, researchers in London verified an idea first suggested in 1970, that M. fermentans is present in the joint fluid of at least one-fifth of rheumatoid arthritis patients tested. Several other studies now have shown that those patients improve and the swelling of their joints diminishes when they are treated with antibiotics known to inhibit mycoplasma, said Tully, the NIH mycoplasma chief. "I think it is a cause of arthritis," Tully said. "It's not there (in the joints) normally." Nicolson and his colleagues also found at least one -- and usually more -- species of mycoplasma in the blood of about half of rheumatoid arthritis patients they tested. The results are expected to be published next month in the British Journal of Rheumatology. There also is evidence, Tully said, that mycoplasmas may cause infertility in some people by infecting either sperm or ova. Mycoplasmas are known to cause infertility in many animals, a problem first discovered in bulls, he said. Infertile couples should be tested for the bacteria and possibly try a course of tetracycline-like antibiotics before they embark on expensive fertility treatments, Tully said. Mycoplasma infection has become a serious threat for transplant recipients, who must take drugs to suppress their immune systems so they will not reject the transplanted organs, and for other people with genetically deficient immune systems. Even "bucketsful of antibiotics" can't completely kill mycoplasmas without the help of immune defenses, Tully said. In several cases published in scientific journals, children and adults with suppressed immune systems have needed years of multiple high-dose antibiotics to control mycoplasma infections. With their defenses down, some have become infected with strains they had carried as part of the normal human bacterial mix and some with animal strains they acquired when bitten or licked by cats or dogs. In 1996, doctors in Denver reported that two lung transplant recipients became infected with mycoplasma carried in the tissue of a donor lung. They each had received half the lung. Both survived, with long-term antibiotics. Starting in 1995, Nicolson and Dr. Darryl See, an immunologist formerly at UC Irvine, have separately reported finding high levels of M. fermentans in the blood of chronic fatigue and fibromyalgia patients. Last year, Nicolson reported at a chronic fatigue conference in Australia that he had found M. fermentans in 41 percent of 203 chronic fatigue and fibromyalgia patients and other mycoplasmal infections in an additional 30 percent, while 32 healthy control subjects had no such infections. Some chronic fatique patients have reportedly taken the antibiotic and gotten better, but Nicholson said he has not followed their cases systematically. A Beverly Hills company, Immunosciences Lab Inc., published a study last year finding M. fermentans in 32 of 100 chronic fatigue patients tested and in only eight of 100 healthy people. Lo, using a slightly different test, said he has not found significant amounts of M. fermentans in the blood of chronic fatigue patients he has tested. Mycoplasma fermentans was found in the bone marrow of children with leukemia in the 1970s, but a connection with the cancer has not been further established. In a 1995 study, long-term mycoplasmal infection in mice led to cellular changes that resulted in tumor growth. A species called Mycoplasma pneumoniae has been known since the 1960s to cause a relatively mild form of pneumonia, often called walking pneumonia, as well as other respiratory diseases. It is contagious through airborne particles. In addition, a number of animal and plant diseases have been traced to mycoplasmas. The microorganisms have killed palm trees and alligators. The first mycoplasma was identified in French cattle a century ago. Many insects have their own species of the bug, and some can spread it to plants. Insect transmission to humans has never been shown. Nicolson firmly believes that M. fermentans can be spread in airborne particles, and that it is most likely to infect people whose immune systems are stressed or genetically weak. That's plausible, other scientists say, but the evidence is not in.
GENETICALLY ALTERED
Nicolson reports finding a genetic alteration -- the addition of one gene from HIV -- in the mycoplasma he finds in Gulf War veterans but not in other people, such as chronic fatigue patients. Therefore, he believes that the organism may have been altered for use as a biological weapon. Other scientists scoff at that conclusion, partly because mycoplasma is too slow-acting to be very effective at disabling soliders on the battlefield. Nicolson, who has solid scientific credentials as former chairman of tumor biology at the prestigious University of Texas M.D. Anderson Cancer Center in Houston, shifted to mycoplasma research after his personal experience convinced him that Gulf War illness was contagious. His stepdaughter, Sharon, a helicopter crew chief in the Gulf War, returned home in 1991 and gradually became disabled with muscle, joint, vision and cognitive problems. When both Nicolson and his wife developed similar symptoms, he began looking for an infectious agent and experimenting with antibiotics. After months on an antibiotic called doxycycline, all three family members recovered. At first, Nicolson used a gene tracking technique developed by his wife, molecular biophysicist Nancy Nicolson, to identify M. fermentans inside cells. Now, he said he uses a method called forensic PCR, which he developed with another former University of Texas biochemist, Marwan Nasralla. Pressured by the university to halt his unorthodox work, Nicolson left Texas in 1996 and came to Orange County to found his own research center, the Institute for Molecular Medicine. Gulf War veterans and others with similar symptoms come to him from all over the country for mycoplasma testing, usually paying $400 to be tested for four species. Not a physician himself, he provides a list of doctors who are willing to prescribe doxycycline for the condition. Other scientists caution that the drug works against other infections as well, so its success does not prove mycoplasma's culpability in Gulf War syndrome. For that reason and others, they say, the new systematic, placebo-controlled study is urgently needed. Although results are not expected for at least a year, researchers said the study was moving very quickly by normal scientific standards because of the intense political interest. "People are willing now to examine mycoplasma more closely for possible associations with disease," study chief Donta said. "We know next to nothing about fermentans. It should be pursued."
© Copyright 1999 Union-Tribune Publishing Co.
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A MYSTERIOUS MALADY WITH BAFFLING ORIGINS
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- During the worst years, she sprouted skin tumors and ballooning moles, and some days she couldn't summon the concentration to pay the bills. Her husband was hospitalized with pneumonia and had trouble remembering his address. Her children were covered with sores and rashes. The whole family repeatedly suffered from high fevers, wracking coughs, painful joints, exhaustion and various unexplained ailments. The family dog and two cats also started coughing, and died. That was before Carol (her name has been changed) discovered doxycycline, the antibiotic now being tested by the U.S. government as a possible treatment for Gulf War illness. The North County couple -- who feared repercussions if their real names were revealed -- consulted with biochemist Garth Nicolson about five years ago and began taking doxycycline on his recommendation. All four family members improved on the drug, she said, but they still must get new prescriptions every few months when the symptoms return. "None of us have been completely cured from it, but we have learned to manage it," she said. Carol said her husband, a 30-year-old former marathon runner who never even got the sniffles, came home from the Gulf War in 1991 sick and disoriented. "When he came home, within three days I knew something was wrong. He just couldn't think," she said. "There was a time when I wouldn't let my children go with him in the car, because I didn't know if he'd remember where he lived." A Navy officer, he left the military and took an office job, which still exhausts him completely, she said. She and their two young children also got sick shortly after he returned home, although her husband was hardest hit. "My family got sick from my husband," Carol said. "We've had all the symptoms." She also is certain that her family has spread the illness to some friends and relatives. But she has tired of trying to tell them so and being ridiculed. "As soon as you talk to people about this stuff, they look at you like you're a wacko," she said. "People don't want to understand it. Ignorance is bliss." The U.S. Centers for Disease Control and Prevention has identified 35 symptoms associated with Gulf War illness. Grouping the major symptoms into three categories -- fatigue, mood/cognition and musculoskeletal -- the CDC researchers developed a working definition for diagnosing the illness: having at least one chronic symptom from at least two of the categories. In a survey of 3,700 Air Force veterans published last fall, the CDC found that 45 percent of those who had been deployed in the gulf met that definition, as did 15 percent who had not been to the gulf. The researchers termed the condition "chronic multisymptom illness." They noted that it "is accompanied by significant decreases in functioning and well-being." The most common symptoms, which usually lasted more than six months, were: sinus congestion, headache, fatigue, joint pain and stiffness, difficulty remembering or concentrating, difficulty sleeping, abdominal pain and bloating, trouble finding words, irritability, rashes or sores, numbness or tingling, muscle pain, depression, diarrhea, sore throat and cough. One San Diego couple, Sean and Leslee Dudley, say they had all those symptoms and more. As many Gulf War veterans have anecdotally reported, they complained of vision problems and extreme sun sensitivity, as well as mental incapacity. "We didn't have brains," Leslee Dudley said. "It was terrifying, to be that mentally helpless." Testing by Nicolson showed that the Dudleys, like Carol and her husband, both were infected with the bacterium Mycoplasma fermentans, which the military is now investigating as a possible cause of Gulf War illness. And both got better on doxycycline. But neither of the Dudleys was ever anywhere near the Persian Gulf. They believe they caught Gulf War illness from Marines who frequented the Cousins Warehouse store where Sean worked, around the corner from the Marine Corps Recruit Depot on Pacific Highway. And, since they got sick a year before Desert Storm, they believe that the Marines were infected beforehand through contaminated or experimental vaccines. That theory raises hackles among scientists studying Gulf War illness, who say that vaccines are screened for mycoplasmas and that there is no evidence of widespread illness among military personnel before the war. Still, the Dudleys have become outspoken advocates for increased research into the baffling condition. Two years ago, they started a registry of people who have mycoplasma infection and the symptoms. The list now is up to 900 names, about a third of them from the San Diego area, they say. Only 16 percent are Gulf War veterans and their families. "We have lawyers, musicians, waitresses, receptionists," Leslee Dudley said. "Most are too sick to be working anymore. Some are homeless. It's slowly going through our communities and everyone is just quietly dropping out." Christian Heineke of San Diego has been extremely ill since he returned from the gulf in 1994 but said he hasn't passed the disease to his girlfriend, roommates or anyone else. However, Heineke believes that he may have caught it from Marines with whom he worked. He was never on the front lines; he spent three years as a welder on a Navy ship docked in Saudi Arabia during and after Desert Storm. He fought exhaustion and other mysterious symptoms the whole time, he said, and spent six months in bed when he returned. "It makes you feel like hell every day," he said. "You just don't feel like you even want to live. I was developing arthritis and I was only 23. I couldn't surf, I couldn't lift weights, it felt like all my joints were on fire." VA doctors said he was depressed and offered Prozac. Instead, Heineke went to Mexico and bought the antibiotic doxycycline, which he had heard that other veterans were using. He improved, found a part-time job as a nurse's aide and got insurance coverage and a prescription for the antibiotic. He has been taking it every day for 21/2 years. "The days I don't take it are the days I get sick," he said. "I'm much better now. I have my strength back and most of my memory has come back. I still get asthma and bad joint pain." Carol said her family also is beginning to accept that their lives are permanently changed by the illness. "We have to face the fact that we're never going to be the same," she said. "Our minds don't work the same as they used to; it's like if you got old real quick." "It's a nightmare. And it hasn't ended yet."
© Copyright 1999 Union-Tribune Publishing Co.
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LETTER TO THE EDITOR OF SAN DIEGO UNION-TRIBUNE (mailed but not published)
April 15, 1999
Dear Editor,
We wish to thank the Union-Tribune for its excellent articles on Gulf War Illness. Susan Duerksen did a great service for both military veterans and civilians who have this disease but have had no hope until now. We would like to thank Congressman Bob Filner for supporting the Nicolsons and for making sure the VA study went forward. Mr. Filner has been a leader in Congress on Persian Gulf War Illness and was honored as "Legislator of the Year" for his efforts on behalf of these veterans by the National Gulf War Resource Center. As the senior Democrat in the Veterans' Affairs Benefits Subcommittee, he is working to schedule a hearing this year in his Subcommittee on causes, treatments and compensation of Persian Gulf Illnesses. The VA study is a good first step. Our community needs to move quickly with private funding in order to stop this epidemic. Medical research, blood tests and medications are urgently needed by those people who will not be part of the study, including women, children and homeless Vets who go untreated and suffer needlessly. Drs. Garth and Nancy Nicolson performed an extraordinary breakthrough in finding one of the causes of Gulf War Illness, Chronic Fatigue Syndrome and Fibromyalgia. Their pioneering mycoplasma research needs San Diego's support to continue.
Sincerely,
Sean and Leslee Dudley
Mycoplasma Registry for Gulf War Illness & Chronic Fatigue Syndrome
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From: Jef Vde nvdeynde@xxxxxxxxx.xxx
Date: Sat Jan 8, 2000 9:16am
Subject: Fw: San Diego Union-Tribune: Antibiotic May Defeat Gulf
War Syndrome-4 articles, 4/14/99
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Datum: zaterdag 8 januari 2000 16:10
Onderwerp: San Diego Union-Tribune: Antibiotic May Defeat Gulf
War Syndrome-4 articles, 4/14/99 Mycoplasma Registry for gulf war
illness & chronic fatigue syndrome
Sean & Leslee Dudley
303 47th Street, J-10
San Diego, CA 92102-5961
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FRONT PAGE OF THE SAN DIEGO UNION-TRIBUNE APRIL 14, 1999
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VETERANS SET TO BEGIN TRIALS OF MEDICATION HERE, ACROSS
U.S.
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- Eight years after the Persian Gulf War, the government is about to start testing a simple antibiotic as a possible cure for the mysterious health problems plaguing many veterans of that conflict.
Ailing veterans in San Diego and across the country will receive the antibiotic in a major scientific trial, based on the theory that bacterial infection may cause at least some cases of the so-called Gulf War syndrome.
Specifically, the researchers will be looking for strains of a very small, little-understood type of bacteria, called mycoplasma.
A MYSTERIOUS MALADY WITH BAFFLING ORIGINS
Finally, the military is focusing on a likely cause of Gulf War syndrome.
If mycoplasma is the culprit, that's good news: It's treatable.
And it's bad news because it means the debilitating illness is probably contagious -- as some military families already are convinced -- and may well be spreading among nonmilitary communities.
"We're not dealing with a black plague," said Dr. Charles Engel, director of the Gulf War health center at Walter Reed Army Medical Center in Washington D.C. "Most people feel relatively comfortable it is not infectious in the way that would result in some sort of catastrophic epidemic.
"But it may well be that we'll find out micro-organisms are responsible for a lot of these multisymptom illnesses."
Beginning this month, Gulf War veterans can sign up -- at 30 military and veterans' health centers, including one in San Diego -- for the antibiotic study or another study testing exercise and behavior-change counseling.
They are the first potential treatments to be tested for the complex of symptoms afflicting an estimated 100,000 of the 700,000 troops who were deployed in the war against Iraq.
The condition is marked by extreme fatigue, joint and muscle pain, concentration and memory problems, rashes, fever, diarrhea and other symptoms that last six months or more.
For years, Gulf War veterans complained that their health problems were not taken seriously or were considered psychological. Now, the Defense Department and the Veterans Affairs Department have about 120 projects under way trying to pin down the cause, characteristics and prevalence of the illness.
The two departments are spending a combined $20 million to investigate treatments -- $8 million for the antibiotic trial and $12 million to buy exercise equipment and pay therapists for the second study.
The idea that Gulf War illness is infectious still faces skepticism five years after it was first proposed by a maverick biochemist, Garth Nicolson, now based in Huntington Beach. Instead, some scientists suspect veterans are experiencing reactions to chemical exposures, stress or a mixture of wartime conditions.
But Nicolson reports finding Mycoplasma fermentans, a species of the smallest type of bacteria, in the blood of almost half of the 600 sick Gulf War veterans he has tested.
He also finds the bacterium in almost all family members of infected veterans who share the symptoms, he said.
And, most significantly, he reports that getting rid of the mycoplasma usually makes the veterans feel much better.
In 1995, Nicolson began publishing his discovery in a variety of scientific journals that the common antibiotic doxycycline helped Desert Storm veterans recover and cleared M. fermentans from their blood. Of those he has monitored, 75 percent have fully recovered, he said.
"The hypothesis is plausible. It could be true," said Engel, one of the leaders of the Pentagon and VA study. "But most of the evidence Mr. Nicolson has presented is in a very preliminary state. Usually a trial like this, that involves treatment of people, wouldn't go forward based on this level of evidence."
MOVING FAST
In this case, the researchers say, political and public pressure has speeded up science, so that a potential treatment and cause are being tested at the same time.
"We want this study done quickly," said Dr. Sam Donta, an infectious disease specialist at the Boston Veterans Affairs Medical Center who is heading the study. "If it works, it will spawn additional studies."
And if it doesn't work, that won't necessarily eliminate mycoplasmas as the cause, Donta said. "We may not have the right drug or the right dose. You've got to start someplace."
Nicolson said the official study of his methods is long overdue and may not be designed well enough to find accurate answers.
"As a first step, it's OK," he said. "I'm not entirely satisfied with it. I have concerns about the statistical analysis."
A former department chairman at a renowned cancer research center in Texas, Nicolson has a role in the government's study. He taught the researchers the technique he developed for finding mycoplasma in blood, and he will recheck their results on 10 percent of the blood samples tested.
Only veterans who test positive for mycoplasma can participate in the antibiotic study.
Others who are sick probably are suffering from other infections or toxic exposures, Nicolson said. He believes those same factors, along with the multiple vaccines given before deployment, could have weakened some troops' immunity enough to let mycoplasma infection take hold.
The organism may have been present in the gulf either as a biological weapon or as a normal part of the bacterial stew carried in some people's respiratory tracts. It can ride there harmlessly unless impaired immunity allows it to infect the blood system, one theory goes.
Nicolson believes M. fermentans is an airborne bug and "moderately contagious," striking mostly at people with weakened immune systems.
Some species of mycoplasma are known to be transmitted in saliva or through coughing and sneezing, and there's some evidence that fermentans may be spread in similar ways, said Joseph Tully, chief of mycoplasma research for the National Institute of Allergy and Infectious Disease in Bethesda, Md.
However, he said the evidence is not yet strong enough to warrant concern about an epidemic.
"At this point, I don't think that's a real risk," Tully said. "But I tell people, I just don't know."
VETERAN'S VIEWS
Among many veterans' families and advocacy groups, there is no doubt the illness is contagious.
Joyce Riley, an Air Force Reserve nurse from Missouri, tracks more than 10,000 sick Gulf War veterans through the American Gulf War Veterans Association she founded five years ago. She said at least 80 percent of them have family members who also are sick enough to seek medical treatment.
"We know it's communicable," Riley said. "We're very concerned about the spread of this disease."
But Engel said relatively few family members have sought care at VA and military medical clinics. The family members who are sick could have chronic fatigue syndrome, or fibromyalgia syndrome, two other disorders with very similar symptoms, he said.
The VA now is trying to determine whether those families have more such disease than the general population.
One major VA study is exploring whether the illness has spread to veterans' spouses and children, but results are not expected for another two years, said Timothy Gerrity, the VA's chief research and development officer.
The antibiotic study starting this month will include 450 Gulf War veterans who test positive for M. fermentans.
Half of them will take doxycycline daily for a year, while the other half will take a phony pill, or placebo. No one will know who is taking which until the study is over.
All participants will be retested for mycoplasma infection after six months, again after taking the drug for a year and once again six months after they finish the drug.
Donta said he also hopes to give doxycycline to a smaller group of veterans who are sick, but don't have mycoplasma infection. If they get better, the problem could be one of the many other micro-organisms vulnerable to the antibiotic.
Doxycycline, a member of the tetracycline family, is among the most commonly used antibiotics, said Dr. Gregory Gray, of the Naval Health Research Center on Point Loma, who is leading the study locally. He said many people take it for years at a time to treat acne.
It may be difficult to get veterans to sign up for the study, the researchers admitted, because many can get doctors to prescribe doxycycline for them and they may not want to risk the 50 percent chance of wasting a year on a placebo.
"We'd like to appeal to veterans on behalf of the larger veteran community," Engel said. "This is a unique opportunity for them to provide scientific information regarding a treatment that is potentially helpful to other veterans."
ANOTHER APPROACH
The second study starting this month will test whether exercise and "cognitive behavioral therapy" -- either separately or in combination -- can ease the veterans' symptoms and improve their physical functioning. The study will involve 1,360 veterans, including an expected 68 in San Diego.
Some will undertake an aerobic exercise program, some the cognitive therapy, some will get both and some neither.
Engel, a psychiatrist and epidemiologist, said he has been using both types of therapy at the Walter Reed center for four years. He said the patients generally have "a very slight reduction" in physical symptoms and a greater reduction in their distress.
"Most Gulf War veterans come here very actively concerned about many health issues," Engel said. "The concern they have . . . is becoming one of the more debilitating aspects of their illness."
Cognitive behavioral therapy uses relaxation techniques, guided imagery to relax muscles and patients are gradually encouraged to resume activities they believe they can't do, Engel said.
"We're not trying to tell them this is in their head," he said. "Rather than reassuring them, you help them design their life."
In the next few weeks, notices are expected to be mailed to many veterans and veteran organizations, seeking volunteers for both studies. The local Naval Health Research Center has set up a special phone line for interested veterans to call, (619) 524-0069.
Eligible veterans can choose which study they want to take part in, Gray said.
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For more information:
Gulf War veterans who wish to volunteer for the studies using antibiotics, exercise or cognitive therapy can contact the Naval Health Research Center after April 19 at: (619) 524-0069
Military research about Gulf War syndrome: http://www.nhrc.navy.mil/.
U.S. Centers for Disease Control and Prevention: http://www.cdc.gov/.
Garth Nicolson's research: http://www.immed.org/.
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© Copyright 1999 Union-Tribune Publishing Co.
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GERM OF AN IDEA FINALLY, THE MILITARY IS FOCUSING ON A LIKELY CAUSE OF GULF WAR SYNDROME
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- Lean, mean and evasive as a stealth fighter, a stripped-down, parasitic mini-bacterium has emerged as a prime suspect in the disabling illnesses that continue to dog veterans of the Persian Gulf War.
Prodded relentlessly by one very determined biochemist, the military and the Department of Veterans Affairs are spending $8 million to test whether Gulf War illness can be cured with antibiotics and whether it may be, at least in part, caused by a barely known species of an exceedingly tiny bug, Mycoplasma fermentans.
If the treatment works and the mycoplasma disappears from treated veterans' blood, the study may solve a highly controversial medical mystery that has dragged on for eight years. The results also may have profound implications for a number of other infectious diseases.
Mycoplasmas, a large family of the smallest and simplest bacteria, have been known for decades to cause some plant and animal diseases. Some strains have been implicated in a variety of human disorders -- including AIDS, rheumatoid arthritis and infertility -- but the bug is so tricky to find that proof is scarce.
In the last five years, Garth Nicolson, a biochemist based in Huntington Beach, has brought the species Mycoplasma fermentans to the forefront of the search for what ails more than 100,000 Gulf War veterans.
Since his stepdaughter returned ill from service in the gulf -- and he then became sick himself -- Nicolson has tested the blood of hundreds of sick Gulf War veterans and their families. He reports finding M. fermentans in 45 percent of the veterans tested, compared with fewer than 10 percent of healthy people. Among family members who share the veterans' symptoms, almost all have the microorganism in their blood, he says.
The sick veterans who aren't infected with mycoplasma probably are suffering from chemical exposures or other infections, Nicolson believes. In many cases, he said, multiple infections and toxic exposures work along with mycoplasma to overburden the immune system and produce the collection of symptoms known as Gulf War syndrome.
Those symptoms -- joint and muscle pain, extreme fatigue, memory loss, rashes and many other problems -- are shared, in differing proportions, with chronic fatigue syndrome and fibromyalgia, two illnesses of unknown cause. Nicolson said he finds M. fermentans in 60 percent or 70 percent of people with those diagnoses who come to him for testing.
"There's no such thing as Gulf War syndrome -- there's no distinct syndrome," he said. "We have millions of civilians with similar symptoms."
If his theory is right, how did so many Gulf War veterans become infected with mycoplasma at once? That's where Nicolson makes other scientists nervous: He believes that the organism was used as a biological weapon and may also have been contained in vaccines given to soldiers, either through accidental contamination or inept experimentation by the U.S. military.
Military scientists say there is no evidence that biological weapons were used or that vaccines were unsafe.
Another possibility, more plausible to bacterial experts, is that the toxic exposures and other stresses of warfare lowered soldiers' immune resistance enough that mycoplasma, normally dormant in some people's respiratory tracks, became actively infectious and then spread among the troops.
"We think that there were multiple sources of Mycoplasma fermentans," Nicolson said. "It doesn't matter; they've got it. Let's treat it."
And Nicolson believes he has found an effective treatment, the antibiotic doxycycline. He said three-quarters of veterans with M. fermentans infection recover fully after lengthy treatment with doxycycline or other antibiotics.
And, with treatment, the mycoplasma vanishes from their blood. Other scientists are suspicious because most of Nicolson's results have not been duplicated in other researchers' tests and have not been published in the most reputable scientific journals.
But they are intrigued enough -- as are members of Congress who pushed through funding for the study -- to not only test his theory but immediately begin testing his treatment.
"I think you'd have to believe it's probably more real than not," Dr. Sam Donta said of the mycoplasma theory of Gulf War illness. "We can't just keep waiting for more and more evidence while people continue to suffer."
Donta, an infectious diseases specialist at the Boston Veterans Affairs medical center, is leading the $8 million national antibiotic treatment study for the VA and the Department of Defense.
The Naval Health Research Center in San Diego is one of 30 centers that hope to each sign up 15 veterans for the study.
The participants' blood samples will go to Joel Baseman, chief of microbiology at the University of Texas Health Sciences Center in San Antonio, for mycoplasma testing before and after they take antibiotics for a year.
"This theory is without enough substantiated proof and, on the other hand, it's very provocative," Baseman said. "This is certainly a leading theory . . . a hypothesis that really needs to be clarified. I'm excited about it."
However, there is some evidence discrediting the theory. Dr. Shyh-Ching Lo, chief of molecular pathology at the Armed Forces Institute of Pathology in Washington, D.C., tested veterans' blood when Nicolson first proposed the idea in 1994, and found M. fermentans in only 1 percent, the same rate he found in non-veterans.
Nicolson argues that Lo's testing technique is not sufficient to find the organism inside cells. The VA study will use Nicolson's method. Lo has been arguing for 10 years that M. fermentans plays a role in AIDS, but he does not believe that the microbe causes Gulf War illness.
The culprit, he said, might be an as-yet-undetected species of mycoplasma.
"Mycoplasma infection potentially can cause all different kinds of mysterious symptoms . . . often chronic, debilitating illness," Lo said. "It sounds like a good candidate, but we have to see some evidence."
THE VAST UNKNOWNS
The idea that a bacterium could cause the chronic illnesses of Gulf War veterans fits with what Baseman calls "an infectious disease rebirth" now under way. In recent years, bacteria increasingly have been accused of causing diseases previously considered non-infectious; one bacterium is now known to cause ulcers and another looks guilty of promoting atherosclerosis, the clogging of arteries in heart disease.
Mycoplasmas are among the most streamlined of bacteria, nearly as small as viruses. The tiny organisms don't even have a cell wall, just a thin outer membrane. They burrow inside cells, where they are tough to find and tougher still to fight.
Previously considered primitive and not very dangerous, they now are thought to be all the more sinister because of their simplicity; they lack many of the ingredients needed for replication and must scavenge them from inside cells.
"It forces them to be very sophisticated pathogens, because they need the host cell completely in order to survive," Baseman said.
In addition, mycoplasmas' simplicity helps them to evade antibiotics. The drugs normally kill bacteria by targeting certain molecular processes -- such as cell wall development -- that most bacteria have, but that mycoplasmas do not. Mycoplasmas simply use the apparatus of the cells they invade rather than carrying around their own, making them very slim targets.
For that reason, antibiotics can only slow the parasitic organisms, leaving it up to the immune system to finish them off, said Joseph Tully, chief of the mycoplasma lab at the National Institute of Allergy and Infectious Diseases, a part of the National Institutes of Health.
That makes mycoplasma infection particularly dangerous for anyone whose immune system is weakened by disease or, as in transplant cases, must be held in check with drugs, Tully said.
Exactly how mycoplasmas damage cells once they are inside -- whether they excrete toxins, steal the cell's nutrients, trigger autoimmune reactions by mimicking the cell wall or all of the above -- isn't well understood. Scientists who have spent much of their careers studying mycoplasmas believe that they are just beginning to discover what harm the organisms can do.
Those discoveries have been easier in recent years because of the development of a diagnostic technique called polymerase chain reaction (PCR). It is used to find and amplify genetic traces of the organism, which is very difficult to culture and grow to measurable amounts.
The evidence to date is sketchy but sobering: In 1989, Lo and colleagues at the Armed Forces Institute of Pathology fingered M. fermentans in the mysterious deaths of six previously healthy adults from different geographic regions who had developed flulike symptoms and died within a few weeks.
The pathologists found the microorganism in many of the victims' internal organs and could not find signs of any other type of infection or disorder.
Some prominent AIDS researchers believe that M. fermentans paves the way for the human immunodeficiency virus to cause AIDS, and may even be a necessary accomplice. A decade ago, Dr. Luc Montagnier, a French scientist who first identified the human immunodeficiency virus, announced that theory and fought for several years to have it tested.
Lo reached the same conclusion as Montagnier when he found M. fermentans in the brain, blood and other tissues of AIDS patients but not in healthy people. He believes that attacking the mycoplasma with antibiotics could protect many HIV-infected people from developing AIDS.
But no one has been able to get funding to study that theory, Lo said, because of stiff resistance from the many AIDS experts who believe that HIV is the sole cause and mycoplasma just a secondary, opportunistic infection.
"We treat AIDS patients when they have (other) opportunistic infections," Lo said. "We believe the mycoplasma is pathological. . . . it needs to be diagnosed and treated. The HIV proponents say, 'It's just mycoplasma.' It's very absurd."
Other researchers, since 1993, have found a new species, Mycoplasma penetrans, almost exclusively in the urine of HIV-infected patients, raising the possibility that it also may contribute to AIDS.
In new research published last summer, Lo and a group of New Jersey doctors showed that the presence in the genital tract of another species, Mycoplasma genitalium, makes transmission of HIV from one person to another much more likely.
The researchers compared 302 heterosexual couples in which at least one partner was infected with HIV. They found Mycoplasma genitalium more than twice as often among couples who shared the infection as among those in which one partner resisted infection over several years. Many other potential variables were tested; herpes infection was the only other difference that seemed to increase the risk of transmitting HIV.
Again, Lo believes that antibiotic treatment for people infected with HIV could be a relatively easy way to control the spread of the virus.
In 1996, researchers in London verified an idea first suggested in 1970, that M. fermentans is present in the joint fluid of at least one-fifth of rheumatoid arthritis patients tested.
Several other studies now have shown that those patients improve and the swelling of their joints diminishes when they are treated with antibiotics known to inhibit mycoplasma, said Tully, the NIH mycoplasma chief.
"I think it is a cause of arthritis," Tully said. "It's not there (in the joints) normally."
Nicolson and his colleagues also found at least one -- and usually more -- species of mycoplasma in the blood of about half of rheumatoid arthritis patients they tested. The results are expected to be published next month in the British Journal of Rheumatology.
There also is evidence, Tully said, that mycoplasmas may cause infertility in some people by infecting either sperm or ova. Mycoplasmas are known to cause infertility in many animals, a problem first discovered in bulls, he said.
Infertile couples should be tested for the bacteria and possibly try a course of tetracycline-like antibiotics before they embark on expensive fertility treatments, Tully said.
Mycoplasma infection has become a serious threat for transplant recipients, who must take drugs to suppress their immune systems so they will not reject the transplanted organs, and for other people with genetically deficient immune systems.
Even "bucketsful of antibiotics" can't completely kill mycoplasmas without the help of immune defenses, Tully said.
In several cases published in scientific journals, children and adults with suppressed immune systems have needed years of multiple high-dose antibiotics to control mycoplasma infections. With their defenses down, some have become infected with strains they had carried as part of the normal human bacterial mix and some with animal strains they acquired when bitten or licked by cats or dogs.
In 1996, doctors in Denver reported that two lung transplant recipients became infected with mycoplasma carried in the tissue of a donor lung. They each had received half the lung. Both survived, with long-term antibiotics.
Starting in 1995, Nicolson and Dr. Darryl See, an immunologist formerly at UC Irvine, have separately reported finding high levels of M. fermentans in the blood of chronic fatigue and fibromyalgia patients.
Last year, Nicolson reported at a chronic fatigue conference in Australia that he had found M. fermentans in 41 percent of 203 chronic fatigue and fibromyalgia patients and other mycoplasmal infections in an additional 30 percent, while 32 healthy control subjects had no such infections. Some chronic fatique patients have reportedly taken the antibiotic and gotten better, but Nicholson said he has not followed their cases systematically.
A Beverly Hills company, Immunosciences Lab Inc., published a study last year finding M. fermentans in 32 of 100 chronic fatigue patients tested and in only eight of 100 healthy people.
Lo, using a slightly different test, said he has not found significant amounts of M. fermentans in the blood of chronic fatigue patients he has tested.
Mycoplasma fermentans was found in the bone marrow of children with leukemia in the 1970s, but a connection with the cancer has not been further established. In a 1995 study, long-term mycoplasmal infection in mice led to cellular changes that resulted in tumor growth.
A species called Mycoplasma pneumoniae has been known since the 1960s to cause a relatively mild form of pneumonia, often called walking pneumonia, as well as other respiratory diseases. It is contagious through airborne particles.
In addition, a number of animal and plant diseases have been traced to mycoplasmas. The microorganisms have killed palm trees and alligators. The first mycoplasma was identified in French cattle a century ago.
Many insects have their own species of the bug, and some can spread it to plants. Insect transmission to humans has never been shown.
Nicolson firmly believes that M. fermentans can be spread in airborne particles, and that it is most likely to infect people whose immune systems are stressed or genetically weak.
That's plausible, other scientists say, but the evidence is not in.
GENETICALLY ALTERED
Nicolson reports finding a genetic alteration -- the addition of one gene from HIV -- in the mycoplasma he finds in Gulf War veterans but not in other people, such as chronic fatigue patients. Therefore, he believes that the organism may have been altered for use as a biological weapon. Other scientists scoff at that conclusion, partly because mycoplasma is too slow-acting to be very effective at disabling soliders on the battlefield.
Nicolson, who has solid scientific credentials as former chairman of tumor biology at the prestigious University of Texas M.D. Anderson Cancer Center in Houston, shifted to mycoplasma research after his personal experience convinced him that Gulf War illness was contagious.
His stepdaughter, Sharon, a helicopter crew chief in the Gulf War, returned home in 1991 and gradually became disabled with muscle, joint, vision and cognitive problems.
When both Nicolson and his wife developed similar symptoms, he began looking for an infectious agent and experimenting with antibiotics. After months on an antibiotic called doxycycline, all three family members recovered.
At first, Nicolson used a gene tracking technique developed by his wife, molecular biophysicist Nancy Nicolson, to identify M. fermentans inside cells. Now, he said he uses a method called forensic PCR, which he developed with another former University of Texas biochemist, Marwan Nasralla.
Pressured by the university to halt his unorthodox work, Nicolson left Texas in 1996 and came to Orange County to found his own research center, the Institute for Molecular Medicine.
Gulf War veterans and others with similar symptoms come to him from all over the country for mycoplasma testing, usually paying $400 to be tested for four species. Not a physician himself, he provides a list of doctors who are willing to prescribe doxycycline for the condition.
Other scientists caution that the drug works against other infections as well, so its success does not prove mycoplasma's culpability in Gulf War syndrome.
For that reason and others, they say, the new systematic, placebo-controlled study is urgently needed. Although results are not expected for at least a year, researchers said the study was moving very quickly by normal scientific standards because of the intense political interest.
"People are willing now to examine mycoplasma more closely for possible associations with disease," study chief Donta said. "We know next to nothing about fermentans. It should be pursued."
© Copyright 1999 Union-Tribune Publishing Co.
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A MYSTERIOUS MALADY WITH BAFFLING ORIGINS
By Susan Duerksen
UNION-TRIBUNE STAFF WRITER
April 14, 1999
SAN DIEGO -- During the worst years, she sprouted skin tumors and ballooning moles, and some days she couldn't summon the concentration to pay the bills.
Her husband was hospitalized with pneumonia and had trouble remembering his address. Her children were covered with sores and rashes.
The whole family repeatedly suffered from high fevers, wracking coughs, painful joints, exhaustion and various unexplained ailments.
The family dog and two cats also started coughing, and died.
That was before Carol (her name has been changed) discovered doxycycline, the antibiotic now being tested by the U.S. government as a possible treatment for Gulf War illness.
The North County couple -- who feared repercussions if their real names were revealed -- consulted with biochemist Garth Nicolson about five years ago and began taking doxycycline on his recommendation. All four family members improved on the drug, she said, but they still must get new prescriptions every few months when the symptoms return.
"None of us have been completely cured from it, but we have learned to manage it," she said.
Carol said her husband, a 30-year-old former marathon runner who never even got the sniffles, came home from the Gulf War in 1991 sick and disoriented.
"When he came home, within three days I knew something was wrong. He just couldn't think," she said. "There was a time when I wouldn't let my children go with him in the car, because I didn't know if he'd remember where he lived."
A Navy officer, he left the military and took an office job, which still exhausts him completely, she said. She and their two young children also got sick shortly after he returned home, although her husband was hardest hit.
"My family got sick from my husband," Carol said. "We've had all the symptoms."
She also is certain that her family has spread the illness to some friends and relatives. But she has tired of trying to tell them so and being ridiculed.
"As soon as you talk to people about this stuff, they look at you like you're a wacko," she said. "People don't want to understand it. Ignorance is bliss."
The U.S. Centers for Disease Control and Prevention has identified 35 symptoms associated with Gulf War illness. Grouping the major symptoms into three categories -- fatigue, mood/cognition and musculoskeletal -- the CDC researchers developed a working definition for diagnosing the illness: having at least one chronic symptom from at least two of the categories.
In a survey of 3,700 Air Force veterans published last fall, the CDC found that 45 percent of those who had been deployed in the gulf met that definition, as did 15 percent who had not been to the gulf.
The researchers termed the condition "chronic multisymptom illness." They noted that it "is accompanied by significant decreases in functioning and well-being."
The most common symptoms, which usually lasted more than six months, were: sinus congestion, headache, fatigue, joint pain and stiffness, difficulty remembering or concentrating, difficulty sleeping, abdominal pain and bloating, trouble finding words, irritability, rashes or sores, numbness or tingling, muscle pain, depression, diarrhea, sore throat and cough.
One San Diego couple, Sean and Leslee Dudley, say they had all those symptoms and more. As many Gulf War veterans have anecdotally reported, they complained of vision problems and extreme sun sensitivity, as well as mental incapacity.
"We didn't have brains," Leslee Dudley said. "It was terrifying, to be that mentally helpless."
Testing by Nicolson showed that the Dudleys, like Carol and her husband, both were infected with the bacterium Mycoplasma fermentans, which the military is now investigating as a possible cause of Gulf War illness. And both got better on doxycycline.
But neither of the Dudleys was ever anywhere near the Persian Gulf. They believe they caught Gulf War illness from Marines who frequented the Cousins Warehouse store where Sean worked, around the corner from the Marine Corps Recruit Depot on Pacific Highway.
And, since they got sick a year before Desert Storm, they believe that the Marines were infected beforehand through contaminated or experimental vaccines.
That theory raises hackles among scientists studying Gulf War illness, who say that vaccines are screened for mycoplasmas and that there is no evidence of widespread illness among military personnel before the war.
Still, the Dudleys have become outspoken advocates for increased research into the baffling condition. Two years ago, they started a registry of people who have mycoplasma infection and the symptoms. The list now is up to 900 names, about a third of them from the San Diego area, they say. Only 16 percent are Gulf War veterans and their families.
"We have lawyers, musicians, waitresses, receptionists," Leslee Dudley said. "Most are too sick to be working anymore. Some are homeless. It's slowly going through our communities and everyone is just quietly dropping out."
Christian Heineke of San Diego has been extremely ill since he returned from the gulf in 1994 but said he hasn't passed the disease to his girlfriend, roommates or anyone else.
However, Heineke believes that he may have caught it from Marines with whom he worked. He was never on the front lines; he spent three years as a welder on a Navy ship docked in Saudi Arabia during and after Desert Storm.
He fought exhaustion and other mysterious symptoms the whole time, he said, and spent six months in bed when he returned.
"It makes you feel like hell every day," he said. "You just don't feel like you even want to live. I was developing arthritis and I was only 23. I couldn't surf, I couldn't lift weights, it felt like all my joints were on fire."
VA doctors said he was depressed and offered Prozac. Instead, Heineke went to Mexico and bought the antibiotic doxycycline, which he had heard that other veterans were using. He improved, found a part-time job as a nurse's aide and got insurance coverage and a prescription for the antibiotic.
He has been taking it every day for 21/2 years. "The days I don't take it are the days I get sick," he said. "I'm much better now. I have my strength back and most of my memory has come back. I still get asthma and bad joint pain."
Carol said her family also is beginning to accept that their lives are permanently changed by the illness.
"We have to face the fact that we're never going to be the same," she said. "Our minds don't work the same as they used to; it's like if you got old real quick."
"It's a nightmare. And it hasn't ended yet."
© Copyright 1999 Union-Tribune Publishing Co.
______________________________________________________________
______________________________________________________________
LETTER TO THE EDITOR OF SAN DIEGO UNION-TRIBUNE (mailed but not published)
April 15, 1999
Dear Editor,
We wish to thank the Union-Tribune for its excellent articles on Gulf War Illness. Susan Duerksen did a great service for both military veterans and civilians who have this disease but have had no hope until now.
We would like to thank Congressman Bob Filner for supporting the Nicolsons and for making sure the VA study went forward. Mr. Filner has been a leader in Congress on Persian Gulf War Illness and was honored as "Legislator of the Year" for his efforts on behalf of these veterans by the National Gulf War Resource Center.
As the senior Democrat in the Veterans' Affairs Benefits Subcommittee, he is working to schedule a hearing this year in his Subcommittee on causes, treatments and compensation of Persian Gulf Illnesses.
The VA study is a good first step. Our community needs to move quickly with private funding in order to stop this epidemic. Medical research, blood tests and medications are urgently needed by those people who will not be part of the study, including women, children and homeless Vets who go untreated and suffer needlessly.
Drs. Garth and Nancy Nicolson performed an extraordinary breakthrough in finding one of the causes of Gulf War Illness, Chronic Fatigue Syndrome and Fibromyalgia. Their pioneering mycoplasma research needs San Diego's support to continue.
Sincerely,
Sean and Leslee Dudley
Mycoplasma Registry for Gulf War Illness & Chronic Fatigue Syndrome
Section 7 subsection 4
http://www.egroups.com/message/cfs_mycoplasma/6
From: Viviane nvdeynde@xxxxxxxxx.xxx
Date: Sun Jan 9, 2000 1:34am
Subject: Article about Mycoplasma from NBC
Interseting Info about Mycoplasma from :
http://www.healthsurfing.com/1999/12/24/
CHRONIC INFECTION: Evasive mycoplasma may cause fatigue and more story by Julianne Remington reported by Lucky Severson produced by Fran Murphy
Everyday tasks seem overwhelming when the exhaustion of chronic disease drains a person’s life
“Your friends, your colleagues, your boss, your family all have to take on faith that you have an illness, and that you are telling them the truth about the way you feel,” says Sophie Wilkinson, who has suffered with chronic fatigue syndrome for 12 years. Just in the last 6 months, a doctor finally confirmed that Sophie has an illness.
A tiny bacteria called mycoplasma may play a role in the puzzling conditions that defy easy diagnosis and treatment, but persist tenaciously over time. Patients with chronic fatigue and Gulf War illness, and other chronic disorders experience exhaustion, muscle and joint pain, and a lack of mental acuity dubbed “brain fog.” Resistant to treatment, the diseases cause some formerly active people to become bedridden. Others can barely work or attend school part time.
THREE MAIN SYMPTOMS
“It’s not the kind of disease that you would make up,” says Sophie. “You have no life. There’s a whole constellation of symptoms that wax and wane, depending on the particular episode. The lack of stamina is a consistent feature.”
The elusive array of complaints shared by chronic illness patients generally comprise a triad of symptoms. Lack of stamina, muscle or joint aches, and neurologic problems like poor memory and concentration.
It’s not clear how mycoplasma drive these symptoms, but the tiny bacteria leave clues that researchers are beginning to decipher. “We can now identify the DNA of mycoplasma in the blood of some Gulf War syndrome patients,” says Sam Donta, M.D., specialist in infectious diseases at Boston University School of Medicine. “But just finding the DNA footprint doesn’t tell us if that’s the cause of the disease.”
Yard work and other tasks that once took very little energy can consume nearly all of a CFS patient’s strength
“Clearly, it’s not something like cancer that’s life threatening,” says Sophie, “but it sort of quenches your taste for life and the activities you want to do.”
TRICKY AND STICKY
Mycoplasma represent the tiniest free-living bacteria. They can thrive on open surfaces of the body including the mouth, respiratory system, the genital tract, and the urinary tract. Unlike viruses that need to reproduce themselves inside living cells, mycoplasma can replicate on their own. But, they lack a cell wall like most bacteria.
“They have finger-like projections that stick out, and researchers have begun to identify the chemicals that make mycoplasma sticky,” says Dr. Donta. “That stickiness helps them live on the open surfaces of the body.”
Mycoplasma proved very difficult to grow in the laboratory for research purposes, and remained a mystery for years. “They were first associated with pneumonia, an unusual kind of pneumonia,” says Dr. Donta. “They’re tricky, because if you didn’t know about mycoplasma, you might think a patient had a viral form of pneumonia. There aren’t very good drugs for the treatment for viral pneumonia, but antibiotics work against bacterial pneumonia.”
LIKE HIBERNATION
Today’s antibiotics kill active bacteria, but mycoplasma grow too slowly, and antibiotic treatment doesn’t wipe them out. “Apparently, mycoplasma go through very slow periods of growth with low metabolic activity, kind of like hibernation,” says Dr. Donta.
Many antibiotics either interfere with the metabolism of the bacteria, or destroy their cell walls. Neither approach, however, works well against the ultra slow metabolizing mycoplasma, which lack cell walls.
Dr. Donta explains that scientists recently identified a couple more mycoplasma, in addition to the well-known mycoplasma pneumonii. Some were renamed, like ureaplasma, which is associated with the urinary tract. Ureaplasmas have been link to small birth weights and miscarriages as well as genital-urinary diseases.
“There is strong evidence that mycoplasma species are associated with many illnesses including chronic fatigue syndrome, rheumatoid arthritis, and other chronic infectious diseases,” says Dr. Donta.
Researchers discovered that mycoplasma get into the body’s tissues and just sit for a while. Periodically they become more active and take some nutrition. Then they go into a resting phase again with low metabolism. “That’s why an antibiotic doesn’t kill them,” says Dr. Donta. “Antibiotics either target the cell wall, which mycoplasma lack, or they block metabolic pathways used to make new proteins.”
Simple jobs like just picking up the leaves can deplete energy stores in patients with chronic diseases
LONGER TREATMENT NEEDED
“It could be that slow metabolic activity is the mycoplasma’s staying power,” says Dr. Donta. “Like a turtle, it may be slow, but it hangs on.” Researchers think prolonged antibiotic treatment may improve symptoms for some chronic sufferers of Gulf War illness.
“We set up a Gulf War illness study to track mycoplasma DNA,” says Dr. Donta. “We’re trying to see if the mycoplasma disappear in patients whose illness improves after taking the antibiotic doxycyclene. The purpose is to learn what role, if any, mycoplasma play in the illness.”
In the study, which is being conducted at 30 Veterans Affairs Medical Centers around the country, patients take either the antibiotic, or a placebo for one year. During 6 months of follow up care, doctors will try to determine if patients taking the antibiotic improved, and if they stayed better.”
“DNA analysis will be done so researchers can determine if the patients who got better showed a decrease in mycoplasma DNA,” says Dr. Donta, who leads the study.
MULTIPLE SYMPTOM DISORDERS
There’s a lot of controversy about chronic disorders like chronic fatigue syndrome and Gulf War illness. “Some doctors think they are psychological,” says Dr. Donta, “But I have long since given up the ‘evil humor’ theory of disease. Patients are suffering from these diseases even when physical exams don’t reveal anything of note.”
“I spent thousands of dollars on medical tests,” says Sophie. “And I had doctors tell me that I was healthy when I was sitting in their office feeling miserable.”
The National Institutes of Health recognize chronic fatigue syndrome as a serious illness. Still many people with the disease fail to receive disability or insurance benefits because doctors and employers don’t believe they suffer from a debilitating condition.
Research studies in immunology, endocrinology and other fields keep probing the mysteries of chronic illnesses in a search for urgently needed therapies.
“Wouldn’t it be nice if we could wake up all of the mycoplasma bacteria, and keep them from slowing down. And then slam them with an antibiotic,” says Dr. Donta. “We need more research to develop drugs that work against mycoplasma.”
Section 7 subsection 5
http://www.alienzoo.com/features/m/200011230001.cfm
Chemtrails
A report from a Canadian research foundation concluded that the much discussed, but little publicized Chemtrails, may be an attempt to hide a sickening military secret.
Professor Donald Scott, president of the Common Cause Medical Research Foundation, claimed that Chemtrails are a belated attempt by U.S. military and intelligence chieftains to stop the spread of a debilitating disease first concocted in the early 1980s.
According to Scott’s account, the military began developing diseases in the 1970s which were infectious but not contagious. In other words, an ailment which could be spread to enemy troops but would not pass into other populations.
One such disease was based on a zoonosis, a disease which can be transmitted to humans by animals, in this case brucellosis. Brucellosis is a bacterial disease usually found in cattle, which can cause undulant fever in humans.
By manipulating this disease, researchers were able to design a disabling bacteria which disappeared following infection. Troops could be infected yet exhibit no signs of the bacteria when examined by a doctor.
In the early 1980s, secret government labs worked to produce a brucellosis pathogen which could disable enemy troops without the risk of infecting friendly forces. This pathogen reportedly was based on brucellosis bacteria in a crystalline form first developed by researchers in 1945.
According to Scott’s report, such a bacteria was tested during the summer of 1984 at Tahoe-Truckee High School in California, where individual rooms were fitted with an independent recycling air supply. A teacher’s lounge was designated as the infection target. Seven of eight teachers assigned to this room became very ill within months.
The high school was only one of several locations where the specially designed pathogens were tested, some distributed by aerosol sprays and others by the use contaminated mosquitoes.
Scott reported that one hundred million mosquitoes a month were bred at the Dominion Parasite Laboratory in Belleville, Ontario, during the 1980s, then tested by both Canadian and U.S. military authorities after being infected with brucellosis.
Some observers believe the viral epidemic reported around New York City in recent years may have been the result of these infected mosquitoes.
The testing of unsuspecting victims was conducted by both the military and CIA, according to Scott, and monitored by the National Institutes of Health as well as the Center for Disease Control.
Encouraged by what they felt was a successful test, military leaders reportedly passed the brucellosis bio agent to none other than Saddam Hussein, who in the mid-1980s was fighting a protracted war against Iran at the behest of the CIA.
George Bush
In 1986, with the approval of Vice-President George Bush, Saddam received shipments of both brucella abortus, biotypes 3 and 9, and brucella melitensis, biotypes 1 and 3.
After Saddam obtained a stockpile of the brucellosis, a terrible discovery was made - these designer bacteria mutated and became contagious.
Saddam Hussein
According to Scott’s report, Saddam used this pathogen on American troops during the Persian Gulf War in 1991, resulting in the illness referred to as Gulf War Syndrome. More than 100,000 Gulf War vets now suffer from this syndrome, which causes chronic fatigue, loss of appetite, profuse sweating even at rest, joint and muscle pain, insomnia, nausea, and damage to major organs.
Much of this information may be found in a 1994 report by Senator Donald W. Riegle, Jr., titled, "U.S. Chemical and Biological Warfare-related Dual Use Exports to Iraq and Their Possible Impact on the Health Consequences of the Persian Gulf War."
Troops initially were told that no such infection existed and that the problem was mostly in their mind. Slowly, over the years, authorities were forced to admit that something had triggered severe illness in many Gulf War veterans.
By then, a variant of the brucellosis had spread to the civilian population. Many people began suffering from general debilitation and tiredness.
When it became know that the contagion was spreading into the general population, top officials with the National Institutes of Health and Center for Disease Control, as well as the Defense Department and the Department of Health and Human Resources began a program of misrepresentation of the disease to mask their role in its origin. The illness was claimed to be connected to the Epstein-Barr virus and was labeled "Chronic Mononucleosis."
This has now become known as Chronic Fatigue Syndrome. Like the veterans before them, victims of this ailment were told it was merely a psychological condition.
One victim, Dr. Martin Lerner of William Beaumont Hospital in Royal Oak, MI, told his peers in the American Society of Microbiology that his bout with this mysterious disease left his heart damaged. Dr. Lerner and others suspected that Chronic Fatigue Syndrome is caused by viral infection.
Top-level officials, concerned both with the spread of the contagion and with the risk that their role in its origin would become publicly known, moved to counteract the pathogen. This program may explain the mysterious Chemtrails which have been noted over major population centers during the past couple of years.
As explained by Scott, "We have learned . . . that a patent was issued in 1996 for an aerosol vaccination process which would permit the vaccination of wildlife and domestic herds by spraying them or their disease vectors (birds) from the air. . . .
"We have noted that many of the sightings of Chemtrails are over migratory bird flight paths. We are currently preparing a report on this subject for release in January 2001.
"The Chemtrails program may well be a belated effort by the
U.S. and Canadian governments to get the brucellosis genie back
in its bottle."
To learn more about who may be behind nefarious activities such as Chemtrails, read Rule by Secrecy: The Hidden History That Connects The Trilateral Commission, The Freemasons and The Great Pyramid by Jim Marrs, now available from finer bookstores everywhere and from JimMarrs.com. Read Alien Agenda by Jim Marrs, for an in-depth look at UFOs, available at this Web site. Also Jim Marrs’ book on the U. S. Army’s remote viewing program,Psi Spies, which was suppressed in 1995, is now available online right here at AlienZoo. Order yours today.
©2000 AlienZoo, Inc.
Section 7 subsection 6
Blood is preferably collected by venipuncture, though finger tip puncture with sterile lancet may sometimes suffice. The tests to be performed determine which anticoagulant if any, should be in the collection tubes. Vacuum tubes which have double-ended needles for ease in specimen collecting and which contain suitable amounts of the appropriate anticoagulants for most routine hematologic procedures available. However, most commercially available vacuum tubes are non sterile and backflow of blood from the filled tube to the vein may occur, permitting the entry of bacteria. Several maneuvers may help to avoid such infections:
- It is essential to remove the tourniquet well before blood flow into the tube has stopped and, preferably, before the tube stopper is completely punctured.
- Moving the patient’s arm during sampling should be avoided; even few centimeters' elevation after the tube draw is complete may lower the pressure sufficiently to produce backflow.
- No pressure should be exerted on the stopper end of the tube. Whenever possible, sterile tubes or needle and arrangements that have a check valve in the system should be used.
EDTA (ethylenediaminetetraacetic acid) is the preferred anticoagulant blood counts are desired since morphology is less distorted and platelets are preserved. It can be added to clean test tubes, or vacuum tubes containing EDTA may be obtained commercially. Slides should be prepared within 3 to 4 h after blood has been drawn, or within 1 to 2 h for platelet counts.
When small quantities of blood are required or venipuncture is not feasible, the finger or, in infants, the plantar surface of the heel is punctured quickly ~ sterile disposable lancet, piercing deeply enough to ensure spontaneous flow blood. Undue pressure which might cause dilution of the blood with tissue fluids should be avoided while collecting the specimen.
This test is easy to perform but difficult to standardize. A stab wound with a No. 11 scalpel blade is made on the earlobe. The time is recorded and the wound is blotted with filter paper at 30-second intervals until all bleeding has stopped. This usually occurs within 6 min. Alternatively, the forearm may be used as puncture site after application of a blood pressure cuff inflated to 40 mm pressure, as in the Ivy method. Normal bleeding time with this method is 2 to 3 min. Bleeding time is prolonged in thrombocytoperna, von Willebrand’s disease and some disorders of platelet function.
Bone marrow aspiration is not difficult and should be done early in suspected hematologic diseases. About 1 ml of marrow is withdrawn by aspiration from the marrow space of the sternum, iliac crest, or dorsal spine of a lumbar vertebra. A few drops are smeared directly on slides and the rest is placed in a tube either heparin or EDTA. If larger volumes of marrow are withdrawn, there usually is dilution with peripheral blood, making interpretation difficult. The anticoagulated marrow may be spun in a centrifuge to separate the plasma from and myeloid-erythroid layers. Additional smears of the concentrated myeloiderythroid layer help in interpretation. The smears are stained with Wright’s and then examined under the microscope. Thicker smears are made for iron stores and stained with Prussian blue.
Bone marrow examination is helpful in anemia, other cytopenias, unexplained leukocytosis, thrombocytosis, or when leukemia or myelophthisis is suspect since it permits evaluation of the site of blood production and an assessment iron stores.
This procedure consists of collecting about 5 ml of blood in a tube with anticoagulant. The clot usually starts to separate from the walls of the tube in to 60 min and is usually completely separated in 12 to 24 h. The retracted clot should not change significantly for 72 h.
Since proper clot retraction depends upon normal platelet number and function, clot retraction is delayed, impaired, or absent when platelets are decreased or function abnormally. If a clot forms and then becomes fluid, clot lysis has occurred. More elaborate studies for fibrinolysis (euglobulin lysis time, thrombin time, tests for split products of fibrin) should then be considered.
This simple test detects gross blood coagulation defects. It is used to monitor heparin therapy although it has been replaced in many hospitals by the partial thromboplastin time for this purpose. Patients with mild coagulation defects, inciuding mild hemophiliacs, may have a normal coagulation time.
Four ml of blood are collected from a vein with a 5-ml sterile syringe, and the time that blood first appears in the syringe is recorded. The needle is removed from the syringe and 1 ml of blood is placed in each of three sterile 8-mm test tubes. After 3 min, the first tube is tilted slightly to see if clotting has taken place. The second tube is examined in the same way 30 seconds later. Alternately, the first and second tubes are tilted until coagulation occurs. The third tube is then tilted in the same manner. The time at which the third tube can be inverted without disturbing the clot is recorded. The time elapsing between the appearance of blood in the syringe and clot formation in the third tube is the coagulation time. The normal range is 6 to 17 min.
The CBC, along with the urinalysis, is a basic ”screening” test in all patients. The CBC usually includes determination of Hb, Hct, WBC count, WBC differential count, an estimation of platelet number, and a description of the blood smear~ including RBC morphology: An RBC count is frequently included, especially when calculation of RBC indices is desired. Anemia, erythrocytosis, inflammation, leukemia, bone marrow failure, and adverse drug reactions may be detected.
Examination of the blood smear can aid in detecting certain abnormalities (e.g., thrombocytopena, malarial parasites, significant rouleau formation, and the presence of nucleated RBCs or immature granulocytes) which may occur despite normal counts. It is important in evaluating RBC morphology and abnormal WBC
Blood counts are normally made by dlilutiuig a measured volume of blood with an appropriate diluent or lysing agent and counting in a chamber under the microscope. Hb can be measured colorimetrically after treatment with dilute hydrochloric acid or with Drabkin’s reagent, which will permit colorimetric or spectrophotoinetric comparison with standards of hematin or cyanmethemoglobin, respectively. The Hct is measured by centrifuging a volume of blood and determining the percastage which is RBCs. From a knowledge of the RBC count, Hb, and Hct, one may calculate RBC indices, namely MCV (mean corpuscular volume), MCII (mean corpuscular hemoglobin), and MCHC (mean corpuscular hemoglobin coacastration). These indices may be useful in helping to establish the character of anemia.
All of the CBC values except the WBC differential count, but including the RBC indices, can be measured very quickly on venous blood by automated equipment. The WBC differential count is made by spreading a small drop of blood on a glass slide and staining with Wright’s stain. The smear is examined by oil immersion microscopy and a count kept of each type of leukocyte identified. A minimum of 100 cells are counted and the various types are reported as a percentage. Automated equipment is becoming available to do differential counts by computerized pazzan recognition. The number of platelets is estimated.
The RBCs ane studied for the presence of anisocytosis, poikilocytosis, hypochromia, stippling, and other abnormalities. Occasionally the RBC indices may be anticipated from such an inspection. The cells should be studied in an area of the smear where they just touch one another. -
Venous blood, collected in anticoagulant, is added to a Wintrobe hematocrit tube to the 10-cm mark and placed in a vertical position. The distance the RBCs fall in 1 h is the ESR. Alternatively, a Westergren tube is filled to the 200-mm mark and read at the end of 1 h.
This is a nonspecific screening test and may be elevated in infection, inflammatory disease, and malignancy. An elevated ESR frequently signifies an increase in fibrinogen and y-globulin. The test is useful in the follow-up evaluation of rheumatoid arthritis and acute rheumatic fever, and may help to distinguish between serious disease and functional symptoms when other findings are unremarkable.
Small amounts of fdp/FDP are present in normal serum but fdp/FDP is markedly elevated in the serum of patients with thromboembolic conditions such as myocardial infarction, deep vein thrombosis, pulmonary emboli, and disseminated intravascular coagulation. Resting levels of fdp/FDP are about 5 jig/mI; levels rise slightly after exercise or stress.
The determination may be made by hemagglutination inhibition (HI) immuno assay, by the use of sensitized latex particles which agglutinate at concentrations >2 ug/ml, or by radioimmunoassay (RIA). The blood specimen must be collected in tubes that contain thrombin to enhance clotting and trypsin inhibitor to prevent fibrin degradation in the specimen after collection. The test may also be done on urine and shows increased levels with kidney disease. It may aid in distinguishing renal from bladder infections, the value being normal in the latter.
Haptoglobin is an a2-globulin with a specific affinity for Hb. It is ordinarily reduced in the presence of hemolysis. The determination may be useful in distinguishing Hb from myoglobin. While many methods for measuring haptoglobin are available, immuno diffusion is the simplest.
Serum iron determination and iron-binding capacity should both be performed since the relationship between their values is important. In iron deficiency, the serum iron is low and the iron-binding capacity high. Both values are decreased in various chronic disorders, such as inflammatory diseases. The serum iron is elevated and may equal the iron-binding capacity in severe hemolysis, megaloblastic anemias, aplastic anemias, and hemochromatosis. Though serum iron may be normal in patients with treated iron deficiency, iron-binding capacity usually remains elevated for several weeks.
LE cells when treated with Wright’s stain appear as amorphous inclusions about the size of a lymphocyte nucleus, lavender in color, with the lobes of the neutrophil nucleus displaced to the cell margin. This nonspecific test is positive in SLE and is also often positive during therapy with certain drugs, including hydralazine and procainamide. Determination of antinuclear antibodies has become the preferred test for the diagnosis of SLE since the technic and interpretation of the “LE prep” are so variable.
This is an excellent screening test for single or multiple coagulation defects. It detects most patients with hemophilia and Christmas disease. More precis and sensitive than the venous clotting time, the FIT has a fixed range of normal values and no significant variability. Unexplained abnormalities can be clarifled by assays of specific coagulation factors and by other tests which are usually performed in a coagulation laboratory. FIT is used to monitor heparin therapy. The patient’s plasma and a normal control plasma are treated with activated partial thromboplastin. The time in seconds that it takes for each to clot is recorded and compared
The ability of platelets to aggregate and stick together may be measured; it provides a useful tool for elucidating some coagulation defects.
Diluting fluid is prepared by dissolving 1 Gm ammonium oxalate in 100 ml distilled water. Venous blood is drawn to the 0.5 mark of a white cell pipet (with tubing) and diluting fluid is added to the 11 mark. The pipet is shaken for 3 min. The first 5 drops are discarded and a counting chamber is filled. The counting chamber is placed in a Petri dish containing moist filter paper, is covered, and is left to stand for 15 min to permit settling. The platelets are then counted as if doing an RBC count, using the high-power objective or phase microscope. The number of platelets counted multiplied by 1000 equals the total number of platelets/cu mm. Automated platelet counters are available. Normal values range between 200,000 and 400,000/cu mm.
The time in seconds that it takes for clotting to occur when a small amount of thromboplastin extract is added to plasma is the prothrombin time. This is performed on a control specimen as well as on the patient’s specimen.
The prothrombin time is useful for following therapy with coumarin anticoagulants. It is also a valuable screening test for disordered blood coagulation in a variaty of acquired conditions (e.g., liver disease, disseminated intravascular coagulation). It should be emphasized that a “minor” prolongation of the prothrombin time may signify a major coagulation defect since certain clotting factors may greatly reduced without significantly prolonging the prothrombin time. Whenever the prothrombin time is consistently 4 or more seconds longer than the control time, further investigation is indicated.
These are helpful in identifying iron deficiency and macrocytic anemias. See in Blood Count, above.
An increase in the number of reticulocytes (immature erythrocytes) indicates increased RBC production by the bone marrow. This response is characteristic in hemolytic anemias and in acute and severe bleeding. Reticulocytosis is also seen in response to specific treatment of vitamin B12, folic acid, and iron deficiencies, may indicate the onset of remission in aplastic anemia or leukemia. A “normal” reticulocyte count in anemia indicates failure of the bone marrow to fully respond.
A few drops of blood are initially stained with fresh methylene blue, counter stained with Wright’s stain, and then counted under oil immersion. One thousand consecutive RBCs are counted and the number having a blue-staining reticulum are expressed as a percentage. The normal range is 0.5 to 1.5%.
This test is positive when hemoglobin S (Hb S) is present in the RBCs; it identifies sickle cell anemia, sickle cell trait, and sickle cell variants. When the sickle cell preparation is positive or when a hemoglobinopathy is suspected, Hb electrophoresis is indicated.
Sickling may be produced in susceptible RBCs by subjecting them to contact with a reducing agent such as sodium metabisulfite. It may also be produced by reduced 02 tension. Sealing a drop of blood under a cover slip with petroleum jelly provides such an environment, which may be viewed microscopically. A rapid tube test which depends upon the differential solubility of Hb S is widely used as a screening method.
This test consists of inflating a blood pressure cuff around the patient’s arm to a pressure midway between systolic and diastolic for 5 mm. A subjective evaluation of the number of petechiae over the surface of the forearm and hand is recorded as negative (no petechiae) to 4+ (confluent petechiae). This test demonstrates capillary fragility but may also be positive in thrombocytopenia.
| Determination | Normal Value | Material Analyzed | Minimal ml of Blood Required | Note |
|---|---|---|---|---|
| Coagulation factors | ||||
| Factor I(fibrinogen) | 0.15—0.35 Gm/100 ml | Plasma | 4.5 | Collect in vacuum tube containing sodium citrate |
| Factor II (prothrombin) | 70—130% of control | Plasma | 4.5 | Collect in plastic tubes with 3.8% sodium citrate |
| Factor V accelerator globulin) | 70—130% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor VII-X (proconvertin-Stuart) | 70—130% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor X (Stuart factor) | 70—130% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor VIII (antihemophilic globulin) | 50—200% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor IX (plasma thromboplastic mctor) | 70—130% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor Xl (plasma thromboplastic antecedent) | 70-130% of control | Plasma | 4.5 | Collect as for Factor II |
| Factor XII(Hageman factor) | 70-130% of control | Plasma | 4.5 | Collect as for Factor II |
| Coagulation screening tests | ||||
| Bleeding time | 3-8 mm | Whole-blood | 6 | Collect in 3 glass tubes (10 x 75 mm) |
| Clotting time | <15 mm | Whole-blood | 6 | Collect in 3 glass tubes (10 x 75 mm) |
| Prothrombin time (Quick) | < 2-sec deviation from control | Plasma | 4.5 | Collect in vacuum tube containing 3.8% sodium citrate |
| Partial thrombo plastin time (activated) | 22-37 sec | Plasma | 4.5 | Collect in vacuum tube containing 3.8% sodium citrate |
| Whole blood clot lysis | No clot lysis in 24 h | Whole-blood | 2 | Collect in sterile tube; incubate at 37 C |
| Fibrinolytic studies | ||||
| Euglobulin lysis | No lysis in 2 h | Plasma | 4.5 | Collect as for Factor II |
| Fibrinogen split products | ||||
| Method I (latex agglutination with anti-D and E antibody) | Negative reaction at > 1:2 dilution | Serum | 4.5 | Collect in special tube containing thrombin & e-aminocaproic acid |
| Method II (staphylococcal clumping) | Positive reaction at >1:8 dilution | Serum | 4.5 | Collect as for Method I |
| Plasminogen | 3-5 casein u/ml | Plasma | 4.5 | Collect as for Factor II |
| Thrombin time | <5-sec deviation from control | Plasma | 4.5 | Collect as for Factor II |
| Complete blood count | ||||
| Hematocrit | Male: 42-50% Female: 40-48% |
Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| Hemoglobin | Male: 13-16 Gm/100 ml Female: 12-15 Gm/100 ml |
Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| WBC count | 4,800-10,800/cu mm | Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| RBC count | 4.2-5.9 million/cu mm | Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| MCV | 80-94 cu microns | Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| MCH | 27-32 uug | Blood | 1 | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| MCHC | 33-38% | Blood | I | Use EDTA as anticoagulant. Use Coulter Counter Model S. The machine directly determines cell counts, Hb (as the cyanmethemoglobin derivative), & MCV, & computes Hct, MCH, & MCHC. |
| ESR | Male: 1-13 mm/h Female: 1-20 mm/h |
Blood | 5 | Use EDTA as anticoagulant |
| Erythrocyte enzymes | ||||
| Glucose-6- phosphate dehydrogenase | 5-15u. | Blood | 9 | Use special anticoagulant (3.8% sodium citrate) |
| 6-Phospho- gluconate dehydrogenase | 2-5u. | Blood | 9 | Use special anticoagulant (3.8% sodium citrate) |
| Glutathione reductase | 9-13u. | Blood | 9 | Use special anticoagulant (3.8% sodium citrate) |
| Pyruvate kinase | 2-3u. | Blood | 8 | Use special anticoagulant (5% polyvinyl pyrrolidine & 3.8% sodium citrate) |
| Folic acid | 6-15 mpg/ml | Serum | 1 | |
| Haptoglobin | 100-300 mg/ 100 ml | Serum | 1 | |
| Hemoglobin studies | ||||
| Electrophoresis for abnormal Hb | Blood | 5 | Collect with anticoagulant | |
| Electrophoresis for A2Hb | 2.0-3.0% | Blood | 5 | Use oxalate as anticoagulant |
| Fetal Hb (alkali resistant) | <2% | Blood | 5 | Collect with anticoagulant |
| Met-and sulf-Hb | 0 | Blood | 5 | Use heparinized blood |
| Serum Hb | 2-3 mg/lO0 ml | Serum | 2 | |
| Thermolabile Hb | Negative | Blood | 1 | Any anticoagulant |
| Lupus anticoagulant | Absent | Plasma | 4.5 | Collect as for Factor II |
| LE cell preparation | ||||
| Hargraves method | Negative | Blood | 5 | Use heparinized blood |
| Barnes method | Negative | Blood | 5 | Use defibrinated blood |
| Leukocyte alkaline phosphatase | 15-40 mg of phosphorus liberated/h/10to10th cells | Isolated blood leukocytes | 20 | Special handling of blood necessary |
| Muramidase | Serum: 4-12 ug/ml | Serum | 1 | |
| Muramidase | Urine: 0-2 ug/ml | Urine | 1 | |
| Osmotic fragility of erythrocytes | Increased if hemolysis Blood 5 occurs in >0.5% saline; decreased if hemolysis is incomplete in 0.3% saline | Blood | 5 | Use EDTA as anticoagulant |
| Peroxide hemolysis | <10% | Blood | 5 | Use heparin as anticoagulant |
| Platelet count | 200000-350,000/cu mm | Blood | 0.5 | Use EDTA as anticoagulant. Counts are performed on Coulter Counter Model B. Low counts are confirmed by hand counting |
| Platelet function tests | ||||
| Clot retraction | 50-100% at 2 h | Plasma | 4.5 | Collect as for Factor II |
| Platelet aggregation | Full response to ADP, epinephrine, & collagen | Plasma | 18 | Collect as for Factor II |
| Platelet Factor 3 | 33-57 sec | Plasma | 4.5 | Collect as for Factor II |
| Reticulocyte count | 0.5-1.5% of red cells | Blood | 0.1 | |
| Vitamin B12 | 200-800 uug/ml | Serum | 12 | Special handling of blood necessary |
Section 7 subsection 7
BBC News World Service
Scientists in the southern Indian state of Kerala have begun examining an unusual phenomenon: colored rainfall in some parts of the state. Its southern and central districts have witnessed spells of colored rain over the past week, prompting researchers to launch a formal investigation.
It all started with scarlet rain showers last Thursday on some villages in the southern districts of Kottayam and Idukki. Soon, a similar phenomenon was reported from eight other districts of the state. These areas witnessed spells of green, yellow, brown and black rains.
Almost the entire state, except for two northern districts, have reported these unusual rains over the past week.
Scientists from the Trivandrum-based Centre for Earth Science Studies are now studying the rain waters collected by local people. The institute's Director, M Baba, said scientists believe the colored rain was caused by dust from a burning meteorite that threw over 2,000 pounds of extraterrestrial dust into the atmosphere.
Section 7 subsection 8
International Herald Tribune
Barry James
Nobody knows how it started. Nobody knows how it will end. Nobody knows how many people eventually will die from it. Those are among the frightening mysteries scientists are discovering about "mad cow" disease, or BSE, the bovine form of transmissible spongiform encephalopathy.
The disease can arise out of nowhere and lie dormant for years, which the official British BSE Inquiry believes is how it started in England. Perhaps only one cow spontaneously developed the disease at first. To become an epidemic it needed an amplifier, which in Britain was the practice of feeding grazing animals the ground-up remains of others of their species.
In Europe, 91 people are known to have contracted variant Creutzfeldt Jakob disease, the fatal neurodegenerative affliction that humans can develop when exposed to infected meat. Creutzfeldt Jakob disease, which leads to dementia and eventually leaves the brain pitted with holes and resembling a sponge, was first identified independently by two German doctors in the 1920s, but until recently it was a condition of the elderly. Variant Creutzfeldt-Jakob disease also attacks younger people, some of them in their teens.
The human toll might seem small when compared with diseases like malaria, 0which kills millions of people every year. But the prospect of turning loose a stealthy, deadly and largely unknown pathogen is what most concerns scientists across Europe. The mad cow scare has touched off a panicky reaction against eating beef, but the worrisome fact is that many people already may be infected, perhaps because proteins known as prions that had somehow become aberrant were lurking in their baby food or hamburger many years ago.
The danger to humanity, scientists say, is that the general level of potential infection will rise, making it easier for the disease to emerge in future generations. This threat is illustrated by the speed at which bovine spongiform encephalopathy amplified among cattle in Britain in just a few years. There have now been more than 180,000 cases, with many others doubtlessly undiscovered among the 4.8 million cows culled and destroyed since 1996 in an attempt to check the disease. An article in the science journal Nature estimated that 975,000 infected cows entered the food supply.
Here is a chilling catalogue, drawn from two dozen interviews with experts and a review of scores of scientific documents, including Britain's recent 16-volume official BSE report, which illustrates why scientists are so concerned about BSE and related spongiform diseases that can affect most species of mammals and birds:
The pathogen that wipes out memory, personality and physical functions is extraordinarily tenacious. It resists heat, alcohol, boiling, ultraviolet light and ionizing radiation. Surgical instruments that come in contact with it can remain contaminated after normal sterilization procedures, and researchers don body protection before handling it.
The pathogen can survive years of being buried in the soil, which is worrisome given that cattle remains often end up in landfills. Iceland in the 1950s slaughtered all its sheep to eliminate a related disease called scrapie. When it brought in healthy animals, scrapie soon reappeared. Some scientists believe that scrapie can mask low levels of BSE in sheep.
While they take time to emerge, perhaps over many decades in humans, the spongiform diseases are highly infectious. According to British scientists, a cow can get BSE by eating one gram of infected material - a speck the size of a peppercorn - from another cow. Even a minute trace of the material in meat and bone meal, the protein supplement produced from rendered animal remains, can infect a cow.
The European Union's Standing Scientific Committee says that "the minimal infective dose considered to be valid for animals should also be applied for humans." Nobody knows what a minimal dose is, but British scientists discovered that a piece of wire that had been in contact with the pathogen for five minutes became as infectious as a solution made from infected brain.
Although the spongiform diseases are most infectious among members of the same species, they can jump the barrier to other species with varying levels of ease. Much has still to be learned about this species barrier, particularly so far as humans are concerned. Scrapie, for example, is believed not to infect humans. But in the United States, doctors identified several cases of variant Creutzfeldt Jakob disease among people who had eaten squirrel brains, and scientists warn that a spongiform encephalopathy called chronic wasting disease, found among deer and elk in the United States, is another potential threat to humans.
Once the pathogen has adapted to a new species, it can infect other members of that species with a much lower dose. In zoos, the pathogen has caused an outbreak of spongiform diseases among primates, big cats, antelope and other species, through the feeding of infected material. One study last year identified 82 cases in zoos. Bovine spongiform encephalopathy can be experimentally provoked in sheep, and domestic cats have acquired a similar encephalopathy from pet food. A 12-year old lion in the Newquay zoo in England was put down recently and found to be suffering from a form of transmissible encephalopathy.
The spongiform encephalopathies are surreptitious. An animal can harbor a spongiform disease and show no symptoms. Mice infected with hamster prions remain apparently healthy throughout their normal life span, but in fact become highly infectious. Cattle are believed to be infectious at an early stage of incubation as the disease spreads through the central nervous system toward the brain, the most lethal tissue of all. Because the incubation period in cows is thought to be longer than three years, the European Union this week decided to destroy cattle for market older than 30 months unless tested after slaughter and found to be free of BSE.
The possibility that an animal can be infectious and show no symptoms raises the question whether people can as well. Scientists fear, for example, that a patient with undetected Creutzfeldt-Jakob disease who was undergoing surgery treatment for another disease might pass it along through surgical instruments. Since nobody knows the average incubation period in man, blood transfusion services in several countries, including the United States and Canada, are turning away donors who have lived in Britain although it is not certain that the defective prions can be passed on through blood.
When the mad cow epidemic emerged in Britain in the 1980s, Stanley Prusiner, a U.S. neurologist and Nobel laureate, had already published his findings that the spongy condition of victims' brains was caused by "proteinaceous infectious particles," or prions. Proteins are the body's primary component and the basis of all enzyme reactions. As they are produced, they fold or coil three- dimensionally.
The agent that causes spongiform disease is a protein that has folded wrongly, and which is able to pass this defect to normal proteins. Because the defective prions resist breakdown by enzymes, they build up within nerve cells and eventually the brain.
The Prion Principle
It is as though bricks told an architect how to build a house. Kurt Vonnegut described the prion principle in his novel "Cat's Cradle," in which a crystal of Ice-IX "taught the atoms the novel way in which to stack, lock and crystallize" until the oceans turned to ice. Unlike viruses, proteins contain no genetic material and therefore provoke no immune response. This is why it is so difficult to detect prion disease in a living being. A brain or tonsil biopsy might find Creutzfeldt-Jakob disease in a human, for example, but only if doctors examine an infected part. The defective proteins survive the rendering process that turns an animal's carcass into industrial fats and gelatin on the one hand, and meat and bone meal on the other. The meal is an effective and cheap protein that helps animals grow and produce milk. When it became apparent that turning herbivores into carnivores was the likely cause of BSE, Britain forbade feeding ruminant meat and bone meal to cattle in 1988, but continued to export the material, thus spreading the disease to other countries.
Scientists consider the inexpensive meat that comes from old dairy cows to be the most dangerous. It is pooled in beef patties, meat pies and pasta fillings; meat from as many as 60 animals may go into a hamburger mix. Some of the cheapest meat is stripped by machines and high- pressure jets from the bone, which is likely to be highly infectious in a sick cow. Each cow provides about seven kilograms (15 pounds) of machine-recovered meat that is incorporated into five- to seven-ton batches of material. The EU's standing scientific committee estimated that each batch contains meat from about 1,000 animals, any one of which could infect the whole, and expose as many as 400,000 persons to the agent. Even the most dedicated vegetarian cannot avoid cattle products, which enter a vast range of goods from cigarette filters to soap. Tallow made from animal fat is used in everyday objects from carpets to television sets. In general, only between one-third and a half of the animal is eaten. "The real market is in the by-products," said Paola Colombo, an EU Commission official.
Ballanchine Was a Victim
"Cosmetics, pharmaceuticals, Gucci handbags - that's animal waste."
People daub their faces with anti-aging creams made from lightly processed bovine materials, an undefined danger indeed, but the choreographer George Ballanchine died of Creutzfeldt-Jakob disease after using a bovine glandular product to preserve his youthful looks.
The first French victim of variant Creutzfeldt-Jakob disease was a body-builder who used a muscle-boosting preparation of the kind still sold virtually unregulated in health food stores in the United States. One contains "freeze dried bovine brain, spleen, pituitary glands and eye tissue," said Michael Hansen, a microbiologist with the U.S. Consumers' Union. "It's almost a cow in a pill."
Questionable cattle products have gone into baby food, pet chow, beauty preparations and vaccines. Only last month, Britain withdrew supplies of polio vaccine after discovering that they were cultivated from British bovine serum produced when mad cow disease was at its height. Eleven million children and travelers have received the oral vaccine. Vaccines against measles, mumps, rubella, diphtheria and whooping cough also were made from British-sourced bovine material until at least 1993.
The government said the risk of contracting variant Creutzfeldt-Jakob disease from vaccine was "incalculably small," but this is not what was said by the author of the first major British mad cow investigation, Sir Richard Southwood. He warned in an internal memorandum that the danger of infection from vaccines was "moderately high." He recommended that the removal of bovine material from vaccines should be a priority area for action.
If the number of people who have been exposed to and perhaps even infected by prions is unknown and unknowable, the number of people likely to die will become known only with time. The victims will suffer from insomnia, memory loss, depression, anxiety, withdrawal and fearfulness, and eventually loss of coordination, incontinence and blindness. Estimates of eventual deaths from Creutzfeldt-Jakob disease range from "several dozen" by the French health secretary, Dominique Gillot, to 250,000 in a recent British government study.
"We might be seeing an epidemic that involves hundreds of thousands of people," said John Collinge of Britain's advisory committee on spongiform encephalopathies. "Let's hope that is not the case, but it's still possible. We need to guard against false optimism and wishful thinking, which has bedeviled this field for too long."
John Kent, a professor of statistics at Leeds University who has tried to quantify the crisis, said that the mathematical models were not to be trusted because scientists do not know how much is an infectious dose and do not know how many people ate infected meat. "Those are two really big variables," he said. "All we can do is to set out a range of possibilities."
The LAURA LEE SHOW.
Copyright © 1997-2000 LL Broadcasting Inc. All rights
reserved.
Revised: December 18, 2000.
Section 7 subsection 9
MERCK MANUAL 13th ed. 1977 Ch. 6
Disturbances in Acid-Base Metabolism
pp. 1203-1209
DISTURBANCES IN ACID-BASE METABOLISM
The pH of ECE in health is maintained at about 7.40 (range, 7.35 to 7.45). Acute changes in pH due to acid or alkali loads (or deficits) are immediately damped by interaction with extracellular and intracellular buffer systems. In the absence of pulmonary disease, respiratory compensation further diminishes pH aberrations. Ultimately, however, the kidneys maintain pH homeostasis by excretion or retention of hydrogen ions and regeneration of lost buffers.
The bicarbonate (HCO3-) buffer system, one of several body buffers, is of singular importance. The Henderson-Hasselbaich equation, expressed in terms of the HCO3- systems, reads:
pH -6.1+ log HCO3-
a(Paco2)
where a = .03 mM/L/mm Hg at 38 C
At a pH of 7.4, the ratio of HCO3- to a (Paco2) is 20:1. Their ratio, rather than their concentrations, determines blood pH. The physiologic importance of this buffer system derives from the fact that two mechanisms (renal and respiratory) exist for adjusting the ratio of this major ECF buffer pair, and thus the pH of the ECF. The denominator a (Paco2) can be modified rapidly by changes in respiratory minute ventilation, while the numerator (HCO3- is subject to renal regulation.
Renal regulation of the HCO3- concentration of ECF is accomplished in servral ways. Hydrogen ion may be secreted into the renal tubular lumen in exchange for Na; for each hydrogen ion secreted, a HCO3- ion is added to the ECF. Thus, net reabsorption of filtered HCO3- occurs. Since the pH of the fluid leaving the proximal tubule is about 6.5, most filtered HCO3- is reabsorbed in the proximal tubules. In the distal tubule, hydrogen ion secretion is partially dependent, upon aldosterone-mediated Na reabsorption and can lower the pH to as low as 4.5 to 5. Throughout the nephron, secreted hydrogen ion is buffered by urinary buffers such as phosphate (titratable acid) and ammonia. In this manner, filtered HCO3 operationally is reabsorbed, and also new HCO3- can be generate4 to replace that lost in body buffer reactions. Since filtered Na is reabsorbed either in association with an anion (i.e., chloride) or by cationic exchange (i.e., with hydrogen ion and, to a lesser extent, potassium), the total Na reabsorbed approximates the sum of the chloride reabsorbed and hydrogen ion secreted. Thus, there is an inverse relationship between chloride reabsorption and hydrogen ion secretion. This relationship is highly dependent upon the existing level of Na reabsorption.
The renal HCO3- threshold also is influenced by body potassium stores. There is a general reciprocal relationship between intracellular potassium content and hydrogen ion secretion. Thus, potassium depletion is associated with increased hydrogen ion secretion and attendant HCO3- generation, leading to a HCO3-increase in ECF and metabolic alkalosis. Finally, the renal HCO3- threshold is influenced by the Paco2 and the state of ECF volume. An increased Paco2 leads to increased HCO3- reabsorption, and a decreased ECF volume leads to increased Na reabsorption and HCO3- generation; e.g., in the proximal tubule.
Clinical disturbances of acid-base metabolism classically are defined in terms of the HCO3- buffer system (see Henderson-Hasselbalch equation, above). Rises or falls of the numerator (HCO3-) are teritted, respectively, metabolic alkalosis or acidosis; rises or falls in the denominator (aPaco2) define, respectively, respiratory acidosis and alkalosis. Simple disturbances, include both the primary alteration and the expected compensation (e.g., in metabolic acidosis there is a primary fall in the HCO3- concentration of the ECF and a secondary fall in the Paco2 due to compensatory hyperventilation). Compensation may be classified as uncompensated, partial, or complete. Mixed disturbances are more complex disorder in which two or more primary alterations coexist (e.g., respiratory acidosis with superimposed diuretic-induced metabolic alkalosis).
It may be necessary to refer to a nomogram in order to distinguish simple from mixed disorders. However, measurement of the pH of arterial (or arterialized venous) blood, the Paco2, and the CO2 combining power (CO2 CP) of venous blood (or calculation of HCO3-) along with recognition of a disease entity known to produce an acid-base derangement and knowledge of the expected responses of the blood gases and buffers, including compensatory changes, are usually sufficient to correctly identify most clinical acid-base problems (see Table 11-36).
| Disturbance | pH | Paco2 | co2 Combing Power |
|---|---|---|---|
| Normal | 7.34-7.38 (venous) 7.38-7.42 (arterial) | 43mm Hg (venous) 40mm Hg (arterial) | 21-28 mEq/L |
| Metabolic alkalouis | up | up** | up* |
| Metabolic acldosis | down | down** | down* |
| Respiratory alkalosis | up | down** | down* |
| Respiratory acidosis | down | up* | up** |
| Mixed metabolic and respiratory acidosis | down | up | down |
| Mixed metabolic and respiratory alkalosls | up | down | up |
| Mixed metabolic acidosis and respiratory alkalosis | up down | down | down |
| Mixed metabolic alkalosis and respiratory acidosis | up down | up | up |
METABOLIC ACIDOSIS
A primary fall in extracellular fluid bicarbonate concentration pH and carbon dioxide combining power are reduced
Etiology and Pathogenesls
The principal causes of metabolic acidosis are shown in TABLE 11-37.
Excessive acid production or Ingestion: A common form is diabetic ketoacidosis with increased production of acetoacetic and B-hydroxybutyric acid. Occasionally, diabetic acidosis maybe associated with an altered NADH/NAD ratio leading to lactic aciddsis and elevated levels of B hydroxybutyric acid. The plasma ketone level is not increased when measured by the usual methods which detect only acetoacetic acid. Lactic acidiosis may develop in any state of diminished tissue oxygenation (e.g., vascular shock), with phenformin administration, or ethanol ingestion. Rarely it occurs idiopathically. In salicylate, methanol, or ethylene glycol poisoning, interference with normal intermediary metabolism or accumulation of exogenous organic anions may cause metabolic acidosis.
|
Impaired renal excretion of acid occurs in acute or advanced chronic renal failure due to reduced hydrogen ion excretion. In chronic renal failure, the major defect is insufficient ammonia production (and thus decreased ammonium ion excretion) as the result of progressive diminution in functioning renal mass. In renal tubular acidosis (RTA) with a relatively normal filtration rate, the defect is either proximal tubular HCO3- wasting (proximal RTA) or an inability to generate an acid urine (gradient-limited or distal RTA).
Symptoms, Signs, and Diagnosis
The major symptoms and signs of acidosis are often obscured by or difficult to separate from those of the underlying disease. Mild acidosis may be asymptomatic or may be accompanied by vague lassitude, nausea, and vomiting. The most characteristic finding in severe metabolic acidosis (e.g., pH <7.2 and CO2 CP<10 mEq/L) is hyperpnea, manifested by an early increase in depth and, later, frequency of respiration (Kussmaul breathing). Signs of ECF volume depletion may also be present, especially in patients with diabetic acidosis or gastrointestinal alkali loss. Severe acidosis may cause circulatory shock, due to impaired myocardial contractility and peripheral vascular response to catecholamines, and progressive obtundation.
Laboratory Findings
The urine pH is < 5.5 when the plasma HCO3- concentration falls to low levels with severe acidosis. The blood pH is < 7.35 and CO2 CP < 21 mEq/L. In the absence of pulmonary disease, the Paco2 is <40 mm Hg. Many forms of metabolic acidosis are characterized by an abnormal anion gap (Table 11-37). The anion gap (representing undetermined plasma anions) is estimated by subtracting the sum of the chloride concentration and CO2 CP from the plasma Na concentration (normal up to 15 mEq/L). Diabetic acidosis usually is characterized by the presence of hyperglycemia and ketonemia. In diabetic patients with hyperglycemia and nonketotic acidosis, blood lactic acid and B-hydroxybutyric acid levels are elevated. Ethylene glycol poisoning should be suspected in individuals having unexplained acidosis and oxate crystals in the urine. Sailcylate poisoning is characterized early by respiratory alkalosis with metabolic acidosis developing later; blood levels of salicylate are usually > 30 to 40 mg/ 100 ml; boiled urine gives a positive test (violet color) with ferric chloride.
Since volume depletion often accompanies acidosis, mild azotemia (BUN 30 to 60 mg/ 100 ml) is common. Greater elevations of the BUN, especially in conjunction with hypocalcemia and hyperphosphatemia, suggest renal failure as the cause of the acidosis. Changes in the serum potassium during acidosis were discussed earlier in this chapter.
Treatment
Therapy of chronic renal acidosis is discussed under ANOMALIES IN KIDNEY AND GASTROINTESTINAL TRANSPORT in §11, Ch. 7. The treatment of metabolic acidosis consists of therapy of the underlying disease (e.g., insulin in diabetic acidosis) and IV administration of sodium bicarbonate when acidosis is severe (pH <7.2). This can be given by adding varying amounts of sodium bicarbonate (44 to 88 mEq) to either D/W or hypotonic saline (one fourth or one half isotonic saline), or by using 5% sodium bicarbonate solutions, depending on the clinical setting and attendant water and volume disturbances. The goal of HCO3-therapy is to raise the CO2 CP to about 10 to 12 mEq/L. The amount of sodium bicarbonate necessary can be approximated by the formula:
mEq of NaHCO3 required =(CO2 CP desired - CO2 CP observed) x 25%TBW
The apparent distribution space of HCO3- is> 25% of TBW, due to continuing transfer of intracellularly buffered hydrogen ion out of cells into the ECF. However, it is best to raise the pH of the ECF only to a safe level, such as 7.2, while other measures are instituted to correct the cause of the acidosis, thereby averting some of the cqmplicatlons of alkali treatment. These include volume overload in patients with cardiac and renal disease and the precipitation of acute tetany in patients with renal failure. Too rapid correction of acidosis may also result in a rise in the Paco2 at a time when CSF bicarbonate levels are still low, thus inducing a "relative CSF acidosis". Occasionally, this may be associated with obtundation, coma, or death. In patients with marked overproduction of hydrogen ions (e.g., lactic acidosis), it may be necessary to give very large quantities of sodium bicarbonate IV in conjunction with dialysis to minimize ECF volume expansion.
RESPIRATORY ACIDOSIS
A primary increase in arterial carbon dioxide pressure; pH as low and carbon dioxide combining power increases renal function is intact.
Etiology and Pathogenesis
Respiratory acidosis is the result of alveolar hypoventilation leading to pulmonary CO2 retention.
It occurs with
|
Symptoms, Signs, and Diagnosis
The most characteristic change is metabolic encephalopathy with headache and drowsiness progressing to stupor and coma. It usually develops slowly with advancing respiratory failure, but abrupt, full-blown encephalopathy may be precipitated by sedatives or pulmonary infection in patients with advanced respiratory insufficiency. Asterixis and multifocal myoclonus are generally present; in some patients, dilation of retinal venules and papilledema result from increased intracranial pressure. The encephalopathy may be reversible if hypoxic brain damage has not occurred.
Laboratory Findings
In acute respiratory acidosis, the low pH is due to the acute elevation in Paco2. The CO2 CP may be normal or slightly increased. When renal compensation is fully developed, as in chronic respiratory acidosis, the fall in pH is blunted due to renal HCO3- retention and elevation of the CO2 CP. If diuretic therapy (e.g., for chronic cor pulmonale) causes superimposed metabolic alkalosis, the high Paco2 may be associated with a high CO2 CP, hypochloremia, and a normal or alkaline blood pH.
Treatment
The treatment must improve the underlying pulmonary disturbance. Severe respiratory failure with marked hypoxemia often requires mechanically assisted ventilation. Sedative drugs (narcotics, hypnotics) should be avoided except as necessary to facilitate mechanical ventilation. Although most patients with chronic CO2 retention and hypoxia tolerate modest O2 enrichment of inspired air, some patients respond with a significant fall in respiratory minute volume and further acute elevation of the Paco2. Presumably, such patients have adapted to chronic hypercapnia so that their major respiratory stimulus is hypoxemia. Therefore the lowest O2 concentration required to elevate the Paco2 to acceptable levels (>50mm Hg) should be given. This can be accomplished with O2 administration by a Ventimask, beginning with a 24% concentration. The Paco2 should be carefully monitored and, if it rises to dangerous levels (>50 to 55mm Hg), mechanical ventilation must be considered.
If mechanical ventilation is used in patients with chronic respiratory failure, the Paco2 should be lowered slowly, especially if concomitant metabolic alkalosis (high CO2 CP and normal or alkaline pH) is present. Rapid lowering of the Paco2 will cause severe metabolic alkalosis (pH >7.5).The resultant leftward shift of the oxyhemogiobin dissociation curve and cerebral vasoconstriction may lead to seizures and death. Providing adequate inspired 02, lowering the Paco2 more slowly, and repairing potassium or chloride deficits will prevent such neurologic consequences.
METABOLIC ALKALOSIS
A primary increase in blood bicarbonate; pH and carbon dioxide combining power are elevated.
Etiology and Pathogenesis
Metabolic alkalosis develops as the consequence of loss of acid from the ECF; e.g., loss of acid-containing gastric juice, loss of acid via the urine or stool, transfer of hydrogen ions into cells, excessive loads of HCO3- (e.g., alkali administration to patients with renal failure), or rapid contraction of the extracellular space (e.g., with potent diuretics). Whatever the cause, the kidney tends to correct the alkalosis rapidly by excreting excess HCO3-, unless other factors, such as volume contraction, result in both a Na-acquisitive state and an increased HCO3- threshold. Thus, a diminished effective arterial volume, potassium deficiency, and persistent adrenal steroid excess are common clinical settings for chronic metabolic alkalosis (TABLE 11-37, p. 1205). Perhaps the most frequent and important of these settings is ECF volume contraction and avid renal sodium reabsorption.
Diuretics cause metabolic alkalosis by several mechanisms, including
|
The loss of gastric hydrochloric acid by suction or vomiting produces metabolic alkalosis which is perpetuated by concomitant ECF volume contraction (sodium chloride loss in gastric juice) and development of potassium deficiency, due to secondary aldosteronism and potassium loss in gastric juice.
In states of persistent adrenal steroid excess, alkalosis results from steroid-mediated reabsorption of Na in the distal tubule in exchange for hydrogen ion. Sodium chloride reabsorption in the distal tubule leads to ECF volume expansion and decreased proximal Na reabsorption. Thus, a continuing supply of Na is delivered distally for exchange with hydrogen and potassium ions. Potassium depletion then leads to persistence of the alkalosia.
Symptoms. Signs, and Diagnosis
Metabolic alkalosis should be suspected in the above clinical settings. The most common clinical manifestations are irritability and neuromuscular hyperexcitability, perhaps due to hypoxia from a transient leftward shift of the oxyhemoglobin dissociation curve. When severe, the ionized calcium fraction may fall low enough to provoke tetany, although total serum calcium is unchanged (see HYPOCALCEMIA, above). Muscular weakness, impaired gastrointestinal motility (e.g., gastric retention, ileus), and polyuria should suggest potassium depletion.
Laboratory Findings
The blood pH and CO2 CP are elevated. Striking increases in the Paco3 to levels as high as 50 to 60 mm Hg may occur with compensatory hypoventilation, especially in patients with mild renal insufficiency. The urine is alkaline except in the presence of severe potassium depletion, in which case it may be acid ("paradoxic acidurla"). Hypochloremia and hypokalemia are usual.
Treatment
Correction of the underlying disturbance is desirable when possible. Metabolic alkalosis usually resolves when ECF volume deficits are replaced with oral or IV sodium chloride. However, when potassium deficiency is severe, or in patients with adrenal steroid excess, the alkalosis cannot be corrected until the potassium deficit is repaired (saline-resistant alkalosis). In the post-hypercapnic state, persistent metabolic alkalosis responds to chloride, given as potassium chloride, sodium chloride (if volume depletion is present), ammonium chloride, or arginine hydrochloride. When mild, metabolic alkalosis usually requires no specific therapy. It should be corrected promptly, however, in patients with myocardial irritability and those with neuromuscular hyperexcitability. In such instances, ammonium chloride administration may be desirable along with other measures (e.g., correction of hypokalemia).
RESPIRATORY ALKALOSIS
A primary decrease in carbon dioxide pressure; blood pH is increased and carbon dioxide combining power is reduce.
Etiology and Pathogenesis
Hyperventilation, leading to excessive loss of CO2 in expired air, results in respiratory alkalosis. The Paco2 and cerebral tissue Paco2 fail, and both plasma and cerebral tissue pH rise. Cerebral vasoconstriction results and, along with the Bohr effect, may produce cerebral hypoxia and the characteristic symptom complex.
This develops following stimulation of the respiratory system
|
Symptoms, Signs, and Diagnosis
Obvious hyperventilation may be present although the breathing pattern in the anxiety-induced syndrome is variable. Tetany, circumoral paresthesias, acroparesthesias, giddiness or lightheadedness, and syncope may occur. In such patients, the symptoms often can be reproduced by voluntary overventilation. Blood lactate and pyruvate levels increase and ionized calcium falls. In all situations, the diagnosis of hyperventilation is confirmed by finding a low Paco2.
Treatment
Respiratory alkalosis due to anxiety resolves on rebreathing expired CO2 from a paper bag (plastic bags may cause accidental suffocation). Other measures aimed at amelioration of chronic anxiety may be helpful (e.g., sedative or tranquilizing drugs). Overventilation with mechanical respirators can be corrected by diminishing minute ventilation, when excessive, or by adding dead space. When hyperventilation is due to hypoxemia, O2 enrichment of inspired air and treatment aimed at correction of abnormal pulmonary gas exchange is appropriate. Correction of respiratory alkalosis by increasing the inspired CO2 concentration may be dangerous in patients with CNS disturbances (which may be associated with a low CSF pH). The treatment of salicylism is given in §lO, Ch.4
Section 7 subsection 10
http://www.sightings.com/general2/frenzy.htm
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Rense.com
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Report Of Chemtrail
Spraying Frenzy In Croatia
From Izakovic Rolando rolando.izakovic@kvarner.net
6-5-00
UPDATE
From Izakovic Rolando rolando.izakovic@kvarner.net
Dear Jeff,
Here are some exclusive images featuring still ongoing chemtrail spraying operation ower town of Rijeka and it's region in Croatia, as was reported on your page http://www.sightings.com/general2/frenzy.htm on 06-05-00. They were taken by me with a simple automatic 35 mm camera on several occasions, during usual everyday activities. Most had to be taken in direction of the sun because chemtrails are sprayed upwind of the aimed location, if possible during a calm and sunny day.
As was stated in earlier post, all started in the morning on Saturday, 05-27-2000, a single day after Croatia signed Partnership for Peace with NATO. At 16:20 CET, sky above my garage (view towards east) looked like this, shoving a very low, spread chemtrail:
At 16:25, some 4 km to the North an 'X' marking the center of a new chemtrail layer, was placed above well-spread old one:
To the East scene looked like this. Notice three fresh chemtrails layered low over the nearby hills:
You could touch chemtrail sailing over my rooftop. Being unfamiliar with local ever-changing wind direction, jet zoomed over it laying a fresh one:
In the same time, from the opposite side of my house, you could see 20 km wide Kvarner bay with clear skies. In order to save on chemicals jets have simply cut the spraying when over the sea. This confirms recent reports that the chemtrail spraying system is a separated one.
On the Thursday morning, 06-02-2000, at 09:30 CET, on the plateau 130 m above Rijeka, where my company is located (I am Chief Designer and Marketing Manager of the main genset manufacturing company in Croatia) the "X marks the spot" sign was placed by two low-flaying jets, after the wind have blown away the earlier efforts. It looked like this:
I drove to the town to develop the first film reel and took this images on the main parking lot, 500 m from the city center:
Again, old chemtrails were hundred meters above the ground, and new ones were placed upwind. They had a "no" day because of the constant wind direction changes and sky above Rijeka remained clear. After I have loaded a new reel, while walking over the city square I have taken this photo showing a chemtrail laid by a nervous pilot. Birds got nervous, but people around me are not noticing anything. Or they do, but it is too strange for them to be pointed at:
Next Friday morning, 06-09-2000, sky above my company's parking lot looked like this:
This time they flew in the straight lines from the North, starting in neighboring Slovenia (those mountains on the horizon). State borders are not a factor for this kind of operation.
Weather was perfect for chemtrail spraying. Around noon I took this close-up in the sky above the main city parking lot:
Around 14:00 CET, heavy, low chemtrail clouds drifted to the city center:
Unfortunately, this is not all. There is more. All the best. IZAKOVIC, CROATIA----
Dear Jeff,
Watching your site, I saw that chemtrails are on again.
This world-exclusive news which, because of its frequently used theme, shall probably be of low interest to your public, is important in that it points out the existence of the significant pressure under which particular Western agencies currently operate:
On 5-26-00, merit of the new social democratic/ liberal government elected last January, after ten-year rule of the Croatian Democratic Union, Croatia finally entered NATO's 'Partnership for Peace.'
Immediately, the NEXT day, Saturday morning 5-27-00, heavy aerial spraying of Croatian main port town Rijeka commenced. Being the first time-ever, foreign aeroplane pilots had the worst luck in guessing the direction of local, constantly changing winds, which they partially-compensated for, in a typically Western way, by working hard all day long.
Pressed by the forces unknown to us, they had to come again second time next Tuesday afternoon, 5-30-00. They start spraying just one hour after the skies have cleared from the day-long rain (they probably waited on the red alert somewhere near).
Third spraying, starting Thursday morning, 6-1-00, was shambles. It had all gone wrong right from the start, when the ' X' marking the centre of the chemtrail-laying effort, suddenly found itself downwind.
Even the transfer of spraying to the opposite side of the town, at the time upwind, did not help because the wind had swiftly changed direction again. So, during the next Saturday night, 6-3-00, they had to increase their efforts dramatically, and the town of Rijeka woke up with a low, thick chemtrail cover.
Operations continued all day long, resulting with incredible chemtrail fog cowering everything from the sea level up to the heavens, if there were any. It was really spectacular because, in these parts, anything remotely resembling fog occurs only during the winter, once in a ten-fifteen year period, or so.
Locals are totally unaware of the origin, state and ramifications of this whole affair and are content to be a joint member of the Brave New World.
All the best, IZAKOVIC,
CROATIA
SIGHTINGS HOMEPAGE
http://www.sightings.com
This Site Served by TheHostPros
Section 7 subsection 11
William R. Platt, ND., F.C.A.P., F.A.C.P. Chief of
Pathology,
U. S. Public Health Service Hospital;
Lecturer in Pathology,
The Johns Hopkins University School of Medicine Baltimore,
Maryland;
Associate Professor of Pathology (Visiting Staff)
Washington University School of Medicine
St. Louis, Missouri
Chapter 1 pp. 1-10
There are certain embryologic-morphologic criteria, pathophysiologic data and diagnostic laboratory procedures involving blood that provide hematologic knowledge that is essential to the complete clinical study of any patient.
Simply stated, blood is a unique bright (arterial) to dark (venous) red fluid of variable composition circulating through the transport vessels of the body with a total volume of approximately 30 ml./kg. body eight. It participates in the physiologic and pathologic activities of all organs and is imposed of a liquid called plasma in which are suspended erythrocytes (red blood cells), leukocytes (white blood cells), and rombocytes (platelets), collectively called hemocytes. These elements of the blood have differing functions. The red blood cells are intimately associated with cardiac output, pulmonary and kidney activity, and blood vessel response in order to oxygenate body tissues. The white blood cell components participate in phagocytosis, utilizing the granulocytes and monocytes together with coexistent factors in the plasma. The lymphocvtes and successor plasma cells function in the elaboration of gamma globulin fractions, which are intimately associated with antibody formation and tissue alterations. The eosinophils and basophils participate in hypersensitivity phenomena.
The platelets are initiators and co-sponsors of the coagulation process.
Clinical hematology is the division of medicine associated with diagnostic laboratory procedures and morphologic interpretations related to blood, and with the correlation of this hematologic data with the entire clinical condition of the patient. Hematology is concerned with the sum total of the interaction of the hematopoietic and the vascular systems. The hematopoietic system is that organ complex associated with the morphologic components of the blood and the manner and loci of their pathophysiologic formation and function. The vascular system can be defined as the entire arrangement of vessels operative in the circulation of all body fluids, including the heart, arteries, capillaries, veins, and lymphatics. If blood coagulation (clotting) is prevented after blood is withdrawn from the vascular system, the formed cellular elements of the blood (hemocytes) can be separated from the noncellular liquid portion (pale straw-colored plasma). Serum, on the other hand, is the amber-colored fluid that remains after separation of the clot associated with blood coagulation. It differs from plasma only by the loss of the protein fibrinogen, which is removed together with the blood cells as insoluble fibrin threads in the coagulation process.
The individual cytologic components of the blood may be defined as follows:
The erythrocyte (red blood cell) is an elastic non-nucleated biconcave discoid cell usually found in the lumina of peripheral blood vessels. It has an average life span of 80 to 120 days, an average diameter of approximately 7.2 u, and is a pale greenish yellow when unstained (it stains eosin red with the Romanowsky or Wright stain). The main function of the erythrocyte is the carrying of hemoglobin with its associated 02 and CO2.
The leukocyte (white blood cell) is a nucleated living cell 8 to 12 u in diameter and is found in the bone marrow and peripheral blood. It has an indefinite, variable life span. In the peripheral blood, leukocytes are mainly composed of polymorphonuclear cells (with a life span of 3 to 4 days), lymphocytes (with a life span of approximately 4.4 years or longer), monocytes (life span of approximately 2 days to 2 weeks), and occasionally plasma cells (long life span of unknown duration). Leukocytes also have certain nuclear and cytoplasmic staining and morphologic qualities when the Romanowsky stains are used. Each type of leukocyte plays some part in the protection of the body from disease— by phagocytosis and immune body formation.
The thrombocyte (platelet) is a morphologically irregular fragment (with an average life span of 8 to 11 days) derived from the cytoplasmic portion of megakaryocytes (parent cell usually situated in the bone marrow). It has a purple-red color with Romanowsky stains (for example. Wright’s stain) and is essential for the proper coagulation of shed blood, clot retraction, and adhesion to the wall of a damaged blood vessel for the purpose of repair. Thrombocytes have recently been reported to be able to attract submicroscopic particles, and they therefore may enhance the removal of solid particles from the blood.
Any moderate to marked variation in the number, morphologic alteration, and function of one or more of the cytologic components of the blood will produce a hematologic symptom called a blood dyscrasia.
In order to understand the significance of qualitative and quantitative variations in bone marrow and peripheral blood, a brief review of the physiology of the blood and blood-forming organs seems appropriate at this point.
The main organs of hematopoiesis are the bone marrow, liver, spleen, thymus, and lymph nodes. Hematopoiesis begins during fetal life; however, under specific situations of stress the liver, spleen, thymus, and lymph nodes may revert to their fetal function and demonstrate extramedullary hematopoiesis. Fatty material occupies most of the bone marrow spaces in adult life except in the flat bones, where blood cell formation remains physiologically active: the fatty areas serve as foci of reserve hematopoiesis as the need may arise in various diseases. The main functions of the cells of the hemabopoietic system are those of oxygen transport. resistance to infection, antibody production, hemorrhage cessation, and reaction to foreign material.
Reductions in cell proportions are occasionallv related to physiologic aberrations — for example. reduction in oxygen supply to tissues due to reduction in hemoglobin or in red blood cells. overwhelming infection ~ with poor host response due to a reduction in leukocytes. and petechial and hemorrhagic manifestations due to platelet deficiency. In addition. these cytopenias may affect the interinvolvement of coagulation factors I to XIII, the integrity of capillary endothelium. and the action of thrombocytes in hemorrhagic diseases. The knowledge of the relationships of the basophil to heparin and histamine production, neutrophil to bacterial phagocytosis; of the lymphocyte and plasma cell to antibody production; of the eosinophil to stress (adrenocortical activity); and of the eosinophil and basophil to hypersensitivity phenomena is still complex but is rapidly developing through the impetus of immunobiologic phenomena. Hyperplasia of hematologic cellular elements may result in disturbed physiologic functions—for example, thrombotic tendencies associated with thrombocythemic and polycythemic states. organ enlargement, and pain in leukemic and lymphomatous states. Finally, atypical cytologic function may be associated with hemolysis in intrinsic red blood cell disease and with hyperglobulinemia in lymphocyte and plasma cell diseases.
Cellular elements of blood may be defined as follows (Plate I):
In the erythrocyte, hemoglobin is the main functioning constituent and has a molecular weight of approximately 66,000. The function of hemoglobin is the transportation of oxygen to the tissues, the removal of carbon dioxide from the tissues, and the buffering of blood, which aids the maintenance of the constant reaction of blood. The last is accomplished by the intraerythrocytic enzyme, carbonic anhydrase, which catalyzes the carbon dioxide and transforms it into carbonic acid. The hydroiten ions of carbonic acid are then buffered by the moderately alkaline deoxyhemoglobin, and the bicarbonate ion diffused back into the plasma. In the pulmonary capillary the same process, in reverse, liberates carbon dioxide for pulmonary elimination. In addition, the amino groups of the globin fraction of hemoglobin form reversible carbamino groups with carbon dioxide and are responsible for approximately 10 per cent of carbon dioxide transport and excretion. Reticulocytes are young, slightly enlarged red cells in which the reticular or uranular network is revealed by supravital stains counterstained with Romanowsky’s stain.
Thrombocytes and leukocytes have been briefly discussed above. The following are various types of leukocytes.
Granulocytes are motile polymorphonuclear cells having ameboid activity, variegated nuclear shape, and cytoplasmic granules. A juvenile or band form is a transitional cell type that developmentally is between the marrow metamyelocyte and the mature granulocyte of the peripheral blood. This form is characterized by an elongated C-shaped nuclear pattern without distinct lobe formation; the number of nuclear lobes denotes the age of the cell, with older cells having more lobes. A neutrophilic (polymorphonuclear) granulocyte has an average diameter of about 10 to 12 u with two to four lobes and slightly acidophilic granules in the cytoplasm. An eosinophilic (polymorphonuclear) granulocyte is approximately the same size as the neutrophil, usually with two lobes. It contains large, coarse, round or oval eosinophilic granules that stain a deep pink and usually fill the cell proper. The basophilic (polymorphonuclear) granulocyte, which is functionally and chemically related to the mast cell, has an average diameter of 8 to 10 u It has a kidney-shaped or slightly lobulated nucleus and large, deep purple granules in the cytoplasm that often obscure nuclear detail.
Lymphocytes are mononuclear leukocytes originating and differentiating first in the primary lymphoid structures of the bone marrow and the thymus. They are then distributed to the secondary lymphoid organs (spleen, lymph nodes, tonsils, pharynx, and subepithelial lymphoid tissue in the gastrointestinal tract), where they are characterized by arrangement into follicles with germinal centers and where they function in specific immune responses. They have an average diameter of 12 to 15 u in the large motile type and 7 to 8 u in the small nonmotile type. The circular, deeply basophilic chunky chromatin-containing nucleus occupies practically all available space in the cell and possesses a clear pale blue rim of cytoplasm (Wright's stain) with occasional distinct reddish-purple azurophil granules.
| Age | Hb(gm.) | Hematocrit(%) | RBC(million/cu.mm) | Platelates(thousand/cu.mm) | Reticulocytes(%) | WBC(cu.mm) | PMN adult | Band(%) | Eosinophils(%) | Basophils(%) | Lymphocytes(%) | Monocytes(%) |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Birth | 17.6 | 55 | 5.5 | 350.0 | 5.0 | 9000—30,000(av., 18,000) | 9400(52%) | 9.1 | 2.2 | 0.6 | 31 | 5.8 |
| 24hrs. | 18.0 | 56 | 5.3 | 400.0 | 5.2 | 9400—34,000(av., 19,045) | 9800(52%) | 9.2 | 2.4 | 0.5 | 31 | 5.8 |
| 1 wk. | 17.0 | 54 | 5.0 | 300.0 | 1.0 | 5000—21,000(av., 12,279) | 4700(39%) | 6.8 | 4.1 | 0.4 | 41 | 9.1 |
| 2 mos. | 12.4 | 30 | 4.3 | 260.0 | 0.5 | 5500—18,000(av., 11,000) | 3300(30%) | 4.4 | 2.7 | 0.5 | 57 | 5.9 |
| 6mos. | 11.5 | 34 | 4.6 | 250.0 | 0.8 | 6000—17,500(av., 11,900) | 3300(28%) | 3.8 | 2.5 | 0.4 | 61 | 4.8 |
| 2 yrs. | 12.9 | 40 | 4.8 | 250.0 | 1.0 | 6000—17,000(av., 10,680) | 3200(30%) | 3.0 | 2.6 | 0.5 | 59 | 5.0 |
| 6yrs. | 14.1 | 42 | 4.8 | 250.0 | 1.0 | 5000—14,500(av., 8500) | 4000(48%) | 3.0 | 2.7 | 0.6 | 42 | 4.7 |
| l4yrs. | 15.0 | 45—m 42—f | 5.1 | 250.0 | 1.0 | 4500—13,000(av., 7900) | 4200(53%) | 3.0 | 2.5 | 0.5 | 37 | 4.7 |
| 21 yrs. | 15.0 | 45m 42f | 5.1 | 250.0 | 1.0 | 4500—11,000(av., 7400) | 4200(56%) | 3.0 | 2.7 | 0.5 | 34 | 4.0 |
Monocvtes are occasionally motile, large mononuclear leukocytes originating in the marrow, measuring approximately 14 to 19 u. These cells are the major source of macrophages in sites of inflammation. They have a lobulated kidney-bean- or horseshoe-shaped pale violet nucleus with vesicular chrornatin crisscrossing the nuclear strands. The nucleus is often located to one side of the cell. The cytoplasm is pale grayish blue, sometimes with an irregular outer border, sometimes vacuolated, and occasionally containing red-staining Auer bodies.
Percentageof Cellular Elements in Blood. Quality control studies of the peripheral blood show some variation in the oft-quoted “norm” values given in various texts of hematology. However, a range of values presents a more accurate approach to blood composition. For reference purposes. see Table 1—1.
Percentage of Liquid Constituents. Included among the liquid constituents are diffusible anabolic substances, diffusible catabolic substances, and nondiffusible constituents.
Because blood is the specialized fluid tissue of the transport system of the body, it contains liquid constituents in which its solid elements are suspended (Fig. 1-1). The specific gravity of whole blood averages between 1.048 and 1.066 to 1.057 in males and 1.053 in females. The specific gravity of serum is 1.026 to 1.031 and that of red blood cells is 1.092 to 1.095. The pH of nonnal blood is 7.35 to 7.45 (the range compatible with life is 6.8—7.8). Total blood volume in terms of body weight is greater in males than in females. chiefly owing to the higher red cell volume in the male. Average values are 75.5 ml./kg. in males and 66.5 ml./kg. in females. or a total of 5 to 6 liters or about 7 to 8 per cent of body weight. Blood cells make up 45 per cent by volume of the whole blood, and because they are heavier than plasma, they sink to the bottom of an anticoagulated blood sample. Blood plasma, which is composed of serum plus fibrinogen, makes up 55 per cent of blood volume: water makes 91 to 92 per cent by weight of the plasma, and plasma protein. 6 to 7 per cent by weight of plasma. The plasma proteins, which are formed mainly in the liver, exert an osmotic pressure of 25 to 30 ml. of mercury, are nondiffusible, and are important in regulating blood volume and the body’s fluid balance. Plasma proteins are also responsible for blood viscosity, which is important in maintaming blood pressure. The plasma proteins are composed of:
|
Also present in the plasma are regulatory and protective proteins, such as hormones, enzymes, and antibodies. Diffusible anabolic substances include inorganic material (0.9%), such as sodium chloride, calcium, potassium, acid carbonate (HC03) iodine, and iron. Also included in this category are nutritive organic materials (such as amino acids, glucose, fats, cholesterol, all of which are foodstuffs in solution absorbed from the gastrointestinal tract, from which they go to other body tissues for utilization and storage), plus respiratory gases (02 and C02). Diffusible catabolic constituents (such as urea, uric acid. xanthine. creatine. creatinine, and ammonia) in plasma are products of tissue activity that are transported from tissues to kidney and skin for excretion. From the preceding discussion. one can summarize the functions of blood as respiration. nutrition. excretion, maintenance of water content in tissues. and regulation of body temperature.
| BODY WEIGHT | WHOLE BLOOD (Volume) | FORMED ELEMENTS (number per cubic millimeter) | PLASMA WEIGHT | LEUKOCYTES (Differential) | PROTEINS plasma/serum (Electrophoresis) | GLOBULINS (Electrophoresis) |
|---|---|---|---|---|---|---|
| BLOOD 8% | FORMED ELEMENTS 45% | LEUKOCYTES 5,000-10,000 | PROTEINS 7% | NEUTROPHILS 57-67% | ALBUMIN 55% | ALPHA 14% |
| OTHER FLUIDS AND TISSUES 92% | PLASMA 55% | ERYTHROCYTES 4.2-6.2 MILLION | WATER 91.5% | EOSINOPHILS 1-3% | GLOULINS 38% | BETA 13% |
| - | - | PLATELETS 140,000-340,000 | Inorganic salts, lipids, enzymes, horomones, vitamines, carbohydrates, 1.5% | BASOPHILES 0-0.75% | FIBRINOGEN 7% | GAMA 11% |
| - | - | - | - | LYMPHOCYTES 25-33% | - | - |
| - | - | - | - | MONOCYTES 3-7% | - | - |
When a technician approches the patient for blood withdrawa1, he should radiate an attitude of confidence, self assurance, and poise. He should explain briefly what he is going to do so that the patient will give his full cooperation. It is essential that the request slip with the name of the patient, room number, and physician’s name is checked verbally with the patient, that all tubes and equipment are in readiness and properly numbered, that the patient and operator are both comfortable. and that there is good light. The technician should be sure that he has blood lancets, sharp needles of proper size, and a dry syringe or proper Vacutainer in good working condition. Material for cleansing the arm, tourniquet, containers for blood, and other equipment should be conveniently placed. If the patient is in bed, a disposable towel placed under the arm prevents the soiling of linen. It is desirable that the patient be reclining when the skin puncture is performed because he is more easily controlled if he feels sick or faint. If the patient is seated, the arm should extend over the corner of a table, and be placed on a disposable towel.
In selecting the site for blood withdrawal, consideration must be given to the type of laboratory test requested, the volume of blood required, and the age of the patient. For example, if both blood chemistry procedures and hematologic procedures are ordered, it is more efficient to obtain a suitable quantity of venous blood with only one venipuncture (especially in using the Vacutamer tubes with or without various types of anticoagulants). If the patient is an infant or is severely burned, adequate samples may be obtained from a skin puncture utilizing microtechniques. In the adult and child. the median basilic veins in the antecubital fossae are most suitable. The best right or left vein is selected after observation and palpation of both antecubital fossae.
For small specimens from adults, the usual puncture sites are the lobe of the ear or the end or side of the distal phalanx of the third or fourth finger. The heel, great toe, or skin of the forearm below the elbow are the sites of choice in very young infants. For continued cooperation, older children should be told what type of ”pinprick” to expect when a puncture is made.
The materials needed are blood lancets (heat sterilized, disposable lancets in sealed envelopes, cotton pledgets, and alcohol(70%).
Technique. A free flow of blood should be assured by warming or rubbing the skin of the site chosen with a piece of dry cotton. The puncture site should be cleansed with 70 per cent alcohol applied with a cotton pledget, and allowed to dry. The skin is then made tense, and the needle placed on its surface. A clean, quick jab 2 to 3 mm. in depth is made with the disposable blood lancet. The first drop of blood is wiped away with a dry cotton pledget; the next drop will well up naturally. Blood is then drawn up into the dilution pipettes by capillarity. After the proper amount of blood has been obtained, a cotton pledget moderately soaked in antiseptic (70% alcohol) is lightly pressed over the puncture site until bleeding has ceased. Sterile 2 x 2 inch gauze may be used instead of the cotton pledget.
Advantages. This technique has several advantages. It is a relatively easy and painless method of obtaining volumes of blood adequate for the information desired, especially from infants. Blood may be taken more than once, even if the patient has poor veins, is uncooperative, or if patient is in shock or badly burned over a large part of his body. It is easy to control the flow of blood using this technique in patients who have a hemorrhagic disease, especially from a finger puncture site. The disposable equipment used reduces and possibly eliminates the potential danger of transmitting infection — for example, the virus of homologous serum hepatitis.
Disadvantages. The blood count may be incorrect if:
The finger is squeezed after puncture, and the blood is diluted with tissue fluids or is concentrated by stasis. Also, squeezing enhances clotting. However, moderate pressure some distance above the puncture is allowed.
The blood flow is not free—that is, if a small amount of blood is obtained and further pressure needed. The red blood cell count and hemoglobin may be higher or lower, and hematocrit and platelet count lower (platelets lost by adherence to puncture tissue area).
Collection of the blood will be made difficult if the skin at the puncture site is not dry; that is, the blood will spread along the surface. Also, if alcohol is mixed with the blood collected, the cells will be distorted and a dilution error will be introduced.
For large specimens, in which venous blood is collected, the veins in the bend of the elbow, the back of the wrist, or the ankle region are used. If the technician is confident and experienced and if repeated venipunctures are to be made for repeated tests and infusions, it is wise to use the wrist and ankle areas. However, if the vessels in these sites are not prominent, if the patient is exceedingly apprehensive (with a low threshold for pain), or if the technician is not highly proficient, the median basilic or cephalic elbow vein is best to use. In obese patients, veins that appear as faint blue lines are usually too superficial and too small and should not be used. It is best to have the patient look away as venipuncture is being performed. The patient should be comfortable and lying down, and good light should be present.
The materials needed are cotton pledgets; alcohol (70%); a tourniquet such as one made by using laboratory rubber tubing (18 in. long by 1/4 in. wide) or one of the commercially available flat or tubular tourniquets; and multicolored, rubber stoppered Vacutainers containing anticoagulants such as Sequestrene (dipotassium or tripotassium ethylenediaminetetraacetate (EDTA]), balanced oxalate (ammonium and potassium oxalate) with or without fluoride, or nonanticoagulant tubes. Sequestrene (the dipotassium or disodium salt of ethylenediaminetetraacetic acid, EDTA) is preferred for erythrocyte counts, leukocyte counts, hematocrits, and platelet counts because it maintains good morphology for 3 to 4 hours after blood is drawn. However, if it is refrigerated, blood counts may be performed for as long as 24 hours after collection in EDTA. EDTA also acts as an anticoagulant by binding calcium in the blood in a nonionized form, therefore making the calcium unavailable to the blood clotting mechanism. EDTA is used in a concentration of 1 to 2 mg./ml. of blood. The most widely used anticoagulant is a mixture of ammonium and potassium oxalate (6 and 4 parts respectively), a total of 2 mg./ml. of blood. It may be used for hemoglobin and other tests for which EDTA is used; double oxalate, not EDTA, must be used for the "sucrose hemolysis” test for paroxysmal nocturnal hemoglobinuria.4 However, the ammonium potassium oxalate mixture cannot be used for the study of blood film preparations after remaining in the blood film for more than 2 or 3 minutes because there is rapid artifact formation and other malformations in lymphocyte and monocyte nuclei, vacuolation in granulocyte cytoplasm, oxalate crystal phagocytosis. and red cell crenation. This balanced oxalate anticoagulant also cannot be used for nitrogen (BUN) or potassium determinations in blood chemistry. Disodium citrate (1 part of 3.8% solution and 4 parts of blood) is only useful in determining sedimentation rates and in the investigation of clotting mechanisms. The oxalate and citrate anticoagulants act as EDTA does in preventing the coagulation of blood. Heparin (o.1 mg./ml. of blood) acts as an anticoagulant by neutralizing thrombin. It is best for preventing hemolysis in osmotic fragility tests and does not affect the corpuscular size and hematocrit. It is not good for blood films in which Wright’s stain is used, because it produces a bluish background. The Vacutainer tubes are desirable because tbey are disposable and only one needle stick is needed for as much blood as is desired. Vacutainers and similar preparations are test tubes vacuum sealed by a flexible rubber stopper, which is punctured by the rear end of a special needle held in its own adapter when the front end of the needle has entered the vein (see following section). The collection tube, which utilizes this technique, also serves as a syringe. However, if this equipment is not available, sterile dry Luer syringes with standard center tips are suitable (5—10 cc. volume). Sharp needles should be 19- to 22-gauge and I to 1.5 inches in length. Disposable needles are preferred for patient’s comfort, ease of venipuncture, and avoidance of risk of transmitting homologous serum hepatitis. Time is also saved because sharpening and beveling needles are eliminated.
Technique and Selection of Vein. Adults and Children. The puncture area is cleaned with an alcohol sponge. A tourniquet is placed about 2 inches above the site of puncture so that it may be released easily. The tourniquet should not be tightened enough to cut off arterial circulation; that is, the radial pulse at the wrist should be palpable. The patient should open and close his fist a few times and then close it tightly. Vacutainer tubes are used. If these are not available, the plunger of a regular syringe is pulled back to make sure that the needle is open. The needle is checked to make certain that it is attached tightly, and the plunger is depressed to its closed position. The patient’s arm is grasped with the technician’s free hand (usually the left), and the technician places his left thumb directly over the vein approximately 1.5 inches away from the intended puncture site. Gentle traction is then applied.
The syringe is held between the right thumb and the last three right fingers. With the needle bevel up, above, and directly in line with the course of the vein, the needle is inserted quickly and steadily under the skin and then into the vein. Some prefer to insert into the skin and vein in one complete motion. When the needle has entered the lumen of the vein, penetration is felt to be easier, and blood will flow freely into the syringe. The amount of needed blood is withdrawn by exerting gentle traction on the plunger. Frothing and hemolysis are avoided by withdrawing blood slowly.
The tourniquet is released and the needle is then slowly withdrawn. A sterile gauze or alcohol cotton pledget is applied to the entry site and held tightly. The patient is told to maintain pressure with his free hand for 3 to 5 minutes to prevent bleeding and hematoma formation. According to some sources, it is better to elevate the patient’s arm slightly and, with a piece of dry sterile gauze or cotton over the entry site, to apply thumb pressure at the site. The needle is removed from the syringe, and the blood is carefully transferred to the proper containers. Each container is tilted so that the blood runs down the side. thus minimizing trauma and frothing. The containers are gently inverted several times to mix the blood and anticoagulant. This is especially important in cases of hypergiobulinemia, anemia. and hyperfibrinogenemia, in which leukocytes and platelets will tend to settle upon standing. Prior to manual or automated counting, the specimen should be inspected for macroscopically visible autoagglutination of erythrocytes, platelet aggregation, and the presence of clots. The plunger is pulled back, and the syringe and needle are immediately rinsed with cold water.
Infants. When the infant is crying, the external jugular vein in the neck is easily visible. The infant is wrapped in a blanket up to and including his shoulders, thus completely immobilizing his chest, trunk, and extremities. The infant is placed flat on a table with his shoulders on the edge of the table and his head turned to the side and stretched slightly downward. The external jugular or internal jugular vein becomes more prominent in this position.
A syringe with a 21-gauge needle is then placed just lateral to the outer border of the smernocleidomastoid muscle pointed toward the chest area and midway between the tip of the mastoid process and the clavicle. The needle. with bevel up, is then inserted in a direction aimed at the sternoclavicular junction just beneath the sternomastoid muscle. The needle is then withdrawn slowly, and traction is maintained on the plunger until blood begins to enter the syringe barrel.
If the foregoing procedure is not feasible, puncture of the femoral vein may be performed. The femoral artery is palpated with the index finger as it passes through the femoral canal area. With the index finger over the pulsating femoral artery, the needle, bevel up, is inserted just medial to the finger down toward the superior ramus of the ischium (bone). The needle is then pulled back slowly, and continuous traction is maintained on the plunger until blood begins to come into the syringe barrel.
Advantages. This is the easiest and most convenient method of obtaining a volume of blood adequate for a variety of tests; more than one type of test can be done with the large volume of blood obtained using this procedure—for example, hematologic, chemical, and serologic.
The sample may be divided and treated as the prescribed investigations demand. Thus, some of the sample may be mixed with anticoagulant to provide plasma or whole blood; some may be allowed to clot to provide serum and to determine accurately clotting time; some may be used to make blood films and blood cultures.
In addition, this is the fastest method of collecting samples from a large number of patients, for it allows accurate dilutions to be carried out with more leisure once the morning collection rush is over. This method also reduces the amount and variety of apparatus needed in the hospital wards.
By providing sufficient blood, this method allows various tests to be repeated in case of accident or error, or for the all important checking of a doubtful result. It frequently allows the performance of additional tests that may be suggested by the results of those already ordered or that may occur to the clinician or clinical pathologist as after thoughts. It reduces the possibility of error associated with the finger puncture technique, which results from dilution with tissue juices or constriction of skin vessels by cold or emotion.
Disadvantages. This method may cause hemoconcentration with subsequent erroneous hematologic and biochemical results, all due to prolonged application of the tourniquet. Blood may fail to enter the syringe owing to collapse of a small vein. the outer coat of the vein without entering the lumen may lead to hematoma formation and subsequent pain around the puncture site. When this technique is used, blood may not be obtainable from the veins of a patient with circulatory failure. Syncope may occur in some patients after venipuncture, and continued venous oozing may occur in patients with a bleeding tendency.
Thrombosis of a vein may occur as a result of trauma or infection with the possible subsequent development of thrombo phlebitis. Homologous serum jaundice may be transmitted to patients by improper handling and contamination of needle or of syringe. Arterial puncture may occasionally occur, especially in children.
Bone marrow is the heterogeneous organ located within the interstices in cancellous bone and between the trabeculae of the marrow cavities in long bones. On aspiration, bone marrow has a rusty red color and normally has a thick fluid like consistency with varying amounts of fatty material and pale gray white marrow fragments.
Section 7 subsection 12
http://www.moreton.com.au/ana/handbook/leakygut.htm
Recent scientific evidence has given credence to a theory of auto intoxication that was proposed at the turn of the century. Many studies have shown that an inflamed gut is more permeable to partially digested food and bacterial fragments. eg. lipid polysaccharides from bacterial breakdown, partially digested food products and other endotoxins.
This increase in permeability results in an inflammatory cascade in various tissues as well as increasing the toxic insult to the liver. Depending on the individual and his ability to detoxify these leaky gut metabolites, a number of symptoms can arise, from neurological, endocrine and metabolic eg. mood changes, memory lapses, irritable bowel, cancer, loss of energy, reduced immune response, arthritis, malnutrition, bloatedness etc.
There are many conditions that may be associated with leaky gut. These include food allergies or intolerances, atopy, chronic urticaria, Crohn's disease, ulcerative colitis, irritable bowel, acute gastroenteritis, cystic fibrosis, exocrine pancreatic defects, poor digestion, iron deficiency and bowel cancers.
To restore the gut barrier and reduce symptoms the following needs to be considered:
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The herbs and nutrients mentioned above reflect the major nutritional supplements that may help the condition. Please do remember however that nutritional supplementation is an adjunct to medical treatment and in no way replaces medical treatment.
Return to the Nutritional Supplement Index?
http://www.moreton.com.au/ana/default.htm
Return to the Access n Able home page ?
http://www.moreton.com.au/ana/default.htm
Section 7 subsection 13
INTRODUCTION
Molecular Genetics of Mycoplasmas UNC Microbiology
European Journal of Clinical Microbiology and Infections
Diseases
MYCOPLASMAS by Shmuel Razin
Chemtrails? Mycoplasma?
What are they?
About a year ago, that would be around the new millennium, I stared to get hits on my web page. People were wanting information on chemtrails. I did a search and did not find much. Then Flier's Filesmailto:MajorStar@aol.com stared to do some on chemtrails and the dam broke. Thus chemtrails caught me. It turns out that a secret organizations or governments world wide possibly the New World Order known as NWO. These black operations are using civilian and military aircraft to spray the air similar to contrails but not. Chemtrails are thick and wide and do not disperse and linger around for long a period of time in all areas of the world. These chemtrails are different from contrails in that contrails are thin and wispy and dissipate in a short time less than an hour. They are sprayed from great altitudes and low as well. They often produce foggy or hazy conditions that last the rest of the day. The spraying is done day and night. Sometimes people see other aircraft accompany the missions some suspect to be of UFO nature. The fallout from the chemtrails spraying produces gels that are sticky and angle hair a web like material that is often white. The fallout often get many people sick and they don't know why. It is said that chemtrails were seen in the Gulf War and produced the Gulf War Illness
It is said all kinds of stuff from jet fuel to secret biological and chemical agents. I really don't know since I have not seen a chemtrail. Mycoplasma is said to be included.
It was brought to my attention of late through this post tapa-chemtrails@egroups.com that chemtrails were spraying Mycoplasma. I was a lab tech in the AF and I never heard of it. We called it walking pneumonia, and treated it as atypical pneumonia. It was not known as Mycoplasma to me. I was discharged in 82. I have done some research and it seems it was first isolated in 81 from two homosexual men and in 62 in Seattle in some children, and even to W.W. II. One source said to go back a hundred years. It is in blood plasma and serum, and affects similar to a fungi infection. It is still mysterious some say it is gram positive and some say it does not gram stain. It reacts with h2o2 and is very difficult to culture and it has no vaccine. It takes all shapes, but mostly coccus, and is the smallest living organism with unusual properties, smaller than bacteria and have no cell wall all it's life. T strains are very tiny colonies of Mycoplasma. L forms are non Mycoplasma bacteria, have no sterols, that at one point in their life they have no cell wall. Mycoplasma is classified as a bacteria and has been sequenced. Some sources say it is in between a bacteria and a virus. It has many test and by electrophoresis. It has no cell walls but a plasma membrane. It is similar to yeast. Thus it's name Mycoplasma. The coccus is the basic form of all Mycoplasmas in culture. The diameter of the smallest coccus capable of reproduction is about 300 nm. In most Mycoplasma cultures, elongated or filaments forms (up to 100 µm long and about 0.4 µm thick) also occur. The filaments tend to produce truly branched mycelioid structures, hence the name Mycoplasma (myces, a fungus; plasma, a form).
Mycoplasmais a minimal free living pathogen, a parasite, gram positive species can take on all shapes mostly coccus,and can affect the skin, genitals, lungs and even the mouth much like a fungi and is in blood plasma, serum, resembles plasmodium thus it's name Mycoplasma. First cultured around 1981 in two homosexual men, and in 62 in some children in Seattle, even in W.W.II and as far back as a hundred years ago. It is identified or a physical map of the chromosome using Pulsed Field Gel electrophoresis.
Mycoplasmas are wall less bacteria that exist in nature as parasites on some higher species of plant, animal or insect. These smallest of all living species have never been found free living,they can be cultivated in the absence of a host. Mycoplasma division is controversial, by fragmentation of filamentous cells containing several discrete DNA components. Mycoplasma are often grouped with or associated with Rickettsia, Chlamydia, and AIDs.
I have come across some testing procedures from below source.
European Journal of Clinical Microbiology and Infections
Diseases
ISSN: 0934-9723 (printed version) ISSN: 1435-4373 (electronic
version).
Volume 17 Issue 4 (1998) pp 255-263.
Polymerase Chain Reaction Assay with Culture for Detection of Genital Mycoplasmas in Perinatal Infections. PCR is a valuable tool for rapid detection of genital mycoplasmas in clinical samples. It is fast, sensitive, specific, and easy to perform, requiring minimal preparation of the clinical sample.
Dna-reagents, mycoplasma spp. Mycoplasma spp. serological reagents are devices that consist of antigens and antisera used in serological tests to identify antibodies to Mycoplasma spp. in serum. Additionally, some of these reagents consist of Mycoplasma spp. antisera conjugated with a fluorescent dye (immunofluorescent reagents) used to identify Mycoplasma spp. directly from clinical specimens. The identification aids in the diagnosis of disease caused by bacteria belonging to the genus Mycoplasma and provides epidemiological information on diseases caused by these microorganisms. Mycoplasma spp. are associated with inflammatory conditions of the urinary and respiratory tracts, the genitals, and the mouth. The effects in humans of infection with Mycoplasma pneumoniae range from inapparent infection to mild or severe upper respiratory disease, ear infection, and bronchial pneumonia. Mycoplasma pneumoniae attaches to the epithelial cells of the respiorty tract. Destruction is due to release of hydrogen peroxide and superoxide anion. Cultures are possible from sputum, swabs and other specimens.
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M. mycoides subsp. mycoides
http://www.mycoplasma-exp.com.
MYCOPLASMA EXPERIENCE LIMITED
source of photos
Mycoplasma Pneumoniae
http://www.kcom.edu/faculty/chamberlain/Website/Lects/Rickett.htm
RICKETTSIA, CHLAMYDIA, MYCOPLASMA
A. T. Still University of Health Sciences/Kirksville College of
Osteopathic Medicine.
MEDICAL MICROBIOLOGY Spring 1999
Dr. Tritz's Lectures
Course Director
Professor and Chairman of the Department of
Microbiology/Imunology
Kirksville College of Osteopathic Medicine
An excerpt from his lecture
"The Rickettsia, Chlamydia & Mycoplasma"
April 14 1999
Mycoplasma and L-Forms
General Characteristics
The mycoplasmas are essentially bacteria lacking a rigid cell wall during their entire life cycle, although they are also much smaller than bacteria. The first organism of this type was associated with pleuropneumonia of cattle, and was originally called the pleuropneumonia organism (PPO). Since that time, a number of organisms with similar morphological characteristics and cultural properties have been isolated. These are commonly referred to as pleuropneumonia-like organisms or PPLO.
A certain group of mycoplasmas produce extremely tiny colonies on agar plates, and are called the T-strains.
Some bacteria readily give rise spontaneously to variants that can replicate in the form of small filterable protoplasmic elements with defective or absent cell walls. These organisms, called L-forms, can also be formed by many species when cell wall synthesis is impaired by antibiotic treatment or high salt concentration. These organisms differ from Mycoplasma in that they contain a rigid cell wall, at least at one stage of their life cycle and contain no sterols in their cytoplasmic membrane.
These organisms are the smallest known free-living organisms. Because of the absence of cell walls, they do not stain with the Gram stain, and they are more pleomorphic and plastic than eubacteria. With Giemsa stain, they appear as tiny pleomorphic cocci, short rods, short spirals, and sometimes as hollow ring forms. Their diameter ranges from 0.15 u to 0.30 u.
Most mycoplasmas require a rich medium containing a sterol and serum proteins for growth. Despite the lack of a cell wall, they do not require a medium of very high osmotic pressure. On solid media, they form minute, transparent colonies. When viewed under low-power magnification, the colony looks like a fried egg. The different strains vary in their growth rate and may take from two days to several weeks to form a colony.
Structure
The cell is enclosed by a limiting membrane which is more similar to that of animal cells than that of bacterial cells because of sterols present in the membrane. The cytoplasm contains ribosomes, but lacks mesosomes. There is no nuclear membrane. In some strains, amorphous material on the outer surface of the membrane suggests the existence of a capsule.
Metabolism
The parasitic mycoplasmas have truncated respiratory systems, lacking quinones and cytochromes. Another indication for the simplicity of the electron transport chain is the finding that the reduced nicotinamide adenine dinucleotide (NADH) oxidase activity is cytoplasmic. Complex electron transport chains are usually membrane bound, since they depend on the spatial organization of their components. Ruling out oxidative phosphorylation as an ATP-generating system leaves only two proven ways of ATP generation, both based on substrate level phosphorylation. The major source for ATP is the arginine dihydrolase pathway.
ARGININE DIHYDROLASE PATHWAY
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Another mechanism for ATP generation is:
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*Acetyl CoA is produced by oxidative decarboxylation of pyruvate.
A few species derive their energy from the degradation of glucose or the hydrolysis of urea. All species synthesize DNA, RNA, lipids and proteins. However, it is not known if they can synthesize amino acids. Those species that require sterols incorporate these sterols (mainly cholesterol) into the cell membrane up to concentrations of 65%.
Multiplication
In the absence of a rigid cell wall, the pattern of replication is quite different from that of typical bacteria, whose division starts with the formation of a well-defined septum. Though the mechanism of division in mycoplasmas is controversial, sequential microscopic observation suggests that new elementary particles arise by fragmentation of filamentous cells containing several discrete DNA components.
Pathogenesis
M. pneumoniae is an extracellular pathogen that adheres to the respiratory epithelium by a specialized terminal protein attachment factor. This adherence protein interacts specifically with neuraminic acid residues on the epithelial cell surface. Ciliastasis occurs following attachment and then destruction of the superficial layer of epithelial cells. Destruction is due to release of hydrogen peroxide and superoxide anion.
Laboratory Diagnosis
The laboratory diagnosis of Mycoplasma infection can be accomplished by:
1. Culturing the organism from sputum, mucous membrane swabbings or other specimens by direct inoculation into liquid or solid media containing serum, yeast extract and penicillin to inhibit contaminating bacteria. Colonies will become detectable in one to three weeks. They stain intensely with neutral red or tetrazolium or methylene blue. The organism can be presumptively identified by its hemabsorption or B-hemolysis of guinea pig red blood cells. It is conclusively identified by staining its colonies with homologous fluorescein-labelled antibody.
2. Quantitation of the patient antibody response to mycoplasma by complement fixation tests on acute and convalescent serum. Cold agglutinins to human O erythrocytes may also be measured.
Diseases
The human diseases caused by mycoplasmas are shown on table 4.
Table 4
| DISEASE OR SYMPTOM | AGENT | HOST |
|---|---|---|
| Primary atypical pneumonia | Mycoplasma pneumoniae | Man |
| Genital infection | Mycoplasma genitalium | Man |
| Rheumatoid arthritis | Mycoplasma fermentans | Man* |
| Nongonococcal urethritis (NGU) | Ureaplasma urealyticum | Man* |
| Stillbirth | Mycoplasma hominis | Man* |
| Spontaneous abortion | Mycoplasma hominis | Man* |
| Infertility | Mycoplasma hominis | Man* |
Chemotherapy
Diseases caused by mycoplasma are usually self limiting and do not require antibiotic treatment. However, if antibiotics are needed, the drug of choice is erythromycin.
Summary
1. The rickettsia are extremely small gram-negative rod-shaped, coccoid or pleomorphic bacteria with limited metabolic capabilities.
2. The Family Rickettsiaceae contains three genera: Rickettsia, Ehrlichia, and Coxiella.
3. All of the members of the Family Rickettsiaceae are obligate intracellular parasites due to a highly permeable cytoplasmic membrane.
4. Confirmative diagnosis of rickettsial diseases is accomplished via the Weil-Felix test, a complement fixation test and/or an indirect fluorescent antibody test.
5. The drugs of choice for the treatment of rickettsial diseases are chloramphenicol and tetracycline.
6. Louse-borne rickettsial diseases include European epidemic typhus, and Brill's disease. Man is the sole reservoir for louse-borne diseases.
7. The only flea-borne rickettsial disease is endemic murine typhus.
8. Mite-borne rickettsial diseases include scrub typhus and rickettsialpox.
9. Tick-borne rickettsial diseases include Rocky Mountain spotted fever, North Asian tick typhus, Fievre boutonneuse, Queensland tick typhus, Q fever, spotted fever and ehrlichiosis.
10. The major target tissue of the rickettsia is vascular endothelium.
11. The chlamydia are extremely small, gram-negative, coccal-shaped, obligate intracellular parasites with limited metabolic capability which are classified as bacteria.
12. The chlamydia lack flavoproteins and cytochromes.
13. Chlamydia undergo a unique developmental cycle which is an alternation in size between the small elementary body and the relatively large reticulate body.
14. The elementary body is relatively metabolically inactive, adapted for extracellular survival and is the infectious unit.
15. The reticulate body is metabolically active, adapted for intracellular growth and is not infectious.
16. The major target tissue of the chlamydia is mucous membranes.
17. Serological diagnosis of chlamydial diseases is via a fluorescent antibody test, complement fixation test or a delayed type hypersensitivity test (Frei test) for lymphogranuloma venereum.
18. Chlamydial diseases include trachoma, inclusion conjunctivitis, lymphogranuloma venereum, bronchitis, pneumonia, sinusitis and meningopneumonitis, hepatic and renal dysfunction, abortion and endocarditis.
19. The mycoplasma are extremely small free-living bacteria which lack a cell wall and cytochromes.
20. Mycoplasma can be cultured on agar media but colonies take up to three weeks to develop.
21. Serological identification of mycoplasma disease relies upon the quantitation of cold agglutinins to human O erythrocytes or a complement fixation test.
22. The only human diseases proven to be of mycoplasma etiology are primary atypical pneumonia and a certain type of genital infection.
http://www.md.huji.ac.il/
The Hebrew University of Jerusalem.
Mycoplasma pneumoniae infection is a disease of the upper and lower respiratory tracts. Cough, fever, and headache may persist for several weeks. Convalescence is slow. Ureaplasma urealyticum infection causes nongonococcal urethritis in men, resulting in dysuria, urgency, and urethral discharge.
Mycoplasmas are spherical to filamentous cells with no cell walls. There is an attachment organelle at the tip of filamentous M pneumoniae, M genitalium, and several other pathogenic mycoplasmas. Fried-egg-shaped colonies are seen on agar. The mycoplasmas presumably evolved by degenerative evolution from Gram-positive bacteria and are phylogenetically most closely related to some clostridia. Mycoplasmas are the smallest self-replicating organisms with the smallest genomes (a total of about 500 to 1000 genes); they are low in guanine and cytosine. Mycoplasmas are nutritionally very exacting. Many require cholesterol, a unique property among prokaryotes. Ureaplasmas require urea for growth, another unusual property. Mycoplasmas have surface antigens such as membrane proteins, lipoproteins, glycolipids, and lipoglycans. Some of the membrane proteins undergo spontaneous antigenic variation. Antibodies to surface antigens inhibit growth; various serological tests have been developed and are useful in classification.
Mycoplasmas are surface parasites of the human respiratory and urogenital tracts. Mycoplasma pneumoniae attaches to sialoglycoproteins or sialoglycolipid receptors on the tracheal epithelium via protein adhesins on the attachment organelle. The major adhesin is a 170-kilodalton (kDa) protein, named P1. Hydrogen peroxide and superoxide radicals (O2-) excreted by the attached organisms cause oxidative tissue damage. Pneumonia is induced largely by local immunologic and phagocytic responses to the parasites. Sequelae of M pneumoniae infection (mainly hematologic and neurologic) apparently have an autoimmune etiology. Several fastidious mycoplasmas may act as cofactors in activation of the aquired immunodeficiency syndrome (AIDS). Macrophage activation, cytokine induction, and superantigen properties of some mycoplasmal cell components can be considered as pathogenicity factors.
IgM antibodies, followed by IgG and secretory IgA, are important in host resistance. The importance of cell-mediated immunity is unclear.
Mycoplasma pneumoniae infection occurs worldwide and is more prevalent in colder months. It affects mainly children ages 5 to 9 years. It is spread by close personal contact and has a long incubation period. Ureaplasma urealyticum is spread primarily through sexual contact. Women may be asymptomatic reservoirs.
Culture of M pneumoniae from sputum or a throat swab is possible, but very slow; therefore diagnosis is usually based on serologic tests. Tests using diagnostic DNA probes and amplification of specific genomic mycoplasma sequences by the polymerase-chain reaction (PCR) are being developed.
There is no certified vaccine for M pneumoniae. Treatment with erythromycin or tetracyclines is effective in reducing symptoms in both M pneumoniae and U urealyticum infections.
Mycoplasmas are the smallest and simplest self-replicating bacteria. The mycoplasma cell contains the minimum set of organelles essential for growth and replication: a plasma membrane, ribosomes, and a genome consisting of a double-stranded circular DNA molecule ( Fig. 37-1). Unlike all other prokaryotes, the mycoplasmas have no cell walls, and they are consequently placed in a separate class Mollicutes(mollis, soft; cutis, skin). The trivial term mollicutes is frequently used as a general term to describe any member of the class, replacing in this respect the older term mycoplasmas.
FIGURE 37-1 Electron micrograph of thin-sectioned mycoplasma cells. Cells are bounded by a single membrane showing in section the characteristic trilaminar shape. The cytoplasm contains thin threads representing sectioned chromosome and dark granules representing ribosomes. (Courtesy of RM Cole, Bethesda, Maryland).
Mycoplasmas have been nicknamed the "crabgrass" of cell cultures because their infections are persistent, frequently difficult to detect and diagnose, and difficult to cure. Contamination of cell cultures by mycoplasmas presents serious problems in research laboratories and in biotechnological industries using cell cultures. The origin of contaminating mycoplasmas is in components of the culture medium, particularly serum, or in the flora of the technician's mouth, spread by droplet infection.
The term primary atypical pneumonia was coined in the early 1940s to describe pneumonias different from the typical lobar pneumonia caused by pneumococci. Several common respiratory viruses, including influenza virus and adenovirus, were shown to be responsible for a significant number of these pneumonias. From other cases, many of which developed antibodies agglutinating red blood cells in the cold (cold agglutinins), an unidentified filterable agent was isolated by Eaton and associates and was called Eaton agent. This agent was identified as a new Mycoplasma species after its successful cultivation on cell-free media in 1962. Named Mycoplasma pneumoniae, it was the first clearly documented mycoplasma pathogenic for humans.
The effects of M pneumoniae on humans include subclinical infection, upper respiratory disease, and bronchopneumonia. Most human infections do not progress to a clinically evident pneumonia. When pneumonia occurs, the onset generally is gradual and the clinical picture is one of a mild to moderately severe illness, with early complaints referable to the lower respiratory passages. Radiography frequently reveals evidence of pneumonia before physical signs are apparent. Involvement is usually limited to one of the lower lobes of the lungs, and the pneumonia is interstitial or bronchopneumonic. The course of disease varies; remittent fever, cough, and headache persist for several weeks. One of the most consistent clinical features is a long convalescence, which may extend from 4 to 6 weeks. Few fatal cases have been reported. Several unusual complications have been noted, including hemolytic anemia, polyradiculitis, encephalitis, aseptic meningitis, and central nervous system illness such as Guillain-Barré syndrome. In addition, pericarditis and pancreatitis have been observed. These sequelae may be related to the suspected immunopathology of M pneumoniae disease (see below).
Growing evidence suggests that Ureaplasma urealyticum causes nongonococcal urethritis in men free of Chlamydia trachomatis, an established agent of nongonococcal urethritis. The wide occurrence of U urealyticum in sexually active, symptom-free adults hampers research in this field. Evidence is based primarily on the production of nongonococcal urethritis symptoms in ureaplasma-free and chlamydia-free volunteers by intraurethral inoculation of U urealyticum and on a report that this disease could be cured in a chlamydia-free man only when he and his partner were treated simultanously with tetracycline, which eliminated U urealyticum from both. Ureaplasmas have also been associated with chorioamnionitis, habitual spontaneous abortion, and low-weight infants. Mycoplasma hominis, a common inhabitant of the vagina of healthy women, becomes pathogenic once it invades the internal genital organs, where it may cause pelvic inflammatory diseases such as tubo-ovarian abscess or salpingitis.
It has been suggested that Mycoplasma genitalium, isolated in 1981 from the urethral discharge of two homosexual men, may account for the tetracycline-responsive, nongonococcal urethritis cases in which chlamydias and ureaplasmas cannot be isolated (about 20 percent of all cases). However, M genitalium is so fastidious that very few clinical isolates have so far been made on the best mycoplasma medium available. Only the recent application of specific PCR amplification of the organism's DNA in clinical specimens has provided experimental proof for the relative prevalence of M genitalium in the human urogenital tract and its apparent role in male urethritis.
The question of whether mycoplasmas act as co-factors in the development of AIDS has attracted much attention recently. Several mycoplasms have so far been incriminated: M fermentans, considered until recently a relatively rare mycoplasma of the human urogenital tract, and M penetrans , a newly-discovered human mycoplasma isolated from several AIDS patients. M pirum, a mycoplasma of an unknown host, has been recently isolated from the blood of a few AIDS patients. While, in vitro studies show that these mycoplasmas may markedly enhance pathogenicity of the human immunodeficiency virus, the possibility that the mycoplasmas may simply represent opportunistic agents found in high frequency in patients with AIDS, cannot be ruled out. Yet on the whole, with the increasing incidence of immunocompromised patients (due to AIDS, organ transplantation, etc.) evidence is accumulating for invasion of tissues and the intracellular location of some mycoplasmas, notably M fermentans and M penetrans. Extragenital infections by urogenital mycoplasmas are rather common in neonates, immunosuppressed and/or hypogammaglobulinemic patients; clinical symptoms are expressed frequently as arthritis.
The coccus is the basic form of all mycoplasmas in culture. The diameter of the smallest coccus capable of reproduction is about 300 nm. In most mycoplasma cultures, elongated or filamentous forms (up to 100 µm long and about 0.4 µm thick) also occur. The filaments tend to produce truly branched mycelioid structures, hence the name mycoplasma (myces, a fungus; plasma, a form). Mycoplasmas reproduce by binary fission, but cytoplasmic division frequently may lag behind genome replication, resulting in formation of multinuclear filaments (Fig. 37-2).
FIGURE 37-2 Schematic presentation of the mode of mycoplasma reproduction. Cells may either divide by binary fission or first elongate to multinucleate filaments, which subsequently breakup to coccoid bodies. (From Razin S: Mycoplasmas: the smallest pathogenic procaryotes. Isr J Med Sci 17:510, 1981, with permission).
Some mycoplasmas possess unique attachment organelles, which are shaped as a tapered tip in M pneumoniae and M genitalium. Mycoplasma pneumoniae is a pathogen of the respiratory tract, adhering to the respiratory epithelium, primarily through the attachment organelle. Interestingly, these two human mycoplasmas exhibit gliding motility on liquid-covered surfaces. The tip structure always leads, again indicating its importance in attachment.One of the most useful distinguishing features of mycoplasmas is their peculiar fried-egg colony shape, consisting of a central zone of growth embedded in the agar and a peripheral one on the agar surface (Fig. 37-3).
FIGURE 37-3 Morphology of a typical "fried-egg" mycoplasma colony.
The lack of cell walls and intracytoplasmic membranes facilitates isolation of the mycoplasma membrane in a relatively pure form. The isolated mycoplasma membrane resembles that of other prokaryotes in being composed of approximately two-thirds protein and one-third lipid. The mycoplasma lipids resemble those of other bacteria, apart from the large quantities of cholesterol in the sterol-requiring mycoplasmas.
Membrane proteins, glycolipids, and lipoglycans exposed on the cell surface are the major antigenic determinants in mycoplasmas. Antisera containing antibodies to these components inhibit growth and metabolism of the mycoplasmas and, in the presence of complement, cause lysis of the organisms. These properties are used in various serologic tests that differentiate between mycoplasma species and serotypes and detect antibodies to mycoplasmas in sera of patients (see below).
The mycoplasma genome is typically prokaryotic, consisting of a circular, double stranded DNA molecule. The Mycoplasma and Ureaplasma genomes are the smallest recorded for any self-reproducing prokaryote (Table 37-1). Therefore, there are very few genes; in some mycoplasmas the number is estimated at fewer than 500, about one sixth the number of genes in Escherichia coli. Mycoplasmas accordingly express a small number of cell proteins and lack many enzymatic activities and metabolic pathways. Their nutritional requirements are correspondingly complex, and they are dependent on a parasitic mode of life.
The dependence of mycoplasmas on their host for many nutrients explains the great difficulty of cultivation in the laboratory. The complex media for mycoplasma culture contain serum, which provides fatty acids and cholesterol for mycoplasma membrane synthesis. The requirement of most mycoplasmas for cholesterol is unique among prokaryotes. The consensus is that only a small fraction of mycoplasmas existing in nature have been cultivated so far. Some of the cultivable mycoplasmas, including the human pathogen M pneumoniae, grow very slowly, particularly on primary isolation. Ureaplasma urealyticum, a pathogen of the human urogenital tract, grows very poorly in vitro, reaching maximal titers of 107 organisms/ml of culture. Mycoplasma genitalium, another human pathogen, grows so poorly in vitro that only a few successful isolations have been achieved.
Glucose and other metabolizable carbohydrates can be used as energy sources by the fermentative mycoplasmas possessing the Embden-Meyerhof-Parnas glycolytic pathway. All mycoplasmas examined thus far possess a truncated, flavin-terminated respiratory system, which rules out oxidative phosphorylation as an ATP-generating mechanism. Breakdown of arginine by the arginine dihydrolase pathway has been proposed as a major source of ATP in nonfermentative mycoplasmas. Ureaplasmas have a requirement, unique among living organisms, for urea. Because they are non-glycolytic and lack the arginine dihydrolase pathway, it has been suggested, and later proven experimentally, that ATP is generated through an electrochemical gradient produced by ammonia liberated during the intracellular hydrolysis of urea by the organism's urease.
The mycoplasma genome is characterized by a low guanine-plus-cytosine content and by a corresponding preferential utilization of codons containing adenine and uracil, particularly in the third position. Most interesting is the use of the universal stop codon UGA as a tryptophan codon in many mycoplasmas, a rare property found so far only in mycoplasmas and in nonplant mitochondria. Resistance of mycoplasmal RNA polymerase to rifampicin is another property distinguishing mycoplasmas from the conventional eubacteria. However, apart from this resistance to rifampicin, the mycoplasmas are susceptible to antibiotics, such as tetracyclines and chloramphenicol, that inhibit protein synthesis on prokaryotic ribosomes.
As the smallest and simplest self-replicating prokaryotes, the mycoplasmas pose an intriguing question: do they represent the descendents of exceedingly primitive bacteria that existed before the development of a peptidoglycan-based wall, or do they represent evolutionary degenerate eubacterial forms that have lost their cell walls? The balance of the molecular evidence, based largely on comparison of base sequences of the highly conserved ribosomal RNA (rRNA) molecules, particularly of the 16S rRNA type, favors the hypothesis of degenerative evolution. According to Woese and his colleagues, the mycoplasmas evolved as a branch of the low-guanine-plus-cytosine Gram-positive bacteria and are most closely related to two clostridia, Clostridium innocuum and C ramosum. However, the marked phenotypic and genotypic variability among mycoplasmas has led some workers to conclude that mycoplasmas evolved from a variety of walled bacteria and accordingly have a polyphyletic origin. Woese maintains that the origin of mycoplasmas is monophyletic and explains the great variety of mycoplasmas by a process of rapid evolution characteristic of the group.
All mycoplasmas cultivated and identified thus far are parasites of humans, animals, plants, or arthropods. The primary habitats of human and animal mycoplasmas are the mucous surfaces of the respiratory and urogenital tracts and the joints in some animals. Although some mycoplasmas belong to the normal flora, many species are pathogens, causing various diseases that tend to run a chronic course (Fig. 37-4).
FIGURE 37-4 Pathogenesis and disease sites of infection by M pneumoniae and U urealyticum.
Most mycoplasmas that infect humans and other animals are surface parasites, adhering to the epithelial linings of the respiratory and urogenital tracts. Adherence is firm enough to prevent the elimination of the parasites by mucous secretions or urine. The intimate association between the adhering mycoplasmas and their host cells provides an environment in which local concentrations of toxic metabolites excreted by the parasite build up and cause tissue damage (Fig. 37-5). Moreover, because mycoplasmas lack cell walls, fusion between the membranes of the parasite and host has been suggested, and some experimental evidence for it has recently been obtained. Membrane fusion would alter the composition and permeability of the host cell membrane and enable the introduction of the parasite's hydrolytic enzymes into the host cell, events expected to cause serious damage. Recent studies have indicated the presence in mycoplasmas of antigenic variability systems. These systems, some of which are already defined in molecular genetic terms, are responsible for rapid changes in major surface protein antigens. The change in the antigenic coat of the parasite helps it to escape recognition by the immune mechanisms of the host.
FIGURE 37-5 Schematic presentation of a M pneumoniae organism attaching to the surface of the ciliary tracheal epithelium, as seen by electron microscopy of a thin section. The clustering of the P1 adhesin on the surface of the attachment organelle at the tip of the mycoplasma is depicted. The H2O2 and O2- excreted by the mycoplasma penetrate into the host cell and cause oxidative damage.
Because attachment of M pneumoniae and M genitalium is affected by pretreatment of the host cells with neuraminidase, sialoglycoproteins and/or sialoglycolipids of the host cell membrane appear to be receptor sites for these mycoplasmas. There is evidence that several M pneumoniae membrane proteins act as adhesins and that they have high affinity for the specific receptors for M pneumoniae on host cells. Monoclonal antibodies to one of these proteins, protein P1 (molecular weight, 170,000 daltons), inhibit attachment of the parasite. Ferritin labeling of the antibodies has shown that P1 concentrates on the tip structure of the mycoplasma, a finding that further supports the notion that the tip serves as an attachment organelle.
The results obtained with M pneumoniae were essentially duplicated recently with M genitalium and showed that in this organism, which closely resembles M pneumoniae morphologically and physiologically, a major adhesin protein, named MgPa, is clustered at the tip organelle. The genes of the major adhesins of M pneumoniae (P1) and of M genitalium (MgPa) were cloned and sequenced, allowing the characterization of these proteins. The two adhesins are alike in many respects and in fact contain extensive areas of homology, as expressed also by shared epitopes. These two proteins may be the product of an ancestral gene that underwent a horizontal gene transfer event.
The nature of the toxic factors that damage the mucosal surfaces infected by mycoplasmas is still unclear. Toxins are rarely found in mycoplasmas. Consequently, researchers considered whether the end products of mycoplasma metabolism were responsible for tissue damage. Hydrogen peroxide (H202), the end product of respiration in mycoplasmas, has been implicated as a major pathogenic factor ever since it was shown to be responsible for the lysis of erythrocytes by mycoplasmas in vitro; however, the production of H2O2 alone does not determine pathogenicity, as the loss of virulence in M pneumoniae is not accompanied by a decrease in H2O2 production. For the H2O2 to exert its toxic effect, the mycoplasmas must adhere closely enough to the host cell surface to maintain a toxic, steady-state concentration of H2O2 sufficient to cause direct damage, such as lipid peroxidation, to the cell membrane. The accumulation of malonyldialdehyde, an oxidation product of membrane lipids, in cells exposed to M pneumoniae supports this notion. Moreover, M pneumoniae inhibits host cell catalase by excreting superoxide radicals (O2-). This would be expected to further increase the accumulation of H2O2 at the site of parasite-host cell contact (Fig. 37-6).
FIGURE 37-6 Proposed mechanism of oxidative damage to host cells by adhering M pneumoniae by increasing concentrations of H2O2 and O2-. (Modified from Almagor M, Kahane I, Yatziv S: Role of superoxide anion in host cell injury induced by Mycoplasma pneumoniae infection. J Clin Invest 73:842, 1984, with permission).
There is evidence that both organism-related and host-related factors are involved in the pathogenesis of mycoplasma infections. Mycoplasmas activate macrophages, and induce cytokine production and lymphocyte proliferation; the rat pathogen, Mycoplasma arthritidis, produces a potent superantigen. Thus, in the case of M pneumoniae, the host may be largely responsible for the pneumonia by mounting a local immune response to the parasite. Syrian hamsters inoculated intranasally with M pneumoniae show patchy bronchopneumonic lesions consisting of infiltration of mononuclear cells. The ablation of thymic function before the experimental infection prevents development of the characteristic pulmonary infiltration, but lengthens the period during which the organisms may be isolated from the lungs. When thymic animals are allowed to recover and then reinfected, an exaggerated and accelerated pneumonic process occurs. Epidemiologic data also suggest that repeated infections in humans are required before symptomatic disease occurs: serum antibodies to M pneumoniae can be found in most children 2 to 5 years of age, although the illness occurs with greatest frequency in individuals 5 to 15 years of age.
An immunopathologic mechanism also may explain the complications affecting organs distant from the respiratory tract in some patients infected with M pneumonia. Various autoantibodies have been detected in the sera of many of these patients, including cold agglutinins reacting with the erythrocyte I antigen, and antibodies reacting with lymphocytes, smooth muscle cells, and brain and lung antigens. Serologic cross-reactions between M pneumoniae and brain and lung antigens have been demonstrated, and these antigens are probably related to the glycolipids of M pneumoniae membranes, which are also found in most plants and in many bacteria. Clearly, host reaction varies markedly, as only about half of the patients develop cold agglutinins and complications are rare, even among individuals with anti-tissue globulins.
Infection with M pneumoniae induces the development of serum antibodies that fix complement, inhibit growth of the organism and lyse the organism in the presence of complement. Generally, the first antibodies produced are of the IgM class, whereas later in convalescence the predominant antibody is IgG. Secretory IgA antibodies also develop and appear to be important in host resistance. The first infection in infancy usually is asymptomatic and generates a brief serum antibody response. Recurrent infections generate a more prolonged systemic antibody response and increasing numbers of circulating antigen-responsive lymphocytes. By late childhood, clinically apparent lower respiratory disease, including pneumonia, becomes more common. Therefore, mycoplasma respiratory disease manifestations appear to vary, depending on the state of local and systemic immunity at the time of reinfection. One hypothesis is that local immunity mediates resistance to infection and that systemic immunity contributes substantially to the pulmonary and systemic reaction characteristic of M pneumoniae pneumonia.
The relative importance of humoral and cell-mediated immunity in resistance to respiratory mycoplasma infections is still unclear. For many mycoplasma infections, such as bovine pleuropneumonia, resistance can be transferred with convalescent-phase serum, but this may not be true for all mycoplasma respiratory diseases. For example, resistance of rats to pulmonary disease induced by M pulmonis can be transferred only with spleen cells obtained from previously infected animals. Although IgA antibody may be important in resistance to mycoplasmas, other factors seem to be involved in resistance to pulmonary disease, and these factors may not be the same for all mycoplasma infections.
One of the most puzzling features of M pneumoniae pneumonia is the age distribution of patients. In a survey conducted between 1964 and 1975 of more than 100,000 individuals in the Seattle area, the age-specific attack rate was highest among 5- to 9-year-old children. Rates of M pneumoniae pneumonia in the youngest age group, 0 to 4 years ol