Thursday, August 09, 2018

Can the mystery of Chronic Fatigue Syndrome be solved by the overlap of HHV-8 and African Swine Fever in Sassari, Sardinia?

Editor's note: The big question we have focused on this site is the relationship between HHV-6/7/8 and African Swine Fever Virus. That question may be answered  by the curious relationship between African Swine Fever and HHV-8 in Sassari, Sardinia.
Is African Swine Fever infecting people in Sassari and being confused with HHV-8? Is HHV-8 the form African Swine Fever  takes in humans?

In the territory of the ASL of Sassari, in 2015, there were 7 outbreak of African Swine Fever (ASF) in domestic pigs that involved 140 pig farms in the protection zones and 765 pig farms in the Surveillance Zone. The messages are promptly arrived to all farmers concerned.

https://www.ijidonline.com/article/S1201-9712(16)31558-2/fulltext



2006 Feb;34(1):39-42.

Infection with human herpesvirus type 8 and Kaposi's sarcoma in Sardinia.

Abstract

BACKGROUND:

A cross-sectional study was conducted in the provinces of Sassari (northern Sardinia, covered by a population-based cancer registry), and of Cagliari (southern Sardinia) to estimate the prevalence of infection with human herpesvirus type 8 (HHV8) and the incidence of classic Kaposi's sarcoma (KS) among HHV8-infected individuals.

PATIENTS AND METHODS:

Sera from 297 hospitalized persons potentially at risk of developing classic KS (i. e., those aged 50 years or older) were tested for antibodies against HHV8. HHV8 seroprevalence rates (with 95% confidence intervals-CI) and yearly incidence rates (IR/100,000) of KS were calculated according to age and sex.

RESULTS:

Of tested individuals, 32.0% had antibodies against HHV8 in Sassari and 30.0% in Cagliari. Estimated IR of KS among HHV8-positive persons and KS:HHV8 ratio were two times higher in Sassari (1:3,891) than in Cagliari (1:8,114), and higher in men (1:2,846 in Sassari; 1:5,483 in Cagliari) as compared to women (1:6,827 in Sassari; 1:12,489 in Cagliari).

CONCLUSIONS:

Although the overall prevalence of HHV8 seemed similar in Sassari and in Cagliari, the risk of KS was higher in Sassari, suggesting that different cofactor(s), or different distribution of the same cofactor(s) between the two provinces of Sardinia, might have played a role in KS development.

All AIDS patients have some form of Kaposi's Sarcoma in this study. Is the same true for Chronic Fatigue Syndrome?

Editor's Note: This following study suggests that Kaposi's 
Sarcoma is universal in AIDS. That is not the conventional wisdom. It would also suggest that HHV-8 is not the real cause of K.S. since not all AIDS patients have it. If Chronic Fatigue Syndrome is just another form of AIDS, one would expect that all Chronic Fatigue Syndrome patients have some form of internal K.S. The presence of crimson crescents in the throats of CFS patients may be a hint that they all have an internal indolent form of Kaposi's Sarcoma.




1985 May;16(5):447-56.

Frequency and anatomic distribution of lymphadenopathic Kaposi's sarcoma in the acquired immunodeficiency syndrome: an autopsy series.

Abstract

Histologic material from 52 autopsies of persons who had died of the acquired immunodeficiency syndrome (AIDS) were reviewed. The study group included 23 Haitians, 19 homosexual men, five intravenous drug abusers, two hemophiliacs (type A), and three persons at unknown risk. Nineteen of the patients (36.5 per cent) had typical Kaposi's sarcoma alone, but 49 (94.2 per cent) had the inflammatory variant of Kaposi's sarcoma as well as typical Kaposi's sarcoma. Inflammatory Kaposi's sarcoma was found in all risk groups studied. In all cases of typical Kaposi's sarcoma, histomorphologic transitions of inflammatory Kaposi's sarcoma to typical Kaposi's sarcoma were observed. Lymph nodes and spleen were the organs most commonly involved by both typical and inflammatory Kaposi's sarcoma. The findings indicate that Kaposi's sarcoma is more common and has a wider morphologic spectrum in AIDS than is generally appreciated.

https://www.sciencedirect.com/science/article/pii/S0046817785800812
Findings and Testimony of Burke A. Cunha, MD., chief, infectious disease division, Winthrop-University Hospital, Mineola, N.Y., USA.
"But the most consistent lab evidence that we look for are elevations of coxsackie B-titers and elevations of HHV-6 titers in combination with the decrease in the percentage of natural killer T cells," Cunha explained. "If the patient has two or three of these abnormalities in our study center, then he or she fits the laboratory criteria for chronic fatigue. Nearly all patients with crimson crescents have two out of three of these laboratory abnormalities," he said.


Crimson crescents may suggest that all Chronic Fatigue Syndrome patients have Kaposi's Sarcoma

Findings and Testimony of Burke A. Cunha, MD., chief, infectious disease division, Winthrop-University Hospital, Mineola, N.Y., USA.
"But the most consistent lab evidence that we look for are elevations of coxsackie B-titers and elevations of HHV-6 titers in combination with the decrease in the percentage of natural killer T cells," Cunha explained. "If the patient has two or three of these abnormalities in our study center, then he or she fits the laboratory criteria for chronic fatigue. Nearly all patients with crimson crescents have two out of three of these laboratory abnormalities," he said.


http://me-ireland.com/scientific/26.htm

Do all Chronic Fatigue Syndrome patients have an indolent form of Kaposi's Sarcoma?

Editor's Note: Although one study found evidence of the Kaposi's Sarcoma Virus in Chronic Fatigue Syndrome patients, there has never been any serious research into the possibility that many or all Chronic Fatigue Syndrome patients have an internal indolent form of Kaposi's Sarcoma. if so that would make it crystal clear that Chronic Fatigue Syndrome is just another face of the AIDS epidemic.


Has R.G. Downing played a major role in the cover-up of African Swine Fever (HHV-6/7/8)?


Did Downing play a role in renaming African Swine Fever? Is HHV-6 really African Swine Fever?

https://www.ncbi.nlm.nih.gov/pubmed/2886840

The Betrayal and Sabotage of Hillary Johnson by the Chronic Fatigue Syndrome Community

A brief excerpt about what happened to Hillary Johnson from The Chronic Fatigue Syndrome Epidemic Cover-up, a bestseller on Amazon available here.


     In the May 6 issue, Neenyah Ostrom wrote a piece about one of the great moments of betrayal in the history of CFS: “The largest chronic fatigue syndrome patient advocate group in the United States has, for all intents and purposes, declared war on the epidemic’s most prominent author over the subject that seems to draw the line in the sand between those who are willing to tell the whole truth about CFS and those who are not: contagion. In its most recently-published CFIDS Chronicle (Spring 1996), the CFIDS Association of America (in Charlotte, North Carolina) has mounted a merciless attack upon Hillary Johnson’s new book, Osler’s Web: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic. Instead of celebrating the publication by a major publishing house of an important book describing in the minutest detail the history of the disease that the CFIDS Association has been attempting to publicize for nearly a decade, the organization has marshalled all its experts to attack Johnson because she writes that there is evidence to prove that CFS is contagious. In the spring issue of the CFIDS Chronicle, the Association consulted numerous physicians and researchers—most of whom are either government employees or receive government funding for their ‘AIDS’ or CFS research—and asked if they considered CFS to be contagious. Only one was brave enough to answer in the affirmative. Never mind that the CFIDS Association has distributed tens of thousands of dollars—collected from sick people, their families, and concerned individuals—for research to identify a causative agent of CFS. Much of this money has been spent investigating various viruses; considerable amounts were invested over the past few years to investigate a retrovirus as a possible cause of CFS.”

Is HHV-6 also causing the eye disease in Alzheimer's patients?

Degenerative eye conditions linked to Alzheimer's in study



https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410290110 






The Role of Natural Killer Cells in Alzheimer’s Disease

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-3083.2012.02769.x



Immune System Problem Linked to Alzheimer's
https://www.webmd.com/alzheimers/news/20050610/immune-system-problem-linked-to-alzheimers
























From Science News


"What we do know is that Alzheimer’s disease is not contagious, Dudley says. You cannot “catch” Alzheimer’s from someone experiencing dementia symptoms. Even if  herpesviruses play a role, many other factors definitely contribute to developing this disease."

https://www.sciencenews.org/article/alzheimers-herpesvirus-possible-link


Herpes may play a role in developing Alzheimer's, a new study suggests — reigniting a controversial theory about what causes the disease 
https://www.msn.com/en-us/health/medical/herpes-may-play-a-role-in-developing-alzheimers-a-new-study-suggests-e2-80-94-reigniting-a-controversial-theory-about-what-causes-the-disease/ar-AAyZM8B


These Slices of Human Brains Revealed an Alzheimer's Clue


Study finds potential link between 2 herpes viruses and Alzheimer's  
http://www.newser.com/story/260972/these-slices-of-human-brains-revealed-an-alzheimers-clue.html

Connections between Alzheimer’s Disease and viruses are building

https://www.popsci.com/herpes-alzheimers-hhv#page-3


Dr. Dudley said he is unsure whether many mainstream Alzheimer’s researchers will endorse the virus idea anytime soon.
“It’s very unpopular,” he said. “I’m sure there’s a lot of people who are secretly unhappy about it.”
Still, he said, Alzheimer’s researchers “come up to me at conferences and say in hushed tones, ‘Oh, I also have a data set that shows viruses, but I’m afraid to publish it.’”
https://www.nytimes.com/2018/06/21/health/alzheimers-virus-herpes.html



Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus

https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5


Robust analysis points to HHV-6A as potential causative agent in Alzheimer’s disease

https://hhv-6foundation.org/alzheimers-disease/robust-analysis-points-to-hhv-6a-as-potential-causative-agent-in-alzheimers-disease



"A new paper in Neuron, though, looks to be the most unignorable one yet with evidence that there’s some sort of viral/bacteial/fungal component to the disease. A team led out of a Mt. Sinai research group has gone over a pretty large sample of Alzheimer’s brain tissue (622 patients who died with the disease, and over three hundred control brains as well), sequencing infectious organism DNA, looking for changes in the proteome, etc. They find that aging brains in normal patients display plenty of viral signatures (as indeed is probably the case in many other tissues). But the AD samples were particularly enriched in herpesviruses 6A and 7, a result that repeated across three independent cohorts from different geographical locations (the brain tissue collections were from more than one previous effort). According to Stat, there’s a paper coming out next month from another group entirely that also implicates HHV6."


http://blogs.sciencemag.org/pipeline/archives/2018/06/22/alzheimers-and-infectious-disease-for-real


Could Herpes Virus Play a Role in Alzheimer's?

https://www.webmd.com/alzheimers/news/20180621/could-herpes-virus-play-a-role-in-alzheimers#1 


"These viruses are becoming activated, and then they put gas on the flame of the Alzheimer's pathology."

http://www.wbur.org/npr/621908340/researchers-find-herpes-viruses-in-brains-marked-by-alzheimers-disease



http://www.health.com/healthday/could-herpes-virus-play-role-alzheimers





https://asunow.asu.edu/20180621-discoveries-asu-new-study-suggests-viral-connection-alzheimers-disease 


For years a newspaper called New York Native warned the world about the HHV-6 epidemic. Read The Chronic Fatigue Syndrome Epidemic Cover-up,  a detailed history of its investigative reporting on HHV-6.

If you have Amazon Prime or Kindle Unlimited, you can immediately begin reading The Chronic Fatigue Syndrome Epidemic Cover-up and you will soon understand why the facts about the HHV-6 and Chronic Fatigue Syndrome epidemics have been hidden from the public for almost four decades.









This is the book causing heated debates about Chronic Fatigue Syndrome and HHV-6, "The Fifty Shades of AIDS Virus," in laboratories, doctor's offices, and homes all over the world.

                                                              


In his bestselling book, The Black Swan, Nassim Nicholas Taleb wrote, "I see the risks of a very strange acute virus spreading throughout the planet." This book by Charles Ortleb warns that the virus causing Chronic Fatigue Syndrome is that virus.

This book belongs in the library of anyone who wants to know the disturbing history of the Chronic Fatigue Syndrome epidemic and the deadly virus HHV-6. Why have the CDC and NIH pretended that the communicable disease fraudulently called "Chronic Fatigue Syndrome" is a mystery for over three decades? By the end of this book of inconvenient truths the answer is crystal clear. The shocking news and bold analysis in this page-turner could lead to a revolution in the science and politics of Chronic Fatigue Syndrome, fibromyalgia, AIDS, autism, and many other illnesses. Scientists, doctors, nurses, patients, journalists, politicians, and historians must begin their journey to a full understanding of the Chronic Fatigue Syndrome epidemic with this book.

As the publisher and editor-in-chief of a small newspaper in New York, Charles Ortleb was the first journalist to devote a publication to uncovering the truth about Chronic Fatigue Syndrome. He assigned Neenyah Ostrom the duty of following every twist and turn of the Chronic Fatigue Syndrome story. No newspaper in the world did more to warn the world about the virus which seems to be triggering Chronic Fatigue Syndrome and many other immunological disorders. Chronic Fatigue Syndrome and AIDS are just the tip of the HHV-6 iceberg.

This provocative book will end the injustice of the silent treatment Neenyah Ostrom's reporting has been getting from the media and The Chronic Fatigue Syndrome community. Ostrom blew the lid off one of the biggest medical secrets of our time: the link between the Chronic Fatigue Syndrome epidemic and AIDS.

Ostrom interviewed most of the major researchers in the field, as well as countless patients and government scientists. She uncovered so many similarities between Chronic Fatigue Syndrome and AIDS that she came to the conclusion that they are part of the same epidemic, and she argued that until their connection is admitted by top government researchers, there is little hope of making real progress in the fight against Chronic Fatigue Syndrome.

Charles Ortleb's book captures all the challenges and excitement of running a small newspaper that was publishing a brilliant journalist who essentially was the Woodward and Bernstein of the Chronic Fatigue Syndrome epidemic. In Rolling Stone, David Black said Ortleb's newspaper deserved a Pulitzer Prize. Randy Shilts praised Ortleb's newspaper in And the Band Played On.

                                                            


This book continues the work Ortleb has been doing to raise awareness about HHV-6 and Chronic Fatigue Syndrome at his website HHV-6 University. Fewer and fewer people now pretend that HHV-6 is harmless. Thanks to Ortleb's efforts, more and more people are abandoning HHV-6 denialism and admitting the virus is at the center of a public health disaster.

 Hillary Johnson, the author of Osler's Web, called it "A rollicking, fascinating and important memoir."









The Human/Animal Interaction of Chronic Fatigue and Immune Dysfunction Syndrome: A Look At 127 Patients and Their 463 Animals


The Human/Animal Interaction of Chronic Fatigue and Immune Dysfunction Syndrome: A Look At 127 Patients and Their 463 Animals


By R. Tom Glass, D.D.S., Ph.D. Professor Emeritus of Oral and Maxilofacial Pathology and Pathology University of Oklahoma, Health Sciences Center Tulsa, OK 74114
Throughout the recognized existence of Chronic Fatigue and Immune Dysfunction Syndrome, anecdotal reports have linked domestic animals with CFIDS, but no formal scientific studies were reported (1,2). Cats and dogs were implicated by their owners most frequently. The usual association with the presence of the animal in the household of a CFIDS patient, followed by the development of strange diseases or dysfunctions in the animal, many of which mimic CFIDS. The severity of the diseases often necessitated euthanasia. In a fewer number of cases, the onset of CFIDS in the patient was associated with an exposure to a domestic animal which was later found to show signs of CFIDS.
Observations from my animal biopsy service demonstrate two interesting findings in animals of CFIDS patients (unpublished findings). Gingival biopsies from cats demonstrated an unusual epithelial viral vesicle associated with an equally unusual submucosal inflammatory response. Several melanomas were found in dogs of CFIDS patients which had the unique feature of a striking progression of the tumor in the absence of an inflammatory response.
Both dogs and cats are known to be susceptible to a wide range of viruses. With the exception of rabies, no zoonotic (animal to human or human to animal) viral infection transmission has been demonstrated between typical domestic animals and humans (3).
These observations and recognitions prompted the following questions:
  1. Do CFIDS patients have domestic animals (pets)?
  2. What is the interaction between CFIDS patients and their pets?
  3. Do the domestic animals have any clinical signs of CFIDS?
  4. What type of signs or manifestations of CFIDS do animals of CFIDS patients demonstrate?
  5. What is the relationship between the interaction of CFIDS patients and their animals and the onset and course of CFIDS?
and resulted in a series of studies to answer the questions.
The first study was a retrospective study of Center for Disease Control and Prevention (CDC) criteria-met CFIDS patient: using a standardized questionnaire which included patient comments. The study subjects came from a university medical center and CFIDS support groups throughout the United States. Appropriate statistical tests, including mean, median, Z test, multivariant analysis, and Chi-square test, were used. This information was compared to national statistical Information on animal interaction compiled by the American Veterinary Medical Association.
One hundred twenty-seven (127) criteria-met CFIDS patients completed questionnaires on their animal Interactions- There were 114 females and 13 males in the study. All respondents were Caucasian with the exception of one Native American. The mean age of the CFIDS patients was 42.4 years with a median age of 43 years. 61.4% of the respondents were married; 311.6% were either single, divorced, or widowed.
The most striking result of this study was the association between CFIDS patients and animals (usually indoor pets) and the number of animals per CFIDS patient. 97% of the CFIDS patients had animal contact [expected normal contact: 57.9% (4)], with only 2 males and 2 females not reporting animal contact. Reported dog ownership per household for CFIDS males was 9.5 and for CFIDS females was 7.9 (expected national average: 1.52). Reported cat ownership per household for CFIDS males was 6.1 and for CFIDS females was 8.7 (expected national average: 1.95). 106 of the respondents (83.5%) reported that their animals (pets) had atypical diseases with signs and symptoms which mimicked CFIDS in humans. Of these 106 CFIDS patients 100 (94.3%) either were the primary caregiver for the sick animals or had intimate contact (sleeping with, being bitten or scratched by, or kissing the animal). The next most common animal contact was birds (parakeets and ducks were mentioned most often), followed by horses, cows, rabbits, goats, and guinea pigs. Two (2) CFIDS patients had contact with primates. The reported mean age of the dogs was 6 years (median = 6 years); of the cats was 6.2 years (median = 5 years); and of other types of animals was 3.2 years (median = 0.4 years).
All of these differences between expected and observed values were found to be statistically significant (p>001) including a statistically significant higher (.02<p£ 05) possession of cats by single, divorced, and widowed persons than married people. Statistical analysis (Chi-square) of the relationship between intimate contact by CFIDS patients and the presence of CFIDS like signs in their animals was highly significant (p£ 001). 67% of the respondents that had such contact stated that the animal showed CFIDS-like signs prior to the human and 33% of the respondents felt that the otherwise healthy animal contracted its CFIDS signs from the CFDS patient. The place where the pet was obtained was as follows: Friends (35%), Commercial (26%), Stray (21%), Pound (15%), Self-bred (3%), 41% of the CFIDS patients had animals that were still alive while 69% of the CFIDS patients had animals that had either died or were moribund at the time of the survey.
Finally, of equal importance were the CFIDS patient’s comments. These comments were often voluminous and detailed the interaction between the animals and the CFIDS patient. It is very clear that the CFIDS patients, in general, are “animal lovers” even though frquently the patient comments spoke of allergies to animals. Simliarly, the respondents gave excellent descriptions of their animal’s(s’) CFIDS-like signs from time of onset to ultimate temination.Respondents also noted that the animals were often the “living being” most consistently in close contact with the CFIDS patient.
The conclusion of this study was that CFIDS patients not only have pets, but that there is a significant animal interaction and that a large number of these animals have atypical or unusual diseases which at least mimic CFIDS.
In the second study, the CFIDS patients reported on a total of 463 animals: 115 healthy animals (which served as a control group for the study) and 348 animals which showed signs of either dysfunction or disease. The control group was comprised of 51 dogs (44%), 39 cats (34%), and 25 animals that were grouped together as “others”. The “others” group was predominantly large animals: horses, cows, goats, and pigs. All the control animals were still living and well at the time of the survey or had died of either traumatic or natural causes.
The group of animals which showed signs of either dysfunction or disease were made up of 189 dogs (54%), 144 cats (41%), and 15 animals that were grouped together as “others”. This “others” group was predominantly small domestic pets: birds, hamsters, and guinea pigs. The mean age of the dogs in this study was 6.5 years (median 6 years); of the cats was 6.2 years (median = 5 years); and of other types of animals was 3.2 years (median = 0.4 years).
The distribution of signs of the animals showing either dysfunction or disease are as follows: 137 animals (59 cats; 64 dogs; 14 others) were classified as having “General Signs.” 36 animals (15 cats; 14 dogs; 7 others) of the general signs category were classified as being “Sick NOS” because the animals were clearly Ill, but no diagnosis could be or had been rendered by a veterinarian. The “Sick NOS” animals were often described as having the same types of clinical signs as their owner. 26 animals (9 cats; 9 dogs; 7 others) in the general signs category died suddenly of unexplained causes. 26 animals (11 cats; 15 dogs) of the general signs category had a variety of altered immune conditions. including allergies, skin rashes, hair loss, systemic lupus erythematosus, and sneezing. 20 animals (3 cats; 17 dogs) developed Parvo or other viral Infections. 11 animals (9 cats; 2 dogs) transmitted their conditions to other animals either by birth or direct contact. 10 animals (9 cats; 1 dog) were listed as having eaten mice, rats, or other wild animals. 9 animals (3 cats; 6 dogs) had non-viral infections.
122 animals (41 cats; 81 dogs) had “Neurological” signs. 32 animals (17 cat.; 15 dogs) of the neurological category had lethargy, weakness, or sleep disorders. 30 animals (9 cats; 21 dogs) in the neurological category had seizures, tremors, or tail twitching. 19 animals (4 cat:; 15 dogs) demonstrated hind limb dragging, myalgia, arthralgia, or Bell’s palsy. 16 animals (6 cats; 10 dogs) were anxious, depressed, moody, or demonstrated inappropriate behavior, including urination and defecation outside their litterbox. 15 animals (4 cats; 11 dogs) had photophobia, ocular discharge, or blindness. 10 animals (1 cat; 9 dogs) had deafness, ear sensitivity, or loss of balance.
36 animals (21 cat.; 15 dogs) demonstrated “Gastrointestinal” signs. 13 animals (9 cats; 4 dogs) in the gastrointestinal category had inflamed gingiva, mouth odor, tooth loss, or drooling. 10 animal, (4 cats; 6 dogs) in the gastrointestinal category had diarrhea or abdominal distention. 9 animals (5 cat.; 4 dogs) demonstrated anorexia. 3 animals (2 cats; I dog) had increased appetite without weight gain. 1 cat had hard stools.
33 animals (18 cats; 14 dogs; 1 other) showed “Reticuloendothelial or Blood Disorders”. 12 animals (3 cats; 8 dogs; 1 other) of this category demonstrated bleeding or blood disorders. 10 animals (9 cats; I dog) in this category developed leukemia. While all of the leukemic cats were positive for feline leukemia virus [FLV], 5 of the cats had been vaccinated against FLV prior to the onset of their feline leukemia. 7 animals (5 cat.; 2 dogs) died of either feline AIDS or canine immune defidency (AIDS). 2 dogs showed massive and generalized lymphadenopathy. 1 cat and 1 dog died of lymphoma (lymphosarcoma).
Excluding leukemia and lymphoma, 15 animals (3 cats;12 dogs) developed tumors (“Neoplasia”). 8 animals (2 cats; 6 dogs) in this category had either fatal and/or multiple tumors which were not further classified, but which resulted in euthanasia of the animal. 4 dogs of this category died from malignant tumors of epithelial origin (3 squamous cell carcinomas and 1 transitional cell carcinoma), while 1 cat developed perianal adenomas, but was still living at the time of the survey. 1 dog died of a functional pituitary tumor and 1 dog died of melanoma.
Only 5 animals (2 cats; 3 dogs) were reported to have “Endocrine Disorders”. 2 cats and 2 dogs in this category had thyroid hyperplasia or thyroid nodules and 1 dog has pituitary hyperplasia.
Of equal importance, 113 of the 127 patients 89%) stated that their own CFIDS symptoms directly related their interaction with animals. Specifically, 79 of the respondents (71%) stated that they either had contact with multiple animals, were farmers, or were caretakers of multiple animals. 18 of these CFIDS patients (16%) note that the onset of their CFIDS symptoms were temporarily associated with the obtaining of a new pet, while 2 CFID patients (1%) noted that their CFIDS symptoms improved after the pet left or died. 9 respondents (8%) stated the other family members also contracted CFIDS in such manner as to implicate the pet as being possibly a common link in etiology. 3 CFIDS patients noted that the onset their CFIDS symptoms directly followed a flea bite episode and 2 CFDS patients reported that the prior owner of the home in which they contracted their CFIDS was inhabited by both CFIDS patients and sick animals.
As was noted in the first study, CFIDS patients care deeply for their animals. This observation can be understood by the detail and thoroughness with which the CFIDS patients filled out the information concerning the symptoms, laboratory results (such as blood count., blood chemistries, biopsy reports, etc.) and the courses of the animal’s(s’) condition. For the most part, it was the CF1DS patient who filled out the questionnaire. It must be remembered that these patients usually have severe fatigue and for them to have given such attention to detail was a major task.
Both studies also noted what an important role the pet plays in the CFIDS patient’s life. An analysis of the comments by the CFDS patients demonstrates unequivocally that the pet was often the CFIDS patient’s major contact with a living being. While it is imperative to consider the results of this study, it is equally imperative not to isolate CFIDS patients from their pets Rather, prevention of intimate contact, such as sharing food or kissing between the CFIDS patient and the pet, should be encouraged.
While the results of this study have certain subjective elements, such as reliance upon CFIDS patient and fault observations or the possibility of “symptom transference” (e.g., arthralgia in a pet is more likely to be noted by an arthralgic patient than a person free of joint pain), the recurrent finding of certain symptoms that may be common to both the CFIDS patient and the animal warrant attention It is important to consider the possibility that CFIDS may be transmitted from human to animal and/or from animal to human. If one considers the symptom of lethargy in the animals, the 32 CFIDS patients who observed this symptom all noted that the lack of energy was different than they had observed before in either the affected animal or in other animals in the same household who did not demonstrate the symptom. The seizure disorders and sudden unexplained deaths were more dramatic and objective signs of possible transmission of an agent that affects the nervous system. While seizure disorders and sudden unexplained deaths are not accepted features of CFIDS in humans, others have noted anecdotally a higher than usual number of seizure disorders and even sudden unexplained deaths in CFIDS patients.
While this study demonstrates the multiplicity of CFIDS-like signs in the animals, it is this same multi-organ involvement in the CFIDS patients that makes CFIDS so difficult to diagnose in humans. As with CFIDS in humans, the animals usually showed no laboratory evidence of a specific disease entity. There was, however, a predominance of neumlogic, neuromuscular, and rheumatologic symptoms in the animals just as there are in CFIDS patients. The result of these studies need to alert the veterinary profession of the need to inquire as to the health of the animal owner and their family. Conversations with a number of clinical veterinarians have pointed out that they are commonly confronted with conditions in domestic animals which do not fall into well established disease patterns. The most common of these deal with neurological and infectious diseases. These two areas were the most often reported as the pet signs found by CFIDS patients. Somewhat confounding was the low number of animals demonstrating endocrine disease. This under-reporting may be more of a lack of testing than a lack of disease as these tests are expensive and CFIDS patients are often financially unable to afford their own diagnostic tests., much less their animal’s(s’).
The results of these studies also need to alert the veterinaray profession that should there be a possibility of animal to human transmission of CFIDS, veterinarians might want to consider the wearing of protective clothing, gloves, eyewear, and masks when examining animals. We have received a number of reports from veterinarians around the country, especially from female veterinarians, that they have had to substantially limit their practices due to fatigue and other CFIDS-like symptoms. Similarly, precautions need to be taken to prevent CFIDS from being transmitted from one animal to another.
The conclusions of the second study were that animals of CFIDS patients demonstrated a wide range of disease and dysfunctional signs, similar to their CFIDS owners. The interactions between the animal and the CFIDS patients was often intimate. The study showed that the course of CFIDS in the animals varied widely, but after more thorough analyses of the data and of subsequent data, it appears that the animals have two distinct courses: 1. Their CFIDS signs produce progressive deterioration and the animal dies or 2. The animals appear to completely recover, usually after about five years.
In closing, both of the above studies had one common conclusion: animal interaction is a very important part of CFIDS patients’ lives’. I am often asked by CFIDS patients, knowing what I do about the CFIDS patient/animal interaction, if I would recommend that CFIDS patients have pets. While there is no way for me to survey animals, from my interaction with my own pet. and with the way CFIDS patients love their pets’ I would say that any pet would willingly run the risk of contracting CFIDS for the love, care and attention they will receive from CFIDS patients.
REFERENCES:
1. Ostrom, N. 50 Things You Should Know About the Chronic Fatigue Syndrome: New York: That New Magazine, 1992: pp 25, 26, 36, 37
2. Ostrom, N. What Really Killed Gilda Radner? New York: That New Magazine, Inc., 1991 pp. 159-164, 345-352
3. Cotran, RS., Kumar, V., Robbins, SL. Robbins Pathological Basis of Disease, 4th ed. Philadelphia: W. B. Saunders Co., 1989; pp. 309-310
4. Wise, JK. The Veterinary Sevice Market for Companion Animals. Schaumburg, IL; American Veterinary Association, 1992; pp. 5-65.
AUTHORS NOTE: This article is the first of three articles on my experiences with Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS; aka CFS). The first article deals with the interaction between CFIDS patients and their animals. The second article will deal with the actual autopsy findings of sick animals owned by CFIDS patients, the transmission of the CFIDS infectious agent to healthy animals, and the autopsy results of these animals. The third article will deal with the oral and head and neck manifestations of CFIDS, a lip biopsy of minor salivary glands for the confirmation of CFIDS, and some interesting therapy for the head and neck pain so often experienced by CFIDS patients [The second and third articles by Dr. Glass will he published in the next two consecutive issues of MPWC News – Ed. note.] In the early 1990’s, the following studies were conducted on CFIDS patients and their animals. The articles were sent to a number of both medical joumals and veterinary medical journals. The response from the editor of the medical journals was that while the articles were well-written, thorough and timely, they were better placed in veterinary medical journals. The veterinary medical joumal editors agreed with the medical journal editors in terms of the validity of the studies; however, they felt that if they published the articles, they might jeopardize the entire practice of veterinary medicine as small animals comprise the largest segments of such practices.
Source: This article appeared in the Spring 1998 Vol 3 Number 2 Edition of the Medical Professionals With CFIDS (MPWC) News

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