I can give you another example:
A certain dean of a certain veterinary school in a certain Midwest state is
an expert on toxicology and has almost 200 published papers, 80 of which
have to deal with safe exposure to toxic chemicals. The format is the same,
they are all peer reviewed, and are scientific trash. It goes thusly: Rats
are fed or exposed to a specific chemical for 13 weeks in varying
concentrations, usually four. The safe level is declared as the level
directly below the exposure that caused cellular or measurable blood value
Where is the flaw in this? Actually there are several.
1. Laboratory rat diets are optimized and are costly as animal feeds go.
They are also not subject to the variants most animal feeds are. Nutrient
levels are carefully maintained. One cannot extrapolate to humans who are
consuming fast food on a regular basis with no supplementation. It would
have been interesting to see what a safe level would be on diets as chaotic
as the average American, diets supplemented with liver detoxifiers, or rats
exposed to stress, and far more valid.
2. Some of the enzymes measured are so obscure they are not even found in
biochemistry texts and are therefore not recognized as important measures of
3. The time frame is far to short to declare a safe level. Autoimmune
disorders take years to manifest.
4. Only one toxin is introduced at a time which is not a real life scenario.
Therefore, the only conclusion that can be made is that there are no
discernible physiological changes in rats exposed to X chemical at X level
for 13 weeks in a controlled laboratory environment. Declaring a "safe"
level is irresponsible, but these papers have passed the review process.
The peer review process is a good-ole-boy network and they support each
other. It is not as pristine as it may seem and sometimes the word fraud is
Here is the submission to pro-Med challenging the new disease proclamation:
The statement that PEMS is "a deadly combination of viruses" is pure
speculation, not science. The ratite (ostrich, rhea) industry went through
a long grocery list of bacteria and viruses as causative agents, all of
which failed the simple test of consistency.
Now, the turkey owners are experiencing the same economic devastation and
all the ARS has to offer is a viral speculation. One of the researchers
listed did write a paper on the profound hypophosphatemia in the rhea and
his conclusion was to supplement with phosphorus. Feed companies
redeveloped feed with high levels of phosphorus and injectable phosphorus
became the standard treatment for acute cases. It didn't work and the birds
still were horribly deformed and dying while injecting large numbers of
easily stressed animals repeatedly is simply neither commercially feasible
nor economically sound. The “solution” offered nothing in the way of an
explanation that why animals that have survived on the planet for 80 million
years would evolved with such a metabolic quirk.
So, here are portions of the introduction to the approved patent
application, which will be published in the fall, supporting my allegation
that the new disease is not new at all. There are few specific references
to rheas because there only a dozen published papers on any aspect of the
rhea. Furthermore, since I have been black-balled, my laboratory facilities
for the last two years have consisted of a glucose tester from K mart and a
surplus Russian microscope. I can't even get blood values done.
This is not a frivolous patent. The patent office has significantly
tightened the rules for medical patents to try to stem the tide of plant and
DNA patents, but once they were satisfied with the science presented (after
numerous rebuttals and queries) and understood that I was not a biotech
company, but just a tenacious, sole researcher, they assisted me in every
way possible. Under the new rules, I could not be granted a patent
specifically for human autoimmune disorders without a double-blind clinical
trial (an impossibility at this point), so I was granted a patent on the
production of the product with specific claims for animals. Call it a
peasant’s revolt, if you wish.
These charts, which are the heart and soul of this patent, are on the
website, and show the path from ATP to autoimmune symptoms through a
competitive and rate-limiting detoxification pathway.
Wasting Syndrome Manifestations in Infant Rheas and Ostriches
Rhea americana (rhea) and Struthios camelus (ostrich) chicks are notoriously
frustrating to raise, often succumbing to a wasting disease from one of
three bewildering syndromes which develop between one week and two months of
age. Birds that survive to three months of age generally mature. Morbidity
and mortality can be 100% (1). Since no single pathogen can be found
consistently, the syndrome is, in our opinion, metabolic in origin, and
perhaps a successful evolutionary adaptation in the wild that becomes a
suicide mechanism in confinement.
1. Rubber Rhea Syndrome, currently believed to be unique to the South
American ostrich, is characterized by severe hypophosphatemia, mildly
depressed blood glucose, low thyroxin levels, with stunting, pliable bills,
softened bones, and many chicks exhibiting widening of the proximal
tibiotarsus, poor feathering, depleted adipose, and ultimately, death.
Bone histopathology, decreased bone ash, gross lesions, and decreased serum
phosphorus characterize moderate to severe rickets (2-4).
2. Post-protozoan stunting syndrome, following successful recovery of
intestinal protozoan overgrowth after a course of treatment with
metronidazole, shows shortened bones and bill, widening of the
tibiometatarsus, hyperkeratinosis, stunting, poor feathering, rounded heads,
and ascites with varying incidence of alopecia, achromotricia,
encephalomyopathy, spontaneous fractures, aneurysms, and paresis. This
syndrome bears a remarkable similarity to aflatoxin poisoning. Chronic
inflammation of the small intestine is apparent at necropsy (unpublished).
This chronic inflammation is not exclusive to this disorder, it is so common
as to be misconstrued as normal (5).
3. Fading Chick Syndrome, recognized by veterinarians and producers alike as
a common problem in the ostrich and rhea, is characterized by extreme weight
loss, muscle degeneration, lethargy, hypothermia, decreased appetite,
stunting, frequent intestinal inflammation, ascites, and death, usually
within the first month with or without secondary infections (6).
The Syndromes as Accelerated Autoimmune Disorders
Inconsistent chick survivability under a wide range of management systems,
climates, feeding programs, and genetics pose a challenge to the commercial
development of rheas and ostriches as livestock animals. These problems
foster the widely accepted, but unsubstantiated view, that ratite chicks are
immunosuppressed and the health problems are therefore multi-factorial
(7-9). Typical efforts to solve these problems through known therapies
utilizing strict biosecurity management or pharmaceutical regimens have
resulted in frustration and increased production costs, threatening the
ability to raise these animals competitively as food animals. Although
ostriches have been raised domestically in South Africa for over 100 years
as the domesticated hybrid commonly referred to as the African Black
ostrich, the rhea and other subspecies of ostriches raised in the United
States are basically ancient wild animals with a long history of successful
evolutionary strategy in the wild state.
Compounding the situation is widespread disagreement and speculation among
veterinarians regarding various causative disease organisms, which upon
closer examination of the symptoms, suggests these “diseases” are variations
of “Fading Chick Syndrome” with an opportunistic bacterial invader of
questionable pathogenicity, Megabacteriosis (10, 11), or viruses such as
coronaviral enteritis (12), rotavirus, or adenovirus (13, 14). Recent
results from the experimental trials at University of Georgia show that two
specific adenovirus isolates are non-pathogenic to ostriches, establishing
that the presence or detection of adenovirus does not implicate
pathogenicity (15), refuting prior claims of adenovirus as the leading cause
of “Fading Chick Syndrome” (16). It may prove to be a synergistic virus,
playing a role in increased adiposity in chickens testing positive for
adenovirus (13). This may be a beneficial synergistic reaction to the birds
in a toxin situation, increasing available adipose sites for toxin
deposition. In our opinion, these syndromes are similar to autoimmune
disorders in humans, where the body attacks itself. However, in the case of
the ostriches these are accelerated autoimmune disorders, rapidly producing
disability and death in weeks rather than decades.
Therefore, the cause of Fading Chick Syndrome and Rubber Rhea Syndrome is
most likely a metabolic imbalance initiated by exposure to environmental
toxins often compounded by stress. This is corroborated by reduced weight
gain during exposure to the feed mycotoxin vomitoxin (16). The nature of the
imbalance and the attempt by the birds to restore homeostasis provides the
basis for utilizing the carcass extract of the ratites in humans and animals
as a therapeutic agent.
The closely related members of the ratite group of flightless birds, rheas
(first), ostriches (second), have a dramatic, crippling, and fatal
evolutionary strategy based on unchecked proteolysis and subsequent cachexia
in a stressed state. These skittish birds are capable of sustained speeds up
to 35 MPH with less than 2% fat available in their muscle. This indicates
an ability to create and manifest an enormous amount of molecular energy in
the form of nucleotides, i.e. ATP (adenosine triphosphate), to meet the
enormous demand of the muscles. ATP assays of dried muscle extract showed
dried rhea muscle extract had sustained ATP 64% higher than chicken and 155%
higher than pork or beef.
1. Shivaprasad HL. Neonatal mortality in ostriches: an overview of possible
causes. Association of Avian Veterinarians, 1993:282-285.
2. Angel CR, Bermudez, A. Serum Vitamin D metabolites and Chemistries from
Healthy Rheas and Rheas with "Rubber Rhea Syndrome". Association of Avian
Veterinarians Session # 4040. Philadelphia, Pennsylvania, 1995.
3. Angel C. Personal Communication. 1995:
4. Grone A, Swayne, D.E., Nagode, L.A. Hypophosphatemic rickets in rheas
(Rhea americana). Veterinary Pathology 1995;32:324-327.
5. Baltmanis B, Blue-McLendon, A, Angel, R. Effect of diet on the ostrich
gastrointestinal tract size. American Ostrich 1997(April):17-24.
6. Speer B. Fading Chick Syndrome. American Ostrich 1994:30-31, 82-85.
7. Wade J. Ratite pediatric medicine and surgery. Association of Avian
8. Raines AM. How to evaluate a ratite facility to aid in diagnosing chick
mortality. Association of Avian Veterinarians, 1994:97-102.
9. Blue-McLendon A. Pediatric Disorders of Ostriches. Proceedings
Association of Avian Veterinarians, 1993:269-271.
10. Peters L. Megabacteriosis. American Ostrich 1995(May):33, 45-48.
11. Huchzermeyer F, Henton, MM, Keffen, RH. High mortality associated with
megabacteriosis of proventriculus and gizzard in ostrich chicks. Veterinary
Record 1993;133(August 7):143-144.
12. Frank R, Carpenter, JW. Coronaviral enteritis in an ostrich (Struthio
camelus) chick. J. of Zoo and Wildlife Medicine 1992;23(1):103-107.
13. Dhurandhar NV, Kulkarni P, Ajinkya SM, Sherikar A. Effect of adenovirus
infection on adiposity in chicken. Veterinary Microbiology
14. Raines A. Adenovirus infection in the ostrich (struthio camelus).
Proceedings of the Association of Avian Veterinarians, 1993:304-311.
15. El-Attrache j, Villegas, P, O'Connor, B, Buhr, JR, Rowland, GN.
Adenovirus Pathogenicity in Immature Ostriches. American Ostrich
16. Scheideler S. Effects of vomitoxin on ostrich growth. American Ostrich
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