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FSF / FAMILIAL SHAR-PEI FEVER

„FAMILIAL SHAR-PEI FEVER“

EXCERPTS FROM MY REPORT ON FSF

FAMILIAL SHAR PEI FEVER

This report summarizes my experiences with FSF in its manifestation as SHS, based on the illness suffered by our Shar-Pei bitch Chilly / Moulin Rouge. This fever episode occurred the first time on February 12, 2006 and again on March 10, 2006, with both events manifested as SHS. Chilly / Moulin Rouge stems from the Cool-Man’s kennel, operated by Uwe Lenk (Andreas Kosbab).

This report includes all the information submitted by many other Shar-Pei owners, describing how their own dogs suffered repeatedly from these complex set of symptoms. My report is complemented by information received from veterinarians. I must point out that, according to the state of current scientific knowledge, this information concerns the disease called Familial Shar-Pei Fever or FSF manifested as the Swollen Hock Syndrome or SHS and/or swollen flews, which is a breed and line related illness that affects Shar-Pei.

The Symptoms:

    - Big eyes begging for help, hanging tail

    - Short fever spike, temperature up to 41.4°C

    - Attacks of shakes throughout the body

    - Labored and fast breathing

    - Inflammatory and highly painful redness of the hocks

    - The dog whimpers and cries out in pain if hocks are touched

    - Dog hobbles, as if walking on eggs

    - Inflammatory and highly painful redness of the flews

    - The dog whimpers and cries out in pain if flews are touched

    - Decreased appetite, refusal to eat

    - No water intake

    - Frequent and heavy urination

    - Fatigued and apathetic behavior

    - Greenish secretion from the eyes

    - Loss of mucin deposits, especially around the head and in particular the flews; hippo-like muzzle of the Shar-Pei disappears and dog begins to look like a shrew.

    - Short-term weight loss

    - Possible light vomiting and diarrhea accompanying the fever.


At first glance, these FSF symptoms remind one strongly of rheumatism.

Therapy:

Unfortunately, no effective treatment has so far been found for FSF or any of its causes.

It is very critical to monitor and lower the body temperature arising from FSF. The symptoms of initial fever episodes are treated with moist cold pads, and with antiphlogistic and antipyretic medication like aspirin, Rimadyl (Pfizer), Metacam (Boehringer), and Zubrin (Essex). Normally, an aspirin meant for adult humans is administered every six hours on day one of the fever spike, followed by one tablet twice a day for the second to fifth day.

It is advisable to administer antipyretics like Rimadyl, Metacam, or Zubrin for acute attacks to ease the pet’s discomfort. Vets consider fluid calcium as a totally ineffective treatment for FSF, although it does not harm the canine.

Giving colchicin in acute attacks of FSF is ineffective and not recommended for treating the fever. A side effect of this treatment could cause bone marrow damage. A Shar-Pei stricken with FSF should be put on a low protein diet of 16% to 20%. Weight loss, water consumption, and food intake must be checked regularly, and the vet notified immediately in case of any change.

I hope that every breeder and dog owner realizes that an FSF episode needs immediate treatment with appropriate antipyretics and analgesics.

My research:

The following are the findings of my research into FSF:

    - The trigger(s) of the disease are unknown, but the cause appears to be an autoimmune system disorder: the levels of immunoglobulin (antibodies) of different classes formed are too low, and this is accompanied by malfunctioning lymphocytes, which are a kind of white blood cells.

    - Stress seems to be one key trigger

    - This disease involves a disorder of the immune system with the above symptomatology.

    - FSF most likely involves a genetic mutation or autosomally recessive disorder, meaning that the carriers need not be stricken, but may transmit the defect.

    - FSF is one of autoimmune polyarthritic disorders.

    - FSF is definitely dependent on the line, since cases in the literature talk about entire families being affected.

    - If the defective gene is inherited from both parents, the offspring is likely to have FSF.

    - If only one parent has the defective gene, the next generation is not likely to get the disease, but it could surface in the following generation.

    - A carrier of the defective DNA will not necessarily become ill, but may transmit the defect.

    - Scientists believe that this disease involves polymeric transmission, i.e. transmission of several genes.

    - The fever episodes are just manifestations of the FSF disease.

    - Mostly puppies are stricken, but adult and old dogs may also suffer from initial episodes of fever and swelling of the heel and carpal joints and inflamed swelling of the muzzle or flews.

    - The health of Shar-Pei is burdened by a series of autoimmune system disorders, which is the primary cause of FSF.

    - During the FSF episode, Shar-Pei have elevated levels of cytokine IL-6 in their blood.

    - Dysfunction of IL-6 appears to be the cause of many of the subsequent illnesses of dogs stricken with FSF.

    - Incestuous breeding and inbreeding of our Shar-Pei is still practiced, in order to obtain preferred traits. Such dubious breeders are thus pursuing an approach that will guaranty promotion of congenital diseases, including FSF.

Many Shar-Pei have mucin deposits in their heel or carpal joints, referred to as socks. This is not synonymous with FSF, which is always accompanied by acute fever spikes.

Scientists agree that about a quarter of the Shar-Pei that gets FSF will begin to develop kidney amyloidosis with the first fever episode.

But, the hereditary disease„FSF“ is „NOT synonymous with amyloidosis!“ !

Nevertheless, the statements by veterinarians in technical articles are worrisome: they state that amyloidosis leads to the deposits of amyloid (protein base pairs) in the kidneys during an FSF episode, and that these are not really treatable. We now know that roughly a quarter of the dogs suffering from FSF develop kidney amyloidosis, which is the death knell for the dogs from premature kidney failure. In addition, these deposits also occur in the liver, lungs, and other organs, causing fatal damage.

I believe that many diseases could be the precursors of fatal amyloidosis. It should be reemphasized that FSF is NOT synonymous with amyloidosis, although each incidence of FSF is a precursor of amyloidosis, which tends to result in premature demise of the Shar-Pei.

None of the vets can really predict the time for premature death of a Shar-Pei from FSF and the consequential amyloidosis. My opinion is that the significant factors are the number of fever incidences and the amount of the deposited protein base pairs or amyloid.

„At the present time, there is no test available for screening a carrier of a defective DNA to control Shar-Pei likely to transmit FSF to their offspring!“

That is why I suggest reading my discourse under:

DEMANDS

Hanspeter Kobold
Bremen,June 2006 2006


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