Mint Creek Valley Kennel

Mint Creek Valley Kennel

CSPCA Charitable Trust

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Dr. Gary Johnson Reports to CSPCA Members

Reprinted from September/October 1996 BARKER

     I have been asked to summarize remarks presented at the recent 
CSPCA National Specialty concerning a disease sometimes called "Swollen 
Hock Syndrome" or "Shar-Pei Fever". Typically, affected Shar-Pei 
experience repeated episodes of fever and/or lameness.  Unfortunately, 
during these inflammatory episodes, amyloid accumulates in the kidneys 
and eventually destroys these organs, leading to premature death.  
Shar-Pei Fever is believed to be an inherited disease because efforts 
to identify an infectious agent have been unsuccessful.

     My involvement in Shar-Pei Fever research began about three years 
ago when I became aware of a theory by Dr. Linda Tintle and her 
colleagues that Shar-Pei Fever is the canine version of a human disease 
known as Mediterranean Fever. This idea seems reasonable because 
symptoms of the human disease closely resemble Shar-Pei Fever.  
Mediterranean Fever was known to be an inherited genetic defect and the 
responsible mutation was known to reside on the short arm of human 
chromosome 16.  As part of an NIH-supported project, I had developed 
some DNA markers for genes from corresponding regions of dog 
chromosomal DNA. I, therefore, contacted Dr. Tintle to see if she could 
supply me with blood samples from families of Shar-Pei so that I could 
determine if these markers would be useful in identifying dogs that 
would eventually develop the disease or pass the disease onto their 
offspring.  As the result of subsequent chromosomal maping experiments,
the position of the Mediterranean Fever mutation is now known much more 
precisely than it was three years ago. As it turned out, our markers 
were from the correct half of chromosome 16, but they were too far away 
from the Mediterranean Fever defect to be useful, even if Dr. Tintle's 
theory is correct.

     A little over a year ago, Dr. Tintle informed me of an effort to 
raise $50,000 to support research on Shar-Pei Fever. Because this money 
could be used to develop additional canine DNA markers closer to the 
Mediterranean Fever mutation, I told her I was interested and, in fact, 
would be able to contribute an addition al $25,000 in discretionary 
funds toward the project.  More recently, we have submitted a success-
ful Shar-Pei Fever grant proposal to the Canine Health Foundation for 
an additional $25,000, bringing the total funds for the project to
$100,000.  These funds are now in the hands of administrators, 
accountants and lawyers; however, I am confident they will become 
available to me soon so that I can begin this project in earnest.

    The discretionary funds mentioned above stem from a project we are
doing for the North American Limousin Foundation which promotes and 
registers a breed of beef cattle. In the past, a substantial number of 
these cattle produced calves with protoporphyria, an inherited severe 
photosensitivity (tendency toward severe sunburn). With support from 
the NALF, we developed a DNA marker that enables us to identify 
symptomless carriers of the disease. By excluding carriers from their 
breeding stock, cattlemen have been able to eliminate protoporphyria 
from their herds. In less than three years, we have tested over 5,000 
head of cattle and greatly decreased the prevalence of protoporphyria 
in Limousin cattle in this country.

     If Dr. Tintle's theory about the relationship of Shar-Pei Fever 
and Mediterranean Fever is correct, we have a good chance of developing 
a DNA marker that identifies carriers of Shar-Pei Fever. If so, a 
simple, reliable and inexpensive blood test could be used to select 
mutation-free Shar-Pei for breeding puppies that should live long, 
healthy lives.

CSPCA Charital Trust

Amoyloidosis/By Dr. Linda J. M. Tintle, DVM

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