Although we at times are not pleased by breeders, the very tight breeding that has went into producing the purebred dogs we
see in practice can make our jobs easier in regard to diagnosing complex internal medicine problems. It is important to know
about these diseases as the breeders are often better informed than veterinarians regarding some of these diseases. This is
especially true with the advent of the Web and the enormous amount of information (and disinformation) available for retrieval.
Thrombocytopenia and femoral artery thrombosis in cavalier king charles spaniels
Most of us are familiar with the huge proportion of the CKCS that develop very early onset mitral and tricuspid valve endocardiosis.
This breed does however have some other peculiarities that are worth mentioning. One such problem is the presence of benign
thrombocytopenia. In this breed dogs have been detected that routinely have platelet counts below 100,000/ul. A bleeding tendency
has not been detected. Part of the thrombocytopenia is spurious if only machine counts are used. Many of the breed have macrothrombocytes
(2 to 3 times normal sized platelets). Automated counts will be falsely low because the platelets are counted as red cells.
Other CKCS actually do have a low platelet count, even when a manual count is performed. A bleeding tendency however is not
always present. This of course does not prevent a CKCS from having immune-mediated thrombocytopenia.
When presented with a CKCS with a low platelet count it is vital to confirm this with a manual count or at least estimate.
The presence of a low platelet count and very large platelets could be consistent with this breed specific problem. A bleeding
tendency should also not be present, in other words no signs of thrombocytopenia (petechia, ecchymoses, epistaxis) should
be present and preferably a buccal mucosal bleeding time should also be in the normal range. Apparently bigger platelets are
hemostatically more active than smaller ones. If in doubt immune suppressive therapy can be tried, if it is the CKCS idiopathic
asymptomatic thrombocytopenia there should be little to no response.
Another newly recognized problem in the breed is the presence of femoral artery thrombosis. This has been detected in 6% of
CKCS investigated. Generally there are no clinical signs other than a weak or absent femoral pulse. Lameness, pain, etc. are
generally not present since collateral circulation can take over supplying blood to the affected limb. The disease appears
to be localized to the femoral arteries, as other vessels have not been found to be involved. Treatment is not needed.
Alabama rot in greyhounds
Certainly not the most flattering name for a disease, however it is easy to remember. The more scientific name is "cutaneous
and renal glomerular vasculopathy of Greyhounds (CRGV). It has also been termed Greenetrack Disease. This is a disease of
undetermined etiology, though it has some resemblance to hemolytic uremic syndrome in humans that is caused by E. coli secreting
shiga-toxin (E. coli O:157). To date infectious agents have not been identified in affected dogs, though they were searched
for. The majority of dogs are racing dogs, however it has been seen in some pet dogs as well. It is uncertain whether the
common practice of feeding racing dogs raw meat is a factor or not.
The disease can present as a multifocal ulceration and edema preferentially of the rear limbs or in combination with acute
renal failure (often anuric or oligouric). Both males and females are affected. The skin lesions tend to be dramatic, initially
just ulcers are present that tend to coalesce so that a large part of the skin of the rear limbs sloughs. Edema can be present
as well. Many dogs also develop renal dysfunction with azotemia. In these dogs, prognosis is guarded to poor as the majority
succumbs to the renal failure, though we have treated one dog successfully. Another common finding in these dogs is the development
of thrombocytopenia, especially in dogs that have or develop renal dysfunction. The thrombocytopenia can be quite pronounced
and cause clinical signs. Anemia also develops as a result of microangiopathic hemolysis, probably in the kidneys (fibrin
strands form in blood vessels and the RBCs are lysed as they go through that vessel).
PKD in persians
Polycystic kidney disease is not a new disease, however efforts are underway to try to eliminate the disease from the breed.
The problem is that the disease tends not to manifest clinically until late in life (usually not before the cat is 6 to 7
years of age) if at all. Fortunately, although clinical manifestations occur late, the cysts can be detected fairly early
in life so that a screening program can be successful. The incidence is high, it may be that 30% of more of the breed is affected.
The reason for this is that the disease is transmitted in an autosomal dominant mode, making for rapid spread within a line.
The cysts develop through apoptosis, that is dying off of the cells, inflammation is not generally involved. The cysts become
progressively bigger, till little renal tissue is left. The liver can also be involved with multiple cysts developing as well,
though this is relatively rare. Diagnosis is best achieved by ultrasonography using a high frequency probe (7.5 mHz). Although
cysts can be identified as early as a few months of age, ultrasound at 1 year is preferable. At this age the cysts have had
time to enlarge so that a skilled ultrasonographer can properly diagnose over 90% of the cases correctly. Unfortunately, there
is no specific treatment available. Once renal failure develops, standard supportive care is indicated.