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Winter 1998 Newsletter


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Canine Mast Cell Tumors

Equine Herpes Virus 1 Myelo encephalopathy
Feline Heart Worm Disease
Surpulinapilosi coli
Vesicular Stomatis in the Horse
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Feline Heartworm Disease

            The first reported case of Dirofilaria immitis in a cat was in 1922 in Virginia.  This cat had 2 adult worms in the right ventricle.  Research into feline heartworm disease has grown significantly since then, and is recognized as a potentially life threatening disease.

            Feline heartworm disease is very important clinically because even a light infection is capable of producing severe, life threatening disease.  The regional prevalence of heartworm infections in domestic cats tends to parallel canine heartworm infections but at a lower rate.  Cats are less easily infected by heartworms.  It has been shown that dogs are the preferred host and there are indications that cats are not the ideal hosts.

            The life span of the parasite is shorter in cats and infections tend to be self-limiting after two to three years.  Cats also have a greater tendency to spontaneously eliminate the infection or die from the infection.  Another reason cats are proven not to be ideal hosts is the aberrant migration of fourth stage larvae which is more likely to occur in cats than in dogs.  Large numbers of ectopic heartworms have been found in the body cavities and central nervous systems of cats.

            Other important differences in feline heartworm disease exist.  Unlike dogs, circulating microfilariae are seldom found in cats.  If found in cats, the average time needed for the worms to produce the larvae is 8 months post-infection with microfilariae persisting for one month.  Cats generally cannot tolerate as many adult heartworms as dogs.  Dogs can potentially maintain a burden of several hundred worms whereas many cats can die from fewer than 10 worms.

            The lesions caused by heartworms is slightly different in cats than in dogs.  While cats can develop interstitial lung disease like dogs, there is also an extensive alveolar type II cell hyperplasia in cats.  These parenchymal lesions may have an important role in the pathogenesis of acute respiratory distress 4-9 months post-infection.  It is thought that cats mount a more intense immune and inflammatory response to the adult heartworms which coincides with the pathogenesis.

            Clinical signs are frequently non-specific and could correlate with many other disease processes.  The most common chronic signs are tachypnea, coughing, and anorexia.  Abnormal lung sounds may be heard but heart mumurs are rare.  Intermittent vomiting that is not associated with eating is another common sign.  There is also a peracute syndrome that can be seen with feline heartworm disease.  The signs associated with this may include acute respiratory distress, ataxia, collapse, seizures, hemoptysis, and sometimes sudden death.

            Diagnostic testing for cats is more difficult than in dogs.  Microfilariae can be detected with the modified Knott's test, however since cats only have microfilariae for a short time, a negative test does not necessarily exclude the diagnosis of heartworms.  Reasons why the results of an ELISA antigen test may produce a false negative result include:  immaturity of parasites, too few female worms to produce detectable levels of antigen, or infection by solely male worms.

            Thoracic radiographs may help confirm a positive heartworm test.  Radiographic evidence of feline heartworm disease includes enlargement of lobar and peripheral branches of pulmonary artery.  This sign may be limited to the right caudal lobar artery where heartworms are most commonly found.  Unlike dogs, right-sided cardiomegaly is seldom seen.  There can be main pulmonary artery enlargement in cats but it is obscured by the cardiac silhouette.  Radiology along with angiography and echocardiography are primarily used to confirm a tentative diagnosis of feline heartworm disease rather than as screening tools.

            Treatment of feline heartworm disease must be based on the clinical signs of the individual cat, not solely on the basis of a positive Knotts or antigen test.  If the cat displays no overt signs of heartworm disease it is best to allow time for spontaneous elimination of the parasites.  These cases can be monitored every 6 to 12 months for worsening of radiographic signs.

            Infected cats with radiographic signs of pulmonary interstitial lung disease may benefit from a diminishing dose of prednisone beginning with a dose of 2 mg/kg per day and gradually reducing it to 0.5 mg/kg every other day by two weeks and then discontinuing after an additional two weeks.  At the end of treatment the cat should be assessed radiographically.  This treatment may be repeated periodically in cats with recurrent respiratory signs.

            In cats that are not controlled by the above regime and are stable clinically, adulticide treatment could be initiated with this acetarsamide at 2.2 mg/kg intravenously twice a day for 2 days.  Post treatment cats should be in caged confinement and under close observation for 3 to 4 weeks.  Owners should be warned that a possible side effect of treatment is potentially fatal pulmonary thromboembolism.

            As always, prevention is the best method of controlling this potentially fatal disease in cats.  Chemoprophylaxis with a monthly dose of ivermectin at 24 mg/kg is recommended to cat owners.  Even though the heartworm antigen test sensitivity is low, it is good medical practice to test for feline heartworm disease before giving chemoprophylaxis for the first time, if at least 8 months have passed since there was an opportunity for infection.

- by Jennifer Keenan, Class of 1999

- edited by Victoria Owiredu-Laast, DVM

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