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Spring 2000 Newsletter

Feline Heartworm
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FINAL DIAGNOSIS - Feline Heartworm

Signalment:  6 year old, neutered male Domestic Shorthair cat

Clinical history:  Cat was adopted as a stray one year ago and presented to rDVM with acute, progressive dyspnea.  The cat died naturally.

Gross necropsy findings:  Dirofilariasis, right ventricle dilation, lung edema, hepatopathy, nephropathy, kidney congestion

Histopathologic findings:  Histopathology of the lung revealed a chronic, diffuse eosinophilic endarteritis with myointimal proliferation and fibrosis.  The walls of all elastic blood vessels within this section were thickened by hyperplasia and hypertrophy of the tunica media.  The smooth muscle cells were swollen and some were vacuolated with pyknotic nuclei.  The internal elastic lamina was disrupted and the tunica intima was infiltrated by moderate numbers of eosinophils and plasma cells.  The endothelial cells were diffusely plump and in some areas, were stratified.  In some affected vessels, the tunica intima was expanded by homogeneous eosinophilic material (collagen) that, in occasional vessels, partially occluded the lumen with villous projections. The surrounding alveoli contained numerous eosinophils and alveolar macrophages.  The alveolar septae were diffusely congested with slight hemorrhage into the alveoli, although few hemosiderin-laden macrophages and erythrophagocytes were observed.  Smooth muscle bundles in the alveolar septae were prominent and rounded (hypertrophy).  The peribronchial glands were increased innumber and the stroma was congested and infiltrated by low numbers of eosinophils.

Morphologic Diagnoses: (1) Chronic, diffuse, proliferative and degenerative, eosinophilic endarteritis  (2) Eosinophilic peribronchiolitis

Pathogenesis: Adult Dirofilaria immitis  inventricle à  pulmonary arteries àeosinophilicendarteritis (Type I hyper-sensitivity) à myointimal proliferation à Type III/IVhypersensitivities à endothelial damage/platelet activation à thrombosis à recanalization à fibrosis

Discussion:  Cats are generally less easily infected with Dirofilaria immitis than are dogs; however, because of small body size, cats with low worm burdens may have severe disease.   Male cats are more frequently and more heavily infected.  Cats have a greater tendency to spontaneously eliminate the parasite or die from infection.  The life span of the parasite is shorter in cats; infections tend to be self-limiting after two years.

  Aberrant migration of fourth stage larvae occurs more frequently in cats; therefore, ectopic heartworms may be found in body cavities and in the central nervous system.  The most severe clinical signs in cats are associated with the arrival of larvae in the pulmonary arteries and with thromboembolism following death of one or more mature worms.  The caval syndrome in dogs, caused partly by large numbers of heartworms interfering with the tricuspid valve, is rarely seen in cats due to light infection.  Arterial intimal proliferation, as occurs in dogs, also develops in the small peripheral and major lobar pulmonary arteries of cats.  Right ventricular hypertrophy or right heart failure due to pulmonary hypertension, however, is rare in cats.  Cats will also develop interstitial pneumonia; however, unlike dogs, may also have extensive alveolar type II cell hyperplasia.  These lesions play an important role in the acute respiratory distress seen in cats at presentation.  Some cats may go into remission and eventually recover; however, sudden death, usually associated with degenerating worms in pulmonary arteries, can occur.

   Similar lesions may be seen with infection by Angiostrongylus vasorum.

-by Kaori Sakamoto,  DVM, ADDL Graduate  Student




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