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 ą pulmonary arteries ąeosinophilicendarteritis
(Type I hyper-sensitivity) ą myointimal proliferation ą
Type III/IVhypersensitivities ą endothelial damage/platelet
activation ą thrombosis ą recanalization ą 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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