7-year-old, neutered, male, cat (Felis domestics).The animal presented with tachypnea and staggering one hour prior to death.
Brain: The animal had blood around the mouth and nostrils.Â The lung lobes had multiple,
sometimes extensive, red to pink, often firm foci, and the cut surfaces exuded bloody froth.Â The right atrium
contained a 14.5 cm slender nematode, which was identified upon microscopic examination as Dirofilaria immitis.
The heart weighed 17.15g and was within normal limits for size and shape.
There is severe villous intimal proliferation involving large and
medium diameter arteries, which is near-occlusive in some instances.Â Slender and broad villous-like projections,
consisting of stalks of collagen covered by prominent endothelial cells, extend into the lumens of affected arteries.
Eosinophils in small to large numbers are dispersed singly or in loose aggregates, accompanied by lesser numbers of
macrophages throughout the expanded tunica intima and are also present in the tunica adventitia and in adjacent
alveolar septae.Â There is mild to moderate hypertrophy and hyperplasia of smooth muscle of the tunica media of
some arteries in the section, with cytoplasmic vacuolation of few myofibers.Â In some sections of the large arteries,
there are deposits of deeply eosinophilic, beaded material, considered to be necrotic remnants of nematodes, which
are surrounded by macrophages and multinucleate giant cells.Â There is diffuse interstitial congestion, focal
hemorrhages, patchy alveolar edema, hyperplasia of bronchial submucosal glands, and smooth muscle hypertrophy
and hyperplasia of terminal bronchioles and alveolar ducts.
Lung: Endarteritis, proliferative and eosinophilic, diffuse, chronic, severe, with medial hypertrophy and hyperplasia, hemorrhage, edema, smooth muscle hyperplasia and hyperplasia of the bronchial submucosal glands.
Heart: Nematode, intraluminal in right atrium, identified as Dirofilaria immitis.
The histologic lesions in the pulmonary arteries are consistent with the endarteritis
reported in feline dirofilariasis caused by Dirofilaria immitis (heartworm), which is characterized by villous
proliferation of the intima together with medial hypertrophy and hyperplasia.Â (9)
Two representative samples of the lung tissue were submitted.Â In one section, there is marked proliferative endarteritis together with granulomatous inflammation consisting of a thin layer of macrophages and multinucleate giant cells surrounding the deeply eosinophilic beaded to granular remnants of the parasite.Â Remnants of the parasite are noted in the adventitia of an affected vessel in the other section.
The marked villous endarteritis in dirofilariasis is reportedly attributable to the presence of live worms in the affected arteries and is of diagnostic importance.(2) In some cases of dirofilariasis, proliferation of intima results in occlusion of pulmonary arteries.(1) A characteristic lesion of canine dirofilariasis is medial hypertrophy of pulmonary arteries, which can be observed in cats, and has been considered a result of D.immitis-mediated stimulation of medial smooth muscle.(9) In cats, medial hypertrophy is often associated with Aelurostrongylus abstrusus and Toxocara cati infections(7,11,12), which can confound interpretation of these changes caused by Dirofilaria infections.(13) Heartworm (HW) disease is primarily a pulmonary vascular disease caused by the filarial organism, Dirofilaria immitis.Â Mosquitoes, e.g.Â Aedes spp., Anopheles spp., and Culex spp.Â are the obligate hosts of the first, second and early third stages of D.Â immitis.Â These mosquitoes can transmit heartworms to numerous wild and companion animal species.Â The infective stage of the parasite develops within the malpighian tubules of the mosquito in 13 days, after which time it migrates to the proboscis or cephalic spaces of head and escapes into the new host when the mosquito feeds.Â The L3 larvae molt to L4s in 2-3 days.Â They remain in subcutaneous tissue for about 60 days, after which develop into L5 larvae.Â At the L5 stage, larvae migrate to the pulmonary arteries (predilection site).Â Microfilariae are produced about 6-7 months post-infection by gravid females.Â If D.Â immitis develops to maturity in hosts other than dogs, microfilaraemia is generally low or absent.(8) Both natural and experimental infections have shown that cats are considerably less susceptible to heartworm disease than dogs.(13) The infective stage (L3) of the parasite when experimentally inoculated into cats caused disease in only 25% of animals, whereas about 44-90% dogs were infected.Â The prepatent period too was found to be longer, e.g.Â 8 months or longer, in cats compared to 6 months in dogs.(5,13)
D.immitis occurs in the right ventricles or pulmonary vessels.Â Right-sided heart failure secondary to pulmonary hypertension is uncommon in cats.(4) Most often in cats, cases have a brief history of dyspnea followed by sudden death.Â These are the result of thromboembolism or acute right-side cardiopulmonary failure.(9) The pulmonary arterial change in heartworm disease of cats can be more severe than that observed in dogs.Â Eosinophilia appear to be more common in cats.(3,13)
Heartworm is enzootic in dogs in the United States.(10) On the other hand, heartworm disease of cats is rare and is mostly detected at the time of necropsy.(13) Diagnosis of heartworm disease in cats can be difficult because of the transient nature of infection and the low numbers of microfilariae seen in circulation(5,13), as well as shorter lifespan of the adult worm in the cat.(5,13) Angiography and serology have been used to detect heartworm infections, especially in cats due to low levels of microfilaremia.(6) ELISA is commonly employed for measurement of anti-D.immitis antibody to adult worms.(6)
Lung, arteries and arterioles: Endarteritis, villar and eosinophilic, diffuse, severe, with mild smooth
muscle hyperplasia and Splendore-Hoeppli material.
The contributor provided an excellent overview of feline pulmonary dirofilariasis.
Domestic felids, ferrets, and California sea lions are dead-end hosts, and are not a source of transmission due to the
absence of microfilaremia(8).
There was some slide variation, and eosinophilic granulomas with Splendore-Hoeppli material were present in some sections.Â Conference participants felt this was the origin of the deeply eosinophilic conglomerations present in some sections.Â Other considerations were necrotic nematode debris, as suggested by the contributor, or conglomerations of fibrin and hemoglobin.Â Conference participants also noticed the presence of hemosiderosis, and attributed this to heart failure.
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