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Dirofilaria immitis (view source)

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==Pathogenesis==

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Heartworm disease is primarily a cardiopulmonary disease. the severity and extent of lesion depends on the number and location of adult worms. The presence of parasites in the pulomnary arteries causes proliferation of the intima, redulting in narrowing and occlusion of the vessels, which leads to pulmonary hypertension. Severe pulmonary arterial disease may cause increased permability of the lung vessls with periarterial oedema, and intersitial and alveolar cellular infiltrate, which can result in irreversible lung fibrosis. Pulmonary thromboembolism, due to platelet aggregation induces by the parasis or in response to the deat (spontaneous or induced by adultidicat treatment) of adult worms is another possible sequela of heartworm disease.

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Heartworm disease is primarily a cardiopulmonary disease. the severity and extent of lesion depends on the number and location of adult worms duration of infection, and host activity level.. The presence of parasites in the pulomnary arteries causes mechanical irritation and proliferation of the intima, redulting in narrowing and occlusion of the vessels, which leads to pulmonary hypertension. perivascular cuffing with inflammatory cells, including infiltration of high numbers of eosinophils. Severe pulmonary arterial disease may cause increased permability of the lung vessls with periarterial oedema, and intersitial and alveolar cellular infiltrate, which can result in irreversible lung fibrosis. Pulmonary thromboembolism, due to platelet aggregation induces by the parasis or in response to the deat (spontaneous or induced by adultidicat treatment) of adult worms is another possible sequela of heartworm disease. chronic lesions and subsequent scarring

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HW-associated inflammatory mediators that induce immune responses in the lungs and kidneys (immune complex glomerulonephritis) cause vasoconstriction and possibly bronchoconstriction. Leakage of plasma and inflammatory mediators from small vessels and capillaries causes parenchymal lung inflammation and edema. Pulmonary arterial constriction causes increased flow velocity, especially with exertion, and resultant shear stresses further damage the endothelium. The process of endothelial damage, vasoconstriction, increased flow velocity, and local ischemia is a vicious cycle. Inflammation with ischemia can result in irreversible interstitial fibrosis.

In some severe cases, worms can migreat to the right ventricle, right artrium and caudal vena cava. This retrografe migration induces incompetence of the tricuspid valve which, in association with concurrent pulmonary hypertension, is responsible for the clinical signs of right-sides heart failure (e.g. jugular distension, liver congestion, ascites). In addition, red blood cell memranes may rupture as the vells flow through the mass of parasits, causing haemolysis and haemoglobinaemia. The concomitant presence of acture right-sided heart failure and intravascular haemolysis is referred to as caval syndrome. Severe cases of caval syndrome can also be characterised by the present of adult worms in the caudal vena cava, thromboembolic events and disseminated intravascular coagulation. Caval syndrom is less common in cats due to the lighter woem burden.

In cats, hertwoms disease generally induces a diffuse plumonary infiltrate and signs of eosinophilis pneumonia. The death od adult worms may cause acute pulmonary embolism with severe haemorrhage and oedema of the affected lobe. Occasionally, immature nematodes cna migrate to sites other than the heart and plumonary areties, causing ectopic infection. Localisation of D. immitis has been repored in the eye, CNS, systemic arteries and subcutaneous tissues. Ectopic infections are more commonly seen in cats than in dogs, suggesting that the parasite is not well adapted to feline hosts.

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The severity of cardiopulmonary pathology in dogs is determined by worm numbers, host immune response, duration of infection, and host activity level. Live adult HW cause direct mechanical irritation of the intima and pulmonary arterial walls, leading to perivascular cuffing with inflammatory cells, including infiltration of high numbers of eosinophils. Live worms seem to have an immunosuppressive effect; however the presence of dead worms leads to immune reactions and subsequent lung pathology in areas of the lung not directly associated with the dead HW. Longterm infections, due to all of the factors noted (ie, direct irritation, worm death, and immune response) result in chronic lesions and subsequent scarring. Active dogs tend to develop more pathology than inactive dogs for any given worm burden. Frequent exertion increases pulmonary arterial pathology and may precipitate overt clinical signs, including congestive heart failure (CHF). High worm burdens are most often the result of infections acquired from numerous mosquito exposures. High exposures in young, naive dogs in temperate climates can result in severe infections, causing a vena caval syndrome the following year. In general, due to the worm size and smaller dimensions of the pulmonary vasculature, small dogs do not tolerate infections and treatment as well as large dogs.

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HW-associated inflammatory mediators that induce immune responses in the lungs and kidneys (immune complex glomerulonephritis) cause vasoconstriction and possibly bronchoconstriction. Leakage of plasma and inflammatory mediators from small vessels and capillaries causes parenchymal lung inflammation and edema. Pulmonary arterial constriction causes increased flow velocity, especially with exertion, and resultant shear stresses further damage the endothelium. The process of endothelial damage, vasoconstriction, increased flow velocity, and local ischemia is a vicious cycle. Inflammation with ischemia can result in irreversible interstitial fibrosis.

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Pulmonary arterial pathology in cats and ferrets is similar to that in dogs, although the small arteries develop more severe muscular hypertrophy. Arterial thrombosis is caused by both blood clots and worms lodged within narrow lumen arterioles. In cats, parenchymal changes associated with dead HW differ from those observed in dogs and ferrets. Rather than type I cellular edema and damage as found in dogs, cats experience type II cellular hyperplasia, which causes a significant barrier to oxygenation. Most significantly, due to restricted pulmonary vascular capacity and subsequent pathology, both ferrets and cats are more likely to die as a result of HW infection

==Signalment==

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