Page 222 - Small Animal Internal Medicine, 6th Edition

194 PART I Cardiovascular System Disorders

HEARTWORM DISEASE IN DOGS The worm distribution and accompanying villous prolif-
eration are most severe in the caudal and accessory lobar
Pathophysiology
VetBooks.ir The presence of adult worms in the pulmonary arteries pro- arteries. Affected pulmonary arteries lose their normal
tapered peripheral branching appearance and appear blunted
vokes reactive vascular lesions that reduce vascular compli-
may occur. The vessels become tortuous and proximally
ance and lumen size. Disease severity depends on several or pruned. Aneurysmal dilation and peripheral occlusion
factors, including the number of worms, how long they dilated as the increased pulmonary vascular resistance
have been present, and the animal’s reaction to the parasites. demands higher perfusion pressures.
Pathologic vessel changes begin within days after young HWs RV dilation and concentric hypertrophy develop in
enter the pulmonary arteries. The host-parasite interaction response to the chronic requirement for increased systolic
may be more important than the worm number alone in the pressure generation. Severe PAH eventually can lead to RV
development of clinical signs, although a large worm burden myocardial failure, increased RV diastolic pressure, and
is generally associated with severe disease. The pathogenesis signs of right-sided CHF, especially in conjunction with sec-
of HWD is modulated by the obligate intracellular bacterium ondary tricuspid insufficiency. Cardiac output progressively
Wolbachia, which is harbored by D. immitis and is integral declines as the RV fails. When cardiac output becomes inad-
to its growth and development. This may involve bacterial equate during exercise, exertional dyspnea, fatigue, and
endotoxins and the host immune response to a major Wol- syncope can occur. PTE, either postadulticide or spontane-
bachia surface protein (WSP), which is thought to contribute ous, can exacerbate PAH and signs of CHF.
to pulmonary and renal inflammation. The increase in pul- HWD can also have systemic complications. Circulating
monary blood flow associated with exercise can exacerbate immune complexes or possibly microfilarial antigens result
the pulmonary vascular pathology. A low worm burden can in glomerulonephritis. Renal amyloidosis has been associ-
produce serious lung injury and a greater rise in pulmonary ated rarely with HWD in dogs. Chronic hepatic congestion
vascular resistance if cardiac output is high. secondary to HWD may lead to permanent liver damage
Villous myointimal proliferation of the pulmonary arter- and cirrhosis. Although the caudal pulmonary arteries are
ies containing HWs is the characteristic lesion. The HW- the preferred site, worm migration “upstream” into the right
induced changes begin with endothelial cell swelling, heart and even to vena cavae is associated with heavy worm
widening of intercellular junctions, increased endothelial burdens. A massive number of worms can cause mechani-
permeability, and periarterial edema. Endothelial sloughing cal occlusion of the RV outflow tract, pulmonary arteries,
leads to the adhesion of activated white blood cells and plate- tricuspid valve region, or venae cavae; this is known as the
lets. Various trophic factors stimulate smooth muscle cell caval syndrome. Caval syndrome results in not only cardio-
migration and proliferation within the media and into the vascular instability but also intravascular hemolysis due to
intima. Villous proliferations consist of smooth muscle and physical shearing of red blood cells flowing past the mass of
collagen with an endothelium-like covering. These prolifera- worms, resulting in anemia and hemoglobinuria. Systemic
tive changes of the intima occur 3 to 4 weeks after adult inflammation and thrombotic complications can lead to
worms arrive; they cause luminal narrowing of the smaller disseminated intravascular coagulation (DIC) or systemic
pulmonary arteries and also induce further endothelial inflammatory response system (SIRS). Aberrant systemic
damage and more proliferative lesions. Endothelial damage arterial worm migration causing embolization of the brain,
promotes thrombosis, as well as a perivascular tissue reac- eye, or other systemic arteries occasionally occurs. Cases of
tion and periarterial edema. However, pulmonary infarction hindlimb lameness, with paresthesia and ischemic necrosis,
is unusual because collateral circulation within the lung is have been described sporadically.
extensive.
Hypersensitivity (eosinophilic) pneumonitis may con-
tribute to parenchymal lung lesions, and inflammation may HEARTWORM DISEASE TESTING
organize into eosinophilic granulomas. Interstitial and alveo- Serologic (Antigen) Tests
lar infiltrates may become radiographically apparent; partial Adult HW antigen (Ag) tests are recommended as the main
lung consolidation develops in some animals. Hypoxic vaso- screening test for HWD in dogs. Although controversy exists
constriction can also play a role in the vascular changes that as to whether yearly testing is necessary, for several reasons
increase pulmonary vascular resistance and consequently the American Heartworm Society recommends yearly
cause PAH. Hypoxia can occur in lung regions where pulmo- testing to ensure that prophylaxis is achieved and main-
nary infiltrates and/or pulmonary thromboembolism (PTE) tained. Currently available Ag test kits are highly accurate.
cause ventilation/perfusion mismatch. Pulmonary vasocon- Circulating Ag is usually detectable by about 6.5 to 7 months
striction may be exacerbated by increased endothelin-1 pro- after infection but not sooner than 5 months. There is no
duction or vasoconstrictive substances elaborated by HWs. reason to test puppies younger than 6 months of age. Ideally,
Dead worms stimulate greater host response and worsen testing of adults is recommended at about 6 to 7 months after
the pulmonary disease. Worm fragments and thrombi cause the preceding transmission season.
embolization and a more intense inflammatory reaction, Commercially available test kits are immunoassays that
which eventually leads to fibrosis. detect circulating HW Ag from the adult female reproductive