HETEROBILHARZIA AMERICANA

Canine schistosomiasis is not an exotic disease. Rather, it is caused by the digenetic trematode H. americana. Its geographic distribution in the United States originally included the southern Atlantic Coast and the Gulf Coast but has now been documented as far north as Kansas. Thus, the distribution of the parasite appears to be the central and southeastern United States.^10,11

Life cycle

There are numerous reservoir hosts for H. americana, but raccoons and nutria appear to be the primary ones. Dogs are the most important domestic definitive host, but red wolves and coyotes may be important wild canid reservoirs. Experimental or natural infections with H. americana have been demonstrated in two species of aquatic snails; however, little information is known about whether additional species can be competent intermediate hosts.

Clinical findings

Passage of the eggs through the tissues provokes a severe granulomatous reaction that is responsible for most of the clinical signs.^11,12 A wide spectrum of disease and presentations occurs in dogs, ranging from subclinical to granulomatous intestinal disease, granulomatous liver disease, or renal failure induced by the hypercalcemia that can result from granulomatous disease. The most common clinical findings include lethargy, weight loss, anorexia, hyporexia, vomiting, hypercalcemia, diarrhea, and polyuria and polydipsia.¹² In severe infections, hepatic disease may also be present.

Complete blood count and serum chemistry profile results are often normal, although hypercalcemia with decreased serum parathyroid hormone or increased serum parathyroid hormone-related protein concentrations may be present. The hypercalcemia in these cases may be misdiagnosed as neoplasia and hypercalcemia of malignancy. Thus, canine schistosomiasis should be included on the differential diagnosis list, particularly in endemic areas, for dogs presenting with unexplained glomerulonephritis or weight loss, gastrointestinal or liver disease, or hypercalcemia.^13-15

Diagnosis

Clinical diagnosis generally comes from the demonstration of the eggs in feces or in intestinal or hepatic biopsy samples. Routine fecal flotations will not detect eggs since they do not readily float. Also, if placed in water, the eggs will hatch within minutes. Thus, fecal sedimentation with 0.85% saline solution is the diagnostic technique of choice for demonstrating these eggs. The examination of direct saline smears may also reveal the presence of eggs.

As with other parasites, eggs are passed intermittently in feces, so multiple fecal examinations may be required. The identity of suspect eggs can be confirmed by resuspending eggs in deionized water, which allows them to hatch, or through a polymerase chain reaction assay. An antigen-capture ELISA is an additional diagnostic choice.¹¹

Treatment

Both praziquantel (25 mg/kg two or three times a day for two or three days) and fenbendazole (40 to 50 mg/kg once a day for 10 days) have been used to treat this infection with variable results.¹¹ In at least one study, hypercalcemia did not resolve unless the animals had been treated with praziquantel.¹² The prognosis is good even in the presence of hypercalcemic-induced renal failure or ascites.¹²