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
Unlike most trematodes, H. americana has separate sexes. The mature trematodes live in the mesenteric veins, where they mate and the female produces eggs. Eggs
in the terminal mesenteric veins penetrate through the vessel, entering the intestinal wall. After traversing the wall, they
are released into the lumen and are passed with feces. The miracidium is fully developed by the time the egg enters the external
environment. If the egg contacts water, the miracidium hatches and enters a freshwater snail. Asexual reproduction occurs,
producing cercariae. These emerge from the snail beginning as early as 25 days after infection. Cercariae penetrate the intact
skin of the definitive host and migrate through the lungs to the liver. The trematodes grow and mature in about 40 days and
then migrate to the mesenteric veins. The prepatent period is about 68 days.
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.
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
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
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