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Compendium March 2010 (Vol 32, No 3)

Canine Schistosomiasis in North America: An Underdiagnosed Disease With an Expanding Distribution

by Eileen M. Johnson, DVM, MS, PhD

    Heterobilharzia americana, a digenean trematode in the family Schistosomatidae, is the etiologic agent of canine schistosomiasis in the southeastern United States.1 A few cases of canine schistosomiasis have been reported in Florida, Louisiana, North Carolina, Texas, and, recently, Kansas.1–6 The natural definitive host for the fluke is the raccoon1; however, infections have been detected in nutrias, bobcats, mountain lions, opossums, white-tailed deer, swamp rabbits, armadillos, coyotes, red wolves, red wolf–coyote crosses, Brazilian tapirs, minks, and beavers.7

    Geographic Distribution

    The geographic distribution of H. americana is believed to be restricted to the south Atlantic and Gulf Coast states (Alabama, Florida, Louisiana, Georgia, North Carolina, South Carolina, Virginia, Mississippi, Texas) due to the environmental requirements of its intermediate host, the freshwater snail Lymnaea cubensis8; however, H. americana infections have been reported in indigenous raccoons7 and three companion dogs in Kansas.6 These cases are likely due to introduction of the fluke with raccoons translocated from Florida before 1983 and transmission by a freshwater snail, Pseudosuccinea columella, experimentally shown to support development of H. americana.9,10 Both L. cubensis and P. columella are present in Oklahoma,11 although schistosomiasis in indigenous dogs or raccoons has not been reported there. P. columella, a North American lymnaeid, has spread worldwide through the trade and transport of aquatic plants.12 L. cubensis is known to be distributed in Florida, Georgia, Louisiana, Texas, Mexico, South America, and the West Indies12; it has also been found in Oklahoma.11

    A retrospective study conducted in Texas discovered a higher rate of H. americana infection in dogs than the previous literature seems to reflect, with a broader distribution than along the Gulf Coast.13 Within a 4-year consecutive period, 127 cases were confirmed in 25 of 254 counties in Texas. Distinct clusters of cases were found along the Gulf Coast and associated with major urban populations. These findings indicate that canine schistosomiasis is not a rare disease and that the distribution of the trematode in Texas has expanded. Another retrospective study of 22 naturally infected dogs in Texas found the infection in younger, larger-breed, indoor dogs that had occasional access to the outdoors. Often, multiple animals in a household were affected.14 Cases have also recently been identified in Alabama, Georgia, North Carolina, and Tennessee.a

    Life Cycle

    Dogs and wildlife are exposed to H. americana while wading or swimming in freshwater areas such as marshes, mud flats, and canals.10 Cercariae discharged from infected snails penetrate the host's skin. The immature schistosomes (schistosomula) first migrate through the body to the lungs, where they are associated with hemorrhage. They are then carried to the liver, where they develop into adult male and female flukes. The adults move into the mesenteric veins, mate, and deposit nonoperculated, spineless eggs (FIGURE 1). The eggs penetrate venules to enter the intestinal wall and are shed into the intestinal lumen. If the eggs reach fresh water, they rapidly hatch, releasing ciliated miracidia (FIGURE 2) that swim for a short period of time in search of a suitable snail. Mother and daughter sporocysts and cercariae develop asexually in the hepatopancreas of infected snails. Cercariae are then shed from the snail to reinitiate the life cycle. Eggs can be detected in the feces of definitive hosts approximately 68 days after exposure to infective cercariae.10

    Diagnosis and Treatment

    Eggs that have been hematogenously disseminated to visceral organs or the intestinal wall provoke a severe granulomatous reaction (FIGURE 3 and FIGURE 4) responsible for most of the clinical signs and pathology.15 Initially, a papular vesicular rash and coughing may be noted. Chronic diarrhea, characterized as mucoid to hemorrhagic, develops and progressively becomes more severe. Fever, anorexia, hypersalivation, lethargy, and weight loss may also be noted.2–6,14 Anemia, dehydration, hyperglobulinemia, hypoalbuminemia, hypercalcemia associated with elevated parathyroid hormone–related protein levels, and eosinophilia are common clinicopathologic findings in infected dogs.2–6,14 Elevated serum alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase activities may also be evident.5 Eggs are not likely to float with centrifugal flotation16; examination of direct saline smears and sedimentation of feces facilitate the detection of H. americana eggs. A miracidia hatching technique that involves resuspending eggs sedimented in saline with deionized water can be employed to verify egg identification.16 An antigen capture ELISA for schistosome circulating anodic antigen5,b and a polymerase chain reaction assay for H. americana are also available for diagnosis.17,c

    Infections in dogs have been treated with high-dose praziquantel (25 mg/kg PO bid or tid for 2 to 3 days) or fenbendazole (40 mg/kg PO sid for 10 days).5 Treatment may result in complete cure or resolution of clinical signs, or it may be ineffective. The protracted course of the disease, poor response to treatment, and diagnostic challenges often lead to euthanasia. Many of the clinical signs and the hypercalcemia associated with elevated parathyroid hormone–related protein levels detected in some cases of canine schistosomiasis are more commonly associated with tumors, endocrine disorders, and other infectious granulomatous diseases.3 Some infections are secondary findings in animals with neoplasms.14 Expensive and invasive procedures may be required to rule out these conditions. Therefore, the definitive diagnosis of schistosomiasis is often delayed, as is initiation of appropriate therapy.

    Conclusion

    Increased awareness of canine schistosomiasis and implementation of appropriate diagnostic parasitology tests in dogs with chronic diarrhea, especially in the southeastern United States, should improve early detection of H. americana infections and could improve therapeutic outcomes. The limited number of reported cases in dogs is incongruent with the high prevalence reported in the natural host (raccoon) and the broad range of naturally infected hosts.7 Geographic distribution of the snail intermediate hosts seems to be expanding.11,12 These factors suggest that canine infections with H. americana are often not detected because routine parasitologic examinations do not include the fecal sedimentation technique or because owners choose euthanasia after exhaustive diagnostic testing fails to determine the etiology of clinical disease.

    Downloadable PDF

    1. Malek EA. Heterobilharzia infection in the dog and other mammals in Louisiana. J Parasitol 1961;47:619-623.

    2. Slaughter JB Jr, Billups LH, Acor GK. Canine heterobilharziasis. Compend Contin Educ Pract Vet 1988;10:606-612.

    3. Rohrer CR, Phillips LA, Ford SL, Ginn PE. Hypercalcemia in a dog: a challenging case. JAAHA 2000;36:20-25.

    4. Fradkin JM, Braniecki AM, Craig TM, et al. Elevated parathyroid hormone–related protein and hypercalcemia in two dogs with schistosomiasis. JAAHA 2001;37:349-355.

    5. Flowers JR, Hammerberg B, Woo SL, et al. Heterobilharzia americana infection in a dog. JAVMA 2002;220:193-196.

    6. Wilson N, Johnson EM, Brunker J, Ritchey J. Heterobilharziasis in a dog [abstract]. Proc 52nd AAVP2007:93.

    7. McKown RD, Veatch JK, Fox LB. New locality record for Heterobilharziaamericana. J Wildl Dis 1991;27:156-160.

    8. Malek EA. Experimental infection of several lymnaeid snails with Heterobilharzia americana. J Parasitol1967;53:700-702.

    9. Malek EA, Short RB, Teehan WH, Jama A. Differential susceptibility of snail hosts to Heterobilharzia americanafrom Texas and Louisiana. J Parasitol 1987;73:872-873.

    10. Lee H. Life history of HeterobilharziaamericanaPrice 1929, a schistosome of raccoon and other mammals in southeastern United States. J Parasitol 1962;48:728-739.

    11. Cheriuyot HC, Jordan HE. Potential for the spread of Fasciola hepatica in cattle in Oklahoma. JAVMA 1990;196:1090-1094.

    12. Madsen H, Frandsen F. The spread of freshwater snails including those of medical and veterinary importance. Acta Tropica 1989;46:139-146.

    13. Snowden K, White S, Barbara L, Craig T. Distribution and characterization of Heterobilharzia americana infections in the dog in Texas [abstract]. Proc WAAVP 2009:99.

    14. Fabrick C, Bugbee A, Fosgate G. Clinical features and outcome of Heterobilharzia americana infection in dogs. J Vet Intern Med 2010;24:140-144.

    15. Bartsch RC, Ward BC. Visceral lesions in raccoons naturally infected with Heterobilharzia americana. Vet Pathol 1976;13:241-249.

    16. Goff WL, Ronald NC. Miracidia hatching technique for diagnosis of canine schistosomiasis. JAVMA 1980;177:699-700.

    17. Bishop MA, Suchodolski JS, Steiner JM. Development of a PCR test for the detection of Heterobilharzia americanaDNA in dog feces. J Vet Intern Med 2008;22:804-805.

    aPersonal communications: Byron Blagburn, MS, PhD, Auburn University; Dana Ambrose MS, University of Georgia; Anne Zajac, DVM, PhD, Virginia Tech; and Sharon Patton, MS, PhD, University of Tennessee; October 2009.
    bAvailable from North Carolina State University College of Veterinary Medicine by request.
    cAvailable from Texas A&M University, College of Veterinary Medicine, Gastrointestinal Laboratory; www.cvm.tamu.edu/gilab/assays/Heterobilharzia%20americana.shtml.

    References »

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