Canine Schistosomiasis in Kansas: Five Cases (2000–2009)

Introduction

Heterobilharzia americana, the causative agent of canine schistosomiasis in the United States, has been reported to occur naturally in the domestic dog in the Atlantic and Gulf Coast states.^1–5 Heterobilharzia has a complex life cycle in which asexual and sexual reproduction occurs in a lymnaeid snail and mammalian host, respectively. Natural mammalian hosts include wild and domestic canids (multiple species), raccoon (Procyon lotor), and nutria (Myocaster coypus) among others. Dogs are infected when wading or swimming in water where infective cercariae penetrate the skin. Adult worms are found in the mesenteric veins where oviposition occurs. Widespread granulomatous disease due to an inflammatory reaction associated with Heterobilharzia eggs can lead to multiorgan damage and hypercalcemia. Although any organ can be affected, the small and large intestine, liver, pancreas, and kidneys are commonly involved.^1–7 Clinical signs of schistosomiasis can include diarrhea with occult or frank blood and mucus, melena, vomiting, weight loss, and lethargy.^1–7 Polyuria can be secondary to hypercalcemia, which might lead to renal failure.² Failure to diagnose schistosomiasis can result in inappropriate treatment, unnecessary client cost, poor clinical outcome, and death. There have been relatively few reported cases of naturally occurring canine schistosomiasis; thus, there remains a paucity of information regarding clinical details.^1–7

The purposes of this report are to describe the clinical presentation, diagnostic test results, treatment, and outcome of dogs with schistosomiasis, and to report that naturally occurring canine schistosomiasis is present in Kansas and, therefore, the Midwestern United States.

Materials and Methods

Medical Records Review

Signalment, historical data, initial physical examination results, diagnostic test results, treatment(s), and outcome were extracted from the medical records of cases included in the study.

Historical information extracted included duration and type of clinical signs at initial presentation, type of home environment (indoor versus outdoor), exposure to and type of surface water (pond, lake, creek, or river), out of state (Kansas) travel, and the presence of clinical signs in other household dogs. Dogs were considered to be from an indoor environment if they were primarily housed indoors with outside exposure limited to a fenced-in yard or leashed walks. Dogs were considered to be from an outdoor environment if they lived primarily outdoors or were allowed to regularly roam free, unsupervised. Initial physical examination information extracted included body condition score (BCS; 1–5 scale), abdominal palpation, and other abnormal physical examination findings recorded in the medical record. Diagnostic test information extracted included results of serum biochemistry, complete blood count, parathyroid hormone (PTH), parathyroid hormone–related peptide (PTHrP), 25-hydroxycholecalciferol, serum protein electrophoresis, fecal flotation, fecal saline sedimentation, miracidium hatching, fecal PCR, abdominal radiographs, abdominal ultrasound, upper and lower gastrointestinal (GI) endoscopy, exploratory laparotomy, and histopathology. Treatment information extracted included type and duration of treatment and outcome.

All abdominal imaging examinations were interpreted by a board certified radiologist. Abdominal radiographs included a right lateral and ventrodorsal view; a left lateral view was made when appropriate. Abdominal ultrasonography included imaging of all intra-abdominal organs, lymph nodes, major vessels, and the peritoneal cavity. Histopathologic examinations were performed by a board certified pathologist.

Schistosomiasis was diagnosed in five dogs during the study period, and all five dogs were included in the final analysis after a review of the medical records concluded that all inclusion criteria were met. Breeds represented included one each of golden retriever (dog 1), Brittany (dog 3), and Labrador retriever (dog 4). Two dogs were mixed breed (dogs 2 and 5). There were two intact males, one neutered male, and two spayed females. Age ranged from 2.5 to 7 yr (median, 4 yr), and body weight ranged from 18 to 37 kg (median, 22 kg).

Home environment information was available for all five dogs, with all being classified as outdoor dogs. Information concerning access to surface water was available for three dogs, with dogs 3 and 4 having regular access to a pond (n=2) and dog 5 to a creek (n=1). Information regarding other dogs in the household was available for three dogs. Dog 3 was an only pet; the housemate of dog 5 had been euthanized within the last 6 mo for persistent hypercalcemia and suspected intestinal lymphoma that was not confirmed via cytology or histopathology; and the housemate of dog 4 was clinically normal but was found to have schistosomiasis via fecal saline sedimentation. All dogs resided in the state of Kansas, with only dog 3 traveling out of state, for sporting purposes, to Nebraska and South Dakota.

Initial examination results were available for all five dogs. Dog 1, initially treated for intestinal lymphoma, was administered a doxorubicin based chemotherapy protocol to which the dog had a positive clinical response (resolution of clinical signs and hypercalcemia). This dog presented a second time 1 yr after the discontinuation of the chemotherapy protocol, approximately 18 mo after initial presentation. This dog received prednisone (1 mg/kg/day, 2.2 mg/kg/lb) during the year between visits. Dog 4 had no clinical signs thought to be associated with schistosomiasis, as small intestinal thickening was found coincidentally via abdominal ultrasonography. This dog presented for surgical evaluation of a periprostatic cyst. Presenting clinical signs for the four symptomatic dogs included diarrhea (dogs 1, 2, 3, and 5), which included frank blood and/or mucus in dogs 1, 3, and 5; vomiting (dogs 1, 2, and 3); lethargy (dogs 1, 2, and 5); anorexia (dogs 1 and 5); weight loss (dogs 1 and 3); polyuria/polydipsia (dogs 1 and 5); and tenesmus in dog 3. Melena was reported in dog 1 at a second visit that was not present at initial examination. Duration of clinical signs at initial examination ranged from 0.5 to 24 mo (median, 3.25 mo). Initial physical examination findings from all five dogs included dehydration (dogs 1 and 5), thickened loops of bowel in dog 1, a heart arrhythmia in dog 1, caudal abdominal pain in dog 4, and generalized abdominal pain in dog 5. The BCS ranged from 1 to 2.5 (median, 2), with dogs 1 and 5 having a BCS of 1. Caudal abdominal pain was found in dog 4, who had a periprostatic cyst. The heart arrhythmia was later found to be premature ventricular contractions.

Biochemistry panel results were available for all five dogs at initial presentation and for dog 1 at a subsequent hospital visit (Table 1). Total calcium was severely elevated in dogs 1 and 5 (19.1 and 19.7 mg/dL, reference range 9.7–12.1 mg/dL). Biochemical changes seen in dog 1 at a subsequent visit showed resolution of hypercalcemia and worsening of azotemia. A complete blood count was available for dogs 1, 2, 3, and 5 at the initial visit and for dog 1 at a subsequent visit (Table 1). In dogs 2 and 5, serum protein electrophoresis showed a polyclonal gammopathy. Results of PTH and 25-hydroxycholecalciferol were available for dogs 1 and 5, and PTHrP was available for dog 5^a. PTH levels were low normal (3.1 and 2.3 pmol/L, reference range 2–13 pmol/L), 25-hydroxycholecalciferol was normal in both dogs (235 nmol/L, reference range 82–285 nmol/L, and 71 nmol/L, reference range 60–215 nmol/L, respectively), and PTHrP was zero^a.

TABLE 1 Biochemistry and Complete Blood Count Results

Parameters in which all patients were within the reference interval were not included.

ALP, alkaline phosphatase; ALT, alanine transaminase; Band Neut., Band neutrophil; BUN, blood urea nitrogen; HCT, hematocrit; HGB, hemoglobin; TCa²⁺, total calcium; RBC, red blood cell concentration; Seg. Neut., Segmented neutrophil; WBC, white blood cell concentration.

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Results of abdominal radiographs were available in dogs 1, 2, 3, and 5. Abnormal findings included mineralization of the small intestine (dogs 1, 2, and 5), mineralization of gastric rugal folds in dog 5, hepatomegaly in dog 1, and a partial intestinal obstruction due to an intraluminal tubular mass in the transverse colon in dog 3. The tubular mass was previously diagnosed as a cecocolic and ileocolic intussusception via endoscopy performed because of tenesmus. Abdominal radiographs taken by the referring veterinarian a few days before referral did not reveal an intestinal obstruction or intussusception. Abdominal ultrasound findings in the five dogs included small intestinal thickening (dogs 1, 2, 4, and 5) that was diffuse in dogs 1, 2, and 4 and isolated to the jejunum in dog 5, primarily affecting the submucosal layer in dogs 1, 4, and 5. In dog 1, the small intestinal mucosa was hyperechoic. Other findings included hepatic hyperechogenicity (dogs 1, 2, and 5), perisplenic/mesenteric lymphadenopathy (dogs 2 and 3), renal hyperechogenicity in dog 5, tortuous and enlarged portal and pancreatoduodenal veins in dog 5, an ill-defined splenic nodule in dog 4, ileocolic and cecocolic intussusception in dog 3, and a periprostatic cyst in dog 4.

Results of upper GI endoscopy were available for dogs 2 and 3. Dog 3 also had colonoscopy. Grossly, the gastric and duodenal mucosa were normal in dog 3, and the duodenal mucosa was reported to appear friable and edematous in dog 2. Colonoscopy in dog 3 showed a smooth, ulcerated, tubular mass that protruded into the lumen of the transverse colon. This was diagnosed as a cecocolic and ileocolic intussusception (Figure 1). Neither of these dogs were hypercalcemic.

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Fecal flotation using Sheather's sugar solution and double centrifugation was negative for parasitic eggs and cysts in all five dogs. Results of fecal saline sedimentation were available for dogs 3 and 4, both of which were positive for Heterobilharzia eggs before treatment, and negative after treatment. Miracidium hatching from the feces of dog 3 demonstrated viable miricidia (Figure 2). Fecal PCR performed on dog 3 was positive for Heterobhilharzia DNA before treatment and negative after treatment^b.

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Gross findings during abdominal exploration or postmortem examination included white circular, infiltrating lesions ranging from 2 mm to 1 cm in diameter on the serosal surface of the small and large intestine in dogs 1 and 4; irregularly shaped, gritty, tan foci in multiple organs in dogs 1 and 5; a firm, irregular, mottled liver in dog 5; a shrunken, irregular pancreas in dog 1; ileocolic and cecocolic intussusception in dog 3; and a periprostatic cyst in dog 4. Histopathology was available in all five dogs via exploratory laparotomy (dogs 2, 3, and 4), GI endoscopy (dogs 2 and 3), or postmortem examination (dogs 1 and 5). All intraabdominal organs were sampled in dogs 1 and 5. In the remaining three dogs, tissues examined included small intestine (dogs 2, 3, and 4), intraabdominal lymph node (dogs 2 and 3), large intestine/cecum in dog 3, and liver in dog 2. Heterobilharzia eggs were found in the small intestine (dogs 1, 3, and 5), large intestine/cecum (dogs 1, 3, and 5), liver (dogs 1, 2, and 5), lymph node (dogs 1 and 5), and pancreas (dogs 1 and 5). In each organ, eggs were associated with primarily granulomatous inflammation characterized by infiltration of macrophages and giant cells, with varying numbers of neutrophils, eosinophils, lymphocytes, and plasma cells, and varying amounts of fibrosis. Occasionally, eggs were partially or completely mineralized. Liver lesions were primarily periportal, with less involvement of the bile ducts and sinusoids. Black pigment was seen within Kupffer cells or extracellularly in dogs 1 and 5. Intestinal lesions included diffuse to multifocal granulomatous enterocolitis with intralesional eggs. Eggs were found in the mucosa (dog 5), submucosa (dogs 1, 3, and 5), and muscular layers (dogs 1, 4, and 5). Dog 2 had no evidence of eggs on small intestinal biopsy but did have disorganized muscle and granulation tissue. Pancreatic lesions included granulomatous and fibrosing pancreatitis in dog 1 and multifocal granulomas with intralesional eggs in dog 5. Lymph node lesions included severe granulomatous lymphadenitis with intralesional eggs in dog 1, lymphoid hyperplasia in dog 2, and subacute hemorrhage in dog 3. Renal lesions included metastatic mineralization in dogs 1 and 5 and severe interstitial and periglomerular fibrosis and tubular ectasia in dog 1. Dystrophic mineralization was also seen in the heart (dogs 1 and 5); small intestine (dogs 1 and 5); skeletal muscle (dog 1); and aorta and pulmonary artery, thyroid gland, stomach, and lung (dog 5). Endoscopically obtained biopsies from the stomach and duodenum were normal in dog 2, whereas dog 3 had evidence of mineralized or partially mineralized fluke eggs found in duodenal biopsies. Adult Heterobilharzia worms were seen in the mesenteric veins in dogs 1 and 5.

Dogs 1 and 5, which had hypercalcemia, were not treated for schistosomiasis. In dog 5, the owner declined additional diagnostics before obtaining a diagnosis, and the dog was euthanized. Dog 1 was treated for intestinal lymphoma and was not definitively diagnosed with schistosomiasis until postmortem examination. Three dogs were treated for schistosomiasis with treatments including fenbendazole^c in dogs 3 and 4 and a combination of fenbendazole and praziquantel^d in dog 2. Dog 4 and a housemate treated with fenbendazole (50 mg/kg/day, 23 mg/lb/day) were found to be negative via fecal saline sedimentation after 10 days of treatment. Dog 3 was treated with fenbendazole (50 mg/kg/day, 23 mg/lb/day) and had evidence of eggs via fecal saline sedimentation after 10 days of treatment but was negative after an additional 7 days of treatment. Fecal PCR was positive for Heterobilharzia DNA in this dog before treatment and was negative after treatment. This dog also had surgical correction of the cecocolic and ileocolic intussusception. Dog 2, treated with fenbendazole (40 mg/kg/day, 18 mg/lb/day) for 10 days and praziquantel (25 mg/kg, 11 mg/lb/day per os q 8 hr) for 2 days, showed improvement but not full resolution of clinical signs until after a second course of combination treatment. All treated dogs had complete resolution of clinical signs, including dog 3 who had surgery to correct cecocolic and ileocolic intussusceptions.

Discussion

This is the first report of naturally occurring canine schistosomiasis outside of the Atlantic or Gulf coast states. Schistosomiasis is a curable disease and should be included on the list of differentials for sporting or outdoor dogs in Kansas and other Midwestern states presenting with a history of diarrhea, weight loss, vomiting, anorexia, or hypercalcemia. In addition, this study presents the first case in which intestinal intussusception may have been secondary to schistosomiasis.

The life cycle of H americana has been well described.^8,9 H americana, a digenetic trematode, requires a mollusk intermediate host and mammalian definitive host in which asexual and sexual reproduction occur, respectively. The lymnaeid snails Lymnaea cubensis and Pseudosuccinea columella are intermediate hosts, although snail susceptibility varies with strain and geography.^8,10 The raccoon is the most important reservoir host.^3,8 Up to 37% of raccoons examined in Kansas were infected with H americana.¹¹ Further, up to 35% of wild canids tested in southeastern Texas and southwestern Louisiana were infected with H americana.¹² To date, only the raccoon (P lotor), nutria (M coypus), swamp rabbit (Sylvilagus aquaticus), and dog (various species) have been found to develop natural patent infections.⁸ Eggs defecated within feces of a definitive mammalian host contain miracidia that emerge quickly once exposed to water (as early as 30 min), with maximum numbers emerging between 1 and 2 hr postwater exposure.⁸ Miracidia are active for about 20 hr at the surface of water, after which they penetrate the head–foot, tentacles, or mantle collar of the snail.⁹ Asexual reproduction occurs within the snail, and after approximately 25–30 days cercariae emerge.^9,13 An average of 600 cercariae emerge from each infected snail.⁸ The cercariae are again active at the water's surface for approximately 18–20 hr, during which time they penetrate the skin of the mammalian host.^8,9 Within 7 days of infecting a mammalian host, immature flukes (schistosomula) may be found in the liver, where most of their growth and maturation occurs.⁹ Adult flukes, with a 4–10 yr life span, migrate to the mesenteric veins, the only place where sexual reproduction is known to occur.¹¹ After oviposition, eggs penetrate the serosal surface of the intestine, migrate through intestine wall, and enter the feces; a patent infection occurs 68–121 days postinfection.¹³ Eggs migrating through the intestinal wall and residing in the mucosa, submucosa, and muscularis invoke severe granulomatous enterocolitis. Other eggs migrate back to the liver and/or various other organs, such as lymph nodes, stomach, pancreas, spleen, kidney, brain, and lung via the portal circulation. In each organ, eggs become embedded and induce a delayed hypersensitivity reaction to antigens released by the eggs.¹⁴ The hypersensitivity reaction leads to formation of granulomas or “pseudotubercles” composed of neutrophils, lymphocytes, macrophages, and giant cells, leading to fibrosis.^13–15 The severity of clinical disease and organ dysfunction is dependent upon the number of mature fluke pairs, the final location of the eggs, and the subsequent inflammation, fibrosis, and degree of hypercalcemia.¹⁵

GI disease has been reported in previously published cases of canine schistosomiasis.^1–6,13 Common clinical signs include persistent to intermittent diarrhea with melena, hematochezia, and mucous, tenesmus, flatulence, vomiting, anorexia, or weight loss.^1–6,13 All dogs in the present study that were clinically ill presented with GI signs. It is common for dogs to present in poor body condition, which may be due in part to GI disease. All dogs had intestinal lesions on histopathologic examination, including one dog that was asymptomatic, although eggs were not found in intestinal biopsies of this dog. It was likely that Heterobilharzia eggs were present within the small intestine but not in the tissue that was sampled. The ileocolic and cecocolic intussusception seen in one dog was not previously reported as arising secondary to schistosomiasis. Although the pathophysiology underlying intestinal intussusception is not completely understood, enteritis and subsequent alterations in GI motility are known to be predisposing factors for intestinal intussusception.¹⁶ Granulomatous enterocolitis associated with schistosomiasis might have played a role in the development of the ileocolic and cecocolic intussusception in this dog.

Kidney failure secondary to hypercalcemia and dystrophic renal mineralization has been reported secondary to canine schistosomiasis.^1,2 Other possible causes of renal dysfunction associated with canine schistosomiasis include immune complex glomerulonephritis secondary to chronic antigenic stimulation, and granulomatous inflammation due to intrarenal eggs.^5,14 Renal disease was seen in two dogs, both of which had histopathologic evidence of dystrophic renal mineralization. In addition, severe diffuse interstitial and periglomerular fibrosis and multifocal tubular ectasia were seen in dog 1. In this dog, azotemia was mild and might have been due to dehydration at the initial visit. At a subsequent visit, the azotemia was much more severe and did not normalize after rehydration, indicating renal dysfunction. Renal fibrosis in this dog could have been due to chronic antigenic stimulation and subsequent glomerulonephritis or hypercalcemia.

In dogs affected with schistosomiasis, periportal fibrosis decreases portal blood flow, although liver function was reported to be unaffected due to neovascularization and the maintenance of normal blood flow.^7,15 Four experimentally infected dogs had normal liver function 2 yr postinfection, as assessed by bromosulphophthalein dye test.¹³ Cirrhosis was reported in raccoons infected with Heterobilharzia, although liver function was not assessed.¹⁷ Decreased portal blood flow and portal hypertension were likely the cause of portal and pancreatoduodenal venous distension seen in dog 5. Histopathological examination performed on liver tissue in three dogs demonstrated granulomatous inflammation with intralesional eggs, similar to previous reports.^1–5,13 Liver inflammation is primarily periportal because of the route of egg migration. Eggs are deposited in the mesenteric veins, swept via portal circulation to the liver, and become lodged in small hepatic veins. Liver enzymes were only mildly elevated in one dog in the present study; an underlying cause was not identified because liver biopsies were not obtained.

Histologic examination of the pancreas of two dogs showed severe, multifocal to coalescing, granulomatous, fibrosing pancreatitis and multifocal granulomas. Although the importance of pancreatitis and subsequent fibrosis as it relates to GI disease in canine schistosomiasis is unknown, reduced exocrine pancreatic function might play a role in the pathogenesis of diarrhea.⁶ Although the pancreas was not sampled in three dogs, it was possible that these dogs also had pancreatitis, contributing to GI disease. Other previously reported clinical signs not noted in this study included cercarial dermatitis, coughing due to worm migration or granulomatous pneumonitis, and neurologic disease.⁷

Hypercalcemia was previously reported in five cases of canine schistosomiasis and was seen in two dogs in this study.^1,2,6 Lymphoma was suspected in dog 1 based on the findings of a diffusely thickened intestine and resolution of hypercalcemia with chemotherapy. Although PTHrP is most commonly increased secondary to malignancy in dogs, it was reported to be elevated in two dogs with schistosomiasis.¹ PTHrP was normal in the only dog in which it was measured in this study. Hypercalcemia associated with granulomatous disease is due to overproduction of calcitriol by activated macrophages.^18–21 Hypercalcemia resolved in the one dog treated for suspected intestinal lymphoma. This might be attributed to the administration of prednisone, which decreases intestinal calcium absorption and corrects aberrant calcitriol production associated with granulomatous disease.^21,22 This dog died as the result of untreated schistosomiasis. The use of prednisone as the sole treatment of canine schistosomiasis is not recommended.

Other common clinicopathologic abnormalities included hyperglobulinemia, hypoalbuminemia, eosinophilia, and anemia.⁷ Hyperglobulinemia secondary to chronic inflammation was seen in three dogs. Hypoalbuminemia in one dog was most likely the result of intestinal loss secondary to granulomatous enterocolitis, because there was no evidence of proteinuria or hepatic failure in this patient. Chronic inflammatory disease or proteinuria due to immune complex glomerulonephritis might be contributing or sole causes of hypoalbuminemia.^4–6,13 Eosinophilia and basophilia were seen in one dog each. This was likely a direct result of inflammation associated with parasitic infections, especially helminth antigens. Anemia in one dog with melena was attributed to GI hemorrhage. Anemia secondary to chronic inflammation was suggested as another possible cause of anemia associated with canine schistosomiasis.⁶

Abdominal imaging is commonly performed in dogs with GI disease or with hypercalcemia of unknown cause. In dogs with schistosomiasis, abdominal radiography has been reported to show no abnormalities, or splenomegaly and/or decreased abdominal detail.^2,6 Abdominal radiographic findings attributed to schistosomiasis in this study were similar, but included hepatomegaly and gastric and small intestinal mineralization. Gastric and intestinal mineralization could be dystrophic mineralization due to hypercalcemia or secondary to long standing granulomatous inflammation. It should be noted that small intestinal mineralization was seen in one dog without hypercalcemia. Poor serosal detail might be secondary to cachexia or abdominal effusion, although no abdominal effusion was noted in the one dog with poor serosal detail in this study.^2,3

Abdominal ultrasonography has been reported to show no abnormalities, hyperechoic kidneys, splenomegaly, diffuse or segmental mural thickening of the small intestine, and abdominal lymphadenopathy.^1–3 Ultrasonographic findings in the dogs in this study were similar to previous reports, although hepatic hyperechogenicity was a common finding. Hepatic hyperechogenicity was most likely the result of granulomatous periportal hepatitis and fibrosis that was seen on histopathology in three dogs. In this study, the thickened small intestine was the result of granulomatous enteritis, and lymphadenopathy was due to granulomatous lymphadenitis and lymphoid hyperplasia.

The diagnosis of canine schistosomiasis may be made based on fecal saline sedimentation, miracidium hatching, fecal PCR, and histopathology.^23,24 Consistent with previously reported cases, fecal flotation did not reveal Heterobilharzia eggs in any dog in which it was performed.^1,3 Canine schistosomiasis will likely not be diagnosed on routine fecal examinations, and for this reason, schistosomiasis should not be excluded based on a negative fecal flotation examination. Diagnosis of schistosomiasis is best obtained via fecal saline sedimentation, fecal PCR, or intestinal or liver biopsies. Although only performed in a small number of dogs, fecal saline sedimentation and fecal PCR were sensitive, noninvasive tests in this study. Research is ongoing, but fecal PCR might be the most sensitive noninvasive test available, with the ability to detect 1.5 eggs/g of feces.²⁵ Schistosomiasis was diagnosed in the housemate of dog 4, and probably present but misdiagnosed in a housemate of dog 5 in this study. For this reason, other dogs in the same household as a dog with schistosomiasis should be tested, as their environmental risk factors are likely similar.

Successful treatment of canine schistosomiasis has been reported with administration of fenbendazole and/or praziquantel.^3,6,24 Fenbendazole at 40 mg/kg (18 mg/lb) body weight by mouth once daily for 10 days or praziquantel at 25 mg/kg (11.4 mg/lb) body weight by mouth three times daily for 3 days has been recommended.^7,24 One dog in this study was treated twice with both fenbendazole and praziquantel, with partial and then complete resolution of clinical signs, respectively. Two dogs receiving only fenbendazole had no eggs found on fecal saline sedimentation after a 10 day course of treatment in one dog, and after a second 7 day course of treatment in the second dog. In addition, a negative fecal PCR and resolution of clinical signs was found after treatment in the second dog. These three cases provided evidence that fenbendazole with or without praziquantel might be an effective treatment of canine schistosomiasis, although the required length of treatment might vary. The authors recommend treating with the previously mentioned fenbendazole protocol and rechecking a fecal saline sedimentation and fecal PCR 2 wk posttreatment. If either fecal PCR or fecal saline sedimentation are positive, repeating a second 7–10 day course of fenbendazole and retesting 2 wk later is recommended.

All dogs with an antemortem diagnosis of schistosomiasis in which specific treatment was pursued achieved complete resolution of clinical signs. This included one dog with a cecocolic and ileocolic intussusception that was surgically corrected. It should be noted that neither dog with hypercalcemia was treated for schistosomiasis, and that clinical outcome would be dependent on the severity and duration of hypercalcemia and subsequent mineralization.

Conclusion

Naturally occurring canine schistosomiasis occurs in Kansas and likely other Midwestern states. Schistosomiasis should be considered in any dog with GI signs (diarrhea, vomiting, anorexia, weight loss), hypercalcemia of unknown cause, or intestinal intussusception. Fecal flotation does not detect Heterobilharzia eggs; therefore, a fecal saline sedimentation and/or fecal PCR should be performed. Fenbendazole with or without praziquantel was an effective treatment in this study. Although no conclusions can be drawn regarding the prognosis of dogs with hypercalcemia, all treated dogs achieved complete resolution of clinical signs.