Heterobilharzia americana infection in dogs | VETgirl Veterinary Continuing Education Podcasts
In this VETgirl online veterinary continuing education podcast, we review Heterobilharzia americana (HA) infections in dogs. As a small animal veterinarian with a fascination for all infectious diseases, I am particularly excited to learn more about this organism. Let’s start with the basics. First, HA is a trematode parasite that can infect our canine patients, causing a condition known as schistosomiasis and potentially severe granulomatous disease. Let’s quickly review the lifecycle. We know that specific snails are the intermediate host, and that dogs swimming in freshwater lakes or streams are often exposed to the free cercariae that have been released by an infected snail. The organisms infect the dog by dermal penetration, and can then migrate via the bloodstream to cause damage elsewhere and eventually to mate. Specifically, the organisms move to the liver and to the lungs, where they sexually mature into adult parasites. These adults can move via the portal system, and they mate and release fertilized eggs in the mesenteric veins. Enzymes facilitate transport of the eggs into the intestines, and they are ultimately excreted in the feces. To round out this process, a new stage of the organism, the flagellated miracidia, is released from the eggs to infect snails if the feces comes in contact with fresh water. And so the cycle continues!
You may be wondering what this infection looks like in dogs. When should this be on a clinician’s radar, how do we test for it, and what does the diagnosis mean for patient care? Rather than diving into the full clinical details of this disease now, instead we will discuss a fascinating study by Graham et al entitled Heterobilharzia americana infection in dogs: A retrospective study of 60 cases (2010-2019) that sought to provide an updated description of the clinical findings, treatment responses, and outcome of dogs diagnosed with HA.
This was a descriptive, retrospective study that involved a detailed medical record review from 2 veterinary hospitals: Texas A&M University Veterinary Medical Teaching Hospital and Gulf Coast Veterinary Specialists. Importantly, this trematode is endemic to the gulf region primarily, though cases have been reported sporadically in other states as well (Lee; Rodriguez). Medical records from March 2010 to December 2019 were searched using the keywords Heterobilharzia and schistosomiasis. To be included, the infection must have been confirmed using either a fecal PCR test, observation of the parasitic ova in fecal samples, or visualization of the organism or its ova on histopathology. Thorough details about the patient, diagnostics, treatment, and outcome were extracted from the medical records by a board-certified internist. Outcome was classified as either dead or alive 6 months following the diagnosis. Some dogs were classified as having an incidental infection. To fit this classification, the dog must have lacked gastrointestinal signs, increased liver enzyme values, or hypercalcemia. Furthermore, if an HA test was only performed due to imaging findings, the authors classified the dog as having an incidental infection.
Okay, let’s hear about some results! How did these dogs present? How were they diagnosed? And what can we expect with this disease? Well, these investigators looked at records from just under a ten-year timespan, and in that period, they found 60 dogs that were diagnosed with HA. More than 80% of this population was diagnosed via a fecal PCR test alone. A smaller subset were diagnosed via GI or liver biopsy, fecal sediments, or fecal direct smears. Of note, 1 dog that had a negative fecal sedimentation test was positive on fecal PCR. Fifty-eight of the 60 dogs (96%) were diagnosed antemortem using one of the tests previously mentioned, and 2 were diagnosed on necropsy. Sadly, these 2 dogs were euthanized without treatment for worsening neurologic signs and for marked hypercalcemia. Of these 60 dogs, 35 were female, and 25 were male. The ages were quite variable, ranging from 7 months to over 17 years! However, the average was 7.5 years, and the average weight was 23.2 kg. The two most commonly represented breeds were Labrador retrievers (n = 11) and German shepherd dogs (n = 6).
Of the 60 dogs, 8 were classified as having incidental infections and lacked any clinical signs of disease. That means that more than 85% of patients were clinically affected by HA. Of these, over 75% had a history of either vomiting or diarrhea. In other words, GI signs are a common manifestation of HA. Another 15% of dogs presented for weight loss, but did not have vomiting or diarrhea. Interestingly, 17% of dogs had polyuria and polydipsia listed as a clinical sign. Testing for HA was usually performed during a chronic enteropathy (53%) or hepatopathy (11.7%) work-up. However, in 15% of dogs, the patient was having an abdominal ultrasound performed for another reason, and sonographic results prompted HA testing. Of note, both hospitals in this study use board-certified radiologists for ultrasonography. You may be wondering what types of ultrasound findings would prompt HA testing. In general, the primary sites of sonographic changes are the GI tract and the liver. Fifty-nine of the 60 dogs in this population had an ultrasound performed, and 83% of those dogs had abnormal findings reported in one or both of these areas. Additionally, 28% of dogs had abdominal effusion noted. Of the GI tract changes, the authors report that two-thirds of dogs had changes in the small intestine, especially the submucosal layer. They also note that pinpoint hyperechoic foci was a common finding. In 64% of dogs, these changes were observed in either the small intestine, liver, mesenteric lymph nodes, or some combination of those sites.
In addition to imaging, 56 dogs had a CBC, serum biochemical, and/or a urinalysis performed, though not all dogs had all tests performed. Of note from the CBC findings, 17.6% of dogs were classified as anemic (hematocrit <30%), but the average hematocrit was 39%. The median neutrophil and eosinophil counts were reported as 6,295/uL and 340/uL, respectively. Eosinophil counts greater than 500/uL were noted in 42% of dogs. Of dogs with total serum calcium levels reported, 11.6% were hypercalcemic, and 16.7% were hypocalcemic. However, one of the hypercalcemic dogs was later diagnosed with primary hyperparathyroidism. Serum creatinine was elevated in 9% of dogs, and median urine specific gravity was 1.018. A quarter of dogs were hypoalbuminemic (albumin <2.4 g/dL), and over 40% of dogs were hyperglobulinemic (globulin >3.7 g/dL). Regarding liver enzymes, interestingly, values were normal in 70% of dogs, and all dogs had serum bilirubin less than 1 mg/dL. Mild increases in alkaline phosphatase and alanine aminotransferase were noted in the dogs with abnormalities.
Let’s move on to treatment! Recall that 2 dogs never received treatment, as they were euthanized and diagnosed with HA post-mortem via necropsy. That leaves 58 dogs that were treated. Of these, 98% were initially treated with praziquantel, and 64% were concurrently treated with fenbendazole. Additionally, 22% of these dogs were given prednisone at the same time, at a median daily dosage of 1 mg/kg. The most common treatment protocol from all dogs was praziquantel (25 mg/kg, q8 hours, for 2-3 days) combined with fenbendazole (50 mg/kg, q24 hours, for 10 days). In 8 of the 33 dogs that received this protocol, the treatment was repeated 3-4 weeks after completion. The authors clarify that, unfortunately, given variations in treatment regimens and follow-up, they cannot provide statistical comparisons between treatment protocols.
When looking at how these treatments performed, the authors found that 65% of all treated dogs had either confirmed or presumed treatment failure. Yikes! A possible explanation for this poor response that is proposed by the authors is poor medication bioavailability given GI tract pathology. Twenty-three dogs had repeated fecal PCR testing 1-2 months after initial therapy. Nearly half of dogs tested negative (47.8%), meaning more than half tested positive. Of those that tested negative, one dog was positive when retested again a month later. The authors note that this dog may have initially tested negative due to intermittent shedding of the ova, or even just reduced shedding in response to treatment. Therefore, the authors suggest follow-up testing at both 1 and 2 months after treatment. Two additional dogs were re-treated because of clinical signs. Note that only 23 dogs had these follow-up PCR results available, and 2 dogs without repeat testing were retreated due to clinical signs. The authors were able to determine survival status in approximately 60% of dogs 6 months following treatment. Overall, 73.5% of dogs were alive after initial diagnosis, and six dogs were euthanized or had died for reasons related to HA. Sadly, two dogs had died acutely during treatment. The authors report that another dog appeared to have an anaphylactoid reaction during treatment, but fortunately this pup responded to fluids and steroids.
So what can we take away from this VETgirl podcast? Well, first of all, it is important to note that the authors acknowledge several limitations to this study, which are largely due to the retrospective study design and questions regarding the validity of the fecal PCR test. That said, hopefully this study gave you some tools to recognize potential HA cases, as prompt diagnosis and treatment are essential. Based on the findings in this study, the authors recommend that clinicians consider HA in dogs with chronic enteropathies or hepatopathies if the dog has lived or travelled in an endemic area. In particular, dogs with eosinophilia, hyperglobulinemia, or sonographic changes consistent with HA should be considered for testing. As mentioned, this study was not designed to draw definitive conclusions on the efficacy or superiority of various therapeutic protocols. However, given the available information, the authors recommend a combination of praziquantel (25 mg/kg, every 8 hours, for 3 days) and fenbendazole (50 mg/kg, every 24 hours, for 10 days). Furthermore, they recommend repeat fecal PCR testing at 4 and 8 weeks after treatment, with concurrent fecal PCR testing for other at risk dogs, such as dogs with shared environments to those testing positive. Since this study recruited dogs from referral hospitals, there is a possibility that the patient population was biased towards more severely affected animals. However, the overall 6-month survival rate in this population was approximately 75%, which at least gives a rough sense of the expectations when managing this challenging disease.
1. Graham A, Davenport A, Moshnikova V, et al. Heterobilharzia americana infection in dogs: A retrospective study of 60 cases (2010-2019). J Vet Intern Med. 2021; 35:1361-1367.
2. Lee HF. Life history of Heterobilharzia americana Price 1929, a schis-tosome of the raccoon and other mammals in southeastern United States. J Parasitol. 1962;48:728-739.
3. Rodriguez JY, Lewis BC, Snowden KF. Distribution and characteriza-tion of Heterobilharzia americana in dogs in Texas. Vet Parasitol. 2014;203(1–2):35-42.
HA – Heterobilharzia americana
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