The patient was a three-year-and-nine-month-old male neutered blue heeler living in Point Cook, Victoria, near the Cheetham Wetlands. The dog arrived at the university’s veterinary hospital after two weeks of unexplained weight gain and noticeable abdominal distension that began following a change in diet. The animal had gained 3.8 kilograms in that short period, reaching 26.8 kilograms, and was passing soft, brown to orange diarrhoea. Otherwise, its energy, appetite, drinking and urination were normal. The dog had never travelled outside its local Melbourne suburbs, had no access to offal, and was current on vaccinations, though regular deworming had lapsed, and the parasite preventatives it had received contained no anticestodal drugs. Notably, frogs were occasionally seen in its yard, and the dog sometimes drank from puddles, a detail that would later prove intriguing.

Initial bloodwork offered only subtle clues. The dog showed mild eosinophilia, an elevation of white blood cells often associated with parasitic disease, alongside mild hypocholesterolaemia, hypoproteinaemia and a mildly raised amylase. Faecal flotation and a Giardia test were both negative, meaning the parasite was not shedding eggs into the intestine. The critical breakthrough came with abdominal ultrasound, which revealed innumerable small, anechoic, oval cysts scattered throughout the peritoneal cavity, ranging from 2 to 18 millimetres in diameter. These fluid-filled structures had thin, smooth, hyperechoic walls, showed no blood flow on Doppler examination, and floated suspended in a large volume of echogenic peritoneal effusion. The surrounding mesentery appeared irregular, with strands connecting the cysts to intestinal loops, and nearby lymph nodes were mildly enlarged. Ultrasound-guided sampling of the fluid yielded serosanguinous material consistent with prior haemorrhage but, crucially, no identifiable parasites.

With parasitic cysts, disseminated neoplasia and chronic peritonitis all on the differential list, the veterinary team proceeded to computed tomography a week later, by which time the dog had become mildly lethargic. The CT confirmed severe abdominal effusion and identified nodular lesions near the gallbladder and along the ventral liver margin, changes compatible with parasitic peritonitis and granulomatous cystic lesions, along with widespread reactive lymph node enlargement. However, the cross-sectional imaging proved less sensitive than ultrasound: only the largest cysts were visible on CT, whereas sonography had demonstrated them in countless numbers. This contrast is one of the report’s most practically valuable findings, suggesting that point-of-care ultrasound, widely available in general practice, may be the superior tool for recognising this rare condition early.

Exploratory laparotomy then transformed suspicion into spectacle. Surgeons suctioned approximately 3.5 litres of serosanguinous, turbid fluid from the abdomen and encountered hundreds of free-floating cystic structures, round and pale white to yellow, measuring 1 to 12 millimetres, each containing fluid and floccular material. The peritoneal surfaces of the diaphragm, mesentery and omentum were studded with petechiae, diffuse redness and dozens of soft white plaques, later understood to be plerocercoid larvae adhering to the serosa. The spleen and liver surfaces were coated in fibrinous membrane, and the parietal peritoneum was thickened. After the abdomen was lavaged with twelve litres of sterile saline, the dog left the operating table 3.7 kilograms lighter. Cytology of the collected peritoneal fluid revealed acoelomic cestode tissue studded with calcareous corpuscles, characteristic mineralised structures found in tapeworm larvae, confirming peritoneal cestodiasis.

Histopathology of omental biopsies showed severe chronic, diffuse, eosinophilic granulomatous peritonitis with intralesional larval cestodes embedded in the tissue. Microscopically, the parasites displayed the hallmark features of pseudophyllidean larvae: a solid, segmented body covered by an eosinophilic tegument, an internal parenchyma containing calcareous corpuscles and excretory canals, and no body cavity. Uniquely, the tegument frequently formed tubular invaginations extending deep into the parenchyma, a feature previously documented in Australian cases whose function remains unknown. The authors suggest that if this morphological signature proves specific to Spirometra, routine histological assessment could enable earlier detection of the disease in tissue sections.

Definitive species identification required molecular tools. Eight cystic structures recovered at surgery were characterised by amplifying and sequencing a 418-base-pair region of the mitochondrial cytochrome c oxidase subunit I gene, the standard DNA barcode for cestode identification. All eight sequences were identical on gel electrophoresis, and BLAST analysis revealed identity to Spirometra mansoni, matching a reference specimen previously recovered from a lowland copperhead snake in Victoria. The sequence has been deposited in GenBank. This molecular confirmation carries taxonomic weight, because Australian Spirometra was historically reported as S. erinacei or S. erinaceieuropaei before recent molecular studies established that the species present in Australia is in fact S. mansoni. The findings also reinforce expert recommendations that morphology alone is unreliable for identifying Spirometra larvae and that genetic testing should be considered the gold standard.

Despite surgery and post-operative treatment that included fenbendazole, praziquantel, nitazoxanide, meloxicam and antibiotics, the disease progressed. Three weeks after the operation the dog returned with lethargy, vomiting, urinary incontinence and further weight loss. Ultrasound now revealed extensive hyperechoic mesenteric strands, intestinal plication, a markedly thickened bladder wall and ongoing peritoneal effusion, consistent with severe adhesions physically obstructing the gastrointestinal tract, accompanied by secondary pancreatitis, cholestasis and cystitis. Faced with a poor prognosis, the owners elected euthanasia. Postmortem examination disclosed a striking pathology: firm, stringy fibrinous adhesions binding the body wall, intestines, omentum, liver and diaphragm into a single coagulum, with dark red plications covering more than seventy percent of the small intestinal serosa. Dozens of cystic spaces within the adhesions contained fluid and cestode fragments, and histology confirmed encapsulated degenerating larvae surrounded by granulomatous inflammation and extensive fibrosis.

The case adds to a globally tiny literature, with previous canine reports from Australia, the United States and Germany, nearly all ending in euthanasia. It also challenges the historical belief that Spirometra larvae cannot replicate asexually, a capability once attributed solely to the genetically distinct Sparganum proliferum, with recent reports in dogs and a cat in Japan demonstrating that Spirometra plerocercoids can indeed proliferate aberrantly. The zoonotic stakes are significant: over 1,600 human sparganosis cases have been reported worldwide, most non-proliferative subcutaneous nodules, but human proliferative sparganosis is rare and associated with high mortality. Because the definitive adult worm lives in wild canids and foxes, with prevalence documented at 36 percent in wild dogs of New South Wales and Queensland, environmental reservoirs sustain the parasite’s multi-host life cycle through copepods, frogs, tadpoles and snakes. The likely infection route for this urban dog remains speculative, possibly frogs or puddle water near the wetlands, though the genetic profile matched the non-amphibian genotype found in dogs, foxes, cats and tiger snakes. Direct animal-to-animal transmission cannot occur, and the authors urge owners to prevent pets from scavenging wildlife and to maintain regular anthelmintic care. Ultimately, the report’s clearest message is a diagnostic one: in a dog with unexplained abdominal distension and countless floating peritoneal cysts on ultrasound, proliferative sparganosis deserves a place on the differential list.

Subject of Research: Proliferative sparganosis caused by Spirometra mansoni in a dog

Article Title: Proliferative Sparganosis Due to Spirometra mansoni in a Dog: A Detailed Diagnostic Picture

Article References: Middlemast, S., Lim, N., Gauci, C. G., & Jabbar, A. (2026). Proliferative Sparganosis Due to Spirometra mansoni in a Dog: A Detailed Diagnostic Picture. Veterinary Medicine and Science, 12(5), Article e71206. https://doi.org/10.1002/vms3.71206

Image Credits: AI Generated

DOI: 10.1002/vms3.71206

Keywords: proliferative sparganosis, Spirometra mansoni, plerocercoid larvae, canine parasitology, peritoneal cestodiasis, abdominal ultrasound, computed tomography, COX1 sequencing, zoonotic disease, granulomatous peritonitis, tapeworm larvae, Veterinary Medicine and Science