Pathology in Practice

Dayna A. Goldsmith Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T3R IJ3, Canada.

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Garrett S. Oetelaar CARE Centre, 7140 12th St SE, Calgary, AB T2H 2Y4, Canada.

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Serge Chalhoub Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T3R IJ3, Canada.

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Claudia Klein Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T3R IJ3, Canada.

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Sarah A. Bramer Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T3R IJ3, Canada.

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Erin P. Locke Antech Diagnostics, 5777 Danbro Cres, Mississauga, ON L5N 6P9, Canada.

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Alessandro Massolo Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T3R IJ3, Canada.

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History

In the fall of 2016, a 19-month-old 25-kg (55-lb) spayed female crossbred German Shepherd Dog was evaluated because of sudden onset of lethargy and inappetence. In March of the same year, the dog had undergone endoscopic biopsy, and examination of the specimen resulted in a diagnosis of eosinophilic inflammatory bowel disease (IBD). At the time of the evaluation, IBD was being managed medically. This dog had regular access to the outdoors and was known to consume coyote feces. Regular deworming was performed including administration of a 14-day course of fenbendazole (50 mg/kg [22.7 mg/lb], PO, q 24 h) in February 2016, application of selamectin in April and July, and administration of a pyrantel pamoate-oxantel-praziquantel combination in May and October.

Clinical and Gross Findings

At the evaluation, abdominal ultrasonography revealed a small amount of anechoic peritoneal effusion and marked hepatomegaly with 5 or 6 moderately well-defined nodules that had an enhanced reticulated pattern. The largest nodule measured 3.5 × 3.9 cm, and all nodules were associated with appreciable distal acoustic enhancement, suggesting a substantial fluid component to their composition. An exploratory laparotomy was performed and liver biopsy specimens were collected. On the basis of subsequent findings and complications of concurrent medical management of the dog's IBD, euthanasia by means of IV injection of pentobarbital was elected.

At necropsy, the liver was markedly enlarged and weighed 2.36 kg (5.19 lb; 9.45% of total body weight); it was connected by multiple fibrous adhesions to the overlying omentum. The abdomen contained approximately 40 mL of serosanguineous fluid. Randomly distributed throughout all lobes of the liver were numerous well-demarcated, unencapsulated, pale yellow, soft masses that ranged from 2.0 to 10.0 cm in diameter and affected approximately 50% of the parenchyma. On cut section, these masses were friable, pale yellow, and porous and exuded small amounts of opaque, pale tan fluid containing flocculent white debris (Figure 1).

Figure 1—
Figure 1—

Photographs of the liver from a 19-month-old 25-kg (55-lb) crossbred German Shepherd Dog that was evaluated because of sudden onset of lethargy and inappetence. A diagnosis of inflammatory bowel disease had been previously made for this dog. At necropsy, the liver was markedly enlarged, weighing 2.36 kg (5.19 lb; 9.45% of body weight). A—Approximately 50% of the parenchyma has been replaced by multifocal to coalescing, poorly demarcated, soft, pale yellow masses (asterisks) that range from 2.0 to 10.0 cm in diameter. B—On cut section, the masses are friable and porous and exude small amounts of opaque, pale tan fluid containing flocculent white debris. Similar fluid was aspirated from the masses.

Citation: Journal of the American Veterinary Medical Association 253, 5; 10.2460/javma.253.5.563

Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page

Additional Necropsy Findings

An examined hepatic lymph node was markedly enlarged, approximately 3 times its expected size; on cut section, the nodal architecture was focally effaced by an approximately 0.5-cm-diameter, pale yellow expansile mass resembling those within the liver. A focal area of fibrous adhesion was present between the liver, diaphragm, and right middle lung lobe. The affected lung lobe was dark red and slightly firm on palpation. Multiple well-demarcated dark red areas were observed within the renal medullae bilaterally. Additional gross findings included 5 raised, ovoid white plaques on the ventral surface of the tongue and 8 small (< 0.4-cm-diameter) white foci rimmed in red along the endocardial surface of the left atrium.

Histopathologic and Microbiological Findings

Histologic examination of the liver biopsy specimens revealed multilocular cysts that caused compression and effacement of the adjacent hepatic parenchyma. The cysts were markedly variable in size and separated by bands of compressed fibrovascular tissue containing residual hepatocytes, proliferative bile ducts, and moderate-to-large numbers of lymphocytes and plasma cells with fewer reactive histiocytes. These cysts were lined by a pink hyaline capsule that was approximately 30-μm wide (laminated layer) and had an inner basophilic layer (germinal epithelium). Many of the observed cysts were collapsed and infiltrated by inflammatory cells. Rare cross-sections of cestode protoscolices, approximately 100 mm in diameter and characterized by an internal parenchyma containing calcareous corpuscles and suckers, were visible within cysts. Protoscolices were frequently degenerate and associated with small numbers of neutrophils and cellular debris that obscured their morphological features.

Similar cysts were observed within both the liver and a hepatic lymph node at necropsy; however, most cysts were ruptured, collapsed, and necrotic and only rarely contained germinal epithelium and calcareous corpuscles. No intact protoscolices were identified within the evaluated tissues. Cysts were highlighted with periodic acid–Schiff stain, which reacted with the hyaline capsule and caused it to appear bright pink (Figure 2). Within the surrounding parenchyma, aggregates of hepatocytes were characterized by lacy cytoplasmic vacuolation (glycogen, consistent with steroid hepatopathy). The absence of a coelom within the observed protoscolices and the presence of calcareous corpuscles identified this parasite as a cestode. Results of a PCR assay performed on liver tissue confirmed the diagnosis of alveolar echinococcosis caused by Echinococcus multilocularis. The invasive pattern of growth in this dog was consistent with E multilocularis infection, and less consistent with Echinococcus granulosus infection, the other cause of hydatid disease in dogs.

Figure 2—
Figure 2—

Photomicrograph of a section of a hepatic lymph node from the dog in Figure 1. Nodules within the hepatic lymph node (and the liver [not shown]) are composed of cystic spaces containing collapsed periodic acid–Schiff reaction-positive laminated membranes that are ≤ 30-μm wide and are associated with a moderate-to-marked lymphocytic and histiocytic infiltrate. Periodic acid–Schiff reaction; bar = 500 μm. Inset—Multiple pale blue round calcareous corpuscles are a defining feature of cestode parasites. H&E stain; bar = 200 μm.

Citation: Journal of the American Veterinary Medical Association 253, 5; 10.2460/javma.253.5.563

Histologic examination of sections of the right middle lung lobe and diaphragm confirmed local extension of inflammation from the abdomen. Histologic examination of sections of the kidneys confirmed multiple areas of acute coagulative necrosis within the renal medulla, possibly secondary to dehydration. The endocardial and tongue lesions were identified as areas of collagen mineralization with minimal associated inflammation and epithelial ulceration. Rare areas of mineralization were also observed within the lungs and skeletal muscle of the diaphragm. A definitive cause for the observed mineralization was not determined in this case in part because of the absence of perimortem clinicopathologic data. However, the sublingual and endothelial distribution was suggestive of mineralization secondary to uremia. Examination of the gastrointestinal tract did not reveal evidence of the previously diagnosed IBD. This could have been indicative of a response to treatment or failure to collect a sample of the lesion if the previously observed inflammation was multifocal.

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: moderate, chronic, multifocal to coalescing multilocular degenerating hydatid cysts with fibrosis and chronic lymphoplasmacytic and histiocytic hepatitis.

Case summary: hepatic alveolar echinococcosis, caused by E multilocularis infection, in a dog.

Comments

Alveolar echinococcosis (AE) involves the formation of large destructive and progressive masses within internal organs as a result of infection with metacestode larvae of the cestode E multilocularis.1 Generally, AE develops in intermediate hosts, primarily rodents; however, infection of accidental hosts including humans and domestic species does occur. The definitive hosts are wild and domestic canids, which carry adult worms in their gastrointestinal tract and are generally immune to infection by the embryonated eggs shed in their feces. On occasion, however, domestic canids have developed AE; in those cases, the metacestode cysts' progressive, destructive, and irreversible pattern of growth can be fatal or require lifelong, expensive, daily treatments with albendazole.2 Recent studies1,3–5 suggest an increasing prevalence of E multilocularis within Europe and North America. Although canine AE is uncommon even in areas that are hyperendemic for E multilocularis, the severity of infection and associated zoonotic potential compels veterinarians to be familiar with E multilocularis infection and its range of clinical signs in dogs.

Alveolar echinococcosis develops after embryonated eggs are ingested by a susceptible host. Within the gastrointestinal tract, eggs mature into oncosphere larvae that penetrate the intestinal mucosa and are transported by the blood or lymphatics to their target organ, typically the liver or, less commonly, the lungs or brain. These oncospheres develop into metacestodes that secrete an inner germinal epithelium and outer acellular laminated membrane, which form the mature hydatid cyst. The germinal epithelium will then bud multiple times into the center of the cyst forming individual protoscolices, each with the capacity to develop into an adult cestode. Maturing cysts progressively invade the hepatic parenchyma through protrusion of the germinal layer.1

In addition to being the definitive host, dogs, like humans, have the capacity to act as dead-end intermediate hosts for E multilocularis. In the case described in the present report, the dog was likely at increased risk of exposure because of its frequent consumption of coyote feces. It is speculated that AE may also develop through self-grooming when dogs have patent intestinal infections. Early diagnosis of AE is essential for successful treatment. Owing to the rarity of this condition and its variable clinical signs, there is the potential for misdiagnosis if histologic examination of suspect masses is not performed. A common differential diagnosis for AE, especially for older dogs, is metastatic neoplasia. The lesions resulting from E multilocularis infection are proliferative, with both expansile and infiltrative growth, and can disseminate along the vasculature to distant organs, a process variably referred to as metastasis. Unlike its counterpart E granulosus that forms distinctly encapsulated cystic masses, the cystic appearance of E multilocularis is only distinct at the microscopic level; macroscopically, E multilocularis–associated lesions can appear quite solid and lack a grossly discernible capsule. In addition, hepatocellular loss and frequent degeneration and collapse of the cysts results in nodules with an umbilicated center, which resemble the lesions of an aggressive carcinoma. As well as metastatic neoplasia, differential diagnoses for AE in dogs include granulomatous liver disease, such as systemic fungal infections, and nonneoplastic proliferative diseases, such as canine hepatic nodular hyperplasia.

Some of the clinical features that are helpful in determining a diagnosis of AE in dogs include a clinical history of exposure to or consumption of canid feces (may contain embryonated eggs), consumption of intermediate hosts (can lead to intestinal infection and the risk of autoinfection through self-grooming), the absence of appropriate deworming (prevention of intestinal E multilocularis infection requires monthly treatment with a cestocide, such as praziquantel), and age (in a young dog, neoplasia as a primary differential diagnosis for AE is less likely). In addition, the distinctive spongy, cystic appearance of the masses, visible both through diagnostic imaging and at necropsy, can help to raise the suspicion for this condition. Examination of aspirate specimens from the masses will often reveal opaque pale tan fluid with suspended flocculent debris. This fluid bears some resemblance to the hydatid sand of E granulosus, and rarely contains protoscolices that can be visualized microscopically. Definitive diagnosis requires histologic examination or PCR assay testing of affected tissue samples.

References

  • 1. Romig T, Deplazes P, Jenkins D, et al. Ecology and life cycle patterns of Echinococcus species. In: Thompson RCA, Deplazes P, Lymbery AJ, eds. Advances in parasitology. London: Academic Press, 2017;1525.

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  • 2. Corsini M, Geissbuhler U, Howard J, et al. Clinical presentation, diagnosis, therapy and outcome of alveolar echinococcosis in dogs. Vet Rec 2015;177:569575.

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  • 3. Weiss AT, Bauer C, Kohler K. Canine alveolar echinococcosis: morphology and inflammatory response. J Comp Pathol 2010;143:233238.

  • 4. Peregrine AS, Jenkins EJ, Barnes B, et al. Alveolar hydatid disease (Echinococcus multilocularis) in the liver of a Canadian dog in British Columbia, a newly endemic region. Can Vet J 2012;53:870874.

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  • 5. Skelding A, Brooks A, Stalker M, et al. Hepatic alveolar hydatid disease (Echinococcus multilocularis) in a boxer dog from southern Ontario. Can Vet J 2014;55:551553.

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