Acute gastrointestinal disease in a young bobcat (Lynx rufus)

Scott D. Mitchell Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK

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Akhilesh Ramachandran Oklahoma Animal Disease Diagnostic Laboratory, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK

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Sushim K. Gupta Oklahoma Animal Disease Diagnostic Laboratory, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK

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Dwight Olson Olson Animal Hospital, Enid, OK

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Alexandra K. Ford Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK

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History

A 6-month-old 5.3-kg castrated male, reportedly indoor-only, pet bobcat (Lynx rufus) presented to a veterinary clinic in Enid, Oklahoma for acute onset of vomiting, diarrhea, and lethargy. The owner had 2 pet raccoons (Procyon lotor) in the same household that recently showed similar clinical signs. One raccoon died despite treatment, and an in-house necropsy performed by the veterinarian revealed segmental reddening of the small intestinal serosa.

Clinical and Gross Findings

Upon presentation to the clinic, the bobcat was febrile, elicited pain on abdominal palpation, and had soft brown stool. Subcutaneous fluids (lactated Ringers, 60 mL/kg, SC), maropitant citrate (Cerenia, 0.5 mg/kg, IM), meloxicam (0.05 mg/kg) and enrofloxacin (Baytril, 2.0 mg/kg, IM) were administered and the patient was hospitalized for overnight observation. Twelve hours later the animal was alert, responsive, and ate small amounts of food. Subcutaneous fluids (60 mL/kg, SC) maropitant citrate (1 mg/kg, IM) and enrofloxacin (3.3 mg/kg, IM) treatments were repeated. Approximately 24 hours later the animal went into cardiac and respiratory arrest. Resuscitation efforts were unsuccessful.

At necropsy, the animal was covered in numerous, live ectoparasites (presumptively diagnosed as Ctenocephalides felis based on host species). The hair of the perineum and tail were covered in liquidous to dried green feces and oral mucous membranes had a diffuse generalized pallor. Approximately 75% of the small intestinal serosa was segmentally red to dark red, and the mucosa was diffusely covered by a layer of tan fibrinous exudate consistent with a diphtheritic membrane (Figure 1). No other significant gross abnormalities were appreciated.

Figure 1
Figure 1

Necropsy photograph of the abdominal cavity of a 6-month-old male bobcat with history of acute- onset vomiting and diarrhea. Segments of small intestine are red to dark red (arrowheads).

Citation: Journal of the American Veterinary Medical Association 262, 1; 10.2460/javma.23.07.0380

Histopathologic and Microbiological Findings

A full set of tissues were collected for histopathologic evaluation. Tissues were fixed in 10% neutral buffered formalin and routinely processed. Microscopically, the small intestine showed diffuse, severe villous blunting and fusion with prominent loss of mucosal architecture (Figure 2). The denuded mucosal surface was frequently replaced by a thick layer of fibrin, necrotic cellular debris, and myriad cocci and coccobacilli. The lamina propria was extensively replaced by fibrin, necrotic cellular debris, small amounts of hemorrhage, and small numbers of neutrophils and mononuclear cells. Approximately 90% of crypts were lost and remaining crypt epithelial cells were frequently swollen with vacuolated cytoplasm (degeneration); shrunken with hypereosinophilic cytoplasm and pyknotic to karyorrhectic nuclei (necrosis); or swollen with vesiculate nuclei, prominent nucleoli, and occasional mitotic figures (regeneration). Lymphoid follicles were not observed. Femoral bone marrow was markedly hypocellular with minimal to absent numbers of erythroid and myeloid precursors (Figure 3).

Figure 2
Figure 2

Photomicrograph of affected segments of small intestine. There is near complete loss of crypts, severe villous blunting and fusion, and myriad bacteria adhered to the denuded mucosal surface. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 262, 1; 10.2460/javma.23.07.0380

Figure 3
Figure 3

Representative photomicrograph of hypocellular bone marrow collected from the femur. There are virtually no erythroid or myeloid precursor cells and abundant, histologically unremarkable adipocytes and erythrocytes. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 262, 1; 10.2460/javma.23.07.0380

Parvovirus real-time PCR assay on a segment of fresh small intestine indicated virus presence in high concentrations (cycle threshold = 7.61). Partial gene sequencing of viral protein 2 showed 100% sequence identity with canine parvovirus type 2a (CPV-2a).

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe, diffuse, fibrinonecrotizing enteritis with villous blunting and fusion and crypt epithelial degeneration, necrosis, and regeneration; severe, diffuse, bone marrow hypocellularity.

Case summary: severe necrotizing enteritis and bone marrow hypocellularity due to parvovirus infection in a bobcat.

Comments

Gross and histopathologic findings were consistent with parvoviral enteritis and secondary bacterial enteritis. A SNAP Canine Parvovirus Test (IDEXX Laboratories) conducted by the referring veterinarian yielded a strong positive result. Additional provided clinical history indicated the 2 raccoons lived in the same household and had similar gastrointestinal signs. These findings were of interest due to the susceptibility of raccoons and felids to canine parvovirus-2 (CPV-2) and feline panleukopenia virus (FPLV) infections. The small intestine submitted for parvovirus PCR was positive with a cycle threshold value of 7.61 indicating very high levels of viral nucleic acids. Because the parvovirus PCR is cross-reactive between feline panleukopenia virus and canine parvovirus, sequencing was pursued to differentiate between the 2 viruses.

Parvoviruses are highly contagious, single stranded DNA viruses that can infect a variety of domestic and nondomestic carnivores. Parvoviral infections in wild felids have been sparsely studied; however, clinical signs are similar to those reported in susceptible domestic animals.1,2 Clinical signs and lesions depend on timing of infection and are chiefly related to the virus’ tropism for rapidly dividing cells, including small intestinal crypt epithelial cells and lymphoid tissues. In utero infection in felids can result in reduced litter sizes and an ataxic syndrome in neonates due to cerebellar hypoplasia.2 Infection in kittens and older felids can result in anorexia, lethargy, pyrexia, epistaxis, vomiting, and variably bloody diarrhea.2,3 Classical gross lesions in susceptible species include segmental reddening and roughening of the small intestine serosa, fibrinous serositis, and watery to mucoid to bloody intestinal contents. Microscopically there is villous atrophy and collapse with necrosis and regeneration of crypt epithelium. Remaining crypt epithelial cells may contain characteristic basophilic to amphophilic intranuclear inclusion bodies early in the disease course. The presence of viral inclusions is highly variable and the lack of these inclusion, as in this case, does not preclude a diagnosis of parvoviral infection.3 Infection of lymphoid tissues results in necrosis and loss of lymphocytes and progenitor cells resulting in lymphopenia or panleukopenia. Histopathology can confirm lymphoid depletion and bone marrow hypocellularity as observed in this case. Definitive clinical and postmortem diagnoses are achieved with molecular diagnostic methods.

Parvoviruses infecting veterinary species have been phylogenetically traced to the original FPLV first described in 1926 including CPV-2, raccoon parvovirus, blue fox parvovirus, and mink enteritis virus.1,2 Canine parvovirus type 2 was initially confined to a canine host range with loss of in vivo replicative ability in fields. The virus has since undergone further antigenic evolutions giving rise to antigenic variants CPV-2a, CPV-2b, and CPV-2c. These antigenic variants have allowed the reintroduction of CPV-2 into the feline host range, and it is suspected that approximately 5% of parvoviral infections of domestic and nondomestic felids are due to CPV-2.1,2

Epidemiologic outbreaks of FPLV in captive and wild felids have been reported, including a recent outbreak in captive-bred juvenile cheetahs and other felids in South Africa.3 Extra-label vaccination of captive nondomestic felids has been recommended, though there are concerns about the use of attenuated modified live vaccines in nondomestic felids due to the potential for vaccine-related parvoviral disease.2 For this reason, vaccination with inactivated or killed vaccines is currently the recommended practice. Some studies investigating the antibody response to the feline panleukopenia vaccine in tigers and lions found variable to insufficient increases in antibody titers.1,4 Furthermore, there are several reports that commercial vaccines for FPLV induce significantly lower antibody titers against CPVs, indicating they may not be cross-protective for CPVs long-term.4,5 In this case, the bobcat was reportedly vaccinated against FPLV a few months prior to death (PUREVAX; Boehringer Ingelheim; modified live vaccine). For these reasons, serologic assessment to determine efficacy of parvoviral vaccines in nondomestic felids may be warranted.

This case provides an excellent clinicopathological example of parvoviral enteritis, an entity that should be considered in domestic and nondomestic carnivores alike. Clinicians involved in care and treatment of animals susceptible to both CPV-2 and FPLV may need to consider a vaccine protocol that provides long-term protection against both viruses.

Acknowledgments

The authors thank the technicians, staff, and management of the histology and molecular diagnostic laboratories at the Oklahoma Animal Disease Diagnostic Laboratory.

Disclosures

The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors have nothing to disclose.

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