Pathology in Practice

Amber R. Olson Michigan State University Veterinary Diagnostic Laboratory, Lansing, MI 48910.

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Annie M. Zimmerman Michigan State University Veterinary Diagnostic Laboratory, Lansing, MI 48910.

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Dodd G. Sledge Michigan State University Veterinary Diagnostic Laboratory, Lansing, MI 48910.

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History

Over a 2-week period, 4 adult animals in a privately owned colony of sugar gliders died. Full necropsies were performed on 3 of those animals. The sugar gliders were fed boiled chicken, sugar glider pellets, dried apples, cantaloupe, other fruits and vegetables, dried crickets, and sugar glider nutrition powder.

Clinical and Gross Findings

Some sugar gliders had no clinical signs prior to death, but others had a 1- to 2-day history of lethargy and anorexia. In the animal that had the least amount of autolysis, the diaphragmatic surfaces of the caudal lung lobes were covered by tan mats of fibrin and there were approximately 20 round (0.5- to 1-mm-diameter), tan foci randomly scattered throughout all liver lobes (Figure 1).

Figure 1
Figure 1

Photographs of the thoracic cavity (A) and the liver (B) of 1 of 4 sugar gliders that died during a 2-week period. The lungs have tan fibrillar material adhered to the pleural surface (visible in the bottom left region of panel A). Throughout the parenchyma of the liver, there are multifocal, round, randomly scattered, tan foci.

Citation: Journal of the American Veterinary Medical Association 258, 11; 10.2460/javma.258.11.1201

Histopathologic Findings

Specimens of various tissues were examined histologically. There was diffuse, variable expansion of the visceral pleura by large numbers of neutrophils, abundant fibrin, and karyorrhectic debris (Figure 2). Alveolar capillaries were moderately congested and contained small numbers of neutrophils and rare megakaryocytes. Alveoli were occasionally filled with flocculent edema fluid, scant fibrin, and rare individualized neutrophils. The submucosa, tunica muscularis, and adventitia of the esophagus were expanded to effaced by large numbers of neutrophils and karyorrhectic to eosinophilic necrotic debris. Small vessels in the lamina propria frequently contained marginating neutrophils, and the esophageal lumen contained sloughed epithelial cells, scant hemorrhage, and a small amount of karyorrhectic debris. The epicardium was similarly expanded by abundant neutrophils, loosely organized fibrin, hemorrhage, and karyorrhectic debris. There was multifocal necrosis of the splenic white pulp characterized by variably sized accumulations of karyorrhectic debris, viable neutrophils, and occasional clusters of extracellular, gram-positive bacterial rods. Similar regions of necrosis containing extracellular bacilli were randomly scattered throughout the hepatic parenchyma. Comparable microscopic changes were present in the liver and spleen of one other necropsied sugar glider, but this animal did not have extensive pleuritis, esophagitis, or epicarditis. Interpretation of the histopathologic findings for the third animal was prevented by the presence of severe autolysis.

Figure 2
Figure 2

Photomicrographs of sections of various tissues obtained for 1 of the 3 sugar gliders that underwent necropsy. A—In this section, the heart (dot), left lung (asterisk), and esophagus (plus symbol) are visible. The visceral pleura and epicardium are variably distended with neutrophils, fibrin, and karyorrhectic debris (arrows). Similar fibrin, karyorrhectic debris, and neutrophils efface the wall of the esophagus. H&E stain; bar = 1 mm. B—The esophageal wall is expanded and effaced by neutrophils and karyorrhectic debris. Submucosal vessels are congested. H&E stain; bar = 50 μm. C—In the heart, the epicardium is expanded by fibrin, neutrophils, and karyorrhectic debris. H&E stain; bar = 50 μm. D—The spleen has necrosis of the white pulp, which is characterized by karyorrhectic debris and neutrophils. H&E stain; bar = 50 μm. E—Affected regions of the epicardium of the heart immunoreact with Listeria O antisera (red labeling). Listeria O antisera labeling with red chromogen and hematoxylin counterstain; bar = 50 μm. F—Similar positive immunoreactivity is evident in the splenic parenchyma. Listeria O antisera labeling with red chromogen and hematoxylin counterstain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 258, 11; 10.2460/javma.258.11.1201

Additional Laboratory Findings

Tissue specimens of the lungs and liver were collected from the least-autolyzed sugar glider for bacterial culture. Cultures of both tissue specimens yielded growth of Listeria monocytogenes. Sections of the esophagus, lungs, pericardium, liver, and spleen underwent immunohistochemical labeling with Listeria O antisera types 1 and 4.a The inflamed or necrotic foci in those tissue sections reacted positively with the antisera (Figure 2).

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: fibrinosuppurative pleuritis, multifocal hepatic necrosis with intralesional bacilli, multifocal splenitis and splenic white pulp necrosis with intralesional bacilli, fibrinosuppurative epicarditis, and necrosuppurative esophagitis.

Case summary: listeriosis in a colony of sugar gliders.

Comments

The gross findings in the lungs and liver of the least-autolyzed sugar glider of the present report were suggestive of bacterial septicemia. Common bacterial pathogens of sugar gliders include Clostridium piliforme, Pasteurella multocida, Klebsiella sp, and L monocytogenes.1,b Histologic examination of specimens from 2 of the 3 animals that underwent necropsy confirmed fibrinosuppurative inflammation with intralesional bacteria in multiple organs. The third animal was severely autolyzed.

Listeriosis in a sugar glider during a 2011 outbreak of the disease that affected 28 states and > 140 people has previously been described.2 That animal had clinical signs including dyspnea, lethargy, and vomiting. Prior to death, it was treated by a veterinarian with fluids SC and sulfamethazine-trimethoprim PO every 12 hours. Although multifocal hepatic necrosis was evident in that sugar glider, it lacked lesions in the lungs, heart, esophagus, and spleen.2 As were the 3 sugar gliders of the present report, that animal had been fed a diet that included cantaloupe, which was ultimately implicated in the 2011 outbreak of listeriosis. There were no known human cases of listeriosis associated with the outbreak in the sugar glider colony of the present report.

Listeria monocytogenes is a zoonotic, gram-positive, facultative anaerobic bacterium that grows in a wide temperature range (4°C to 45°C). Infection generally occurs by consumption of contaminated food. Listeriosis is considered one of the deadliest food-related illnesses of humans and has a 20% to 30% mortality rate.3 In veterinary species, listeriosis most commonly affects ruminants. This disease manifests as 2 forms in adult ruminants: a neurologic form and late-term abortion. The neurologic form is sometimes referred to as circling disease. In this form of listeriosis, the bacteria travel up the trigeminal nerve, elicit microabscess formation in the brainstem, and cause asymmetric neurologic signs including circling, head tilt, drooping of the ear and eyelid, and ptyalism. In the other form, there is hematogenous spread of the bacteria to the placenta, resulting in placentitis and late-term abortion. The dam is often free of clinical signs, but the fetus may have septicemia.

Septic listeriosis often develops in young ruminants. Systemic infection most commonly affects the cerebrum, liver, and heart.4 In the sugar gliders of the present report, the spleen, lungs, and esophagus were also affected; however, there was no involvement of the CNS.

In the colony described in the present report, the source of infection in these sugar gliders was not determined. On the basis of the provided diet history, contaminated food represented a likely source of exposure. Cantaloupe in particular has been linked to previous outbreaks of listeriosis,2 and that fruit may have introduced the pathogen to this colony of sugar gliders. Given the rapid progression of the disease in this group of animals and in the previous reported case, treatment options may be limited. In a suspected outbreak, removal of potentially contaminated feedstuffs from the diet of surviving animals may be warranted.

Footnotes

a.

BD Diagnostic Systems, Hunt Valley, Md.

b.

Garner M. Diseases of pet hedgehogs, chinchillas, and sugar gliders, in Proceedings. 32nd Annu Conf Assoc Avian Vet 2011; session 2585.

References

  • 1.

    Nichols D. Wednesday Slide Conference 2007–2008 Conference 23. The Armed Forces Institute of Pathology Department of Veterinary Pathology 2008;110.

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  • 2.

    Nichols M, Takacs N, Ragsdale J, et al. Listeria monocytogenes infection in a sugar glider (Petaurus breviceps)—New Mexico, 2011. Zoonoses Public Health 2015;62:254257.

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  • 3.

    Jordan K, McAuliffe O. Listeria monocytogenes in foods. Adv Food Nutr Res 2018;86:181213.

  • 4.

    Vázquez-Boland JA, Kuhn M, Berche P, et al. Listeria pathogenesis and molecular virulence determinants. Clin Microbiol Rev 2001;14:584640.

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