Adult, male, sugar glider, Petaurus brevicepsThe owner had seven sugar gliders. Two sugar gliders, one female and one male, became acutely lethargic, dehydrated, and were vomiting. The sugar gliders died and the male was presented for postmortem examination. The diet did contain cantaloupe that had been previously frozen and raw organic soybeans.
The liver was slightly enlarged with multiple pinpoint tan foci of necrosis.Â The lungs were mildly congested.Â
The liver contains numerous random multifocal to coalescing foci of necrosis filled with necrotic cellular debris and variable numbers of degenerate neutrophils.Â The margins of the necrotic foci contain variable numbers of gram-positive intracellular and extracellular rod-shaped bacteria.Â The necrotic foci occasionally extend into portal veins resulting in necrosis of the vascular wall and fibrin thrombi within the lumen.Â Throughout the liver, there are moderate numbers of hepatocytes that contain clear distinct cytoplasmic vacuoles consistent with lipid.Â There are moderate numbers of hepatocytes that contain golden-brown to yellow-green cytoplasmic granular pigment that is consistent with hemosiderin and bile.Â
Liver: Severe multifocal and random necrotizing suppurative hepatitis with rare vascular necrosis and thrombosis and intracellular and extracellular gram-positive rod-shaped bacteria consistent with Listeria monocytogenes.
Listeria monocytogenes was isolated on bacterial culture of the liver.Â
Listeria monocytogenes is a gram-positive, intracellular, non-spore forming, facultative anaerobic, rod-shaped bacterium that causes the disease listeriosis.(2,5,6) It has the ability to infect and cause disease in multiple species including but not limited to humans, ruminants, pigs, horses, rabbits, chinchillas, and birds.(1,2,4,5,6,7,8,9) The bacterium is believed to be distributed worldwide with many animals and people (estimated up to 70% of people in some areas are carriers) being asymptomatic carriers.(2,6,7) In addition, the bacterium has been isolated from sewage, stream water, silage, and soil.(6)
Most incidents of listeriosis occur when the host ingests contaminated soil, water or food.(1,2,5,6,7) The bacterium is internalized into the host cell using the surface protein internalin, which interacts with E-cadherin on the host cells allowing the bacterium to cross the intestine, placenta, and blood-brain barrier.(1,2,5,7,9) Once inside the host cell, the bacterium lyse the phagocytic cell phagolysosome using a pore-forming protein called listeriolysin O and two phospholipases allowing it to gain access to the host cell cytoplasm.Â The bacterium then replicates within the host cell cytoplasm.Â Listeria has the ability to co-opt the host cell actin filaments using the bacterial surface protein ActA to help it migrate to the host cell membrane to induce pseudopod-like protrusions that can be transferred to another host cell.Â The host protection against Listeria appears to be mediated by IFN-Î³ production by NK cells and T-lymphocytes as host macrophages stimulated by IFN-Î³ phagocytose and kill Listeria while host macrophages that internalize Listeria coated by C3 become infected.(1)
Severe disease caused by Listeria monocytogenes tends to manifest as three distinct syndromes in both animals and humans: abortion after infection of the pregnant uterus, septicemia with visceral abscesses, and meningoencephalitis.(1,2,9) The syndromes, particularly the neurologic and genital forms of listeriosis, rarely occur at the same time.(2) Abortions occur most commonly in cattle and sheep, but have also been reported in women and other species.(1,2) Encephalitic listeriosis occurs most commonly in ruminants while people tend to develop suppurative meningitis.(1,2) All species seem to be susceptible to septicemia with Listeria.(5)
In abortions, Listeria crosses the placenta and most likely results in fetal septicemia.(6) The gross lesions in the fetus often include severe placentitis and multiple pinpoint yellow foci in multiple organs, which are most prominent in the liver.Â However, the gross fetal visceral lesions are easily obscured by postmortem decomposition.Â The microscopic lesions in the fetal organs consist of foci of necrosis filled with degenerate neutrophils and macrophages surrounded by bacteria.Â Necrotizing enterocolitis with intralesional bacteria may be present.Â Meningitis can also be seen in the fetus.Â The microscopic placental lesions include necrosis of the cotyledonary villi with a suppurative exudate and many bacteria.
The neurologic form of listeriosis in ruminants is most often the result of feeding contaminated silage.(2,5,7,9) The bacteria travel via the trigeminal nerve and other sensory nerves to the brainstem possibly gaining entry to the nerves through wounds in the oral cavity.Â There usually are no gross lesions associated with neurologic listeriosis in ruminants.Â The microscopic lesions are limited to the brainstem.Â The microscopic lesions can range from small early lesions of accumulations of glial cells to severe encephalitis with macrophages, lymphocytes, plasma cells, neutrophils, and the formation of the characteristic microabscesses.Â Bacteria can be seen in some lesions.
The septicemic form of listeriosis most often occurs in neonates and young animals, but can occur in adult animals.(1,2,8,9) The gross and microscopic lesions consist of multifocal necrosis and microabscesses that can contain bacteria.(2) These lesions occur most frequently in the liver.Â Although the source of the bacterium is often not identified in septicemic cases, potential sources include contamination of the pregnant uterus by Listeria during gestation and the bacterium crossing the intestine after the animal ingesting contaminated soil, water or food.
In the fall of 2011 in multiple states including Colorado and New Mexico, a total of 146 persons were sickened, 30 people died, and one woman miscarried after eating cantaloupe contaminated with Listeria monocytogenes.(3) The sugar glider in this case was known to eat cantaloupe in its diet.Â Listeria monocytogenes has 11 different serotypes that can be distinguished from one another using molecular techniques.Â Using pulse field gel electrophoresis, the serotype of the L.Â monocytogenes isolated from the sugar glider was not the same as the serotype of the L.Â monocytogenes isolated from the cantaloupe associated with the listeriosis outbreak in people.Â Nevertheless, this case illustrates the One Health concept of the potential of infectious agents to infect veterinary species and humans that are sharing the same environment and ingesting the same food and water.Â
Liver: Hepatitis, necrotizing and suppurative, multifocal, severe, with vascular necrosis, thrombosis, and numerous intra and extracellular bacilli.
The contributor provides an excellent review of listeriosis.Â Conference participants discussed the vascular lesions and described them as vascular necrosis due to local inflammation rather than a true vasculitis.Â Participants also commented on the necrotic areas, noting the core of lytic necrosis and inflammation surrounded by a corona-like ring of coagulative necrosis.Â There was speculation that such lesions could be due to either the local effects of listeriolysin O and phospholipase facilitating transfer of the bacteria across cell membranes resulting in coagulative necrosis in advance of inflammation; or to a locally released toxin directly resulting in cell death.Â
1. McAdam AJ, Sharpe AH.Â Infectious Diseases.Â In: Kumar V, Abbas AK, Fausto N, Aster J, eds.Â Robbins and Cotran Pathologic Basis of Disease.Â 8th ed.Â Philadelphia, PA: Elsevier Saunders; 2010: 361.
2. Maxie MG, Youssef S.Â Nervous system.Â In: Maxie MG, ed.Â Jubb, Kennedy, and Palmers Pathology of Domestic Animals.Â 5th ed.Â Vol 1.Â Philadelphia, PA: Elsevier Saunders; 2007: 405-408.
3. Multistate Outbreak of Listeriosis Linked to Whole Cantaloupes from Jensen Farms, Colorado.Â The Centers for Disease Control and Prevention Website.Â http://www.cdc.gov/listeria/outbreaks/cantaloupes-jensen-farms/120811/index.html.Â December 8, 2011 (Final Update).Â Accessed June 11, 2012.Â
4. Percy DH, Barthold SW.Â Rabbit.Â In: Percy DH, Barthold SW, eds.Â Pathology of Laboratory Rodents and Rabbits.Â 3rd ed.Â Ames, IA: Blackwell; 2007: 278-280.
5. Quinn PJ, Markey BK, Leonard FC, FitzPatrick ES, Fanning S, Hartigan PJ.Â Listeria species.Â In: Quinn PJ, Markey BK, Leonard FC, FitzPatrick ES, Fanning S, Hartigan PJ, eds.Â Veterinary Microbiology and Microbial Disease. 2nd ed.Â Ames, IA: Wiley-Blackwell; 2011: 217-221.
6. Schlafer DH, Miller RB.Â Female genital system.Â In: Maxie MG, ed. Jubb, Kennedy, and Palmers Pathology of Domestic Animals. 5th ed.Â Vol 3.Â Philadelphia, PA: Elsevier Saunders; 2007:492-493.
7. Walker RL.Â Listeria.Â In: Hirsh DC, MacLachlan NJ, Walker RL, eds.Â Veterinary Microbiology.2nd ed.Â Ames, IA: Blackwell; 2004:185-189.
8. Warner SL, Boggs J, Lee JK, et al.Â Clinical, pathological, and genetic characterization of Listeria monocytogenes causing sepsis and necrotizing typhlocolitis and hepatitis in a foal. J Vet Diagn Invest. 2012; 24(3):581-586.
9. Zachary JF.Â Nervous System.Â In: Zachary JF, McGavin MD, eds.Â Pathologic Basis of Veterinary Disease.Â 5th ed.Â St.Â Louis, MO: Elsevier Mosby; 2012: 845-846.