Adult, female banded mongoose (Mungos mungo).The whole population of 8 banded mongooses (Mungos mungo) of a zoological park was affected and died within 11 days. Animals were housed in an outdoor enclosure. Some animals showed anorexia, lethargy and staggering gait. Severe dyspnea and swelling of the intermandibular region were regularly observed. Therapy with prednisolone and antibiotics was unsuccessful. There was no previous animal transfer in the population. Similar fatalities in other animal species did not occur. The animal keepers were healthy and free of any skin lesion. Mongooses died about two days after onset of disease. Four mongooses were submitted to our institute for pathomorphological examination.
Animals were in good nutritional condition.Â There were multiple inconspicuous skin lesions predominately at the head and ventral trunk, measuring up to 0.5 cm in diameter.Â Some lesions appeared as small papules or vesicles, others as pustules.Â Single skin lesions were covered by crusts.Â There was a small ulcer on the tongue in one animal.Â Retropharyngeal tissue (including lymph nodes) was replaced by a firm whitish mass compressing the larynx.Â Within liver and spleen there were miliary white foci of necrosis and multiple petechiae.Â
Liver: Multifocally to coalescing there are randomly distributed foci of hepatocellular degeneration and necrosis, characterized by hypereosinophilia, loss of cellular detail, cellular debris, and pyknotic as well as karyorrhectic nuclei (coagulative necrosis).Â Foci vary in size from 40 to 200 Î¼m; in some locations only single hepatocytes are affected.Â In less affected areas, hepatocytes are swollen, have pale eosinophilic cytoplasm and swollen nuclei (degeneration).Â Centrally in the necrotic zone there is extravasation of blood cells (acute hemorrhage) admixed with fibrin and degenerated inflammatory cells.Â Within the cytoplasm of necrotic cells, degenerating cells and unaltered hepatocytes there are up to five, oval or round, bright eosinophilic inclusion bodies (5-10 Î¼m in size).Â Additionally, there is mild portal fibrosis and bile duct proliferation.Â There is a mild portal infiltration of lymphocytes and plasma cells.Â Single hepatocytes show cytoplasmic vacuolization (fatty change) and there is a mild intracanalicular cholestasis.Â
Spleen and lymph node lesions (slides not submitted) were characterized by necrotizing inflammation, and cytoplasmic inclusion bodies were detectable occasionally.Â Skin lesions (slides not submitted) showed hyperplasia and degeneration of epithelial cells (ballooning degeneration) with acantholysis.Â Within the subcutaneous tissue of the neck there was marked edema and necrosuppurative cellulitis and necrotizing lymphadenitis of retropharyngeal lymph nodes.
Liver: Hepatitis, necrotizing, multifocal to coalescing, random, subacute, severe, with intralesional hemorrhage and numerous intracytoplasmic inclusion bodies, banded mongoose, Mungos mungo.Â
Etiology: Consistent with systemic cowpoxvirus infection.
Orthopoxvirus was detected virologically and identified as cowpoxvirus (negative staining, transmission electron microscopy, cell culture, PCR, sequencing).
Poxvirus infections in nonnative hosts are a focus of epidemiological studies and there is an obvious zoonotic potential.(7,11,13,14) The most common sources of human infection are infected cats.(1) Recently, cases of cowpoxvirus infection in humans have been described in France and Germany after transmission from pet rats.(2,9) Wild rodents are suspected as reservoir hosts.(3)
There are several reports on cowpox virus infection in zoo animals.Â Reports of lethal poxvirus infections in elephants (4) and fatal cases in felids (1,8) can be found in the literature.Â Felids usually develop a mild dermal or a fatal pulmonary course of the disease.Â Necrotizing hepatitis due to cowpox virus is rare in felids; however, cases have been described in lions and cheetahs.(8)
In the banded mongooses the most severe lesions were necrotizing hepatitis, splenitis and lymphadenitis with occurrence of characteristic eosinophilic cytoplasmic inclusion bodies.Â In contrast to cases of cowpox virus in other members of the suborder Feliformia, the lungs were unaltered.Â The etiologic diagnosis was confirmed by cell culture, electron microscopy, PCR and sequencing.Â Wild rodents may have served as reservoir and vector in our cases.Â This hypothesis was supported by observation of poxvirus lesions in a captured rat in the surrounding of the outdoor enclosure.
Liver: Hepatitis, necrotizing, multifocal to coalescing, random, severe, with numerous intracytoplasmic eosinophilic inclusion bodies.
Despite its name, cowpox virus infection is neither endemic nor common in cattle.(2,14) The contributors review provides due emphasis on the role of cats in zoonotic cowpox virus infection.Â Many attribute an apparent increase in human infections with cowpox virus to waning immunity to orthopoxviruses in general, associated with the cessation of immunization with Vaccinia virus for smallpox.(2,14)
While many members of the Poxviridae family cause only localized cutaneous disease, the following characteristically produce systemic disease, which may be severe: Sheeppox virus, Ectromelia virus, Monkeypox virus, and Variola virus.(5) Conference participants discussed these and other poxviruses of veterinary importance, which are summarized by genus as follows:
- Avipoxvirus: 10 species, including Fowlpox virus
- Capripoxvirus: Goatpox virus, Lumpy skin disease virus, Sheeppox virus
- Cervidpoxvirus: Deerpox virus W-848-83
- Leporipoxvirus: Myxoma virus, Rabbit (Shope) fibroma virus, Squirrel fibroma virus
- Molluscipoxvirus: Molluscum contagiosum virus
- Orthopoxvirus: Camelpox virus; Cowpox virus; Ectromelia virus; Monkeypox virus; Vaccinia virus (buffalopox virus, rabbit pox virus); Variola virus
- Parapoxvirus: Bovine papular stomatitis virus; Orf virus; Parapoxvirus of red deer in New Zealand; Pseudocowpox virus
- Suipoxvirus: Swinepox virus
- Yatapoxvirus: Tanapox virus; Yaba monkey tumor virus
- Unassigned: Squirrel poxvirus (5,6)
Typical poxviral lesions are both proliferative and necrotizing.Â As poxviruses are epitheliotropic, replication within cells causes degeneration (i.e.Â ballooning degeneration) and necrosis, which is further exacerbated by ischemia when the virus replicates in endothelial cells and causes vascular damage.Â Several virulence factors may account for the ability of poxviruses to induce proliferation, including a gene whose product resembles epidermal growth factor.(5)
Unlike other DNA viruses, poxviruses produce intracytoplasmic, rather than intranuclear inclusion bodies.Â All poxviruses produce small, basophilic, intracytoplasmic inclusion bodies, designated type B or Guarnieris bodies, early in the replication cycle.Â These represent the actual sites of virus replication.Â The numerous, large, prominent, eosinophilic, intracytoplasmic inclusion bodies noted in this case are designated type A or acidophilic-type inclusions (ATI), and they are produced later in the replication cycle.Â In humans, type A inclusions are diagnostically useful, because they are only associated with certain poxviruses (e.g.Â Cowpox and Ectromelia virus, but not Monkeypox, Variola, or Vaccinia virus).Â Capripoxviruses generally produce type A inclusions; the large inclusions in Avipoxvirus infections are known as Bollinger bodies and they contain smaller Borrel bodies representing virus particles.(12)
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