No abstract

Endotheliotropic elephant herpesvirus (elephantid herpesvirus 1; ElHV-1) is apathogenic for African elephants (Loxodonta africana), but causes fatal haemorrhagic disease in Asian elephants (Elephas maximus). This is thought to occur through transmission from African elephants in places where both species are housed, such as zoological gardens. The virus has caused considerable losses in North American and European zoological gardens and thus severely impedes breeding of the endangered Asian elephant. Previously, the ultrastructural and genetic characterization of ElHV-1 from a male Asian elephant that died from the disease at the Berlin zoological gardens in 1998 have been reported. Here, a partial characterization of the ElHV-1 genome is presented. A 60 kbp locus, spanning 34 open reading frames, was analysed. Most of the detected genes were found to be conserved among the herpesviruses and showed an overall arrangement most similar to that of betaherpesviruses, in particular Human herpesvirus 6 and Human herpesvirus 7. Most importantly, in addition to a protein kinase gene that is homologous to the human cytomegalovirus UL97 gene, a thymidine kinase (TK) gene was found, which is generally missing in betaherpesvirus genomes. Thus, ElHV-1 is the only known betaherpesvirus to encode a TK gene. This peculiarity might contribute to the fulminant pathogenicity of ElHV-1, but also provide a crucial enzymic activity for developing an efficient antiviral therapy with currently available nucleoside analogues.

A male Asian elephant (Elephas maximus) died at the Berlin zoological gardens in August 1998 of systemic infection with the novel endotheliotropic elephant herpesvirus (ElHV-1). This virus causes a fatal haemorrhagic disease in Asian elephants, the so-called endothelial inclusion body disease, as reported from North American zoological gardens. In the present work, ElHV-1 was visualized ultrastructurally in affected organ material. Furthermore, a gene block comprising the complete glycoprotein B (gB) and DNA polymerase (DPOL) genes as well as two partial genes was amplified by PCR-based genome walking and sequenced. The gene content and arrangement were similar to those of members of the Betaherpesvirinae. However, phylogenetic analysis with gB and DPOL consistently revealed a very distant relationship to the betaherpesviruses. Therefore, ElHV-1 may be a member of a new genus or even a new herpesvirus subfamily. The sequence information generated was used to set up a nested-PCR assay for diagnosis of suspected cases of endothelial inclusion body disease. Furthermore, it will aid in the development of antibody-based detection methods and of vaccination strategies against this fatal herpesvirus infection in the endangered Asian elephant.

To assess if wild carnivores in Germany play a role in the epizootiology of canine parvovirus (CPV) infection, seroprevalences against CPV in free-ranging carnivores (n=1,496) from selected urban and rural areas were compared. Antibodies against CPV were found in sera from red foxes (Vulpes vulpes; 136 of 1,442; 9%), raccoon dogs (Nyctereutes procyonides; two of 33; 6%), stone martens (Martes foina; four of 13; 31%), and pine martens (Martes martes; one of two) using the hemagglutination-inhibition test and pig erythrocytes. Evidence of CPV infection was detected in all study areas. Antibody titers varied between 10 and 320. In red foxes, the number of reactors did not differ between most urban and rural areas. However, we found significantly more reactors in the most densely populated urban area (Berlin). None of 430 tissue samples (small intestine, spleen, mesenterial lymph nodes) from any species tested for the presence of CPV nucleic acid using polymerase chain reaction yielded an amplification product. Based on our results, we believe that contact between domestic dogs and free-ranging red foxes probably plays a subordinate role in the epizootiology of CPV in Germany.

Pathologic-histologic and immunocytologic as well as serologic findings from a total number of 50 recently dead or euthanatized moribund harbor seals (Phoca vitulina) are described. In 14 of 31 histologically examined brains of affected seals alterations corresponding to canine distemper encephalitis (CDE) were found. Immunofluorescence-serologic tests using polyclonal as well as monoclonal antibodies against canine distemper virus (CDV) resulted in positive findings in organ sections of 24 dead seals. An agent was isolated from organs of dead seals and subjected to several passages in vero cell cultures as well as in primary seal lung-cell cultures. The agent was able to be identified as canine distemper-like virus with both antibodies.CDV neutralising serum-antibodies were detected in 13 out of 19 serum specimens. Further interdisciplinary investigations are required to determine whether the virus induced alterationsstill to be interpretated only in a purely qualitative senseshould be considered as the manifestation of contributing ecological factors, or as the primary cause of the still present deaths of harbor seals.