Das canine Parvovirus (CPV-2)wurde erstmals bei Hunden im Jahr 1978 beschrieben. Dieses Virus verbreitete sich innerhalb weniger Monate weltweit in einer schweren Pandemie. Retrospektiv wird angegnommen, dass es sich aud dem Felinen Panleukopenie-Virus oder einem nah verwandten Virus entwickelt hat. Ziel dieser Arbeit war es, durch Untersuchungen von archivierten paraffineingebetteten Gewebeproben von Hunden und Katzen aus den frühen 1970iger Jahren einen möglichen Anzestor des caninen Parvovirus zu identifizieren und die Hypothese zu überprüfen, dass CPV-2 schon vor 1978 in den Hundepopulationen zirkulierte.

Canine parvovirus type 2 (CPV-2), the aetiological agent of haemorrhagic enteritis in dogs emerged in 1978 worldwide. In the mid 1980’s, the original CPV-2 had evolved and was completely replaced by 2 variants, CPV 2a and 2b. In 2000, a new variant of CPV (CPV-2c) was detected in Italy and now circulates in other countries. Haemorrhagic enteritis in dogs is a major disease in South Africa and Nigeria. Both infection rates with CPV-2 and case fatality rates in young dogs are high. CPV-2 is a small, negative-sense, single-stranded DNA virus of 5.2kb long and a member of the Parvoviridae family, which also includes feline panleukopenia virus (FPV) and mink enteritis virus (MEV). The CPV-2 genome is prone to mutations at the VP2-encoding region. As a result we investigated the genetic composition of the VP2 region in the CPV-2 genome using molecular methods (qPCR) to provide information for comparison of field and vaccine strains of the virus. The conventional PCR detection results yielded 137 (97.85%) of the total of 140 feacal samples screened with diarrhoea positive. One hundred-and-six of 108 samples from South Africa (98.15%) tested positive and two (1.85%) were negative, while 30 (96.77%) from 31 faecal samples from Nigeria were positive and 1 (2.23%) was negative. Results obtained from the genotyping of the CPV- 2 strains using CPV-2a/b and CPV-2b/c TaqMan assays employing minor groove binder (MGB) probes, revealed that out of a total of 106 South African samples, 100 (94.34%) were infected with CPV-2b and 6 (5.66%) with CPV-2a, while all the Nigerian samples [n=30 (100%)] contained only CPV2a. There was no reported case of CPV-2c. The VP2 gene of selected DNA samples (n=27), from South Africa (n=19), Nigeria (n=6) and multivalent vaccines (n=2) were amplified and sequenced. These sequences were originally aligned and edited to a total length of 1,750 bp of the CPV-2 VP2 encoding gene. These selected sequences showed 99% maximum identity to the GenBank sequences from the blast results (NCBI BLASThttp:// www.ncbi.nlm.nih.gov/BLAST/) and alignment of all the sequences was performed using ClustalX. Two phylogenetic analyses showed most South African field isolates distant from viruses from other parts of the world. A few clustered with Asian and European strains, while Nigerian CPV-2 strains clustered with USA and some European isolates. The results of the protein analysis showed seven changes of amino acids at positions 265, 297, 324, 424, 426, 440 and 475 for most of the South Africans strains while the Nigerian CPV-2 had only one field isolate with an amino acid change. / Dissertation (MSc)--University of Pretoria, 2010. / Veterinary Tropical Diseases / unrestricted

Das canine Parvovirus (CPV-2)wurde erstmals bei Hunden im Jahr 1978 beschrieben. Dieses Virus verbreitete sich innerhalb weniger Monate weltweit in einer schweren Pandemie. Retrospektiv wird angegnommen, dass es sich aud dem Felinen Panleukopenie-Virus oder einem nah verwandten Virus entwickelt hat. Ziel dieser Arbeit war es, durch Untersuchungen von archivierten paraffineingebetteten Gewebeproben von Hunden und Katzen aus den frühen 1970iger Jahren einen möglichen Anzestor des caninen Parvovirus zu identifizieren und die Hypothese zu überprüfen, dass CPV-2 schon vor 1978 in den Hundepopulationen zirkulierte.

Inflammation in meninges and/or brain is regularly noticed in red foxes and other wild carnivores during rabies control programs. Despite negative rabies virus (RABV) results, the etiologies of these cases remain unknown. Thus, the aim of this study was to provide an overview of the occurrence of pathogens that may cause diseases in the brains of wild carnivores and pose a risk to humans and other animals. In addition to RABV and canine distemper virus (CDV), a variety of pathogens, including members of Flaviviridae, Bornaviridae, Herpesviridae, Circoviridae, as well as bacteria and parasites can also cause brain lesions. In 2016 and 2017, brain samples of 1,124 wild carnivores were examined by direct fluorescent antibody test for RABV as well as (reverse-transcriptase) quantitative polymerase chain reaction (PCR) for the presence of CDV as part of a monitoring program in Saxony-Anhalt, Germany. Here, we applied similar methods to specifically detect suid herpesvirus 1 (SuHV-1), West Nile virus (WNV), Borna disease virus 1 (BoDV-1), canid alphaherpesvirus 1 (CaHV-1), canine parvovirus type 2 (CPV-2), fox circovirus (FoxCV), and Neospora caninum (N. caninum). Further, bacteriogical examination for the existence of Listeria monocytogenes (L. monocytogenes) and immunohistochemistry of selected cases to detect Toxoplasma gondii (T. gondii) antigen were performed. Of all pathogens studied, CDV was found most frequently (31.05%), followed by FoxCV (6.80%), CPV-2 (6.41%), T. gondii (4/15; 26.67%), nematode larvae (1.51%), L. monocytogenes (0.3%), and various other bacterial pathogens (1.42%). In 68 of these cases (6.05%), multiple pathogen combinations were present simultaneously. However, RABV, WNV, BoDV-1, SuHV-1, CaHV-1, and N. caninum were not detected. The majority of the histopathological changes in 440 animals were inflammation (320/440; 72.73%), predominantly non-suppurative in character (280/320; 87.50%), and in many cases in combination with gliosis, satellitosis, neuronophagia, neuronal necrosis, and/or vacuolization/demyelination, or in single cases with malacia. Thus, it could be shown that wild carnivores in Saxony-Anhalt are carriers mainly for CDV and sometimes also for other, partly zoonotic pathogens. Therefore, the existing monitoring program should be expanded to assess the spill-over risk from wild carnivores to humans and other animals and to demonstrate the role of wild carnivores in the epidemiology of these zoonotic pathogens.