During late summer 2001 in Austria, a series of deaths in several species of birds occurred, similar to the beginning of the West Nile virus (WNV) epidemic in the United States. We necropsied the dead birds and examined them by various methods; pathologic and immunohistologic investigations suggested a WNV infection. Subsequently, the virus was isolated, identified, partially sequenced, and subjected to phylogenetic analysis. The isolates exhibited 97% identity to Usutu virus (USUV), a mosquito-borne Flavivirus of the Japanese encephalitis virus group; USUV has never previously been observed outside Africa nor associated with fatal disease in animals or humans. If established in central Europe, this virus may have considerable effects on avian populations; whether USUV has the potential to cause severe human disease is unknown.

In 2013, several Austrian piglet-producing farms recorded outbreaks of action-related repetitive myoclonia in newborn piglets (“shaking piglets”). Malnutrition was seen in numerous piglets as a complication of this tremor syndrome. Overall piglet mortality was increased and the number of weaned piglets per sow decreased by more than 10% due to this outbreak. Histological examination of the CNS of affected piglets revealed moderate hypomyelination of the white substance in cerebellum and spinal cord. We detected a recently discovered pestivirus, termed atypical porcine pestivirus (APPV) in all these cases by RT-PCR. A genomic sequence and seven partial sequences were determined and revealed a 90% identity to the US APPV sequences and 92% identity to German sequences. In confirmation with previous reports, APPV genomes were identified in different body fluids and tissues including the CNS of diseased piglets. APPV could be isolated from a “shaking piglet”, which was incapable of consuming colostrum, and passaged on different porcine cells at very low titers. To assess the antibody response a blocking ELISA was developed targeting NS3. APPV specific antibodies were identified in sows and in PCR positive piglets affected by congenital tremor (CT). APPV genomes were detected continuously in piglets that gradually recovered from CT, while the antibody titers decreased over a 12-week interval, pointing towards maternally transmitted antibodies. High viral loads were detectable by qRT-PCR in saliva and semen of infected young adults indicating a persistent infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-016-0406-1) contains supplementary material, which is available to authorized users.

A novel pestivirus species was discovered in a piglet-producing farm in Austria during virologic examinations of congenital tremor cases. The emergence of this novel pestivirus species, provisionally termed Linda virus, in domestic pigs may have implications for classical swine fever virus surveillance and porcine health management.

The correlation between parvovirus infections and lesions in the central nervous system other than cerebellar hypoplasia was studied in 100 cats. The animals were necropsied with a history of various diseases, one third showing typical clinical and pathomorphological signs of panleukopenia. In 18 cats polyclonal antiserum against canine parvovirus consistently labeled neurons mainly in diencephalic regions, whereas the cerebellar cortex remained negative in all cases. In situ hybridization with digoxigenin-labeled minus-sense RNA probes, hybridizing with monomer-replicative form DNA or mRNA, revealed positive signals in nuclei of several neurons of the brain, again excluding the cerebellum. PCR applied to formalin-fixed and paraffin-embedded brain tissue and intestinal tissues of the diseased cats and subsequent DNA sequence analysis yielded canine parvovirus type 2 (CPV-2)-like sequences in the central nervous system. Two aspects of these findings are intriguing: (i) parvoviruses appear to be capable of replicating in neurons, cells that are considered to be terminally differentiated and (ii) CPV-like viruses of the old antigenic type CPV-2 appear to be able to infect cats.Canine parvovirus (CPV) and feline panleukopenia virus (FPV) are considered to be host range variants among the feline parvovirus subgroup in the genus Parvovirus (12). Whereas FPV is known to have infected cats for many decades, CPV emerged suddenly in the mid-1970s and spread throughout the world in 1978. It was a new pathogen for the dog, and retrospective studies revealed the first signs of its appearance in 1976. The original virus from 1978, designated CPV type 2 (CPV-2) to separate it from a nonrelated parvovirus isolated in 1973 from skin tissue of a dog (2), was replaced throughout the world between 1979 and 1985 by two different but closely related antigenic variants: CPV type 2a (CPV-2a) and CPV-2b (10). Besides the antigenic differences between CPV-2 and the antigenic types CPV-2a and -2b, they show distinct biological properties. Whereas CPV-2 is only known to infect and replicate in dogs, CPV-2a and -2b can infect, replicate, and cause disease in cats (14). Experimental infections of cats with CPV-2 consistently failed to demonstrate virus replication (14,15).Parvovirus replication is restricted to the nucleus and is dependent on certain helper functions from the host cell. This is due to the single-stranded DNA genome of the virus that needs to be completed to a double-stranded intermediate to start transcription and translation of the viral genome and proteins, respectively. The DNA polymerase responsible for the synthesis of the complementary strand is a cellular polymerase that is only expressed in mammalian cells during the S phase of the cell cycle (1).Replication of FPVs in dogs and cats is predominantly seen in some highly mitotically active tissues, such as the lymphoid tissue, including lymph nodes, spleen, and thymus, as well as bone marrow and the epithelium of the gastrointestinal tract. Infection of the central ner...

Objectives Despite comprehensive diagnostics, the aetiology of meningoencephalitis (ME) in cats often remains undetermined. As a result of recently published surveys, Encephalitozoon cuniculi has gained growing importance in cats not only with ocular disorders, but also with central nervous system disease. Therefore, it was hypothesised that E cuniculi may be an underestimated pathogen in the development of feline non-suppurative and/or granulomatous ME. Methods As a first step, histopathological sections of the brain of cats with encephalopathy were retrospectively reviewed to identify cases of granulomatous ME. In a second step, an immunohistochemical screening for detection of E cuniculi was performed in cases with ME of unknown origin. Results In 59/89 (66.3%) cats with ME, an aetiologically relevant pathogen was detected. Forty-three of 89 (48.3%) cats had a diagnosis of feline infectious peritonitis. In 14/89 (15.7%) cats, protozoan cysts were identified and infection with Toxoplasma gondii was confirmed by immunohistochemistry (IHC) in all cases. In 2/89 (2.3%) cats with granulomatous ME, fungal organisms were identified. Thirty of 89 (33.7%) cats with ME of unknown origin that underwent IHC for the detection of E cuniculi remained negative. Conclusions and relevance The results of this study suggest that E cuniculi is unlikely to be directly associated with (non-suppurative and/or granulomatous) ME in cats in Austria.

No abstract

Encephalitozoon cuniculi is known to infect human beings, dogs, mink, cats, rodents, foxes, goats, horses, non-human primates, rats, ticks and the main host the rabbit (Oryctolagus cuniculus). Reports of E cuniculi in domestic cats (Felis catus) with histopathological changes are rare. This report describes an E cuniculi infection in the brain and kidneys of a six-week-old kitten. Postmortem examination was performed and microscopical examination of the brain and kidney revealed nodular infiltrates associated with Gram-positive microsporidian spores consistent with E cuniculi. PCR and immunohistochemistry confirm the findings. While E cuniculi infection in domestic cats is rare, this case demonstrates that it should be taken into consideration as a differential diagnosis for kittens with poor weight gain. Given the serious course of the disease and the risk of transmission to other littermates or other mammals including human beings, it is important to rule out an E cuniculi infection.