Pharmacogenetic excitation of the median raphe region affects social and depressive-like behavior and core body temperature in male mice.

AIMS: Median raphe region (MRR) is an important bottom-up regulatory center for various behaviors as well as vegetative functions, but detailed descriptions and links between the two are still largely unexplored. METHODS: Pharmacogenetics was used to study the role of MRR in social (sociability, social interaction, resident intruder test) and emotional behavior (forced swim test) parallel with some vegetative changes (biotelemetry: core body temperature). Additionally, to validate pharmacogenetics, the effect of clozapine-N-oxide (CNO), the ligand of the artificial receptor, was studied by measuring (i) serum and brainstem concentrations of CNO and clozapine; (ii) MRR stimulation induced neurotransmitter release in hippocampus; (iii) CNO induced changes in body temperature and locomotor activity. KEY FINDINGS: MRR stimulation decreased locomotion, increased friendly social behavior in the resident intruder test and enhanced depressive-like behavior. The latter was accompanied by diminished decrease in core body temperature. Thirty minutes after CNO injection clozapine was predominant in the brainstem. Nonetheless, peripheral CNO injection was able to induce glutamate release in the hippocampus. CNO had no immediate (<30 min) or chronic (repeated injections) effect on the body temperature or locomotion. SIGNIFICANCE: We confirmed the role of MRR in locomotion, social and depressive-like behavior. Most interestingly, only depressive-like behavior was accompanied by changed body temperature regulation, which was also observed in human depressive disorders previously. This indicates clinical relevance of our findings. Despite low penetration, CNO acts centrally, but does not influence the examined basic parameters, being suitable for repeated behavioral testing.

Salpingitis in geese associated with Mycoplasma sp. strain 1220.

An outbreak of disease in a White Rhine laying goose flock was characterized by increased water uptake, increased mortality, production of eggs with abnormal shells, a 25% drop in egg production and 40% embryo mortality. Affected dead or sacrificed birds had sero-fibrinogranulocytic peritonitis and salpingitis, infiltration of the lamina propria in the uterus and heterophil granulocytes in the isthmus and magnum of the oviduct. Mycoplasmas, mainly identified as Mycoplasma sp. strain 1220, were isolated from the airsac, liver, ovary, magnum and peritoneum of some affected geese. Strain 1220 was originally isolated from a Hungarian gander with phallus inflammation and, according to detailed biochemical and serological examinations, it is expected to represent a new avian species within the genus Mycoplasma.

Poxvirus infection in Hungarian great tits (Parus major): case report.

From a total of 1819 great tits (Parus major) ringed in 2007 in Pilis Mountains, Hungary, 15 birds presented nodular proliferative lesions on different areas of the head and eyelids, suggesting a poxvirus infection. Three birds were submitted for analysis. The presence of avipoxvirus infection was confirmed by histopathology, electron microscopy (EM) and a polymerase chain reaction (PCR) based technique. Nucleotide sequence analysis of a 428 base pairs (bp) fragment of the viral 4b core protein gene revealed 100% identity between two of the Hungarian isolates (PM9 HUN, PM33 HUN) and two great tit poxvirus strains isolated in Norway in 1973 (GTV A256, GTV A311). The third Hungarian isolate (PM34 HUN) was more closely related to a different Norwegian isolate (GTVA310) than to the Hungarian isolates. The nucleotide sequence analysis of a shorter fragment of the viral 4b core protein (227 bp) gene revealed 100% identity between the Hungarian isolates, the same Norwegian isolates and a great tit poxvirus strain detected in Austria in 2007.

Phylogenetic diversity of avian nephritis virus in Hungarian chicken flocks.

Avian nephritis virus (ANV) infection was detected in 4-day-old to 22-day-old chickens collected on Hungarian farms between 2002 and 2005. The animals suffered from diarrhoea, growth retardation, runting-stunting syndrome, and 2 to 6% mortality was reported. Tubulonephrosis, interstitial nephritis and uricosis (gout) was diagnosed. The presence of ANV RNA was detected in chicken carcasses using reverse transcriptase-polymerase chain reaction. The virus was demonstrated in 69% of the investigated farms. The nucleotide sequence of the amplification products (corresponding to part of the genome that encodes the GP1 protein) was determined and phylogenetic analysis was performed. The nucleotide sequences showed 76 to 86% identity to the reference strain isolated in 1976 in Japan. The constructed phlyogenetic tree indicates high diversity of the Hungarian ANV sequences, regardless of their origin and year of sample collection. Analysis of the putative amino acid sequences encoded by the partial GP1 sequences also revealed high diversity of the virus. Even samples collected at the same farm, at the same time but from different flocks, differed in nucleotide and putative amino acid sequences. The possible effects of the sequence diversity on the pathogenicity, antigenicity and diagnostics of ANV are discussed.

Pathology of goose haemorrhagic polyomavirus infection in goose embryos.

Goose embryos were infected with goose haemorrhagic polyomavirus (GHPV) onto the chorioallantoic membrane (CAM) in order to examine the effect of GHPV on the embryos and to obtain data on whether embryos could develop into infected, virus-shedding goslings, as well as to present an accurate biological method for virus titration. The reported method of infection could offer a possibility to express the virus titre as the median embryo infective dose (EID(50)). As a special pathological feature of the disease, extensive cerebral haemorrhages were observed, which protruded the skullcap in many cases. Some embryos infected with 10(1.25) or 10(0.25) EID(50)/0.2 ml were able to hatch; however, they were in poor physical condition and died by post-hatching day 4 showing haemorrhagic nephritis and enteritis of geese. Virus shedding was revealed by polymerase chain reaction. The ability of some of the infected goose embryos to hatch may indicate the potency of GHPV to spread vertically, although this needs further study for confirmation.

Reovirus identified as cause of disease in young geese.

The pathology, epizootiology and aetiology of a specific disease of young geese, which has been seen in Hungary for more than three decades, were investigated. The disease was characterised by splenitis and hepatitis with miliary necrotic foci during the acute phase, and epicarditis, arthritis and tenosynovitis during the subacute/chronic phase. Clinical signs usually appeared at 2 to 3 weeks of age and persisted for 3 to 6 weeks. From different organs of the affected birds, a reovirus was isolated in embryonated eggs and tissue cultures of Muscovy duck or goose origin, as well as in Vero cells. In experimental infections, the dominant features of the disease were reproduced in day-old and young goslings. The biological and partial molecular characterisation of one of the isolated strains (D15/99) showed that it was related to the reovirus described as the cause of a similar disease of Muscovy ducks. An RT-PCR method suitable for the detection of reoviruses was also elaborated and tested. This is the first report on the involvement of reovirus in arthritis of geese.