Cerebellar Abiotrophy in Two Related Lion-tailed Macaques (Macaca silenus)

Cerebellar abiotrophy is a degenerative condition characterized by either early or late onset of severe neurological deficits caused by the marked depletion of Purkinje cells and granule cell neurons of the cerebellar cortex. The condition has been reported in numerous species with a proposed genetic basis of transmission. Here we present the anatomopathological investigation of two closely related lion-tailed macaques. Both cases, a 9-month-old male and a 4-month-old female, shared a long history of progressively worsening ataxia, incoordination and delayed body growth. Based on the characteristic findings, diagnoses of cerebellar abiotrophy were made. The relatedness of the two cases strongly supports an inherited mode of transmission. To the authors’ knowledge, this is the first report of cerebellar abiotrophy in a macaque species

Wave I State Demographic Characteristics, Exclusionary Indices, and Inclusionary Indices

These data provide measures of punishment regime variation in state-based policies, practices, and programs, both in their punitive and non-punitive forms, and some additional state demographic control variables. These data were gathered to use with Add Health for multilevel analyses

Novel Host-Related Virulence Factors Are Encoded by Squirrelpox Virus, the Main Causative Agent of Epidemic Disease in Red Squirrels in the UK

Squirrelpox virus (SQPV) shows little evidence for morbidity or mortality in North American grey squirrels (Sciurus carolinensis), in which the virus is endemic. However, more recently the virus has emerged to cause epidemics with high mortality in Eurasian red squirrels (S. vulgaris) in Great Britain, which are now threatened. Here we report the genome sequence of SQPV. Comparison with other Poxviridae revealed a core set of poxvirus genes, the phylogeny of which showed SQPV to be in a new Chordopoxvirus subfamily between the Molluscipoxviruses and Parapoxviruses. A number of SQPV genes were related to virulence, including three major histocomaptibility class I homologs, and one CD47 homolog. In addition, a novel potential virulence factor showing homology to mammalian oligoadenylate synthetase (OAS) was identified. This family of proteins normally causes activation of an endoribonuclease (RNaseL) within infected cells. The putative function of this novel SQPV protein was predicted in silico

Implications of squirrelpox virus for successful red squirrel translocations within mainland UK

Remnant red squirrel populations in the UK mainland are threatened by squirrelpox viral disease and the reservoir of the squirrelpox virus, the invasive grey squirrel, is expanding its range. Until this threat can be effectively mitigated, there is a high risk from disease outbreaks, following proposed conservation translocation of red squirrels

The drivers of squirrelpox virus dynamics in its grey squirrel reservoir host

Manypathogensofconservationconcerncirculateendemicallywithinnaturalwildlifereservoirhostsanditisimperativetounderstandtheindividualandecologicaldriversofnaturaltransmissiondynamics,ifanythreattoarelatedendangeredspeciesistobeassessed.Ourstudyhighlightsthekeydriversofinfectionandsheddingdynamicsofsquirrelpoxvirus(SQPV)initsreservoirgreysquirrel(Sciurus carolinensis)population.ToclarifySQPV dynamics in this population, longitudinal data from a 16-month mark-recapture study were analysed,combining serology with real-time quantitative PCR to identify periods of acute viraemia and chronic viralshedding. At the population level, we found SQPV infection prevalence, viral load and shedding varied sea-sonally,peakinginautumnandearlyspring.Individually,SQPVwasshowntobeachronicinfectionin>80%ofgreysquirrels,withviralloadspersistingovertimeandboutsofpotentialrecrudescenceorreinfectionoc-curring.AkeyrecurringfactorsignificantlyassociatedwithSQPVinfectionriskwasthepresenceofco-infectingsquirrel adenovirus (ADV). In dual infected squirrels, longitudinal analysis showed that prior ADV viraemiaincreasedthesubsequentSQPVloadintheblood.However,therewasastrong,negativeassociationbetweenpriorADVviraemiaandsubsequentSQPVsheddingfromtheforearm,probablycausedbyADVprolongingtheSQPVacuteviraemicphase,sodelayingonsetofthechronicsheddingphase,andtherebyalteringviralsheddingpatternsoverthetimescalesexaminedhere.Hence,co-circulatingADVinfectionmaybeinvolvedinmediatingboththequantitativelevelsofSQPVinfectionandthetiminganddegreeofsubsequentinfectiousnessofgreysquirrels

Renal trematode infection due to Paratanaisia bragai in zoo housed Columbiformes and a Red Bird-of-Paradise (Paradisaea rubra)

Trematode infections affect a diverse range of avian species and the organs that are parasitised are also very varied. The family Eucotylidae contains seven genera of renal flukes that parasitise various birds. In birds, mild to severe lesions have been reported for species of the genus Paratanaisia, which was originally described from columbiform and galliform specimens collected in South America and has been identified in a number of wild avian species. This paper investigates eight cases of renal trematode infection at Chester Zoo in the UK due to Paratanaisia bragai in five previously unreported species: red bird-of-paradise, Socorro dove, Mindanao bleeding heart dove, laughing dove and emerald dove. Pathological changes, which varied between species, are discussed. A known intermediate snail host Allopeas clavulinum was present in the enclosures but there was no direct evidence of trematode infection. The size of the snails, possible low prevalence and the difficulty of visualising sporocysts contributed to this. Thus the development and application of further molecular diagnostic markers that can be applied to snail tissues is warranted. Parasite identification was confirmed utilizing DNA amplification from formalin-fixed paraffin-embedded tissues using PCR and trematode specific primers. Sequencing full ssrDNA and D1-D3 lsrDNA confirmed the identity in all cases as P. bragai. However, the short 310 bp fragment used provides insufficient variation or sequence length for wider application. The epidemiology, pathology and consequences for the management of these endangered species are discussed. Preliminary work on developing an effective ante mortem diagnostic PCR test kit is also highlighted

Characterisation of Salmonella enterica serotype Typhimurium isolates from wild birds in northern England from 2005 – 2006

<p>Abstract</p> <p>Background</p> <p>Several studies have shown that a number of serovars of <it>Salmonella enterica </it>may be isolated from wild birds, and it has been suggested that wild birds may play a role in the epidemiology of human and livestock salmonellosis. However, little is known about the relationship between wild bird <it>S. enterica </it>strains and human- and livestock- associated strains in the United Kingdom. Given the zoonotic potential of salmonellosis, the main aim of this study was to investigate the molecular epidemiology of <it>S. enterica </it>infections in wild birds in the north of England and, in particular, to determine if wild bird isolates were similar to those associated with disease in livestock or humans.</p> <p>Results</p> <p>Thirty two <it>Salmonella enterica </it>isolates were collected from wild birds in northern England between February 2005 and October 2006, of which 29 were <it>S. enterica </it>serovar Typhimurium (<it>S</it>. Typhimurium); one <it>S</it>. Newport, one <it>S</it>. Senftenberg, and one isolate could not be classified by serotyping. Further analysis through phage typing and macro-restriction pulsed-field gel electrophoresis indicated that wild passerine deaths associated with salmonellosis were caused by closely-related <it>S</it>. Typhimurium isolates, some of which were clonal. These isolates were susceptible to all antimicrobials tested, capable of invading and persisting within avian macrophage-like HD11 cells <it>in vitro</it>, and contained a range of virulence factors associated with both systemic and enteric infections of birds and mammals. However, all the isolates lacked the <it>sopE </it>gene associated with some human and livestock disease outbreaks caused by <it>S</it>. Typhimurium.</p> <p>Conclusion</p> <p>The wild bird isolates of <it>S. enterica </it>characterised in this investigation may not represent a large zoonotic risk. Molecular characterisation of isolates suggested that <it>S</it>. Typhimurium infection in wild passerines is maintained within wild bird populations and the causative strains may be host-adapted.</p

Drowning is an apparent and unexpected recurrent cause of mass mortality of Common starlings (Sturnus vulgaris)

Drowning is infrequently reported as a cause of death of wild birds and such incidents typically involve individual, rather than multiple, birds. Over a 21-year period (1993 to 2013 inclusive), we investigated 12 incidents of mortality of multiple (2-80+) Common starlings (Sturnus vulgaris) in Great Britain that appeared to be due to drowning. More than ten birds were affected in ten of these reported incidents. These incidents always occurred during the spring and early summer months and usually involved juvenile birds. In all cases, circumstantial evidence and post-mortem examinations indicated drowning to be the most likely cause of death with no underlying disease found. A behavioural explanation seems likely, possibly related to the gregarious nature of this species combined with juvenile inexperience in identifying water hazards. A review of data from the ringed bird recovery scheme across Great Britain (1913-2013 inclusive) of both starlings and Common blackbirds (Turdus merula), also a common garden visitor, identified additional suspected drowning incidents, which were significantly more common in the former species, supporting a species predisposition to drowning. For each species there was a marked seasonal peak from April to August. Drowning should be included as a differential diagnosis when investigating incidents of multiple starling mortality, especially of juveniles