Abstract With increasing awareness of disease as an endangering process, an assessment of which pathogens might pose a problem and their patterns of infection in natural hosts is necessary. This paper examines the exposure of sympatric Ethiopian wolves ( Canis simensis ) and domestic dogs to canine distemper virus (CDV), canine adenovirus (CAV) and canine parvovirus (CPV) in the Bale region, Ethiopia and then relates these data to population trends of wolves. Wolves ( n = 30) sampled between 1989 and 1992 had been exposed to CDV, CAV and CPV, but only CAV might be able to persist in this wolf population. Anecdotal and serological evidence suggested that an epidemic of CDV occurred in the dog population of the Bale Mountains National Park (BMNP) in 1992–93. All park dogs born since this time were seronegative to CDV, although some young dogs in the nearby urban population were seropositive. Despite evidence of CAV infection in wolves, none of the dogs sampled in the park were CAV seropositive, although this virus appeared highly seroprevalent and endemic in urban dogs. All dogs tested for CPV antibodies were seropositive. The BMNP wolf population declined in the late 1980s and early 1990s, with rabies responsible for a dramatic population reduction between 1990 and 1992. Although the population declined further up until 1995, it is not possible to assess whether the concurrent canine distemper epidemic in park dogs also affected wolves. Nevertheless, with evidence of rabies, CDV, CAV and CPV infections in sympatric domestic dogs and Ethiopian wolves, canid diseases clearly pose a significant threat to the future persistence of this Ethiopian wolf population.
Abstract To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans, use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni . In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into the mechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)
