Erratum to: Arrhythmogenic right ventricular cardiomyopathy secondary to adipose infiltration as a cause of episodic collapse in a horse.

[This corrects the article DOI: 10.1186/s13620-015-0052-3.].

Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection.

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.

Arrhythmogenic right ventricular cardiomyopathy secondary to adipose infiltration as a cause of episodic collapse in a horse.

A 15-year-old Clydesdale cross gelding was investigated and managed over a 2-year period for intermittent collapse. The horse presented initially after an observed episode of collapse at rest, and had a resting tachycardia, elevated Cardiac Troponin I and polycythaemia. Multiple dysrhythmias were detected on telemetric electrocardiography. Vital parameters, cardiac rhythm and red cell count returned to reference range with prolonged rest but further resting syncopal episodes were observed, and due to safety concerns and limited treatment options the horse was euthanased. Post mortem evaluation identified extensive infiltration and replacement of right and left ventricular myocardial fibres with adipose and fibrous tissue, consistent with arrhythmogenic right ventricular cardiomyopathy. This report provides further information regarding the clinical and pathological features of this rarely reported condition.

Comparison of the 1988 and 2002 phocine distemper epizootics in British harbour seal Phoca vitulina populations.

In 1988 and 2002 dramatic and well-documented phocine distemper epizootics occurred in Europe. While their progression and impact were remarkably similar and consistent over much of Europe, mortality in the UK varied greatly between and within the 2 epizootics. We use antibody levels in blood samples to show that 51% (Bayesian 95% CI: 41 to 61%) of the individuals alive in 5 UK harbour seal populations at the end of the 1988 epizootic had been exposed to the virus, and that the equivalent figure after the 2002 outbreak was 22% (95% CI: 16 to 30%). Antibody prevalence was significantly higher in females than males after the 2002 epizootic. Combining these estimates with information on reductions in the numbers of animals observed hauled out during surveys of the Wash, Moray Firth, and Orkney populations and a simple epidemiological model, suggests that the differences between the 2 epizootics were primarily due to a 27% (95% CI: 8 to 43%) fall in R0, the basic reproductive rate of the virus. The large geographic variation in population effects observed within the UK during each epizootic appears to have been mainly due to differences in case mortality, with R0 being remarkably similar in all the populations investigated.

Identification of a detrimental role for NK cells in pneumococcal pneumonia and sepsis in immunocompromised hosts.

Gram-positive sepsis is a major disease problem. However, the contribution of various immune cell types to pathogenesis remains unclear. By infecting scid and wild type BALB/c mice with Streptococcus pneumoniae we have found a situation in which natural killer (NK) cells can play a detrimental role in the response to infection. scid mice were found to be significantly more susceptible to local and systemic pneumococcal infection than controls; they had significantly higher bacterial loads, elevated inflammatory responses and more widespread lung pathology. Interestingly, depletion of NK cells in scid mice resulted in significantly lower bacteraemia and inflammatory cytokine production. Infection with pneumococci deficient in pneumolysin revealed the toxin was involved in cytokine production. Overall results indicate that elevated NK cell activity during pneumococcal pneumonia amplifies pulmonary and systemic inflammation, increases bacteraemia and results in poor outcome.