Supports for medical students during rural clinical placements: factors associated with intention to practise in rural locations.

INTRODUCTION: Through rural clinical schools (RCSs), medical students may undertake an extended block of clinical training in rural Australia. The premise of these placements is that meaningful rural exposure will facilitate rural career uptake. RCSs offer a range of supports to facilitate student engagement in the program. This study aims to analyse RCS students' perceptions of these supports and impact on intentions to work rurally. METHODS: Between September 2012 and January 2013 RCS students were invited to complete questions regarding perceptions of student support, as a part of the annual Federation of Australian Medical Educators survey. Multivariable logistic regression was used to identify associations between supports and intentions for rural internship or career. RESULTS: There were 454 participants. A majority of students (n=349, 79.1%) felt well supported by their RCS. Students from a rural background (odds ratio (OR)=1.64 (95% confidence interval (CI):1.13-2.38)), or who indicated that their placement had a positive impact on their wellbeing (OR=1.38 (95%CI:1.07-1.80)), were more likely to intend to complete a rural internship. Those who felt socially isolated were less likely to elect this (OR=0.82 (0.70-0.97)). Outcomes were similar for those indicating a preference for rural or remote practice after completing training. CONCLUSIONS: Student perceptions of supports offered by RCSs were generally very positive. Perceptions of financial support were not predictive of rural career intent. Although this does not negate the importance of providing appropriate financial supports, it does demonstrate that student wellbeing is a more important recruitment factor for rural practice.

An experimental study of Bungowannah virus infection in weaner aged pigs.

Bungowannah virus is a pestivirus identified from an outbreak of stillbirth and increased mortality in the first 3-4 weeks of life on a piggery in New South Wales, Australia in June 2003. The aims of this study were to determine if post-natal infection results in any clinical abnormalities and quantify the amount of Bungowannah virus RNA in blood, oropharyngeal, nasal and conjunctival excretions and faeces during the course of infection. Thirty pigs were infected intra-nasally with one of six different doses of Bungowannah virus or a control inoculum and clinical signs and rectal temperatures monitored. Sera, leukocytes and oropharyngeal, nasal, conjunctival, rectal and tissue swabs were tested for Bungowannah virus by qRT-PCR and sera for antibody by peroxidase linked assay and virus neutralisation test. The infectious dose by the intra-nasal route in weaner pigs was determined to be between 1.6 and 3.2 log(10) TCID(50). Few clinical signs could be attributed to infection. Viraemia and viral excretion in oropharyngeal secretions were detected from 3 days post-inoculation and seroconversion from 10 days post-inoculation. Viral shedding was greatest and most frequently detected in oropharyngeal, and to a lesser extent, nasal secretions, and generally detected in lower amounts and less frequently in conjunctival secretions and faeces.

Experimental infections of the porcine foetus with Bungowannah virus, a novel pestivirus.

In 2003 an outbreak of sudden deaths occurred in 2-3-week-old pigs on a piggery in New South Wales, Australia. There was a marked increase in the birth of stillborn pigs and preweaning losses associated with a multifocal non-suppurative myocarditis with myonecrosis. The aim of this study was to amplify any infectious agents present in field material to aid the detection and identification of the causative agent of the porcine myocarditis syndrome (PMC). Foetuses were directly inoculated in utero with tissue extracts from field cases of PMC at 56-60, 70-84 or 85-94 days of gestation and euthanased 7-28 days later. The IgG concentration in foetal sera/body fluids was measured, hearts were examined by light microscopy and selected hearts were examined by electron microscopy. An infectious agent was detected in tissues from cases of PMC and its identification as the novel pestivirus Bungowannah virus has recently been reported (Kirkland et al., 2007). Sow sera, foetal tissues and foetal sera/body fluids were tested for Bungowannah virus RNA by qRT-PCR and antibody by peroxidase-linked assay. Bungowannah virus was detected in numerous organs of the porcine foetus. Following direct foetal exposure it is probable that this virus spreads by direct intra-uterine transmission to adjacent foetuses and by trans-uterine transmission to the dam. Data were obtained for both the replication of the virus in the porcine foetus and the humoral immune response in the foetus and sow.

Building a strong foundation for occupational health and safety: Action research in the workplace.

BACKGROUND: Action research (AR) holds promise as a method to improve occupational health and safety. METHODS: This case study explores the challenges and accomplishments during the first 6 months of an AR occupational health and safety committee at a manufacturing facility. RESULTS: Critical steps in the formative phase of the AR project included: (1) addressing differing power levels and perceived ownership of management and production committee members; (2) developing a collaborative approach to communication and problem solving; and (3) transitioning from dependence on university leadership to shared leadership among the committee. CONCLUSIONS: AR can lead to greater empowerment to address occupational health and safety issues, and to improved dialog between labor and management. AR can increase the likelihood that the problem will be understood, and effective solutions will be developed and their application supported and used throughout the organization.

Field and laboratory evidence that Bungowannah virus, a recently recognised pestivirus, is the causative agent of the porcine myocarditis syndrome (PMC).

In 2003 an outbreak of sudden deaths occurred in 2-3-week-old piglets on a piggery in New South Wales, Australia. There was a marked increase in the birth of stillborn piglets and preweaning losses associated with a multifocal non-suppurative myocarditis with myonecrosis. The aim of this study was to review existing data and to undertake further investigations of specimens from naturally infected pigs to provide evidence to support the hypothesis that Bungowannah virus, a recently recognised pestivirus, causes the porcine myocarditis syndrome (PMC). Sera collected from gilts and sows from affected and unaffected units were tested for Bungowannah virus antibody by a peroxidase-linked assay and Bungowannah virus RNA by qRT-PCR in selected cases. Stillborn piglets from affected and an unaffected unit were also tested for Bungowannah virus antibody and RNA. Body fluid IgG levels and the incidence of myocardial lesions in these stillborn piglets are summarised. Tissue sections from stillborn piglets with myocarditis/myonecrosis were examined for Bungowannah virus RNA by in situ hybridisation. A clear temporal association between the occurrence of PMC on a unit or module and exposure to Bungowannah virus was identified by serological tests in both breeding aged animals and stillborn pigs. In addition, at the individual animal level on affected units, Bungowannah virus RNA was detected in stillborn piglets in large amounts by qRT-PCR and in association with myocardial lesions by in situ hybridisation. The examination of field material from cases of PMC by serology, qRT-PCR and in situ hybridisation provides strong indirect evidence that Bungowannah virus is the causative agent for PMC.