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The role of a slaughterhouse worker (SHW) involves the authorized killing of living beings, yet there is limited understanding of the consequences this behavior has on their well-being. The purpose of this systematic review is to collate and evaluate the current literature on the psychological impact of slaughterhouse employment. Fourteen studies met the specific a priori inclusion criteria. The findings from this review were demarcated by the focus of studies: (1) the prevalence of mental health disorders, (2) the types of coping mechanisms used, and (3) the link between slaughterhouse employment and crime perpetration. It was found that SHWs have a higher prevalence rate of mental health issues, in particular depression and anxiety, in addition to violence-supportive attitudes. Furthermore, the workers employ a variety of both adaptive and maladaptive strategies to cope with the workplace environment and associated stressors. Finally, there is some evidence that slaughterhouse work is associated with increased crime levels. The research reviewed has shown a link between slaughterhouse work and antisocial behavior generally and sexual offending specifically. There was no support for such an association with violent crimes, however. Based on existing research, we suggest future directions for research (i.e., applying more methodological rigor) but highlight key findings for practitioners and policymakers that warrant attention. [ABSTRACT FROM AUTHOR]

Chlamydia trachomatis /HSV-2 vaginal co-infections are seen clinically, suggesting that these sexually transmitted pathogens may interact. We previously established an intravaginal Chlamydia muridarum /HSV-2 super-infection model and observed that chlamydial pre-infection protects mice from a subsequent lethal HSV-2 challenge. However, the mechanism of protection remains unknown. The type I interferon, IFN-β, binds to the type I interferon receptor (IFNR), elicits a host cellular antiviral response and inhibits HSV replication in vitro and in vivo. Previous studies have demonstrated that C. muridarum infection stimulates genital tract (GT) IFN-β production; therefore, we hypothesized that chlamydial pre-infection protects mice from HSV-2 challenge via the IFN-β/IFNR-induced antiviral response. To test this prediction, we quantified IFN-β levels in vaginal swab samples. Detection of IFN-β in C. muridarum singly infected, but not in mock-infected animals, prompted the use of the super-infection model in IFNR knockout (IFNR−/−) mice. We observed that C. muridarum pre-infection reduces HSV-2-induced mortality by 40% in wild-type mice and by 60% IFNR−/− mice. Severity of HSV-2 disease symptoms and viral shedding was also similarly reduced by C. muridarum pre-infection. These data indicate that, while chlamydial infection induces GT production of IFN-β, type I IFN-induced antiviral responses are likely not required for the observed protective effect. [ABSTRACT FROM AUTHOR]