Although bubonic plague is an endemic zoonosis in many countries around the world, the factors responsible for the persistence of this highly virulent disease remain poorly known. Classically, the endemic persistence of plague is suspected to be due to the coexistence of plague resistant and plague susceptible rodents in natural foci, and/or to a metapopulation structure of reservoirs. Here, we test separately the effect of each of these factors on the long-term persistence of plague. We analyse the dynamics and equilibria of a model of plague propagation, consistent with plague ecology in Madagascar, a major focus where this disease is endemic since the 1920s in central highlands. By combining deterministic and stochastic analyses of this model, and including sensitivity analyses, we show that (i) endemicity is favoured by intermediate host population sizes, (ii) in large host populations, the presence of resistant rats is sufficient to explain long-term persistence of plague, and (iii) the metapopulation structure of susceptible host populations alone can also account for plague endemicity, thanks to both subdivision and the subsequent reduction in the size of subpopulations, and extinction-recolonization dynamics of the disease. In the light of these results, we suggest scenarios to explain the localized presence of plague in Madagascar.

Yersinia pestis, the etiologic agent of the disease plague, has been implicated in three historical pandemics. These include the third pandemic of the 19(th) and 20(th) centuries, during which plague was spread around the world, and the second pandemic of the 14(th)-17(th) centuries, which included the infamous epidemic known as the Black Death. Previous studies have confirmed that Y. pestis caused these two more recent pandemics. However, a highly spirited debate still continues as to whether Y. pestis caused the so-called Justinianic Plague of the 6(th)-8(th) centuries AD. By analyzing ancient DNA in two independent ancient DNA laboratories, we confirmed unambiguously the presence of Y. pestis DNA in human skeletal remains from an Early Medieval cemetery. In addition, we narrowed the phylogenetic position of the responsible strain down to major branch 0 on the Y. pestis phylogeny, specifically between nodes N03 and N05. Our findings confirm that Y. pestis was responsible for the Justinianic Plague, which should end the controversy regarding the etiology of this pandemic. The first genotype of a Y. pestis strain that caused the Late Antique plague provides important information about the history of the plague bacillus and suggests that the first pandemic also originated in Asia, similar to the other two plague pandemics.

Autotransporter protein secretion represents one of the simplest forms of secretion across Gram-negative bacterial membranes. Once secreted, autotransporter proteins either remain tethered to the bacterial surface or are released following proteolytic cleavage. Autotransporters possess a diverse array of virulence-associated functions such as motility, cytotoxicity, adherence, and autoaggregation. To better understand the role of autotransporters in disease, our research is focused on the autotransporters of Yersinia pestis, the etiologic agent of plague. Y. pestis strain CO92 has nine functional conventional autotransporters, referred to as Yaps for Yersinia autotransporter proteins. Three Yaps have been directly implicated in virulence using established mouse models of plague infection (YapE, YapJ and YapK). While previous studies from our laboratory showed that most of the CO92 Yaps are cell associated, YapE and YapG are processed and released by the omptin protease Pla. In this study, we identify the Pla cleavage sites in YapG that result in many released forms of YapG in Y. pestis, but not in the evolutionarily related gastrointestinal pathogen, Yersinia pseudotuberculosis, which lacks Pla. Furthermore, we show that YapG does not contribute to Y. pestis virulence in established mouse models of bubonic and pneumonic infection. As Y. pestis has a complex life cycle involving a wide range of mammalian hosts and a flea vector for transmission, it remains to be elucidated whether YapG has a measureable role in any other stage of plague disease.

Studies over the past several decades have dramatically increased our understanding of the immune response to Mycobacterium tuberculosis infection, and advances in proteomics and genomics have led to a new class of immune-diagnostic tests, termed interferon-γ (IFN-γ) release assays (IGRAs), which appear to obviate many of the problems encountered with the tuberculin skin test (TST). Worldwide, 2 IGRAs are currently commercially available. QuantiFERON-TB Gold In-Tube (Cellestis) is a third-generation product that uses an enzyme-linked immunosorbent assay to measure IFN-γ generated in whole blood stimulated with M. tuberculosis-specific antigens. T-Spot-TB (Oxford Immunotec) employs enzyme-linked immunosorbent spot technology to enumerate the number of purified lymphocytes that respond to M. tuberculosis-specific antigens by producing IFN-γ. These in vitro tests measure the host immune response to M. tuberculosis-specific antigens, which virtually eliminates false-positive cross reactions caused by bacillus Calmette-Guérin vaccination and/or exposure to environmental nontuberculous mycobacteria that plague the interpretation and accuracy of the tuberculin skin test (TST). The high specificity of IGRAs, together with sensitivity commensurate with or better than that of the TST, promises an accurate diagnosis and the ability to focus tuberculosis-control activities on those who are actually infected with M. tuberculosis. The Third Global Symposium was held over a 3-day period and was presented by the University of California, San Diego, Continuing Medical Education department; slides and sound recordings of each presentation are available at http://cme.ucsd.edu/igras/syllabus.html . A moderated discussion is also available at http://cme.ucsd.edu/igrasvideo . This document provides a summary of the key findings of the meeting, specifically focusing on the use of IGRAs in screening healthcare worker populations.

Globally, health worker shortages continue to plague developing countries. Community health workers are increasingly being promoted to extend primary health care to underserved populations. Since 2004, Healthy Child Uganda (HCU) has trained volunteer community health workers in child health promotion in rural southwest Uganda. This study analyses the retention and motivation of volunteer community health workers trained by HCU. It presents retention rates over a 5-year period and provides insight into volunteer motivation. The findings are based on a 2010 retrospective review of the community health worker registry and the results of a survey on selection and motivation. The survey was comprised of qualitative and quantitative questions and verbally administered to a convenience sample of project participants. Between February 2004 and July 2009, HCU trained 404 community health workers (69% female) in 175 villages. Volunteers had an average age of 36.7 years, 4.9 children and some primary school education. Ninety-six per cent of volunteer community health workers were retained after 1 year (389/404), 91% after 2 years (386/404) and 86% after 5 years (101/117). Of the 54 'dropouts', main reasons cited for discontinuation included 'too busy' (12), moved (11), business/employment (8), death (6) and separation/divorce (6). Of 58 questionnaire respondents, most (87%) reported having been selected at an inclusive community meeting. Pair-wise ranking was used to assess the importance of seven 'motivational factors' among respondents. Those highest ranked were 'improved child health', 'education/training' and 'being asked for advice/assistance by peers', while the modest 'transport allowance' ranked lowest. Our findings suggest that in our rural, African setting, volunteer community health workers can be retained over the medium term. Community health worker programmes should invest in community involvement in selection, quality training, supportive supervision and incentives, which may promote improved retention.

Since plague is an important natural focus zoonosis, the typing of natural plague foci becomes one of the elements in understanding the nature and developing related prevention program of the disease. Natural foci of plague are composed by four fundamental parts which include Eco-geographical landscape (natural plague foci), hosts, vectors and pathogens (Yersinia pestis) that comprehensively interact through the large temporal scale of evolution. Human activities have had great impact on the foci of natural plague. Based on the published serial research papers, we tried to integrate the knowledge of each factor in natural plague foci and focusing on theoretical aspects, so as to strengthen the prevention and surveillance programs of plague to be extrapolated to other zoonosis.

The evolution from a newly graduated or novice nurse to a competent nurse can be challenging and difficult. This transition involves a tidal wave of emotions along with time needed to develop critical thinking skills, in order to apply their knowledge to patient situations, make decisions and respond with appropriate actions. The purpose of this paper was to explore the existing literature in the area of supports for novice nurses; by determining who is a novice nurse, what can plague a novice's transition, and how to support their successful transition. These results have been compared with the role of Clinical Nurse Expert at The Ottawa Hospital and overall, the findings suggest that a one year coaching program for novices is an effective strategy for supporting their transition, subsequently increasing their retention rates, as well as having a positive influence on the nursing profession, our patients and the healthcare system.

Yersinia pestis causes pneumonic plague, a disease characterized by inflammation, necrosis and rapid bacterial growth which together cause acute lung congestion and lethality. The bacterial type III secretion system (T3SS) injects 7 effector proteins into host cells and their combined activities are necessary to establish infection. Y. pestis infection of the lungs proceeds as a biphasic inflammatory response believed to be regulated through the control of apoptosis and pyroptosis by a single, well-conserved T3SS effector protein YopJ. Recently, YopJ-mediated pyroptosis, which proceeds via the NLRP3-inflammasome, was shown to be regulated by a second T3SS effector protein YopK in the related strain Y. pseudotuberculosis. In this work, we show that for Y. pestis, YopK appears to regulate YopJ-mediated apoptosis, rather than pyroptosis, of macrophages. Inhibition of caspase-8 blocked YopK-dependent apoptosis, suggesting the involvement of the extrinsic pathway, and appeared cell-type specific. However, in contrast to yopJ, deletion of yopK caused a large decrease in virulence in a mouse pneumonic plague model. YopK-dependent modulation of macrophage apoptosis was observed at 6 and 24 hours post-infection (HPI). When YopK was absent, decreased populations of macrophages and dendritic cells were seen in the lungs at 24 HPI and correlated with resolution rather than progression of inflammation. Together the data suggest that Y. pestis YopK may coordinate the inflammatory response during pneumonic plague through the regulation of apoptosis of immune cells.

INTRODUCTION:

Emergency departments are important safety nets for people who live in rural areas. Moreover, a serious problem in access to healthcare services has emerged in these regions. The challenges of providing access to quality rural emergency care include recruitment and retention issues, lack of advanced imagery technology, lack of specialist support and the heavy reliance on ambulance transport over great distances. The Quebec Ministry of Health and Social Services published a new version of the Emergency Department Management Guide, a document designed to improve the emergency department management and to humanise emergency department care and services. In particular, the Guide recommends solutions to problems that plague rural emergency departments. Unfortunately, no studies have evaluated the implementation of the proposed recommendations.

METHODS

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ANALYSIS:

To develop a comprehensive portrait of all rural emergency departments in Quebec, data will be gathered from databases at the Quebec Ministry of Health and Social Services, the Quebec Trauma Registry and from emergency departments and ambulance services managers. Statistics Canada data will be used to describe populations and rural regions. To evaluate the use of the 2006 Emergency Department Management Guide and the implementation of its various recommendations, an online survey and a phone interview will be administered to emergency department managers. Two online surveys will evaluate quality of work life among physicians and nurses working at rural emergency departments. Quality-of-care indicators will be collected from databases and patient medical files. Data will be analysed using statistical (descriptive and inferential) procedures. ETHICS AND DISSEMINATION: This protocol has been approved by the CSSS Alphonse-Desjardins research ethics committee (Project MP-HDL-1213-011). The results will be published in peer-reviewed scientific journals and presented at one or more scientific conferences.

Abstract Yersinia pestis can cause oropharyngeal plague as a result of consumption or handling of meat from infected animals. Thus, food naturally or intentionally contaminated can have a role in the dissemination of oropharyngeal plague. The growth of a conditionally virulent pYV-bearing rifampicin-resistant Y. pestis KIM5 (rif-Y. pestis KIM5) in retail raw ground pork (RGP) was studied at temperatures ranging from 4 to 30°C. At 4°C, rif-Y. pestis KIM5 did not grow but survived. In RGP, rif-Y. pestis KIM5 grew at refrigerated temperatures of 10 and 15°C with growth rates of 0.05 and 0.16 log10 colony-forming units (CFU)/h. The growth rates at abusive temperatures of 20, 25, and 30°C were 0.26, 0.30, and 0.77 log10 CFU/h. The growth rate was increased 15.4-fold with the increase of storage temperatures from 10°C to 30°C. The maximum population density ranged from 6.76 to 8.66 log10 CFU/g. Furthermore, there was no detectable loss of pYV in surviving rif-Y. pestis KIM5 at any of the temperatures tested in retail RGP. This suggests that under these conditions, Y. pestis could cause oropharyngeal plague if the meat was not properly cooked. The individual infected by Y. pestis in food is a potential reservoir who can infect others, leading to outbreaks of plague.