SummaryFor many opportunistic pathogens, it is unclear why their virulence determinants and expression of pathogenic behavior have evolved when damage or death of their host offers no obvious selective advantage to microbial growth or survival [1–3]. Many pathogens initiate interactions with their host on mucosal surfaces and must compete with other members of the microflora for the same niche. Here we explore whether competitive interactions between microbes promote the acquisition of virulence characteristics. During model murine nasal colonization, Haemophilus influenzae outcompetes another member of the local flora, Streptococcus pneumoniae, by recruiting neutrophils and stimulating the killing of complement-opsonized pneumococci [4]. For S. pneumoniae, resistance to opsonophagocytic killing is determined by its polysaccharide capsule [5, 6]. Although there are many capsule types among different S. pneumoniae isolates that allow for efficient colonization, virulent pneumococci express capsules that confer resistance to opsonophagocytic clearance. Modeling of interspecies interaction predicts that these more virulent S. pneumoniae will prevail during competition with H. influenzae, even if production of a capsule is otherwise costly. Experimental colonization studies confirmed the increased survival of the more virulent S. pneumoniae type during competition. Our findings demonstrate that competition between microbes during their commensal state may underlie selection for characteristics that allow invasive disease.
Polymicrobial interactions on mucosal surfaces can influence inflammation, immunity, and disease outcome. Here, we review how host responses to colonization in the upper respiratory tract with the bacterial pathogen Streptococcus pneumoniae can be altered by co-infection. Recent advances provide a mechanistic understanding of how mucosal immunity can be subverted at distinct immunological time-points during pneumococcal colonization by other pathogens such as Haemophilus influenzae, influenza type A and Staphylococcus aureus. These examples use animal models of co-infection to highlight how otherwise effective host responses can be rendered ineffective by co-infection, and vice versa. The complex microbial ecology of mucosal sites must be considered to fully understand how immune responses in a natural setting influence the outcome of host-pathogen interactions.
BackgroundAntimicrobial resistance is under-documented and commensal Escherichia coli can be used as indicator organisms to study the resistance in the community. We sought to determine the prevalence of resistance to broad-spectrum antimicrobials with particular focus on the quinolones, which have recently been introduced in parts of Africa, including Ghana.ResultsForty (13.7%) of 293 E. coli isolates evaluated were nalidixic acid-resistant. Thirteen (52%) of 2006 and 2007 isolates and 10 (66.7%) of 2008 isolates were also resistant to ciprofloxacin. All but one of the quinolone-resistant isolates were resistant to three or more other antimicrobial classes. Sequencing the quinolone-resistance determining regions of gyrA and parC, which encode quinolone targets, revealed that 28 quinolone-resistant E. coli harboured a substitution at position 83 of the gyrA gene product and 20 of these isolates had other gyrA and/or parC substitutions. Horizontally-acquired quinolone-resistance genes qnrB1, qnrB2, qnrS1 or qepA were detected in 12 of the isolates. In spite of considerable overall diversity among E. coli from Ghana, as evaluated by multilocus sequence typing, 15 quinolone-resistant E. coli belonged to sequence type complex 10. Five of these isolates carried qnrS1 alleles.ConclusionsQuinolone-resistant E. coli are commonly present in the faecal flora of Accra residents. The isolates have evolved resistance through multiple mechanisms and belong to very few lineages, suggesting clonal expansion. Containment strategies to limit the spread of quinolone-resistant E. coli need to be deployed to conserve quinolone effectiveness and promote alternatives to their use.
Many early-career researchers are involved in the peer review of manuscripts for scientific journals, typically under the guidance of or jointly with their advisor, but most of the evidence about this activity is anecdotal. Here we report the results of a literature review and a survey of researchers, with an emphasis on co-reviewing and 'ghostwriting'. The literature review identified 36 articles that addressed the involvement of early-career researchers in peer review, most of them about early-career researchers and their advisors co-reviewing manuscripts for the purposes of training: none of them addressed the topic of ghostwriting in detail. About three quarters of the respondents to the survey had co-reviewed a manuscript. Most respondents believe co-reviewing to be a beneficial (95%) and ethical (73%) form of training in peer review. About half of the respondents have ghostwritten a peer review report, despite 81% responding that ghostwriting is unethical and 82% agreeing that identifying co-reviewers to the journal is valuable. Peer review would benefit from changes in both journal policies and lab practices that encourage mentored co-review and discourage ghostwriting.
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