Volume 71, Issue 3, August 2014

The role of a protease secreted by the Chlamydia containing vacuole in processing proteins of human cells has been questioned. Here we further examine whether this protease is actually secreted.

This review summarises the recent advances in the study of Acinetobacter baumannii pathogenesis, with a particular focus on evolutionary and genomic aspects, and proposes new avenues of research.

Type IV pilins of Clostridium difficile: We describe nine type IV pilins or pilin-like proteins identified in the genome of C. difficile. These proteins have relatively conserved N terminal regions, but diverge at the C termini. Analysis of synonymous and nonsynonymous substitutions indicates two pilin proteins contain codons under positive selection. Immunization of mice with six of the pilins resulted in generation of antibodies with varying titer and crossreactivity.

HspX, a protein induced during chronic Mycobacterium tuberculosis infection, is studied as a vaccine candidate and virulence determinant in a relevant model of tuberculosis.

Several toxin–antitoxin modules contribute to persistence in Burkholderia cenocepacia J2315; this contribution depends on the mode of growth and the antibiotic used.

The identification of mutants in a key virulence protease in Chlamydia helps clarify the role that this protease plays in manipulating host cellular functions.

Rhodococcus equi (‘Prescottella equi’) is a pathogenic actinomycete primarily infecting horses but has emerged as an opportunistic human pathogen. We have sequenced the genome of the type strain of this species, R. equi strain C7^T, and compared the genome with that of another foal isolate 103S and of a human isolate ATCC 33707. The R. equi strains are closely related to each other and yet distantly related to other rhodococci and actinomycetes. The comparison of gene contents among R. equi strains revealed minor differences that could be associated with host adaptation from foals to humans.

Demonstration that TLR2 and TLR4 mediate the TNFα response to Vibrio vulnificus may enable the development of novel strategies to block harmful TLR signaling as an adjunct to antibiotic treatment.