Send to

Choose Destination
See comment in PubMed Commons below
Infect Immun. 2010 Aug;78(8):3323-34. doi: 10.1128/IAI.00081-10. Epub 2010 May 3.

Characterization of the role of the pathogenicity island and vapG in the virulence of the intracellular actinomycete pathogen Rhodococcus equi.

Author information

Department of Infectious Diseases, University of Georgia, Athens, GA 30602, USA.


Rhodococcus equi, a facultative intracellular pathogen of macrophages, causes severe, life-threatening pneumonia in young foals and in people with underlying immune deficiencies. R. equi virulence is dependent on the presence of a large virulence plasmid that houses a pathogenicity island (PAI) encoding a novel family of surface-localized and secreted proteins of largely unknown function termed the virulence-associated proteins (VapACDEFGHI). To date, vapA and its positive regulators virR and orf8 are the only experimentally established virulence genes residing on the virulence plasmid. In this study, a PAI deletion mutant was constructed and, as anticipated, was attenuated for growth both in macrophages and in mice due to the absence of vapA expression. Expression of vapA in the PAI mutant from a constitutive promoter, thereby eliminating the requirement for the PAI-encoded vapA regulators, resulted in delayed bacterial clearance in vivo, yet full virulence was not restored, indicating that additional virulence genes are indeed located within the deleted pathogenicity island region. Based on previous reports demonstrating that the PAI-carried gene vapG is highly upregulated in macrophages and in the lungs of R. equi-infected foals, we hypothesized that vapG could be an important virulence factor. However, analysis of a marked vapG deletion mutant determined the gene to be dispensable for growth in macrophages and in vivo in mice.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center