Articles of Significant Interest Selected from This Issue by the Editors

doi:10.1128/IAI.01661-07

DOI: 10.1128/IAI.01661-07

Asymptomatic Bacteriuria Provides Insights into Mechanisms of Commensalism

Escherichia coli, the major cause of urinary tract infections, may also cause asymptomatic bacteriuria (ABU), i.e., a carrier state without causing symptoms. This resembles a state of commensalism with a bacterial monoculture rather than a complex flora. Accordingly, ABU is an interesting model to study mechanisms of commensalism and driving forces in the pathogen and the host. Geno- and phenotypic analyses of ABU isolates by Zdziarski et al. (p. 695-703) show that many ABU strains arise from virulent variants by gene loss while others are nonvirulent. Attenuation may constitute a general mechanism for mucosal pathogens to evolve towards commensalism.

Discovery of Virulence Determinants in Rickettsia rickettsii

Rickettsia rickettsii is the etiologic agent of Rocky Mountain spotted fever, the most severe disease caused by the spotted fever group of rickettsia. Little is known regarding what imparts virulence to the pathogenic strains of rickettsiae. Ellison et al. (p. 542-550) determined the genomic sequence of an avirulent strain of R. rickettsii and compared it to that of a virulent strain. Although the genomes share a high degree of identity, several distinctions were observed, including the deletion of a major surface protein, the rickettsial outer membrane protein A (rOmpA), from the avirulent strain. Infection of guinea pigs with the avirulent strain conferred protection against the virulent strain.

Invasion of the Mammalian Bloodstream by Bartonella quintana Requires a Family of Autotransporter Adhesins

Bartonella quintana invades the human bloodstream, binds erythrocytes, and then persists for months. B. quintana variably expressed outer membrane protein (Vomp) autotransporter adhesins are candidate virulence proteins in this process. Vomps confer virulence phenotypes in vitro, but characterization has been hampered by the lack of tools to accomplish allelic replacement in a wild-type background. MacKichan et al. (p. 788-795) describe a method for generating in-frame deletions in wild-type Bartonella. Using a recently developed macaque animal model, they then demonstrate that the isogenic vomp null mutant is avirulent and incapable of bloodstream infection. These new tools will facilitate study of the Vomps and other virulence factors of Bartonella.

Friendly Fire: Human Plasminogen Coating of Streptococcus pneumoniae through Interaction with Choline-Binding Protein E Facilitates Migration across the Extracellular Matrix

Bacterial virulence often requires the surface recruitment of host proteins. Attali et al. (p. 466-476) present evidence defining the phosphorylcholine esterase domain of the choline-binding protein E (CBPE) of Streptococcus pneumoniae as a receptor for human plasminogen, the precursor of the plasmin protease. The biological relevance of the CBPE-plasminogen interaction is supported by the fact that a pneumococcus with a deletion of the cbpE gene displays a reduced level of plasminogen binding and activation into plasmin as well as a reduced ability to cross an in vitro model of the extracellular matrix. This work supports a physiological role for the CBPE-plasminogen interaction in pneumococcal dissemination into the human host.