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      Small colony variants: a pathogenic form of bacteria that facilitates persistent and recurrent infections.

      Nature reviews. Microbiology

      genetics, Aminoglycosides, enzymology, Staphylococcus aureus, Phenotype, Humans, Genetic Variation, physiopathology, microbiology, drug therapy, Bacterial Infections, pathogenicity, drug effects, Bacteria, Animals, pharmacology

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          Abstract

          Small colony variants constitute a slow-growing subpopulation of bacteria with distinctive phenotypic and pathogenic traits. Phenotypically, small colony variants have a slow growth rate, atypical colony morphology and unusual biochemical characteristics, making them a challenge for clinical microbiologists to identify. Clinically, small colony variants are better able to persist in mammalian cells and are less susceptible to antibiotics than their wild-type counterparts, and can cause latent or recurrent infections on emergence from the protective environment of the host cell. This Review covers the phenotypic, genetic and clinical picture associated with small colony variants, with an emphasis on staphylococci, for which the greatest amount of information is available.

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          Most cited references 85

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          A site-directed Staphylococcus aureus hemB mutant is a small-colony variant which persists intracellularly.

          Although small-colony variants (SCVs) of Staphylococcus aureus have been recognized for many years, this phenotype has only recently been related to persistent and recurrent infections. Clinical S. aureus SCVs are frequently auxotrophic for menadione or hemin, two compounds involved in the biosynthesis of the electron transport chain elements menaquinone and cytochromes, respectively. While this observation as well as other biochemical characteristics of SCVs suggests a link between electron-transport-defective strains and persistent infections, the strains examined thus far have been genetically undefined SCVs. Therefore, we generated a stable mutant in electron transport by interrupting one of the hemin biosynthetic genes, hemB, in S. aureus by inserting an ermB cassette into hemB. We isolated a hemB mutant, due to homologous recombination, by growth at a nonpermissive temperature and selection for erythromycin resistance. This mutant showed typical characteristics of clinical SCVs, such as slow growth, decreased pigment formation, low coagulase activity, reduced hemolytic activity, and resistance to aminoglycosides. Additionally, the mutant was able to persist within cultured endothelial cells due to decreased alpha-toxin production. Northern and Western blot analyses showed that expression of alpha-toxin and that of protein A were markedly reduced, at both the mRNA and the protein level. The SCV phenotype of the hemB mutant was reversed by growth with hemin or by complementation with intact hemB. Hence, a defect in the electron transport system allows S. aureus SCVs to resist aminoglycosides and persist intracellularly.
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            Highly adherent small-colony variants of Pseudomonas aeruginosa in cystic fibrosis lung infection.

            Pseudomonas aeruginosa, an opportunistic human pathogen and ubiquitous environmental bacterium, is capable of forming specialized bacterial communities, referred to as biofilm. The results of this study demonstrate that the unique environment of the cystic fibrosis (CF) lung seems to select for a subgroup of autoaggregative and hyperpiliated P. aeruginosa small-colony variants (SCVs). These morphotypes showed increased fitness under stationary growth conditions in comparison with clonal wild-types and fast-growing revertants isolated from the SCV population in vitro. In accordance with the SCVs being hyperpiliated, they exhibited increased twitching motility and capacity for biofilm formation. In addition, the SCVs attached strongly to the pneumocytic cell line A549. The emergence of these highly adherent SCVs within the CF lung might play a key role in the pathogenesis of P. aeruginosa lung infection, where a biofilm mode of growth is thought to be responsible for persistent infection.
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              Persistent infection with small colony variant strains of Staphylococcus aureus in patients with cystic fibrosis.

              In a 34-month prospective study to determine the prevalence of Staphylococcus aureus small colony variants (SCVs) in cystic fibrosis (CF) patients, S. aureus SCVs or SCVs plus normal S. aureus were recovered from 26 of 78 patients; 27 patients harbored only normal S. aureus. By pulsed-field gel electrophoresis, clonal identity was demonstrated of SCV and normal strains isolated at the same time and of multiple S. aureus SCV and normal strains in consecutive specimens from individual patients. All S. aureus SCVs were resistant to antifolate antibiotics, while the corresponding parent strains were susceptible, and in 11 of 12 SCV/normal pairs, gentamicin was less active against S. aureus with the SCV phenotype than against the normal isolate. Analysis of the underlying auxotrophism of SCVs revealed hemin, thymidine, and/or menadione dependencies. Thus, S. aureus SCVs are highly prevalent in respiratory secretions of CF patients, persist over extended periods, and may contribute to S. aureus persistence in CF patients.
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                Author and article information

                Journal
                10.1038/nrmicro1384
                16541137

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