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Open Access Highly Accessed Research article

A global view of Staphylococcus aureus whole genome expression upon internalization in human epithelial cells

Christian Garzoni, Patrice Francois*, Antoine Huyghe, Sabine Couzinet, Caroline Tapparel, Yvan Charbonnier, Adriana Renzoni, Sacha Lucchini, Daniel P Lew, Pierre Vaudaux, William L Kelley and Jacques Schrenzel

BMC Genomics 2007, 8:171  doi:10.1186/1471-2164-8-171

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Antibiotic resistance

Gavin Koh   (2007-08-09 11:44)  Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand email

The two most common strains of MRSA endemic to UK hospitals are EMRSA-15 and EMRSA-16 (Johnson et al., 2001). EMRSA-16 is particularly well studied because of its success as a nosocomial pathogen (synonymous with ST36:USA200 in the US, and MRSA252 under the international typing scheme) (Holden et al., 2004). It is interesting to note that despite the fact that these two strains arose indepedently, they share the same pattern of resistance to antibiotics (they are both resistant to penicillin, erythromycin and ciprofloxacin), whereas other less successful strains that occasionally appear possess sensitivity patterns that are far less predictable. On the other hand, these two strains have not been as successful in the community. Of note, a similar pattern of antibiotic resistance has been found in US nosocomial isolates (LaPlante et al., 2007).

The persistence of erythromycin resistance in a nosocomial strain may perhaps be explained by the fact that erythromycin is commonly used in intensive care setting as a gut motility agent; the acquisition of resistance to ciprofloxacin may likewise possibly be attributed to the overuse of fluoroquinolones in the healthcare setting. It is not clear, however, that over use of macrolides or fluoroquinolones occurs any less frequently in the community. Even more interesting is the fact that the original EMRSA-16 strain that emerged in Kettering in 1992 was gentamicin-resistant, and that over the following two years after its identification gentamicin resistance was lost from the majority of EMRSA-16 isolates (Murchan et al., 2004).

This paper by Garzoni et al. suggests that an additional factor may also be at play. Erythromycin and ciprofloxacin are both effective against intracellular pathogens, whereas gentamicin is not (indeed, gentamicin was used in this study as part of the protocol to eliminate extracellular bacteria, while preserving intracellular bacteria). The success of MRSA strains with this specific antibiogram may perhaps be explained by its importance in enabling Staphylococcus aureus to exploit an intracellular niche in an environment where there is heavy antibiotic use.

Johnson AP, Aucken HM, Cavendish S, et al. (2001). "Dominance of EMRSA-15 and -16 among MRSA causing nosocomial bacteraemia in the UK: analysis of isolates from the European Antimicrobial Resistance Surveillance System (EARSS)". J Antimicrob Chemother 48: 143-4.

Holden MTG, Feil EJ, Lindsay JA, et al. (2004). "Complete genomes of two clinical Staphylococcus aureus strains: Evidence for the rapid evolution of virulence and drug resistance". Proc Natl Acad Sci U S A 101: 9786–91.

Murchan S, Aucken HM, O’Neill GL, Ganner M, Cookson BD. (2004). "Emergence, Spread, and Characterization of Phage Variants of Epidemic Methicillin-Resistant Staphylococcus aureus 16 in England and Wales". J Clin Microbiol 42: 5154–60.

LaPlante KL, Rybak MJ, Amjad M, Kaatz GW (2007). Antimicrobial susceptibility and staphylococcal chromosomal cassette mec type in community- and hospital-associated methicillin-resistant Staphylococcus aureus. Pharmacotherapy 27: 3-10.

Competing interests

None declared.

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