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Review Article

Molecular characterization of Staphylococcus aureus isolates derived from severe pneumonia: a retrospective monocentre study

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Pages 811-819 | Received 03 May 2021, Accepted 28 Jul 2021, Published online: 12 Aug 2021
 

Abstract

Background

Staphylococcus aureus is endowed with a repertoire of virulence factors potentially implicated in its pathogenicity and ability to cause invasive disease. The main objective of this study was to describe the bacterial genotype, including virulence genes and affiliation to clonal complexes (CCs), encountered in severe pneumonia.

Methods

DNA microarray was used to analyse 18 S. aureus isolates from patients hospitalized with severe pneumonia between 2017 and 2019.

Results

Among 18 S. aureus isolates, 14 were methicillin-susceptible S. aureus (MSSA), and 4 methicillin-resistant S. aureus (MRSA). There were 14 community-acquired, 3 healthcare-associated, and 1 hospital-acquired infections. Different radiological presentations were observed: necrotizing pneumonia (n = 8, 44%), alveolar consolidation (n = 7, 39%), alveolar-interstitial infiltrates (n = 3, 17%). Sixteen patients (89%) required ICU hospitalization, 13 (72%) an invasive mechanical ventilation, and 12 (67%) a vasopressor support. Mortality affected 6 patients (33%). Panton–Valentine leukocidin (PVL), staphylococcal enterotoxins, toxic shock syndrome toxine-1 (TSST-1) encoding genes were documented in nine (50%), 12 (67%), one (6%) of the isolates, respectively. Accessory regulator gene group I was the most reported (n = 9, 50%) and was found in five deaths. The majority of isolates were affiliated to CC152 (n = 6), followed by CC15 (n = 3), CC45 (n = 2), CC30 (n = 2), CC1 (n = 2), CC8 (n = 1), CC9 (n = 1), and CC25 (n = 1). All the CC152 isolates were PVL-positive.

Conclusion

CC152-PVL positive S. aureus strains were the most prevalent in severe pneumonia. Other virulence gene profiles were found coupled to additional clonal lineages. A genotyping strategy contributes to describe the current circulating strains and bacterial genetic backgrounds.

Acknowledgements

The authors thank the National Reference Center for Staphylococci, Lyon, France, for technical assistance with the microarrays.

Disclosure statement

No potential conflict of interest was reported by the author(s).

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