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Cell. 2014 Aug 14;158(4):722-733. doi: 10.1016/j.cell.2014.06.045.

Phenotypic variation of Salmonella in host tissues delays eradication by antimicrobial chemotherapy.

Author information

1
Focal Area Infection Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland.
2
Focal Area Infection Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland; BASF SE, 67056 Ludwigshafen, Germany.
3
FACS Core Facility, Biozentrum, University of Basel, 4056 Basel, Switzerland.
4
Proteomics Core Facility, Biozentrum, University of Basel, 4056 Basel, Switzerland.
5
Focal Area Infection Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland. Electronic address: dirk.bumann@unibas.ch.

Abstract

Antibiotic therapy often fails to eliminate a fraction of transiently refractory bacteria, causing relapses and chronic infections. Multiple mechanisms can induce such persisters with high antimicrobial tolerance in vitro, but their in vivo relevance remains unclear. Using a fluorescent growth rate reporter, we detected extensive phenotypic variation of Salmonella in host tissues. This included slow-growing subsets as well as well-nourished fast-growing subsets driving disease progression. Monitoring of Salmonella growth and survival during chemotherapy revealed that antibiotic killing correlated with single-cell division rates. Nondividing Salmonella survived best but were rare, limiting their impact. Instead, most survivors originated from abundant moderately growing, partially tolerant Salmonella. These data demonstrate that host tissues diversify pathogen physiology, with major consequences for disease progression and control.

PMID:
25126781
DOI:
10.1016/j.cell.2014.06.045
[Indexed for MEDLINE]
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