Key result
The S. aureus mutator phenotype was associated with decreased in vivo fitness and did not significantly increase the acquisition of rifampicin resistance compared to wild-type (12.5% vs 0%; P=0.4).
Why the study?
Does hypermutability in S. aureus affect bacterial fitness and emergence of antibiotic resistance in a rat model of chronic bone infection?
Does hypermutability in S. aureus affect bacterial fitness and emergence of antibiotic resistance in a rat model of chronic bone infection?
Absolute Event Rate: 12.5% vs 0%
p-value: p=0.4
In a rat model of chronic bone infection, the S. aureus mutator phenotype was associated with decreased in vivo fitness and did not confer a significant advantage in acquiring antibiotic resistance.
Mutator S. aureus shows reduced fitness without resistance advantage in rat osteomyelitis; hypothesis-generating and leaves open human relevance.
This study was designed to investigate the role of hypermutability of Staphylococcus aureus on bacterial fitness and antibiotic resistance in a model of chronic bone infection. An isogenic pair of strains, S. aureus RN4220 and its mutator counterpart inactivated in the mutL gene were used in a rat model of osteomyelitis of the tibia. The effect of the mutator phenotype in the emergence of antibiotic resistance was assessed in rats infected by each strain separately and treated with rifampicin for 5 days. No difference between the two strains was found in bacterial growth in vitro and in bacterial survival in the animal model, indicating no fitness defect in the mutator strain. In competition studies performed in rats coinfected with the two strains at a same ratio and sacrificed at different times from day 3 to day 42 postinoculation, the mutator strain was clearly disadvantaged because it was found in all rats and at all study times at lower counts (P<0.05 from day 14 to day 42). Two of the 16 rats infected by the mutator strain and none of the 14 rats infected by the wild-type strain had acquired rifampicin-resistant mutants (P=0.4). Data suggest that the S. aureus mutator phenotype was associated with a decreased bacterial fitness in vivo and did not confer significant advantage in the acquisition of antibiotic resistance in a model of chronic bone infection.
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Daurel et al. (2007) studied Osteomyelitis due to Staphylococcus aureus (n=30). S. aureus mutator phenotype (inactivated mutL gene) vs. Wild-type S. aureus RN4220 was evaluated on Acquisition of rifampicin-resistant mutants (p=0.4). The S. aureus mutator phenotype was associated with decreased in vivo fitness and did not significantly increase the acquisition of rifampicin resistance compared to wild-type (12.5% vs 0%; P=0.4).
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