cfr-mediated, linezolid-resistant MRSA outbreak
Investigators from Madrid report in CID a 15-patient outbreak during April to June 2008 caused by linezolid-resistant MRSA. As if the outbreak wasn't scary enough, they report that it's mediated through a new mechanism, the cfr gene. Since linezolid is a synthetic antibiotic with no analog in nature, linezolid resistance was thought to be rare and only result when a point mutation occurred at the drug target site. These investigators report that all strains in this outbreak lacked the point mutation but rather each had the cfr gene.
The cfr gene is naturally occurring in bovine staphylococci and mediates resistance to chloramphenicol, florfenicol and clindamycin. It has also been found in porcine isolates. In animals the gene is found on plasmids and is thought to be transferable between staphylococci; there is a suggestion that in human strains, while it is chromosomal it is likely on an integrated plasmid capable of excision/mobilization/transmission to other pathogens and could spread quickly.
It's possible that this type of resistance will be more difficult to control since the gene can hop aboard non-pathogenic species that we don't screen for, like coagulase-negative Staph, evade our detection and spread resistance to otherwise linezolid-sensitive strains, be they MSSA or MRSA. In addition, this type of transmission, of genes not bacteria, may be the Achilles' heal for antimicrobial use in livestock. If you are going to argue that pig strains are different from human strains as a reason to allow antimicrobials in animals, this argument doesn't seem to hold water if it's the genes that spread and lead to resistance. I take that back. It may not be an Achilles heal but rather a Trojan Horse.
The cfr gene is naturally occurring in bovine staphylococci and mediates resistance to chloramphenicol, florfenicol and clindamycin. It has also been found in porcine isolates. In animals the gene is found on plasmids and is thought to be transferable between staphylococci; there is a suggestion that in human strains, while it is chromosomal it is likely on an integrated plasmid capable of excision/mobilization/transmission to other pathogens and could spread quickly.
It's possible that this type of resistance will be more difficult to control since the gene can hop aboard non-pathogenic species that we don't screen for, like coagulase-negative Staph, evade our detection and spread resistance to otherwise linezolid-sensitive strains, be they MSSA or MRSA. In addition, this type of transmission, of genes not bacteria, may be the Achilles' heal for antimicrobial use in livestock. If you are going to argue that pig strains are different from human strains as a reason to allow antimicrobials in animals, this argument doesn't seem to hold water if it's the genes that spread and lead to resistance. I take that back. It may not be an Achilles heal but rather a Trojan Horse.
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