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Whole‐genome comparison of meticillin‐resistant Staphylococcus aureus CC22 SCC mec IV from people and their in‐contact pets
Author(s) -
Loeffler Anette,
McCarthy Alex,
Lloyd David H.,
Musilová Eva,
Pfeiffer Dirk U.,
Lindsay Jodi A.
Publication year - 2013
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/vde.12062
Subject(s) - mobile genetic elements , staphylococcus aureus , biology , gene , genome , microarray , host (biology) , microbiology and biotechnology , staphylococcal infections , genetics , medicine , bacteria , gene expression
Background Meticillin‐resistant Staphylococcus aureus ( MRSA ) infections remain important medical and veterinary challenges. The MRSA isolated from dogs and cats typically belong to dominant hospital‐associated clones, in the UK mostly EMRSA ‐15 ( CC 22 SCC mec IV ), suggesting original human‐to‐animal transmission. Nevertheless, little is known about host‐specific genetic variation within the same S. aureus lineage. Hypothesis/Objectives To identify host‐specific variation amongst MRSA CC 22 SCC mec IV by comparing isolates from pets with those from in‐contact humans using whole‐genome microarray. Methods Six pairs of MRSA CC 22 SCC mec IV from human carriers (owners and veterinary staff) and their respective infected in‐contact pets were compared using a 62‐strain whole‐genome S. aureus microarray ( SAM ‐62). The presence of putative host‐specific genes was subsequently determined in a larger number of human ( n = 47) and pet isolates ( n = 93) by PCR screening. Results Variation in mobile genetic elements ( MGE s) occurred frequently and appeared largely independent of host and in‐contact pair. A plasmid ( SAP 078A) encoding heavy‐metal resistance genes ( arsR , arsA , cadA , cadC , mco and copB ) was found in three of six human and none of six animal isolates. However, only two of four resistance genes were associated with human hosts ( P = 0.015 for arsA and cadA ). Conclusions and clinical importance The variation found amongst MGE s highlights that genetic adaptation in MRSA continues. However, host‐specific MGE s were not detected, which supports the hypothesis that pets may not be natural hosts of MRSA CC 22 and emphasizes that rigorous hygiene measures are critical to prevent contamination and infection of dogs and cats. The host specificity of individual heavy‐metal resistance genes warrants further investigation into different selection pressures in humans and animals.