Staphylococcus Aureus Pneumonia: Emergence of MRSA in the Community

Suzanne F. Bradley, MD


Semin Respir Crit Care Med. 2005;26(6):643-649. 

In This Article

How Does CA-MRSA Differ from HA-MRSA? Clues from the Laboratory

All MRSA are characterized genotypically by the presence of mecA, which encodes for altered penicillin binding proteins (PBPs) (PBP2A) on their cell walls. The low affinity binding of PBP2A to antistaphylococcal penicillins results phenotypically in resistance to all β-lactam antibiotics.[8] It is possible that MRSA arose when mecA was transferred from coagulase-negative staphylococci on a mobile genetic element termed SCCmec and incorporated into the chromosome of a methicillin-susceptible S. aureus (MSSA) strain by recombination.[2,8,9,10]

There are at least five types of SCCmec now identified that may carry genes in addition to mec required for recombination [cassette chromosome recombinase (ccr)], antibiotic resistance, and virulence factors.[2,8,9] HA-MRSA has been associated with SCCmec types I to III. These HA-MRSA SCCmec types may contain resistance elements for numerous antibiotic classes, including macrolides, lincosamides, aminoglycosides, fluoroquinolones, tetracyclines, and sulfonamides. These health care-associated SCCmec types are so large that they cannot be incorporated into a phage, or they lack the genes required for recombination. It has been suggested that these large genetic elements may actually impair the growth and fitness of HA-MRSA to the point where they might not survive without the selective pressure of antibiotics. Perhaps as a result, the spread of mecA throughout S. aureus has been inefficient with only five phylogenetically distinct MRSA lineages worldwide.[3,8,9,10]

In contrast, CA-MRSA is characterized by the presence of SCCmecIV, and more recently SCCmecV.[2,8,9] SCCmecIV has been present in coagulase-negative staphylococci since the 1970s but was not found in S. aureus until decades later.[2] Discovery of recent clusters of severe MSSA and MRSA infection with identical pulsed gel electrophoresis (PFGE) types suggests that insertion SCCmecIV might have occurred in highly virulent MSSA strains.[9,10]

SCCmecIV from CA-MRSA contains primarily mecA, ccr, and on some occasions, genes that encode for various toxins. SCCmecIV is small enough that efficient transfer by phage or transposon into MSSA is possible. In addition to the increased efficiency of transfer of a smaller cassette, CA-MRSA has been associated with more rapid growth rates than HA-MRSA, which may confer some survival advantage that might facilitate spread of these organisms. As a result, there is the potential that the horizontal transfer of SCCmecIV from CA-MRSA to multiple MSSA clones could occur efficiently with the potential for rapid dissemination worldwide.[8,9] Outbreaks of CA-MRSA have been associated primarily with PFGE strains types USA400 and USA300 and multiple locus sequence typing (MLST) types ST1 and ST8 in the United States; ST80 and ST30 have been found in Europe.[2,9,11,12]


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