Chapter 129. Staphylococcal Infections (Part 2)

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S. aureus Infections Epidemiology S. aureus is a part of the normal human flora; ~25–50% of healthy persons may be persistently or transiently colonized. The rate of colonization is higher among insulin-dependent diabetics, HIV-infected patients, patients undergoing hemodialysis, and individuals with skin damage. The anterior nares are the most frequent site of human colonization, although the skin (especially when damaged), vagina, axilla, perineum, and oropharynx may also be colonized. These colonization sites serve as a reservoir of strains for future infections, and persons colonized with S. aureus are at greater risk of subsequent infection than are uncolonized individuals. ...

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Chapter 129. Staphylococcal Infections (Part 2) S. aureus Infections Epidemiology S. aureus is a part of the normal human flora; ~25–50% of healthy persons may be persistently or transiently colonized. The rate of colonization is higher among insulin-dependent diabetics, HIV-infected patients, patients undergoing hemodialysis, and individuals with skin damage. The anterior nares are the most frequent site of human colonization, although the skin (especially when damaged), vagina, axilla, perineum, and oropharynx may also be colonized. These colonization sites serve as a reservoir of strains for future infections, and persons colonized with S. aureus are at greater risk of subsequent infection than are uncolonized individuals. Overall, S. aureus is a leading cause of nosocomial infections. It is the most common cause of surgical wound infections and is second only to CoNS as a
cause of primary bacteremia. Increasingly, nosocomial isolates are resistant to multiple drugs. In the community, S. aureus remains an important cause of skin and soft tissue infections, respiratory infections, and (among injection drug users) infective endocarditis. The increasing prevalence of home infusion therapy is another cause of community-acquired staphylococcal infections. Most individuals who develop S. aureus infections are infected with their own colonizing strains. However, S. aureus may also be acquired from other people or from environmental exposures. Transmission most frequently results from transient colonization of the hands of hospital personnel, who then transfer strains from one patient to another. Spread of staphylococci in aerosols of respiratory or nasal secretions from heavily colonized individuals has also been reported. In the past 10 years, numerous outbreaks of community-based infection caused by methicillin-resistant S. aureus (MRSA) in individuals with no prior medical exposure have been reported. These outbreaks have taken place in both rural and urban settings in widely separated regions throughout the world. The reports document a dramatic change in the epidemiology of MRSA infections. The outbreaks have occurred among such diverse groups as prisoners, athletes, Native Americans, and drug users. Risk factors common to these outbreaks include poor hygienic conditions, close contact, contaminated material, and damaged skin. The community-associated infections have been caused by a limited number of MRSA
strains. In the United States, strain USA300 has been the predominant clone and is also responsible for an increasing number of nosocomial infections. Of concern has been the apparent capacity of community-acquired MRSA strains to cause serious disease in immunocompetent individuals. This ability may be due to the presence of different toxin-producing genes in these strains. Pathogenesis General Concepts S. aureus is a pyogenic pathogen known for its capacity to induce abscess formation at sites of both local and metastatic infections. This classic pathologic response to S. aureus defines the framework within which the infection will progress. The bacteria elicit an inflammatory response characterized by an initial intense polymorphonuclear leukocyte (PMN) response and the subsequent infiltration of macrophages and fibroblasts. Either the host cellular response (including the deposition of fibrin and collagen) contains the infection, or infection spreads to the adjoining tissue or the bloodstream. In toxin-mediated staphylococcal disease, infection is not invariably present. For example, once toxin has been elaborated into food, staphylococcal food poisoning can develop in the absence of viable bacteria. In staphylococcal toxic shock syndrome (TSS), conditions allowing toxin elaboration at colonization
sites (e.g., the presence of a superabsorbent tampon) suffice for initiation of clinical illness. The S. aureus Genome The entire genome has been sequenced for numerous strains of S. aureus. Among the interesting revelations are (1) a high degree of nucleotide sequence similarity among the different strains; (2) acquisition of a relatively large amount of genetic information by horizontal transfer from other bacterial species; and (3) the presence of unique "pathogenicity" or "genomic" islands—mobile genetic elements that contain clusters of enterotoxin and exotoxin genes or antimicrobial resistance determinants. Among the genes in these islands are those carrying mecA, the gene responsible for methicillin resistance. Methicillin resistance– containing islands have been designated staphylococcal cassette chromosome mecs (SCCmecs) and range in size from ~20 to 60 kb. To date, five SCCmecs have been identified. Type 4 and type 5 SCCmecs have been associated with community-acquired MRSA strains. A limited number of MRSA clones have been responsible for most community and hospital-associated infections worldwide. A comparison of these strains with those from earlier outbreaks (e.g., the phage 80/81 strains from the 1950s) has revealed preservation of the nucleotide sequence over time. This
observation suggests that these strains possess determinants facilitating survival and spread.