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In the mid-1800s, Louis Pasteur and Robert Koch first observed and cultured staphylococci, the bacterial ?bad boys,? causing numerous life-threatening infections. Staphylococci?gram-positive nonmobile cocci that divide in irregular grape-like clusters?are facultative anaerobes, but they prefer aerobic conditions. Two are common: Staphylococcus epidermidis, which normally colonizes skin and mucous membranes, and S aureus (so called because of its yellow-to-orange colony pigment1), which normally colonizes human nares and perineum and can cause disease.2 Less common causes of foreign-body infections, bacteremia, endocarditis, bone infections, and organ abscesses are S epidermidis, S saprophyticus, S lugdunensis, and S schleiferi. S aureus? invasive character is partially the result of a loose-fitting polysaccharide capsule that may impede phagocytosis.
In 1946, penicillin became a viable weapon against S aureus, but resistance developed rapidly because of this organism?s ability to produce beta-lactamase. In the early 1960s, discovery of methicillin gave new hope.3 Subsequently, other semisynthetic penicillins and better infection-control measures slowed S aureus? epidemic spread. Soon, however, methicillin-resistant S aureus (MRSA) appeared.
Where Infection Starts
Neonates are susceptible to S epidermidis and S aureus colonization. S aureus may start in the umbilical area and move into the nose.4,5 With age, some people become permanent carriers. S aureus may spread to close contacts, but established nasal flora usually prevents acquisition of new strains.6 Unfortunately, antibiotic treatment may eliminate that protection and allow other strains to colonize.
Up to 40% of community-dwelling people carry S aureus in their nares. Hospital patients and personnel have higher carriage rates. Carriers who are dispersers spread staphylococci on clothes and bedding and by airborne transmission. Dust particles containing staphylococci may travel considerable distances.
Hemodialysis patients, diabetics, drug addicts, and patients with various dermatologic conditions are at highest risk.7,8 Postsurgically, carriers develop more infections than noncarriers.9
Prescribers controlled early MRSA epidemics with aminoglycosides. In the late 1970s, however, gentamicin resistance developed, and a new wave of hospital outbreaks started.10 Since then, MRSA strains have been reported globally,11 in both hospitals and communities.12 Today, nearly 40% of S aureus in the United States is MRSA. Globally, incidence varies widely.13 Patients at highest risk are described in Table 1. Person-to-person transmission of MRSA usually occurs via health care workers? hands.8
Staphylococcal infections often are intensely purulent. The infected area tends to encapsulate, leading to abscess formation.14 Table 2 describes several specific staphylococcal infections.15
Simple drainage usually is sufficient to address uncomplicated superficial and chronic staphylococcal lesions. Acute serious staphylococcal infections (eg, pneumonia or bacteremia) require immediate antibiotic therapy after antibiotic-susceptibility testing. Pending culture results, empiric treatment with a penicillinase-resistant penicillin or a cephalosporin is acceptable. Cell-wall-active antibiotics and aminoglycosides are synergistic when the organism is susceptible to both. Combinations of a beta-lactamase-stable semisynthetic penicillin and an aminoglycoside often are used for severe systemic infections, particularly in immunocompromised hosts. Clindamycin and rifampin possess good anti-staphylococcal activity. Some chronic or recurrent infections can be controlled with an oral penicillinase-resistant penicillin over months or years.
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