ABSTRACT
Staphylococci are gram-positive cocci that grow in grape-like clusters and produce the enzyme catalase. Many species are members of the endogenous microbiota of the skin and mucous membranes of the gastrointestinal (GI) and genitourinary tracts of humans. The anterior nares are the reservoir of S. aureus. As many as one-third of the US population are colonized in the anterior nares by this organism. From this site, it is readily transferred to the hands. S. aureus is easily transferred horizontally (person to person) by direct contact (bacteria on the hands) or by contact with fomites (inanimate objects) such as bed linen, and medical instruments. It’s extensively cross-linked cell wall renders it very resistant to drying. S. aureus is unique among staphylococci because it produces a cell-associated and secreted coagulase, which converts fibrinogen to fibrin and it expresses protein A on its surface, which binds the Fc region of human IgG. S. aureus (and other species of staphylococci) produce an extracellular polysaccharide capsule or slime that enables them to form a biofilm on catheters and other prostheses. S. aureus requires a breach in the skin or mucosa such as produced by a catheter, a surgical incision, a burn, a traumatic wound, ulceration or viral skin lesions to facilitate its entry into the tissues. S. aureus has several enzymes that aid in invasion of the barrier epithelia and serve as spreading factors. Intact barrier epithelia, together with innate immune factors at these surfaces, are effective in preventing invasion of S. aureus. If S. aureus breaches the epithelial barrier, the bacteria are phagocytosed by neutrophils but have various mechanisms to resist phagocytosis and intracellular killing. S. aureus is a versatile pathogen that causes a wide range of infections from superficial skin lesions to serious systemic infections. S. aureus is readily identified by its Gram-stain morphology, production of catalase and coagulase. Prevention of staphylococcal infection relies on the practice of good hygiene. The infectious dose of S. aureus required to initiate a wound infection in a healthy person is high unless the wound contains a foreign body of some sort. In the hospital setting, attempts have been made to eliminate nasal carriage of S. aureus by hospital personnel by the use of antibiotic regimens. Intravascular devices, such as catheters, should be promptly removed if infection is suspected. Abscesses must be drained and, usually, if the infection involves a prosthetic joint, it should be removed. Antibiotic therapy is problematic for staphylococcal infections because of broad antibiotic resistance. Currently, less than 10% of staphylococcal isolates are susceptible to penicillin. About half of S. aureus and CNS isolates are resistant to semi-synthetic penicillins (methicillin, nafcillin, oxacillin) that are resistant to β-lactam ring hydrolysis. Methicillin-resistant S. aureus are termed MRSA. In MRSA, the gene mecA encodes the protein PBP2A (penicillin-binding protein 2A), a transpeptidase involved in the assembly of the cell wall. Serious infections with methicillin-sensitive S. aureus (MSSA) infections are treated with parenteral penicillinase-resistant penicillins or first- or second-generation cephalosporins with clindamycin. Vancomycin is reserved for staphylococcal strains that are resistant to penicillinase-resistant penicillins and clindamycin. Mupirocin may be used to treat superficial or localized skin infections caused by S. aureus. Low-level resistance to vancomycin, an antibiotic to which staphylococci had been uniformly sensitive, has been recognized.
