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Staphylococci 

Staphylococci

Chapter:
Staphylococci
Author(s):

Bala Hota

, Kyle J. Popovich

, and Robert A. Weinstein

DOI:
10.1093/med/9780199204854.003.070604_update_006

Update:

Pathogenesis – genome sequencing can identify toxins associated with worse clinical outcomes.

Prevention – discussion of factors associated with recent decline in incidence of hospital-onset S. aureus bacteremias.

Treatment – discussion of (1) early modification of therapy if blood cultures fail to clear rapidly; (2) a new antibiotic, tedizolid; (3) recent study comparing 6 vs 12 weeks of therapy for pyogenic vertebral osteomyelitis.

Updated on 30 Jul 2015. The previous version of this content can be found here.
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date: 30 March 2017

Staphylococci are Gram-positive cocci that form clusters, but can occur singly, in pairs, chains, or tetrads. They are classically distinguished from other Gram-positive cocci by presence of catalase, an enzyme that degrades hydrogen peroxide (H2O2). S. aureus is distinguished from other coagulase-negative staphylococci, which are generally less virulent, by the presence of coagulase, an enzyme that coagulates plasma. Many toxins and regulatory elements enhance virulence in staphylococci.

Epidemiology

Colonization—staphylococci are skin commensals. About 20% of adults are persistently colonized by S. aureus, 60% are intermittently colonized, and 20% are never colonized. High-risk groups for S. aureus colonization include infants, insulin-dependent diabetics, intravenous drug users, HIV-infected patients, and renal dialysis patients.

Methicillin-resistant S. aureus (MRSA)—risk factors for MRSA colonization and infection among hospitalized patients include antibiotic exposure, surgery, nursing-home residence, or high MRSA ‘colonization pressure’, i.e. frequent exposure to colonized or infected patients. However, MRSA is no longer only a hospital-related infection, with community-associated MRSA affecting individuals without health care exposures.

Clinical features

S. aureus infection—clinical syndromes can be divided into three groups: (1) Illness due to release of toxins, leading to disease at sites often remote from infection—including (a) staphylococcal scalded skin syndrome—release of epidermolytic toxins leads to bullae and desquamation; (b) food-borne illness due to preformed toxin—a heat-stable superantigen toxin produces sudden vomiting and diarrhoea; (c) toxic shock syndrome—superantigen toxins cause multisystem organ dysfunction; may be menstrual (e.g. tampon-associated) or nonmenstrual. (2) Illness due to local tissue destruction and abscess formation—including (a) impetigo, folliculitis, and cellulitis; (b) furuncles and carbuncles; (c) mastitis; (d) pyomyositis; (e) septic bursitis; (f) septic arthritis; (g) osteomyelitis; (h) epidural abscess; (i) pneumonia; (j) urinary tract infection. (3) Hematogenous infection—including bacteraemia and endocarditis.

Coagulase-negative staphylococci—most infections with these skin commensals are the consequence of medical interventions leading to foreign bodies, e.g. prosthetic joints or heart valves, indwelling intravascular catheters or grafts, or peritoneal catheters. Conditions include endocarditis (5–8% of native valve infections, c.40% of prosthetic valve infections), intravascular catheter infections (6–27% of vascular-catheter infections), prosthetic joint infections (up to 38% of arthroplasty infections), peritoneal dialysis, catheter infections, and postoperative ocular infections.

Diagnosis

Diagnosis relies on characteristic clinical and epidemiological features, supported by positive cultures from the relevant clinical site, with identification (when appropriate) of exotoxin-positive strains. Outbreak and epidemiological investigations use molecular fingerprinting techniques to assess relatedness of staphylococci.

Treatment

Aside from supportive care, the mainstays of therapy are (1) prompt drainage of infected foci; and (2) antimicrobials—(a) coagulase-negative staphylococci—vancomycin is the mainstay of therapy because of the high rates of methicillin resistance; (b) S. aureus—antimicrobial choice should be based on the local prevalence of MRSA and the clinical severity of illness; a bactericidal agent, preferably a β‎-lactam, is used whenever possible; oral agents active against MRSA include clindamycin, trimethoprim/sulfamethozaxole, doxycycline, minocycline, linezolid; glycopeptides (i.e. vancomycin or teicoplainin) have been the usual therapy of severe infections due to MRSA, but vancomycin resistance is emerging.

Prevention

Prevention of illness due to S. aureus, particularly MRSA, relies on proactive infection control measures, including (1) surveillance for MRSA colonization; (2) imposed grouping (cohorting) of infected and colonized patients; (3) barrier precautions—e.g. gowning and gloving by health care staff; (4) improved hand hygiene; (5) cleaning patients—e.g. with chlorhexidine; (6) improved environmental cleaning; (7) antimicrobial stewardship.

Better strategies for treatment and salvage of infected catheters or methods for treatment of biofilm may improve treatment of coagulase-negative staphylococcal infections. No vaccines are available.

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