General Concepts
Clinical Manifestations
Staphylococci can cause many forms of infection. (1) S aureus causes superficial skin lesions (boils, styes) and localized abscesses in other sites. (2) S aureus causes deep-seated infections, such as osteomyelitis and endocarditis and more serious skin infections (furunculosis). (3) S aureus is a major cause of hospital acquired (nosocomial) infection of surgical wounds and, with S epidermidis, causes infections associated with indwelling medical devices. (4) S aureus causes food poisoning by releasing enterotoxins into food. (5) S aureus causes toxic shock syndrome by release of superantigens into the blood stream. (6) S saprophiticus causes urinary tract infections, especially in girls. (7) Other species of staphylococci (S lugdunensis, S haemolyticus, S warneri, S schleiferi, S intermedius) are infrequent pathogens.
Structure
Staphylococci are Gram-positive cocci 1μm in diameter. They form clumps.
Classification
S aureus and S intermedius are coagulase positive. All other staphylococci are coagulase negative. They are salt tolerant and often hemolytic. Identification requires biotype analysis.
Natural Habitat
S aureus colonizes the nasal passage and axillae. S epidermidis is a common human skin commensal. Other species of staphylococci are infrequent human commensals. Some are commensals of other animals.
Pathogenesis
S aureus expresses many potential virulence factors. (1) Surface proteins that promote colonization of host tissues. (2) Factors that probably inhibit phagocytosis (capsule, immunoglobulin binding protein A). (3) Toxins that damage host tissues and cause disease symptoms. Coagulase-negative staphylococci are normally less virulent and express fewer virulence factors. S epidermidis readily colonizes implanted devices.
Host Defenses
Phagocytosis is the major mechanism for combatting staphylococcal infection. Antibodies are produced which neutralize toxins and promote opsonization. The capsule and protein A may interfere with phagocytosis. Biofilm growth on implants is impervious to phagocytosis.
Treatment
Infections acquired outside hospitals can usually be treated with penicillinase-resistant β-lactams. Hospital acquired infection is often caused by antibiotic resistant strains and can only be treated with vancomycin.
Antibiotic Resistance
Multiple antibiotic resistance is increasingly common in S aureus and S epidermidis. Methicillin resistance is indicative of multiple resistance. Methicillin-resistant S aureus (MRSA) causes outbreaks in hospitals and can be epidemic.
Epidemiology
Epidemiological tracing of S aureus is traditionally performed by phage typing, but has limitations. Molecular typing methods are being tested experimentally.
Diagnosis
Diagnosis is based on performing tests with colonies. Tests for clumping factor, coagulase, hemolysins and thermostable deoxyribonuclease are routinely used to identify S aureus. Commercial latex agglutination tests are available. Identification of S epidermidis is confirmed by commercial biotyping kits.
Control
Patients and staff carrying epidemic strains, particularly MRSA, should be isolated. Patients may be given disinfectant baths or treated with a topical antibiotic to eradicate carriage of MRSA. Infection control programs are used in most hospitals.
