ABSTRACT
The family Micrococcaceae includes two genera of clinical importance, Staphylococcus and Micrococcus. The genus Staphylococcus contains 14 species, of which coagulase-positive S. aureus and the coagulase-negative species, S. epidermidis, S. hemolyticus, S. saprophyticus, and S. lugdunensis have been most frequently incriminated in human infections. Staphylococci are colonizers of the anterior nares and skin, from which they may gain access to normally sterile tissues, and through which staphylococci may be transferred from one individual to another. S. aureus is the predominant cause of pyogenic infections and several toxin-mediated syndromes, while S. epidermidis (and other coagulase-negative species) is usually associated with device-related infections, e.g. indwelling catheters, prosthesis and other foreign bodies. S. saprophyticus is mainly associated with spontaneous urinary tract infections in sexually active young women. The cell wall of S. aureus contains a unique substance, termed protein A. It is an immunologically active substance which binds the FC fragment of immunoglobulin G. S. aureus, in addition to coagulase and catalase, produces a variety of exoenzymes, including hemolysins, extracellular deoxyrobinuclease, fibrinolysin, hyaluronidese, lipase, and a leukocidin. Among the protein exotoxins are those responsible for food poisoning (enterotoxin), toxic shock syndrome (toxic shock syndrome toxin 1, TSST1), and scalded skin syndrome (exfoliatin). Strains producing TSST 1 are almost universally associated with menstrual cases and for about 50% of nonmenstrual cases, while strains producing enterotoxins B (47%) and C (3%) account for the remaining cases. These toxins behave as superantigens that react directly with receptors on macrophages and
lymphocytes, resulting in release of inflammatory cytokines. Toxic shock syndrome (TSS) strains belong largely to bacteriophage group I. Staphylococcal scalded-skin syndrome is produced by select strains of bacteriophage group II, and originates from a focus of infection where the toxin is produced and disseminates to cause cleavage of the middle layers of the epidermidis, with resultant desquamation. Infants are most commonly affected but the syndrome occasionally occurs in adults. Methicillin resistant S. aureus (MRSA) and strains with intermediate resistance to vancomycin are being documented and these complicate the course of antibiotic treatment. S. aureus causes infections, either by direct invasion from a carrier site, usually through a break in the skin or mucosal integrity, or by production of extracellular toxins. The hallmark of staphylococcal infection is abscess formation. Primary or secondary bacteremia may result in
Figure 376 Staphylococcus aureus Gram-positive to Gram-variable cocci, singly and in ‘grape-like’ clusters in smear of agar culture
Figure 379 Staphylococcus aureus Pulsatile scalp abscess in patient with AIDS which developed at site of varicella-zoster reactivation
Figure 377 Staphylococcus aureus Cocci singly, in pairs and clusters, some intracellular, in polymorphonuclear leukocyte in smear of abscess exudate
Figure 378 Staphylococcus aureus Yellow-pigmented, smooth, hemolytic colonies on 5% sheep blood agar after 24-h incubation
dissemination to multiple organs and bone and may lead to bacteremic pneumonia and endocarditis. Endocarditis caused by S. aureus and S. epidermidis is a special risk in intravenous drug abusers who use contaminated needles and syringes.
