Staphylococcus

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Chapter 174 Staphylococcus

Staphylococci are hardy, aerobic, gram-positive bacteria that grow in pairs and clusters and are ubiquitous as normal flora of humans and present on fomites and in dust. They are resistant to heat and drying and may be recovered from nonbiologic environments weeks to months after contamination. Strains are classified as Staphylococcus aureus if they are coagulase positive or as 1 of the many species of coagulase-negative staphylococci (e.g., Staphylococcus epidermidis, Staphylococcus saprophyticus, Staphylococcus haemolyticus, etc). Often, S. aureus produces a yellow or orange pigment and β-hemolysis on blood agar and S. epidermidis produces a white pigment with variable hemolysis results, although definitive species confirmation requires further testing. S. aureus has many virulence factors that mediate various serious diseases, whereas coagulase-negative staphylococci tend to be less pathogenic unless an indwelling foreign body (e.g., intravascular catheter) is present. Emerging antimicrobial resistance has become important, especially to the β-lactam antibiotics and less often to vancomycin.

174.1 Staphylococcus aureus

S. aureus is the most common cause of pyogenic infection of the skin and soft tissue, causing impetigo, furuncles (boils), cellulitis, abscess, lymphadenitis, paronychia, omphalitis, and wound infection. Bacteremia (primary and secondary) is common and can be associated with or result in osteomyelitis, suppurative arthritis, deep abscesses, pneumonia, empyema, endocarditis, pyomyositis, pericarditis, and rarely meningitis. Toxin-mediated diseases, including food poisoning, staphylococcal scarlet fever, scalded skin syndrome, and toxic shock syndrome (TSS), are caused by certain S. aureus strains. Methicillin resistance is a global problem.

Etiology

Disease may result from tissue invasion or injury caused by various toxins and enzymes produced by the organism. Strains of S. aureus can be identified by the virulence factors they produce and can be classified by various molecular techniques.

Adhesion of S. aureus to mucosal cells is mediated by teichoic acid in the cell wall; exposure to the submucosa or subcutaneous sites increases adhesion to fibrinogen, fibronectin, collagen, and other proteins. Different strains of S. aureus produce many different virulence factors that have 1 or more of 4 different roles: protect the organism from host defenses, localize infection, cause local tissue damage, and act as toxins affecting noninfected tissue sites.

Most strains of S. aureus possess factors that protect the organism from host defenses. Many staphylococci produce a loose polysaccharide capsule, or slime layer, which may interfere with opsonophagocytosis. Production of coagulase and/or clumping factor differentiates S. aureus from S. epidermidis and other coagulase-negative staphylococci. Clumping factor interacts with fibrinogen to cause large clumps of organisms, interfering with effective phagocytosis. Coagulase causes plasma to clot by interacting with fibrinogen and this may have an important role in localization of infection (abscess formation). Protein A is present in most strains of S. aureus but not coagulase-negative staphylococci and reacts specifically with immunoglobulin G1 (IgG1), IgG2, and IgG4. It is located on the outermost coat of the cell wall and can absorb serum immunoglobulins, preventing antibacterial antibodies from acting as opsonins and thus inhibiting phagocytosis. Other enzymes elaborated by staphylococci include catalase (inactivates hydrogen peroxide, promoting intracellular survival), penicillinase or β-lactamase (inactivates penicillin at the molecular level), and lipase (associated with skin infection).

Many strains of S. aureus produce substances that cause local tissue destruction. A number of immunologically distinct hemolysins that act on cell membranes and cause tissue necrosis have been identified (α-toxin, β-hemolysin, δ-hemolysin). Panton-Valentine leukocidin (PVL), which is produced by many current strains of S. aureus and has been associated with invasive skin disease, combines with the phospholipid of the phagocytic cell membrane, producing increased permeability, leakage of protein, and eventual death of the cell.

Many strains of S. aureus release 1 or more exotoxins. Exfoliatins A and B are serologically distinct proteins that produce localized (bullous impetigo) or generalized (scalded skin syndrome, staphylococcal scarlet fever) dermatologic complications (Chapter 651). Exfoliatins produce skin separation by splitting the desmosome and altering the intracellular matrix in the stratum granulosum.

One or more staphylococcal enterotoxins (types A, B, C1, C2, D, E) are elaborated by most strains of S. aureus. Ingestion of preformed enterotoxin A or B is associated with food poisoning, resulting in vomiting and diarrhea and, in some cases, profound hypotension. By 10 yr of age, almost all individuals have antibodies to at least 1 enterotoxin.

Toxic shock syndrome toxin-1 (TSST-1) is associated with TSS related to menstruation and focal staphylococcal infection. TSST-1 is a superantigen that induces production of interleukin-1 and tumor necrosis factor, resulting in hypotension, fever, and multisystem involvement. Enterotoxin A and enterotoxin B also may be associated with nonmenstrual TSS.

Clinical Manifestations

The signs and symptoms vary with the location of the infection, which is most commonly the skin but may be any tissue. Disease states of various degrees of severity are generally a result of local suppuration, systemic dissemination with metastatic infection, or systemic effects of toxin production. Although the nasopharynx and skin of many persons may be colonized with S. aureus, disease due to this organism is relatively uncommon. Skin infections due to S. aureus are considerably more prevalent among persons living in low socioeconomic circumstances and particularly among those in tropical climates.

Respiratory Tract

Infections of the upper respiratory tract due to S. aureus are rare, in particular considering the frequency with which the anterior nares are colonized. In normal hosts, otitis media (Chapter 632) and sinusitis (Chapter 372) are rarely caused by S. aureus. S. aureus sinusitis is relatively common in children with cystic fibrosis or defects in leukocyte function and may be the only focus of infection in some children with toxic shock syndrome. Suppurative parotitis is a rare infection, but S. aureus is a common cause. A membranous tracheitis that complicates viral croup may be due to infection with S. aureus, but other organisms are also possible. Patients typically have high fever, leukocytosis, and evidence of severe upper airway obstruction. Direct laryngoscopy or bronchoscopy shows a normal epiglottis with subglottic narrowing and thick, purulent secretions within the trachea. Treatment requires careful airway management and appropriate antibiotic therapy.

Pneumonia (Chapter 392) due to S. aureus may be primary (hematogenous) or secondary after a viral infection such as influenza. Hematogenous pneumonia may be secondary to septic emboli from right-sided endocarditis or septic thrombophlebitis, with or without the presence of intravascular devices. Inhalation pneumonia is caused by alteration of mucociliary clearance (see cystic fibrosis, Chapter 395), leukocyte dysfunction, or bacterial adherence initiated by a viral infection. Common symptoms and signs include high fever, abdominal pain, tachypnea, dyspnea, and localized or diffuse bronchopneumonia or lobar disease. S. aureus often causes a necrotizing pneumonitis that may be associated with development of empyema, pneumatoceles, pyopneumothorax, and bronchopleural fistulas.

Central Nervous System

Meningitis (Chapter 595.1) caused by S. aureus is not common; it is associated with penetrating cranial trauma and neurosurgical procedures (craniotomy, cerebrospinal fluid [CSF] shunt placement) and less frequently with endocarditis, parameningeal foci (epidural or brain abscess), diabetes mellitus, or malignancy. The CSF profile of S. aureus meningitis is indistinguishable from that in other forms of bacterial meningitis.

Heart

S. aureus is a common cause of acute endocarditis (Chapter 431) on native valves. Perforation of heart valves, myocardial abscesses, heart failure, conduction disturbances, acute hemopericardium, purulent pericarditis, and sudden death may ensue.

Kidney

S. aureus is a common cause of renal and perinephric abscess (Chapter 532), usually of hematogenous origin. Pyelonephritis and cystitis due to S. aureus are unusual.

Toxic Shock Syndrome (TSS)

S. aureus is the principal cause of TSS (Chapter 174.2), which should be suspected in anyone with fever, shock, and/or a scarlet fever-like rash.

Intestinal Tract

Staphylococcal enterocolitis rarely follows overgrowth of normal bowel flora by S. aureus, which can occur as a result of broad-spectrum oral antibiotic therapy. Diarrhea is associated with blood and mucus. Peritonitis associated with S. aureus in patients receiving long-term ambulatory peritoneal dialysis usually involves the catheter tunnel. Removal of the catheter is required to achieve a bacteriologic cure.

Food poisoning (Chapter 332) may be caused by ingestion of preformed enterotoxins produced by staphylococci in contaminated foods. Approximately 2-7 hr after ingestion of the toxin, sudden, severe vomiting begins. Watery diarrhea may develop, but fever is absent or low. Symptoms rarely persist longer than 12-24 hr. Rarely, shock and death may occur.

Diagnosis

The diagnosis of S. aureus infection depends on isolation of the organism from nonpermissive sites such as cellulitis aspirates, abscess cavities, blood, bone or joint aspirates, or other sites of infection. Swab cultures of surfaces are not as useful, as they may reflect surface contamination rather than the true cause of infection. Tissue samples or fluid aspirates in a syringe provide the best culture material. Isolation from the nose or skin does not necessarily imply causation because these sites may be normally colonized sites. Because of the high prevalence of MRSA, the increasing severity of S. aureus infections, and the fact that bacteremia is not universally present even in severe S. aureus infections, it is usually important to obtain a nonpermissive culture of any potential focus of infection as well as a blood culture prior to starting antibiotic treatment. The organism can be grown readily in liquid and on solid media. After isolation, identification is made on the basis of Gram stain and coagulase, clumping factor, and protein A reactivity. Patterns of susceptibility to antibiotics should be assessed in serious cases, as antimicrobial resistance is increasingly common.

Diagnosis of S. aureus food poisoning is made on the basis of epidemiologic and clinical findings. Food suspected of contamination should be cultured and can be tested for enterotoxin.

Treatment

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