The Staphylococci: Pathogenesis, Pathology, Clinical Findings, Diagnostic Laboratory Tests, Treatment, Epidemiology and Control.

Question 1

Pathogenesis

Answer 1

Staphylococcus aureus causes disease through a combination of invasive enzymes, surface proteins, and exotoxins. It colonizes the skin and mucosal surfaces, especially the anterior nares. Adhesins (MSCRAMMs) promote attachment to host tissues. Protein A, capsule, and catalase help evade the immune system. Enzymes such as coagulase, hyaluronidase, and staphylokinase facilitate tissue invasion. Toxins like TSST-1 and enterotoxins act as superantigens, stimulating massive cytokine release. Exfoliative toxins disrupt skin integrity. Disease may result from direct infection, toxin production, or both.

Question 2

Pathology

Answer 2

Pathologic effects include suppurative inflammation and tissue necrosis. Local infections (e.g., boils, abscesses) show neutrophil infiltration, pus formation, and tissue destruction. Toxin-mediated diseases involve systemic inflammatory responses, such as in toxic shock syndrome or scalded skin syndrome. S. aureus can also cause metastatic abscesses by hematogenous spread, particularly in the lungs, bones, or brain. Chronic infections may involve biofilm formation on medical devices (especially by S. epidermidis).

Question 3

Clinical findings

Answer 3

Staphylococcal infections are categorized as: 1) Pyogenic: skin infections (impetigo, boils, carbuncles, cellulitis), wound infections, osteomyelitis, septic arthritis, pneumonia (especially post-influenza), endocarditis, bacteremia. 2) Toxin-mediated: a) Food poisoning (rapid-onset vomiting, diarrhea from preformed enterotoxin). b) Scalded skin syndrome (diffuse exfoliation in infants). c) Toxic shock syndrome (fever, hypotension, rash, desquamation, multiorgan failure). Coagulase-negative staphylococci (e.g., S. epidermidis) cause prosthetic device infections; S. saprophyticus causes urinary tract infections in young women.

Question 4

Diagnostic laboratory tests

Answer 4

Diagnosis involves: 1) Microscopy: gram-positive cocci in clusters from pus, sputum, or blood. 2) Culture: golden-yellow colonies on blood agar (S. aureus), often beta-hemolytic; mannitol salt agar helps isolate and differentiate S. aureus (mannitol fermenter). 3) Catalase test: differentiates Staphylococcus (+) from Streptococcus (-). 4) Coagulase test: distinguishes S. aureus (+) from other species (-). 5) PCR or MALDI-TOF may be used for rapid identification. Blood cultures and sensitivity testing are essential for systemic infections.

Question 5

Treatment

Answer 5

MSSA (methicillin-sensitive S. aureus) is treated with nafcillin or oxacillin. Alternatives include cefazolin or clindamycin. MRSA (methicillin-resistant S. aureus) is treated with vancomycin, linezolid, daptomycin, or newer agents like ceftaroline. Abscesses require surgical drainage. For toxin-mediated diseases, supportive care and antitoxin antibiotics (e.g., clindamycin) are used. Coagulase-negative staphylococci are often resistant to many antibiotics and treated based on susceptibility testing.

Question 6

Epidemiology and control

Answer 6

Staphylococci are part of normal skin flora but are opportunistic pathogens. S. aureus colonizes the nares in ~30% of people. Transmission occurs via direct contact or contaminated fomites. Hospital-acquired infections involve MRSA and coagulase-negative staphylococci on catheters, prosthetic devices, and surgical wounds. Risk factors include surgery, indwelling devices, immunosuppression, and chronic illness. Control includes hand hygiene, contact precautions, decolonization with mupirocin (nasal) and chlorhexidine (skin), and screening high-risk patients for MRSA carriage.