9.3 SST Pathogenicity and Virulence Mechanisms

9.3 SST Pathogenicity and Virulence Mechanisms

Quick Answer: S. aureus: coagulase, protein A, PVL in some CA-MRSA, exfoliative toxins (SSSS), TSST-1. S. pyogenes: M protein, streptolysin, Spe superantigens. P. aeruginosa: pyocyanin, elastase, biofilm on burns. C. perfringens: alpha toxin (lecithinase, Nagler). Pasteurella: rapid cellulitis after a bite. Correlate the wound Gram stain with culture, and interpret mixed flora against specimen quality.

Outline II.G.4 tests organism pathogenicity: etiology, transmission, and virulence mechanisms for the SST and bone organisms already named. The exam item is often a mechanism paired with a syndrome (SSSS, toxic shock, necrotizing fasciitis, gas gangrene, burn-wound biofilm, bite cellulitis) plus a Gram stain/culture correlation question.

Staphylococcus aureus

Etiology and transmission. S. aureus is a human skin and anterior-nares colonizer. Transmission is by direct contact, fomites, and autoinoculation into hair follicles, surgical wounds, and breaks in skin. Community strains cause abscesses and purulent cellulitis; hospital strains cause surgical-site and device infections.

Virulence factors the exam names:

• Coagulase (bound clumping factor and free coagulase) clots plasma. It is the species-level identifier and a virulence factor that helps wall off abscesses.
• Protein A binds the Fc portion of IgG, inhibiting opsonophagocytosis. Rapid latex kits detect protein A plus clumping factor.
• Panton-Valentine leukocidin (PVL) is a pore-forming bicomponent toxin enriched in some community-associated MRSA (CA-MRSA) lineages associated with recurrent skin abscesses and, less often, necrotizing pneumonia. PVL is not present in every MRSA isolate; do not equate oxacillin resistance with PVL.
• Exfoliative toxins (ETA/ETB) cause staphylococcal scalded-skin syndrome (SSSS) in young children: sterile, Nikolsky-positive sheets of desquamation. The toxin is hematogenous; bullae are culture-negative, while the focus (often nasopharynx or a small skin lesion) grows S. aureus.
• TSST-1 is a superantigen that causes toxic shock syndrome (fever, rash, hypotension, multiorgan failure), historically tampon-associated and also after wounds and sinus packing.

Abscess formation is the clinical signature of S. aureus SST disease. A Gram stain of pus showing GPC in clusters that culture as coagulase-positive staphylococci is concordant.

Streptococcus pyogenes

Etiology and transmission. Group A streptococci colonize the throat and skin and spread by respiratory droplets and contact. Minor trauma, varicella, and surgical wounds are portals for invasive SST disease.

Virulence:

• M protein (encoded by emm) is the major antiphagocytic surface protein. It defines serotypes and helps GAS persist in tissue. Rheumatic fever follows pharyngitis, not pyoderma; post-streptococcal glomerulonephritis can follow either.
• Streptolysin O and streptolysin S lyse cells and produce beta hemolysis (streptolysin S is oxygen-stable and accounts for surface hemolysis on blood agar). ASO titers are used serologically for nonsuppurative sequelae, not for acute wound diagnosis.
• Streptococcal pyrogenic exotoxins (Spe) are superantigens. SpeA and SpeC are associated with streptococcal toxic shock and scarlet fever; they help explain the fulminant course of type II necrotizing fasciitis.

GAS cellulitis and erysipelas are often non-purulent. Culture of intact cellulitis is low-yield; when tissue is obtained in necrotizing disease, expect a monomicrobial Gram stain of GPC in chains rather than mixed fecal flora.

Pseudomonas aeruginosa

Etiology and transmission. An environmental gram-negative rod of water and moist surfaces. Transmission to SST is from burns, hydrotherapy, hot tubs, wet shoes, and hospital sinks—not person-to-person in the staphylococcal sense.

Virulence:

• Pyocyanin (blue-green phenazine) generates reactive oxygen species and gives many colonies their color. It is a recognition clue, not an excuse to sniff plates.
• Elastase (LasB) and related proteases destroy tissue and evade immune proteins.
• Biofilm on burns, catheters, and chronic wounds produces the mucoid, treatment-refractory phenotype. Burn-wound sepsis is the historic Pseudomonas SST disaster.

Etiology on the Gram stain is GNR in a burn or wet wound; culture should be oxidase-positive. Not every isolate is obviously green, so do not wait for pigment before considering Pseudomonas in a burn-unit wound.

Clostridium perfringens

Etiology and transmission. Spores in soil and the GI tract contaminate traumatic or surgical wounds with reduced redox potential (devitalized muscle, vascular injury).

Virulence. Alpha toxin is a lecithinase (phospholipase C) that hydrolyzes cell-membrane phospholipids, producing the outer hemolytic zone and the Nagler reaction on egg-yolk agar (lecithinase precipitate inhibited by antitoxin on one half of the plate). Theta toxin (perfringolysin O) contributes to the inner complete hemolytic zone. Together they drive gas gangrene: myonecrosis, gas, and shock. Stormy fermentation is a metabolic demonstration in litmus milk, not the toxin assay. The Nagler plate is the virulence demonstration the exam pairs with alpha toxin.

Pasteurella multocida

Etiology and transmission. An oral commensal of cats and dogs, inoculated by bite or scratch. Virulence includes a capsule and endotoxin, but the exam-level fact is rapid cellulitis—often within 3–24 hours—at the bite site. That speed distinguishes it from slower mixed human-bite infections in which Eikenella may appear later and in mixed culture.

Correlate Gram stain of the wound with culture

Mixed-flora interpretation depends on specimen quality. Mixed organisms from a surface swab of a chronic wound are colonization until proven otherwise—do not report five pathogens with full AST. Mixed organisms from deep surgical tissue in a diabetic foot, Fournier gangrene, or human bite are a true polymicrobial infection; report the predominant aerobes (staphylococci, streptococci, Enterobacteriaceae, P. aeruginosa) and the anaerobic group. A single unexpected GNCB from a toddler's bone is Kingella until ruled out, not mixed flora.

If the Gram stain and culture disagree, troubleshoot: prior antibiotics, overgrowth of skin flora, failure to use anaerobic transport, or a fastidious organism (Kingella, Eikenella, Francisella) that overnight aerobic blood agar did not recover. That correlation is as testable as any toxin name.

On the exam

Pair the toxin with the disease: PVL with some CA-MRSA abscesses, exfoliative toxin with SSSS, TSST-1 with staphylococcal toxic shock, M protein and Spe with invasive GAS, pyocyanin/elastase/biofilm with Pseudomonas burns, alpha-toxin/Nagler with C. perfringens, and Pasteurella with same-day bite cellulitis. Then insist that the Gram stain and the culture tell the same story, and that mixed swab flora is not invasive polymicrobial disease.