Staphylococcus
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Direct answer
Staphylococcus aureus is the gram-positive coccus in clusters that is catalase-positive and coagulase-positive, ferments mannitol to golden-yellow colonies on Mannitol salt agar, and owns a toxin wardrobe the exam raids every year — toxic shock syndrome toxin 1 acting as a superantigen, exfoliative toxin causing staphylococcal scalded skin syndrome, enterotoxins causing vomiting within hours of contaminated food, and Panton–Valentine leukocidin linked to necrotising pneumonia and abscesses. Methicillin resistance, mediated by the mecA gene encoding PBP2a, converts a flucloxacillin-treated organism into one needing vancomycin, teicoplanin or linezolid. The coagulase-negative staphylococci, long dismissed as contaminants, cause two textbook diseases: Staphylococcus epidermidis with its slime biofilm on prosthetic valves, shunts and catheters, and Staphylococcus saprophyticus producing dysuria in young sexually active women, identified by novobiocin resistance.
What you must remember
- Identification ladder: catalase separates staphylococci (positive) from streptococci (negative); coagulase and mannitol fermentation then separate S. aureus from the coagulase-negative species.
- Local arsenal of enzymes: coagulase (clots plasma), protein A (binds Fc of immunoglobulin G, defeating opsonisation), catalase, hyaluronidase, staphylokinase.
- Toxic shock syndrome toxin 1 is a superantigen bypassing antigen processing to polyclonally activate T cells; the classic setting is prolonged tampon use, presenting with fever, rash, desquamation and hypotension.
- Staphylococcal food poisoning: preformed heat-stable enterotoxin in food, vomiting and cramps within 1–6 hours, no fever — contrast the 12–24 hour delay of salmonella gastroenteritis.
- Scalded skin syndrome (Ritter disease) in neonates: exfoliative toxin splits the epidermis at the stratum granulosum, Nikolsky positive, mucosa spared — distinguish from Stevens–Johnson syndrome, which involves mucosa.
- Methicillin-resistant S. aureus: treat with vancomycin (trough-guided), teicoplanin, linezolid or daptomycin; flucloxacillin and cloxacillin remain the choice for sensitive strains.
- Staphylococcus epidermidis is the commonest organism on prosthetic devices because biofilm slime (polysaccharide intercellular adhesin) shields it from antibiotics and neutrophils.
- Staphylococcus saprophyticus is the second commonest cause of uncomplicated cystitis in young women — novobiocin-resistant, coagulase-negative.
From a boil to toxic shock — one organism, five diseases
A carrier in the anterior nares develops a furuncle: local pyogenin, hyaluronidase spreading the pus, drained and treated expectantly. The same strain on an improperly stored custard produces enterotoxin, and the family vomits within four hours — the incubation period is the enterotoxin's, not the bacterium's. If the strain carries toxic shock syndrome toxin 1 and the setting is a prolonged tampon or a wound pack, fever, conjunctival injection, a sunburn rash, diarrhoea and refractory hypotension follow, with desquamation of palms and soles a week later; management is removing the source, aggressive fluids and supportive care, with clindamycin added to suppress toxin. In a neonate, exfoliative toxin instead produces widespread erythema and sheet-like peeling with a positive Nikolsky sign — the clinician must resist labelling it a drug reaction, because mucous membranes are spared and the answer is anti-staphylococcal therapy. Each disease is toxin-led, which is why source control, not antibiotics alone, decides outcomes.
Where students slip
The timing question decides food-poisoning marks: one to six hours of incubation means preformed staphylococcal enterotoxin, eight to sixteen means Clostridium perfringens, over a day means salmonella — examinees who anchor on "bacteria in food" miss the toxin logic. The second slip is catalase versus coagulase as the first dividing test: clusters versus chains under the microscope divide genera, but catalase is the bench test separating staphylococcus from streptococcus. Third, the scalded-skin versus Stevens–Johnson stem: mucosal involvement points to Stevens–Johnson, toxin-mediated peeling with spared mucosa to staphylococcus. Finally, a "growth in multiple bottles of coagulase-negative staphylococcus" in a line-related fever is a pathogen, not a contaminant — dismissing it is the clinical trap the viva sets.
Frequently asked questions
Which test separates Staphylococcus aureus from coagulase-negative staphylococci?
The coagulase test — slide (bound clumping factor) or tube (free coagulase) — positive in S. aureus; mannitol salt agar fermentation and golden pigment corroborate.
Why does toxic shock syndrome toxin 1 cause hypotension?
It acts as a superantigen, binding directly to major histocompatibility complex class II and T-cell receptors to release massive cytokines — interleukin-1, interleukin-2 and tumour necrosis factor — bypassing normal antigen specificity.
How quickly does staphylococcal food poisoning present?
Within one to six hours of ingesting preformed, heat-stable enterotoxin, with prominent vomiting and cramps but no fever; the short interval distinguishes it from bacterial invasion syndromes.
Which staphylococcus causes urinary infection in young women?
Staphylococcus saprophyticus — coagulase-negative and novobiocin-resistant — a common cause of uncomplicated cystitis in young, sexually active women.
How is methicillin resistance detected and treated?
Cefoxitin disc diffusion or PBP2a/mecA detection; treatment options are vancomycin, teicoplanin, linezolid or daptomycin, since all conventional beta-lactams fail against PBP2a.
Why does Staphylococcus epidermidis infect prosthetic valves?
It produces slime biofilm (polysaccharide intercellular adhesin) that anchors it to foreign material and shields it from antibiotics and immune cells, often needing device removal.