Gram Positive Cocci: Staphylococci

Staphylococci are Gram positive cocci arranged in irregular clusters, described as grape-like, and are catalase positive, the key test distinguishing staphylococci from streptococci, which are catalase negative.

They are facultative anaerobes, nonmotile, non-spore-forming, and tolerate high salt concentrations, a property exploited diagnostically via mannitol salt agar, a selective medium for staphylococcal isolation.

Three species are of principal medical importance: Staphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus saprophyticus, differentiated primarily by coagulase status and, among the coagulase-negative group, by novobiocin susceptibility.

Catalase separates Staphylococcus, positive, from Streptococcus and Enterococcus, negative. Coagulase separates S. aureus, positive, coagulase positive staphylococcus, from all other staphylococci, coagulase negative staphylococci, CoNS. Novobiocin susceptibility separates the two clinically important CoNS species: S. epidermidis is susceptible, S. saprophyticus is resistant, the standard laboratory method for distinguishing them when clinically relevant.

Morphology. Gram positive cocci in clusters.

Important laboratory features. Catalase positive, coagulase positive, beta-haemolytic on blood agar, golden-yellow colony pigmentation, the origin of the species name.

Reservoir. Human anterior nares, nasal carriage present in roughly a third of the population, skin, and moist body sites. Humans are the principal reservoir.

Transmission. Direct contact, autoinoculation from a colonised site, fomites, and healthcare-associated spread via hands of staff.

Virulence factors. Protein A binds the Fc portion of IgG, preventing opsonisation and phagocytosis. Coagulase converts fibrinogen to fibrin, forming a protective fibrin wall around the organism, contributing to abscess formation. Alpha-toxin, alpha-haemolysin, is a pore-forming membrane damaging toxin.

Panton-Valentine leukocidin, PVL, is a pore-forming toxin targeting leukocytes, associated with severe necrotising skin and soft tissue infection and necrotising pneumonia, particularly in community-acquired MRSA strains. Toxic shock syndrome toxin-1, TSST-1, is a superantigen, causing toxic shock syndrome. Exfoliative toxins cleave desmoglein-1 in the epidermis, causing staphylococcal scalded skin syndrome.

Enterotoxins are preformed heat-stable toxins, causing rapid-onset, one to six hour, staphylococcal food poisoning. Biofilm formation is important in prosthetic device and catheter-associated infection.

Major diseases. Skin and soft tissue infection: impetigo, folliculitis, furuncles and carbuncles, cellulitis, abscess.

Toxin-mediated disease: toxic shock syndrome, scalded skin syndrome, food poisoning.

Invasive disease: bacteraemia, infective endocarditis, a leading cause of acute native and prosthetic valve endocarditis, osteomyelitis, septic arthritis, necrotising pneumonia.

Diagnosis. Gram stain and culture, blood agar, mannitol salt agar for selective isolation, coagulase test for confirmation, MALDI-TOF or molecular methods for rapid identification.

Resistance patterns. MRSA, methicillin-resistant S. aureus, resistance is mediated via the mecA gene, encoding an altered penicillin-binding protein, PBP2a, with low affinity for beta-lactams, conferring resistance to essentially the entire beta-lactam class.

VISA and VRSA, vancomycin-intermediate and vancomycin-resistant S. aureus, are rare but clinically significant emerging resistance patterns.

Community-acquired MRSA strains are often distinguished from healthcare-associated strains by PVL toxin carriage and a different resistance gene cassette pattern.

Prevention. Hand hygiene, contact precautions for known MRSA colonisation or infection, nasal decolonisation protocols, topical mupirocin, in selected surgical or high-risk populations, and chlorhexidine bathing in some ICU settings.

Morphology. Gram positive cocci in clusters, indistinguishable from S. aureus on Gram stain alone.

Important laboratory features. Catalase positive, coagulase negative, novobiocin susceptible.

Reservoir. Normal skin flora, present essentially universally.

Transmission. Endogenous, from the patient's own skin, in the great majority of clinically significant infections, introduced during device insertion or surgery.

Virulence factors. Low intrinsic virulence. The dominant virulence mechanism is biofilm formation on foreign material, catheters, prosthetic joints, heart valves, cerebrospinal fluid shunts, conferring both antimicrobial tolerance and immune evasion.

Major diseases. The classic opportunistic pathogen of medical devices: catheter-associated bloodstream infection, prosthetic joint infection, prosthetic valve endocarditis, cerebrospinal fluid shunt infection.

Diagnosis. Frequently isolated as a blood culture contaminant, skin flora introduced at venepuncture, so interpretation requires clinical correlation: growth in multiple separate blood culture sets, in a patient with an indwelling device and a compatible clinical picture, supports true infection rather than contamination.

Resistance patterns. A high proportion of S. epidermidis isolates are methicillin-resistant, often higher than S. aureus MRSA rates in the same institution, relevant to empirical antibiotic choice when device infection is suspected.

Morphology. Gram positive cocci in clusters.

Important laboratory features. Catalase positive, coagulase negative, novobiocin resistant, the key distinguishing feature from S. epidermidis.

Reservoir. Periurethral area, gastrointestinal tract, and genital flora, particularly in young sexually active women.

Transmission. Endogenous ascent from periurethral colonisation into the urinary tract.

Virulence factors. Adhesins mediating attachment to uroepithelium. Relatively low overall virulence outside the urinary tract.

Major diseases. A classic cause of uncomplicated urinary tract infection, cystitis, in young, sexually active women, the second most common cause of community-acquired UTI in this population after E. coli.

Diagnosis. Urine culture. Novobiocin resistance confirms the identification when a coagulase-negative staphylococcus is isolated from urine in a compatible clinical context. Some automated urinalysis systems can under-detect this organism given its slower growth, so clinical suspicion in a young woman with typical cystitis symptoms and a negative rapid urine screen should prompt formal culture.