Staphylococcus Overview and Characteristics

Staphylococcus Overview

  • Family: MICROCOCCACEAE

  • Genus: Micrococcus

  • Genus: Staphylococcus

  • Family: STREPTOCOCCACEAE

  • Genus: Streptococcus

  • Genus: Enterococcus

  • Classification: GRAM POSITIVE COCCI

General Characteristics of Staphylococcus Aureus

Basic Properties

  • Morphology:

    • Gram-positive cocci observed as individual organisms, in pairs, and in irregular, grapelike clusters.

  • Motility: Nonmotile

  • Formation: Non–spore-forming

  • Catalase: Positive

  • Coagulase Positive:

    • Bound Coagulase:

    • Clumping factor reacts with fibrinogen causing aggregation

    • Extracellular Coagulase:

    • Converts prothrombin to thrombin, leading to fibrinogen to fibrin conversion

  • Resistances:

    • Tolerant to temperatures (~50°C), high salt concentrations, and drying.

  • Colony Appearance:

    • Golden/yellow colonies that are strongly β-hemolytic on blood agar.

Distribution and Carriage

  • Found in human flora in:

    • Axillae

    • Inguinal and perineal areas

    • Anterior nares

  • Carriage is more common in children than in adults.

  • Carriers are divided into:

    • Persistent carriers: High risk of infection

    • Intermittent or Noncarriers: Low risk of infection

  • Molecular typing via pulsed-field gel electrophoresis (PFGE) shows that the isolate from blood in most patients with S. aureus bacteremia is identical to that from the anterior nares.

Decolonization strategies include:

  • Topical mupirocin

  • Chlorhexidine gluconate washes

  • Oral rifampin plus doxycycline for 7 days

Virulence Factors of Staphylococcus Aureus

Surface Proteins

  • Adhesins:

    • Protein A (SpA)

    • Fibronectin-binding proteins A and B

    • Collagen-binding protein

    • Clumping factor A and B proteins

Enzymes

  • Coagulase

  • Lipase

  • Hyaluronidase

  • Staphylokinase

  • Nuclease

Toxins

  • Cytotoxins:

    • α-Toxin

    • β-Toxin

    • γ-Toxin

  • Panton-Valentine Leukocidin (PVL):

    • Induces pore formation and affects leukocyte cell membranes

  • Enterotoxins

    • Various types (A, B, C, D, E, G, H, I, J)

  • Exfoliative Toxin

  • Toxic Shock Syndrome Toxin

  • Superantigens:

    • Cause nonspecific T-cell stimulation leading to severe clinical disease

Tissue Invasion and Effects on Host Immunity

Tissue Invasion Mechanisms

  • Major toxin: α-Toxin induces pore formation leading to breaches in epithelial and endothelial cells by breaking adherens junctions and compromising the cytoskeleton.

Effects on Host Immunity

  • Inhibition of neutrophil-mediated killing:

    • Neutrophil activation is reduced.

    • Decreased migration to infection sites.

    • Reduced opsonization and phagocytosis of bacteria.

Small-Colony Variants (SCVs)

  • Persistent deep-seated infections linked to these variants.

  • Exhibit slow-growing, quasi-dormant characteristics:

    • Smaller colonies on agar plates

    • Quiescent metabolism

    • Reduced haemolytic and coagulase activities

    • Decreased carbohydrate utilization

    • Low virulence and increased antibiotic resistance

  • Triggered by environmental stress factors such as reactive oxygen species, low pH, cationic peptides, and limited nutrition.

  • Notably described in cystic fibrosis patients, contributing to persistent S. aureus infection.

Types and Presentation of S. Aureus Infections

Skin and Soft Tissue Infections

  • Impetigo: Small erythematous area evolving to bullae.

  • Folliculitis: Tender pustule around hair follicles.

  • Furuncles: Abscesses with purulent material.

  • Carbuncles: Clusters of connected furuncles.

  • Paronychia: Infection around fingernail evolving from cellulitis to abscess.

  • Scalded Skin Syndrome (Ritter disease): Fragile blisters, fever, and possible mucopurulent discharge.

  • Deep Tissue Abscess and Infections: Pain and tenderness in infected sites.

Other Clinical Presentations

  • Pneumonia: Positive blood cultures associated with secondary disease.

  • Osteomyelitis: Sudden onset with bony tenderness; diagnosis through blood culture.

  • Septic Arthritis: Joint pain with fever; diagnosis via joint fluid examination.

  • Bacteremia: Systemic infection indicating S. aureus presence in the bloodstream.

  • Endocarditis: Fever and malaise; diagnosis requires multiple blood culture sets.

  • Thrombophlebitis: Localized infection near intravenous lines.

  • Toxic Shock Syndrome: Rapid onset fever and erythema affecting multiple organ systems.

Treatment Considerations

  • MSSA (Methicillin-Susceptible S. aureus):

    • Treatment includes parenteral penicillins (e.g., nafcillin), 1st/2nd-generation cephalosporins, and clindamycin.

  • MRSA (Methicillin-Resistant S. aureus):

    • Requires treatment with vancomycin, daptomycin, or linezolid.

Prevention

  • Focus on cleanliness and disinfection, especially in hospital settings.

  • Nosocomial pathogens commonly found in nurseries and intensive care areas.

Coagulase-Negative Staphylococci (CNS)

  • Examples include S. epidermidis, S. saprophyticus, S. lugdunensis.

  • Characteristics: Opportunistic pathogens, associated with biofilm formation.

  • Commonly implicated in infections related to catheters and prosthetic devices.

Summary of Treatment Options for CNS

  • Effective against oxacillin-resistant strains: Vancomycin, linezolid, teicoplanin, and others.

Laboratory Diagnosis for Staphylococci

  • Utilize microscopic examination, culture techniques, biochemical reactions (catalase, coagulase), and automated identification methods (ID32Staph, bioMerieux, MALDI TOF) for accurate diagnosis.