Staphylococcus Overview
Staphylococcus Overview
Taxonomy
Family: MICROCOCCACEAE
Genus: Micrococcus
Genus: Staphylococcus
Family: STREPTOCOCCACEAE
Genus: Streptococcus
Genus: Enterococcus
Classification: GRAM POSITIVE COCCI
Basic Characteristics of Gram Positive Cocci
Staphylococcus and Streptococcus
Divide into:
Catalase Positive: Staphylococcus
Catalase Negative: Streptococcus
Staphylococcus aureus
General Properties
Morphology: Gram-positive cocci
Seen individually, in pairs, or in irregular, grapelike clusters
Characteristics:
Nonmotile
Non-spore-forming
Catalase-positive
Coagulase-positive
Bound Coagulase (Clumping Factor): Reacts with fibrinogen causing aggregation of organisms.
Extracellular Coagulase: Converts prothrombin to thrombin, thus converting fibrinogen to fibrin.
Resilience:
Resistant to temperatures around ~50°C
Able to withstand high salt concentrations and drying
Colony Characteristics:
Golden/yellow colonies
Strongly β-hemolytic on blood agar
Colonization and Carriage
Human Flora Locations:
Found in the axillae, inguinal, perineal areas, and anterior nares
Patterns of Carriage:
Persistent carriers (higher risk of infection) typically seen in children
Intermittent or noncarriers (lower risk of infection) seen more in adults
Molecular Typing
Technique Used: Pulsed-field gel electrophoresis (PFGE)
Findings: In S. aureus bacteremia, isolates from patients' blood are often identical to those found in anterior nares
Decolonization Strategies
In hospitalized patients with methicillin-resistant S. aureus (MRSA) strains:
Topical Mupirocin
Chlorhexidine Gluconate Washes
Oral Rifampin plus Doxycycline for 7 days
Virulence Factors of Staphylococcus aureus
Key Adhesins
Protein A (SpA)
Fibronectin-binding Proteins A and B
Collagen-binding Protein
Clumping Factor A and B Proteins
Enzymes Produced
Coagulase
Lipase
Hyaluronidase
Staphylokinase
Nuclease
Toxins
α-Toxin
β-Toxin
γ-Toxin
Panton-Valentine Leukocidin (PVL)
Enterotoxins
Exfoliative Toxin
Toxic Shock Syndrome Toxin (TSST)
Superantigens
The toxins can lead to severe immune responses via nonspecific T-cell stimulation.
Tissue Invasion
Mechanism of the Major Toxin
α-Toxin Function:
Causes pore formation in cell membranes
Interrupts epithelial and endothelial integrity by breaching adherens junctions and compromising the cytoskeleton
Panton-Valentine Leukocidin (PVL)
Pore Formation: Induces damage in leukocyte membranes
Epidemiology: Found in less than 5% of S. aureus strains, prevalent in those causing necrotic skin lesions and severe pneumonia
Associations: Frequently linked with community-associated MRSA (CA-MRSA) infections, particularly affecting skin and soft tissue
Effects on Host Immunity
Immunosuppression Mechanisms:
Decrease in neutrophil-mediated killing
Reduced neutrophil activation and migration to the infection site
Impaired bacterial opsonization and phagocytosis
Small-Colony Variants (SCVs)
Description: Quasi-dormant, slow-growing bacteria linked to persistent infections
Characteristics:
Smaller colonies on agar plates
Quiescent metabolism
Reduced hemolytic and coagulase activities
Decreased carbohydrate utilization
Low virulence potential and increased antibiotic resistance
Emergence Triggers: Reactive oxygen species, low pH, cationic peptides, and nutrient limitation can induce SCVs
Clinical Relevance: Associated with cystic fibrosis patients
Summary of Virulence Factors
All Strains Include:
Leukocidin
Enzymes: Lipases, hyaluronidase, cytotoxins (α, β, γ, δ), enterotoxins (various types), exfoliative toxins, nucleases, proteases, collagenase
Mechanism: Convert local host tissues into nutrients for bacteria
Pyrogenic Toxin Superantigens: Bind major histocompatibility complex II, inducing severe clinical diseases via nonspecific T-cell activation
Types and Presentations of Staphylococcus aureus Infection
Common Infections:
Skin and Soft Tissue: Impetigo, folliculitis, furuncle, carbuncle, paronychia
Invasive: Pneumonia, osteomyelitis, septic arthritis, bacteremia, endocarditis, thrombophlebitis, deep tissue abscess
Toxin-Related: Classic food poisoning, toxic shock syndrome, scalded skin syndrome (Ritter disease)
Specific Presentations
Impetigo: Small erythematous area progressing to bullae that heal with honey-colored crusts
Folliculitis: Tender pustule at hair follicle
Furuncle: Abscesses exuding purulent material from a single opening, affecting skin and subcutaneous tissues
Carbuncle: Aggregate of furuncles with multiple pustular openings
Paronychia: Infection around fingernail starting as cellulitis, can progress to abscess
Acute: Frequently caused by S. aureus
Chronic: Usually of fungal origin
Treatment: Warm water soaks, surgery, antibiotics
Osteomyelitis: Sudden fever and painful limp in children, severe presentation may be subtle in neonates
Diagnosis: Blood cultures (positive in only 30-50% of pediatric cases) and culture of bone aspirate
Minimum treatment duration: 4-6 weeks
Septic Arthritis: Symptoms include decreased motion, warmth, tenderness of join, often absent in infants
Diagnosis: Joint fluid examination and culture
Endocarditis: Presents with fever, malaise, and potential peripheral emboli; diagnosis by blood culture
Imaging Examples
Findings in Endocarditis:
Large vegetation on mitral valve visible via echocardiography
Specific Infections by S. aureus
Pneumonia: Blood cultures more positive in secondary than primary cases; specimens should be adequate (e.g., lung tap, pleural fluid)
Thrombophlebitis: Affects IV catheter sites, diagnosed through blood cultures
Abscess Formation: Painful puss collections; S. aureus is the common cause; management includes drainage
Scalded Skin Syndrome (Ritter Disease): Fragile blisters with tender bases, may accompany fever; treatment with high-volume antibiotics
Toxic Shock Syndrome: Progresses rapidly with severe symptoms; involves T-cell stimulation and cytokine release leading to shock
Treatment Strategies
MSSA Treatment
Regimens:
Penicillinase-resistant penicillin (nafcillin, oxacillin)
First or second generation cephalosporins
Combination therapy with clindamycin
Other agents: fluoroquinolones, tetracycline, tigecycline, aminoglycosides
MRSA Treatment
Options:
Vancomycin, teicoplanin for bacteremia
Daptomycin
Linezolid and tedizolid (pneumonia)
Quinupristin/dalfopristin
Telavancin
Ceftaroline
Local antibiotics (mupirocin)
MecA Detection: Via PCR
Prevention and Control
Source: Skin and nasal colonization
Transmission: Hands, objects, surfaces
Prevention Strategies:
Hand hygiene
Use of mupirocin to reduce nasal colonization
Important Sites for Infection Control: Newborn nurseries, ICUs, operating theaters
Coagulase-Negative Staphylococci (CNS)
Species Examples:
S. epidermidis
S. haemolyticus
S. hominis
S. capitis
S. saprophyticus (novobiocin resistant)
S. warneri
S. xylosus
S. lugdunensis
Clinical Role
Characteristics: Opportunistic pathogens; biofilm producers on plastic surfaces (e.g., prosthetic appliances)
Associated Conditions: Catheter-associated sepsis, infections following immunosuppression
Staphylococcus lugdunensis
Key Features:
Coagulase-negative but produces bound coagulase
Causes SSTI, infective endocarditis (high mortality associated)
Treatment: Generally sensitive to oxacillin
Treatment Options for CNS Infections
Resistance: 50-60% oxacillin resistant; treat with:
Vancomycin, teicoplanin (glycopeptides)
Tigecycline, linezolid, tedizolid
Quinupristin/dalfopristin
Laboratory Diagnosis for Staphylococci
Methods:
Microscopy
Culture
Biochemical reactions (catalase, coagulase tests)
Automatic identification systems (e.g., ID32Staph, bioMerieux)
MALDI-TOF (mass spectrometry)