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Immune defense mechanisms (skin)
Physical barrier: Unbroken skin effectively blocks pathogen entry.
Chemical defenses: Salt, a slightly acidic environment, dryness.
Biological defenses: Dead skin cells shed regularly, making colonization hard; normal microbiota outcompete pathogens.
SALT (Skin-Associated Lymphoid Tissue): Immune cells present to detect invaders.
Pathogens that cause skin infections
Bacteria: Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus spp., Rickettsia, Bacillus anthracis
Viruses: Varicella zoster virus (chickenpox, shingles), HSV, HPV, parvovirus B19
Fungi: Candida albicans, dermatophytes (cause tineas/ringworm)
Factors that establish infection
Skin barrier breaches: cuts, burns, insect bites, etc.
Immune status of host
Pathogen virulence
Environmental exposure (e.g. hospital setting)
Characteristic of Staphylococcus aureus
Gram-positive cocci in clusters
Salt-tolerant, survives on skin and in nasal passages
Spread easily via contact
Often causes pus, inflammation, fever
Can lead to toxic shock syndrome, scalded skin syndrome
Staphylococcus aureus
Gram stain: Gram-positive cocci
Catalase test: Positive (helps differentiate from Streptococcus)
Mannitol salt agar: Ferments mannitol (turns media yellow)
Coagulase test: Positive
Antibiotic sensitivity testing (e.g., Kirby-Bauer)
Virulence factors of Staphylococcus aureus
Capsule: Blocks phagocytosis
Coagulase: Forms clots, slowing immune response
Hyaluronidase, proteases, lipases: Break down host tissues
Alpha-toxin, leukocidins, hemolysins: Kill cells
Protein A: Binds antibodies inappropriately to avoid immune detection
MRSA
Methicillin-Resistant Staphylococcus aureus
Two types: HA-MRSA (hospital-acquired) & CA-MRSA (community-acquired)
Resistant due to mecA gene
MecA gene
Codes for PBP2a, a penicillin-binding protein
PBP2a has low affinity for beta-lactam antibiotics (e.g., penicillin), making them ineffective
Transferred via bacteriophage transduction
Staphylococcus aureus infections
Hair follicle infections, wound infections
Scalded skin syndrome (via exfoliatin toxin)
Impetigo, cellulitis, erysipelas, necrotizing fasciitis
Staphylococcus or Streptococcus infections
Impetigo
Erysipelas (more often S. pyogenes)
Cellulitis
Necrotizing fasciitis (also Clostridium, E. coli, Aeromonas)
Characteristics of Pseudomonas aeruginosa
Gram-negative rod, aerobic, has polar flagellum
Forms biofilms, produces pigments (e.g., pyocyanin)
Common in soil, water, hospital environments
Highly opportunistic and resistant to many antibiotics
Pseudomonas infections
Wound infections, especially in burn patients
Lung infections, skin rashes, eye, ear, and foot infections
C. perfringens
Anaerobic, causes gas gangrene via alpha-toxin, collagenase, hyaluronidase
C. tetani
Produces tetanospasmin toxin (causes spastic paralysis/lockjaw), vaccine-preventable
Infections by Viral pathogens
Varicella zoster: Chickenpox, shingles
HSV-1: Cold sores
HPV: Warts
Roseola (HHV-6), Fifth disease (Parvovirus B19): Mild rashes
Fungal pathogens
Dermatophytes (cause ringworm, tineas)
Candida albicans: Causes cutaneous candidiasis
Varicella virus
Enveloped dsDNA virus, part of Herpesviridae
Chickenpox: Respiratory spread, lesions on skin
Shingles: Reactivation of latent VZV in sensory ganglia
Vaccine available; can be severe in adults and immunocompromised