BIOL2420 – Wound Infections Review

Wound Infections – General Concepts

  • The Human Body = Mostly Anaerobic
    • Deep tissues, avascular areas, necrotic pockets → O$_2$ falls to essentially 0 mmHg0\,\text{mmHg}.
    • Enables growth of obligate-/facultative-anaerobes that are harmless on skin but lethal inside.
  • Typical Routes of Entry
    • Traumatic injury (lacerations, punctures, crush, burns, surgery, IV lines, animal/human bites).
    • Hematogenous spread from another focus (e.g., endocarditis → septic emboli).
  • Types of Wounds
    • Clean surgical incision
    • Contaminated traumatic wound (soil, feces, saliva)
    • Crush / devitalized tissue (compartment syndrome risk).
    • Burn (intense protein coagulation, wide‐open vascular channels → large inoculum).
    • Anaerobic wound = any wound where circulation/O$_2$ is compromised (pressure sores, diabetic foot, frostbite, necrotic tumors, etc.)
  • Debridement
    • Defined as “removal / cleansing of all diseased tissue”.
    • Purposes: eliminate bacterial bioburden, reduce toxin load, relieve pressure, stimulate perfusion, create margin for antibiotics/immune response, & promote wound healing.
  • Abscess
    • Localized collection of pus within a newly formed cavity.
    • “Gigantic pus pocket deep in skin.”
    • MUST be drained; antibiotics alone fail (no vascular supply).
  • Clinical Importance of Anaerobic Wounds
    • Rapid toxin accumulation, extensive necrosis, systemic sepsis, limb-/life‐threatening.
    • Delay in recognition → exponential tissue loss (e.g., S. pyogenes\text{S.\ pyogenes} can advance 1 inch hr−11\,\text{inch hr}^{-1}).

Staphylococcal Wound Infections

  • Two Common Species
    • Staphylococcus aureus\textbf{Staphylococcus aureus} – more virulent
    • Golden-yellow ("aurum") colonies; yellow-tinged purulent exudate.
    • Produces multiple toxins: leukocidins, exfoliatin, TSST-1 superantigen ⇒ cytokine storm.
    • Staphylococcus epidermidis\textbf{Staphylococcus epidermidis} – opportunistic, less virulent
    • Normal skin flora; white colonies & white pus.
    • Virulence tied mainly to biofilm on plastic/metal (catheters, prostheses).
  • Shared Clinical Picture
    • Erythema, pain, warmth, purulent drainage, local abscess formation.
    • Both pyogenic (pus-forming) & trigger robust inflammation.
  • Pathogenesis Comparison
    • S. aureus → direct tissue damage via cytolytic toxins + superantigens.
    • S. epidermidis → indirect damage; inflammation from immune response to biofilm.
  • Epidemiology
    • Source = patient’s own microbiota or cross-contamination by HCWs/fomites.
    • Risk factors: surgery, trauma, diabetes, immunosuppression, foreign bodies.
  • Treatment / Prevention
    • Empiric oral β\beta-lactams → adjust per susceptibility.
    • Severe: IV therapy (vancomycin, linezolid, daptomycin, ceftaroline, etc.).
    • Antibiotic resistance:
    • MRSA (Methicillin-Resistant S. aureus) → used to be treated w/ vancomycin.
    • VRSA/VISA (Vancomycin-Resistant/Intermediate).
    • No licensed vaccine; infection control + proper wound care essential.

Necrotizing Fasciitis ("Flesh-Eating Disease")

  • Hallmark S/S
    • Sudden, disproportionate pain; erythema rapidly turning violaceous → black necrosis.
    • Bullae – large fluid-filled blisters; rupture → skin sloughs.
    • Fulminant course: hours to spread along fascial planes.
    • Systemic: fever, hypotension, toxic shock.
  • Causative Agents
    • Streptococcus pyogenes\textbf{Streptococcus pyogenes} (Group A β-hemolytic) – MOST common.
    • Polymicrobial (GAS + anaerobes), or other monomicrobial (V. vulnificus, S. aureus).
  • Pathogenesis
    • Bacteria introduced into fascia (via cut, surgery, blunt trauma, idiopathic).
    • Indirect damage: exotoxins (streptolysin, streptokinase, hyaluronidase, Spe superantigens) → ischemia, liquefaction of fascia, thrombosis of vessels.
    • Gas may or may not be produced (distinguish from clostridial myonecrosis).
  • Epidemiology
    • Incidence low but mortality high (20–40 %).
    • Comorbidities: DM, obesity, alcoholism, NSAID use (masking pain), varicella lesions.
  • Management
    • ALWAYS high-dose, broad-spectrum IV antibiotics (e.g., β\beta-lactam + clindamycin).
    • Emergent surgical debridement; delay >24 h24\,\text{h} doubles mortality.
    • Hyperbaric O$_2$ & IVIG considered adjuncts.
    • Amputation if uncontrolled.

Pseudomonas Wound Infections

  • Signature Sign
    • Purulent discharge tinted green (mix of blue "pyocyanin" + yellow-green "pyoverdin").
  • Agent
    • Pseudomonas aeruginosa\textbf{Pseudomonas aeruginosa} – aerobic Gram-negative rod; ubiquitous in soil & water.
  • Metabolism & Niche Shift
    • Strict aerobe unless NO3−\text{NO}_3^{-} present → uses nitrate as terminal e- acceptor → can thrive in otherwise anaerobic tissues (burn eschar, necrotic muscle, contact-lens solution, etc.).
  • Key Virulence Factors
    • Exotoxin A – ADP-ribosylates EF-2 → blocks host protein synthesis
      ⇒\Rightarrow impaired healing, necrosis.
    • Exoenzyme S – type III-secreted; interferes w/ phagocytosis & induces apoptosis.
    • Pigments (pyocyanin, pyoverdin) → generate ROS, sequester iron; also diagnostic.
  • Clinical Contexts
    • Burn wounds, ventilator-associated pneumonia, swimmer’s ear, hot-tub folliculitis, contact-lens keratitis, catheter infections.
    • Eye involvement can follow minor trauma + contaminated water.
  • Therapy & Prevention
    • Empiric anti-pseudomonal β-lactam (piperacillin-tazobactam/cefepime) + aminoglycoside or fluoroquinolone.
    • Multidrug resistance + biofilm formation complicate therapy.
    • Surgical debridement; amputation in refractory limb infections.
    • Strict infection-control in hospitals; no vaccine.

Clostridial Myonecrosis (Gas Gangrene) – preview

  • Caused mainly by Clostridium perfringens\textit{Clostridium perfringens}.
  • Alpha-toxin (lecithinase) → destroys muscle cell membranes.
  • Gas (H$2$, CO$2$) production = crepitus.
  • Therapy = STAT high-dose IV penicillin + clindamycin, extensive debridement, possible HBO.

Human Bite Wounds – preview

  • Polymicrobial mix: Aerobes (S. aureus, Eikenella corrodens) + anaerobes (Fusobacterium, Bacteroides).
  • Crush + inoculum → septic arthritis, osteomyelitis.
  • Empiric: amoxicillin-clavulanate; thorough irrigation.

Bartonellosis – preview

  • Cat-scratch disease (Bartonella henselae) can involve inoculation papule, adenitis; bacillary angiomatosis in AIDS.
  • Azithromycin / doxycycline.

Sporotrichosis – preview

  • “Rose-gardener’s disease.” Fungus Sporothrix schenckii\textit{Sporothrix schenckii}.
  • Lymphocutaneous nodular spread.
  • Itraconazole; saturated KI.

High-Yield Integrations & Exam Tips

  • Always think oxygen tension:
    • P. aeruginosa\text{P. aeruginosa} thrives when nitrate substitutes for O$_2$.
    • Clostridia & Streptococci multiply in totally anoxic fascia/muscle.
  • Debridement is the cornerstone for all necrotic, purulent, or biofilm-laden wounds; antibiotics alone fail where perfusion is absent.
  • Beware superantigens (S. aureus TSST-1; S. pyogenes SpeA/SpeC): can produce systemic shock in otherwise localized infections.
  • Monitor antibiotic resistance patterns:
    • MRSA →\rightarrow vancomycin/linezolid.
    • P. aeruginosa →\rightarrow combination therapy guided by MIC.
  • Differentiating Pus Color:
    • Yellow-gold ⇒\Rightarrow S. aureus.
    • White ⇒\Rightarrow S. epidermidis.
    • Green/Blue-green ⇒\Rightarrow P. aeruginosa.
  • Equation to remember – relationship of diffusion of O$2$ into tissue (Fick’s law): J=−D ΔCΔxJ = -D\,\frac{\Delta C}{\Delta x} ⇒ As thickness (Δx\Delta x) of necrotic tissue increases, flux (JJ) of O$2$ plummets (\Rightarrow) anaerobiosis.