Chapter 23: Microbiology of Wound Infections

A Glimpse of History

This section highlights the historical discoveries that shaped our understanding of wound infections, particularly tetanus and diphtheria.

• Shibasaburo Kitasato (1856–1931): Studied tetanus (lockjaw) in Robert Koch's laboratory.

• Identified Clostridium tetani spores in soil and dust.

• Determined C. tetani is an obligate anaerobe and developed cultivation methods.

• Showed that bacterial toxins (not the bacteria themselves) cause disease symptoms.

• Emil von Behring demonstrated that Corynebacterium diphtheriae also causes disease via toxin production.

23.1 Anatomy, Physiology, and Ecology of Wounds

Wound Types and Characteristics

Wounds differ in their nature, severity, and risk of infection. Understanding these differences is crucial for clinical management.

• Incisions: Clean cuts by sharp objects (e.g., knife).

• Punctures: Deep, narrow wounds from small sharp objects (e.g., nails).

• Lacerations: Irregular tears in tissue.

• Contusions: Tissue damage from blunt force (bruises).

• Abrasions: Superficial scraping of the epidermis.

• Gunshot wounds: Caused by projectiles.

• Burns: Result from heat, chemicals, electricity, radiation, or friction.

Wound Healing and Tissue Exposure

Wounds expose normally protected tissues, initiating a complex healing process.

• Collagen: Main supportive protein in skin, tendons, and scars.

• Fibronectin: Glycoprotein involved in tissue binding and repair.

• Fibrinogen: Blood protein converted to fibrin for clot formation.

• Granulation tissue: New connective tissue and capillaries that fill wound space, later replaced by collagen (scar tissue).

Wound Abscesses

An abscess is a localized collection of pus surrounded by inflamed tissue, representing a defensive response to infection.

• Pus: Contains living and dead leukocytes, tissue debris, and proteins.

• Abscesses help localize infection but can allow some bacteria to escape.

• Treatment is difficult due to poor blood supply and the presence of clots, which limit antimicrobial penetration.

• Abscesses often require surgical drainage.

Anaerobic Wounds

Some wounds create environments with low oxygen, favoring the growth of anaerobic bacteria.

• Obligate anaerobes like Clostridium tetani thrive in such conditions.

• Deep punctures, extensive tissue damage, or contamination with dirt increase risk.

• Facultative anaerobes can deplete oxygen, further supporting anaerobic growth.

23.2 Common Bacterial Infections of Wounds

Consequences of Infected Wounds

• Delayed healing and abscess formation.

• Spread of bacteria or toxins, potentially leading to systemic infection.

• Infected surgical wounds may compromise medical devices, necessitating removal.

Table: Leading Causes of Wound Infections

Staphylococcal Wound Infections

Staphylococcus aureus and S. epidermidis are the most common causes of wound infections.

• Signs and Symptoms:

  • Pyogenic (pus-forming) infections.

  • Inflammatory reaction, fever, and in severe cases, toxic shock syndrome (high fever, muscle aches, hypotension).

• Causative Agents:

  • Gram-positive cocci, facultative anaerobes, cluster formation.

  • Coagulase test distinguishes S. aureus (coagulase-positive) from others.

  • S. epidermidis is a major cause of healthcare-associated infections (HAIs).

• Pathogenesis:

  • S. aureus: Multiple virulence factors (clumping factor, enzymes, capsules, protein A).

  • Can evade immune response, cause intense inflammation, and form abscesses.

  • Some strains produce superantigens, leading to systemic effects.

  • S. epidermidis: Less virulent, forms biofilms on medical devices, can cause subacute endocarditis.

• Epidemiology:

  • S. aureus carriers at higher risk; risk factors include age, health status, and hospital stay.

  • S. epidermidis is part of normal skin and mucous membrane microbiota.

• Treatment and Prevention:

  • Methicillin-resistant S. aureus (MRSA) is a major concern; some strains are also vancomycin-resistant (VISA, VRSA).

  • Thorough wound cleaning is essential.

Group A Streptococcal "Flesh-Eating Disease" (Necrotizing Fasciitis)

• Causative Agent: Streptococcus pyogenes, β-hemolytic, Gram-positive, chain-forming.

• Signs and Symptoms: Sudden onset, severe pain, swelling, skin discoloration, fever, confusion, rapid progression to shock and death if untreated.

• Pathogenesis:

  • Virulence factors: M protein, SPEs (streptococcal pyrogenic exotoxins), enzymes (streptokinase, hyaluronidase, deoxyribonuclease, streptolysins).

  • Destruction of tissue, intense inflammation, systemic toxicity.

• Epidemiology: Rare, sporadic cases; risk factors include chronic diseases, immunosuppression, recent surgery, and trauma.

• Treatment and Prevention: Immediate surgery to remove dead tissue; penicillin effective early but not against toxins or bacteria in necrotic tissue.

Pseudomonas aeruginosa Infections

• Opportunistic pathogen: Major cause of healthcare-associated and burn wound infections.

• Signs and Symptoms: Chills, fever, skin lesions, shock, greenish wound color due to pigments (pyoverdin, pyocyanin).

• Causative Agent: Gram-negative rod, polar flagellum, found in soil and water, aerobic but can respire anaerobically with nitrate.

• Pathogenesis:

  • Tissue damage, delayed healing, risk of septic shock.

  • Exotoxin A inhibits host protein synthesis; Exoenzyme S disrupts cell membranes.

  • Pyocyanin pigment acts as a siderophore and impairs respiratory epithelium.

• Epidemiology: Widespread in moist environments; can contaminate medical equipment and solutions.

• Treatment and Prevention: Few effective antimicrobials; infection control and removal of dead tissue are critical.

23.3 Diseases Due to Anaerobic Bacterial Wound Infections

Tetanus (Lockjaw)

• Signs and Symptoms: Difficulty swallowing, jaw muscle contractions, painful spasms, breathing difficulty, abnormal heart rhythms, possible fractures.

• Causative Agent: Clostridium tetani, anaerobic, Gram-positive, spore-forming rod.

• Pathogenesis:

  • Not invasive; remains localized in wound.

  • Produces tetanospasmin (an AB exotoxin) that blocks inhibitory neurotransmitter release, causing uncontrolled muscle contraction.

• Epidemiology: Spores widespread in soil, dust, and animal intestines; risk from puncture wounds, poor immunization, and improper wound care.

• Treatment and Prevention: Tetanus immune globulin (TIG), wound cleaning, antibiotics, and vaccination with inactivated tetanus toxoid.

Clostridial Myonecrosis (Gas Gangrene)

• Signs and Symptoms: Severe pain, swelling, bloody or brownish fluid, gas bubbles, skin discoloration, rapid progression to delirium and coma.

• Causative Agent: Clostridium perfringens (most common), other Clostridium species.

• Pathogenesis:

  • Requires dead or poorly oxygenated tissue.

  • Produces alpha-toxin (lecithinase) that destroys cell membranes, collagenase, and hyaluronidase.

  • Gas production (hydrogen, CO2) leads to tissue swelling.

• Epidemiology: Common in soil and animal feces; risk factors include trauma, surgery, diabetes, and cancer.

• Treatment and Prevention: Surgical removal of dead tissue, antibiotics, hyperbaric oxygen; no vaccine available.

Actinomycosis (Lumpy Jaw)

• Signs and Symptoms: Slow-growing, sometimes painful swellings that burst and drain pus, often on jaw or neck.

• Causative Agent: Actinomyces israelii, Gram-positive, filamentous, slow-growing anaerobe.

• Pathogenesis: Infection requires tissue injury; forms dense yellowish colonies ("sulfur granules").

• Epidemiology: Part of normal oral and intestinal microbiota; not transmitted person-to-person.

• Treatment and Prevention: Prolonged antibacterial therapy; prevention by avoiding tissue injury.

23.4 Bacterial Infections of Bite Wounds

Human Bites

• Signs and Symptoms: Initially minor, but can become painful, swollen, and produce foul-smelling pus.

• Causative Agents: Mixed aerobic and anaerobic oral microbiota, including Streptococcus, Staphylococcus aureus, Bacteroides, and others.

• Pathogenesis: Synergistic infection due to combined action of multiple species and their enzymes/toxins.

• Treatment and Prevention: Immediate cleaning, surgical opening, and broad-spectrum antibiotics.

Pasteurella multocida Bite Wound Infections

• Signs and Symptoms: Rapidly spreading redness, swelling, pus, possible abscesses, risk of bloodstream invasion.

• Causative Agent: Pasteurella multocida, Gram-negative, facultative anaerobic coccobacillus.

• Treatment and Prevention: Penicillin (with β-lactamase inhibitor), immediate wound cleaning.

Bartonellosis (Cat Scratch Disease)

• Signs and Symptoms: Pus-filled pimple, enlarged lymph nodes, fever; usually self-limiting.

• Causative Agent: Bartonella henselae, curved Gram-negative rod.

• Treatment and Prevention: Antibacterial medications for severe cases; avoid stray cats and fleas.

Streptobacillary Rat Bite Fever

• Signs and Symptoms: Fever, chills, rash, joint pain after rat bite or ingestion of contaminated food.

• Causative Agent: Streptobacillus moniliformis, Gram-negative, pleomorphic rod.

• Treatment and Prevention: Penicillin; prevention by rodent control and safe handling.

23.5 Fungal Wound Infections

Sporotrichosis (Rose Gardener's Disease)

• Signs and Symptoms: Chronic ulcers and nodules along lymphatic vessels, usually on hands or arms.

• Causative Agent: Sporothrix schenckii, a dimorphic fungus found in soil and vegetation.

• Pathogenesis: Spores enter via plant material injury, cause local and lymphatic infection.

• Treatment and Prevention: Oral potassium iodide, itraconazole, or amphotericin B; prevention by wearing gloves and protective clothing.

Additional info: This chapter integrates concepts from microbial pathogenesis, host defense, and clinical microbiology, providing a comprehensive overview of wound infection etiology, mechanisms, and management.