This document summarizes several bacterial and fungal pathogens that can cause wound infections. Staphylococcus aureus is the leading cause and produces virulence factors like coagulase and protein A. Pseudomonas aeruginosa commonly causes nosocomial infections through drug resistance. Clostridium tetani causes tetanus through tetanospasmin toxin. Treatment involves vaccination, antitoxin, and antibiotics depending on the pathogen.

3.  Penetration of the skin by micro-organisms is
difficult—Part of the innate defense
 Wounds provide the most common access
through the skin.
 Disease production in infected wounds
depends on
› How virulent infecting organisms are
› How many organisms infect the wound
› Is the host immunocompetent
› Nature of the wound
 Does it contain crushed material or foreign material

4.  Leading cause of wound
infections
 Symptoms
› Bacteria are pyogenic
› Infection causes
 Inflammation
 Fever
› Some strains produce
toxic shock syndrome
 More than 30 recognized
strains

5.  Causative Agent: S. aureus
 Virulence due to the production of extracellular
products
 Coagulase
 Causes blood clotting to evade phagocytosis
 Clumping factor
 Aids in bacterial wound colonization
 Protein A
 Hide bacteria from phagocytic cells
  toxin
 Produces hole in host cell membrane

6.  Treatment
› Many strains develop resistance to antibiotics
 Many strains treated with anti β lactamase penicillins and
vancomycin
 Vancomycin resistant strain identified in 1997
 Epidemiology
 30% to 100% due to patient’s own flora
› Factors associated with infection include
 Advanced age
 Immunosupression or poor general health
 Prolonged postoperative hospital stay

7.  Primary pathogen is S. pyogenes
› Also known as “flesh eaters”
 Β hemolytic, Gram-positive cocci in chains
› Can cause rapidly deteriorating disease and death
 Common cause of wound infections
› Not a lot of antimicrobial resistance: early penicillin
 Two extracellular products
are responsible for
virulence
 Pyrogenic exotoxin A
 superantigen : toxic
shock
 Exotoxin B
 necrotizing fasciitis

8.  P. aeruginosa
 Major cause of
nosocomial infections
› Lung infections
› Burn infections
 Community acquired
infections include
› Rash and external ear
infections
› Infection of foot bones
› Eye infections
› Heart valve infections
› Lung biofilms

9.  Pathogenesis
› Some strains produce enzymes and toxins to enhance virulence
 Exoenzyme S
 Toxin A
 Phosphlipase C
 Epidemiology
› P. aeruginosa is widespread in nature
 Prevention and Treatment
› Prevention involves elimination of sources of bacteria
› P. aeruginosa is multi-drug resistant
› Medications must be administered intravenously at high
doses

10.  Symptoms
› Divided into early and late symptoms
› Early symptoms
 Restlessness
 Irritability
 Difficulty swallowing
 Contraction of jaw muscles
 Convulsions
 Particularly in children
› Later symptoms
 Increased muscle involvement
 Pain
 Difficulty breathing
 Death

11.  Causative Agent
› Clostridium tetini
 Anaerobic
 Gram-negative
 Bacillus
 Spore former
 25% mortality rate; rare in the developed world
› tetanospasmin toxin
 blocks inhibition of motor neurons, causing paralysis
 Prevention: vaccination, treatment: antitoxin
 Bacterial spores prevalent in dirt and dust and
gastro intestinal tract of humans and other animals

12.  Causative Agent
› Several species of Clostridium
 Most common offender, C. perfrigens
 Encapsulated, Gram-negative bacillus
 Endospores of causative bacillus are innumerable
› Spores found in nearly all soil or dusty surface
› Normal flora of intestinal tract and vagina
 Primarily disease of wartime
› Due to neglected wounds containing debris
› Treat with hyperbaric oxygen, antibiotics (penicillin)

13.  Causative Agent
› Actinomyces israelii
 Filamentous, anaerobic, slow growing
 Pathogenesis
› A. israelii cannot penetrate healthy mucosa
› Infection is characterized by cycles
 Abscess formation → scarring → formation of sinus tracts
› Disease progresses to skin and can penetrate bone or central
nervous system
 Epidemiology
› Can be normal flora
 Prevention and Treatment
› No proven prevention
› Responds to numerous antibacterials
 Penicillin and tetracycline

14.  Causative Agent
› Pasteurella multocida
 Gram-negative
 Coccobacillus
 Rounder bacillus shape
 Most are encapsulated
 Bite infections from numerous animals
› Fowl Cholera, animal reservoir
 Symptoms
› Spreading redness
› Tenderness
› Swelling of adjacent tissues
› Pus discharge

15.  Causative Agent
› Bartonella henselae
 Gram-negative bacillus
 Symptoms
› Disease begins within a week
› Painful enlargement of lymph nodes
› Fever
 Epidemiology
› Zoonotic disease
 Cats infected by flea
bite
› Infections treated
with amipicillin

16.  Causative Agent
› Streptobacillus moniliformis
 Gram-negative,Bacillus
 Symptoms
› Bite wound usually heals without complication
› Development of chills, fever, head and muscle ache and
vomiting 2 to 10 days after healing
 Majority of cases are self limiting
 7% - 10% of untreated cases are fatal

17.  Causative Agent
› Sporothrix schenckii
 Dimorphic fungus
 Lives in soil and on vegetation
 Associated with puncture wound
from vegetation
 Sporadic:
› rare in healthy people
› Untreated cases may become chronic
› Itroconazole and amphotericin B