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