1. Consequences include: –Delay in healing –May result in localized infection (abscess) –Bacteria or their products may migrate to adjacent tissues or bloodstream Wound Infections

2. Causative Agent –Streptococcus pyogenes “flesh eating bacteria” –Dramatic but rare Small epidemics occur –Generally easily treated Not a lot of antimicrobial resistance Necrotizing Fasciitis

3. Signs and symptoms –Nausea, and other flu- like symptoms –Intense pain and swelling at infection site –Discoloration and distortion of skin –Skin hot to the touch –Fever, malaise,

4. Epidemiology –Usually spread through direct contact –Pathogen enters through wound and produces enzymes and toxins that destroy tissue several cm per hour may cause organ failure –Severe infections termed invasive Pneumonia Meningitis Streptococcal toxic shock Death

5. Prevention –No proven prevention measures –Wounds increase risk –Difficult to diagnose in the early stages because the symptoms are nonspecific and flulike

6. Treatment –clindamycin and penicillin treatment must be given early has little or no effect on bacteria in necrotic tissues No effect on toxin –Urgent surgery required Removal of necrotic tissue Amputation

7. Pseudomonas Infections Causative agent: –Pseudomonas aeruginosa –G-, aerobic bacillus –Opportunistic pathogen –Major cause of nosocomial infections Burn and lung infections –Occasional cause of community acquired infections Contaminated pools and hot tubs

8. Signs & Symptoms –Change in tissue color pyocyanin –Chills, fever, skin lesions and shock

9. –Multiple virulence factors Endotoxin Exoenzyme S Toxin A Elastase Neuramindase Polysaccharide capsule Fimbriae

10. Epidemiology –Rarely part of the microbiota –Widespread in nature Found extensively in soil, water and on plants –Introduced in hospitals on shoes, on plants and flowers and on produce –Contaminates soaps, ointments, eye drops, swimming pools and hospital equipment

11. Prevention –Prevention involves elimination of source –Prompt wound care –Debridement of burns Removal of eschar followed by application of antibacterial cream like silver sulfadiazine

12. Treatment –Established infections are extremely difficult to treat P. aeruginosa is multi-drug resistant Typically combine aminoglycosides and beta- lactam drugs Polymyxin last resort drug

13. Clostridial Myonecrosis gas gangrene Causative agent: –Species of Clostridium, most commonly C. perfrigens Encapsulated; anaerobic, gram + bacillus Produces endospores

14. Signs and symptoms –Begins abruptly with rapidly increasing localized pain and swelling –Thin, foul smelling fluid leaks from wound Fluid is often brownish and frothy –Frothy appearance is due to gas production by infection bacteria –Crepitation –Skin becomes stretched and mottled with black spots Ishemia and necrosis –Delirium and coma followed by death Mortality ~ 40%

16. –C. perfringens unable to grow in healthy tissue Survives well in dead or poorly oxygenated tissue Releases toxin in tissue –Bacteria produces gas through fermentation Gas accumulates in tissue contributing to spread Crepitation

17. Gas-filled spaces produced by C. perfringens.

18. Bacteria produces neurotoxin Toxin attacks host cell membrane –Toxin diffuses and kills tissue cells Other enzymes breakdown dead tissues –Collagenase –Hyaluronidase (spreading factor)

19. –Factors that increase susceptibility to clostridial myonecrosis Presence of dirt and dead tissue in wound –Spores found in nearly all soil or dusty surface Poor circulation –encourages poor oxygenation of tissues Long delays in treatment –Immediate medical attention in severe wound is especially important

20. Prevention and treatment –Vaccine unavailable –Prompt cleaning and debridement of wound –Surgical removal of dead and damaged tissue Amputation may be required –Hyperbaric oxygen treatment Inhibits growth of clostridia –Stops release of toxin –Penicillin or cephalosporin are given to halt bacterial growth No growth = no toxin production