Wound Infections: Chapter 24- Wounds can be classified aso incised (incision) knife/other sharp object surgical wound infections = large healthcare costo puncture small sharp objecto laceration tissue is torno contusion crushed tissue by impacto burn a.k.a thermal burns are initially sterile- Wound Infectionso Wounds are infected by microbes from fingers, air, object causing wound, normal flora => attach to exposed underlying tissue parts: fibrin, fibrinogen, collagen…o wound abscess localized collection of pus surrounded by body tissue abscess helps localize infection to prevent spread in body to resolve: abscess must rupture to a body surface or be surgically drainedCommon Bacterial Wound Infections- Consequences of wound infection:o delay in healingo formation of abscess: localized damageo spread of bacteria or their products to tissues and bloodstream: systemic damage- Staphylococcal Wound Infectionso staphylococci are the leading cause of wound infectionso commonly in nose, on skino two species account for most human infections S. aureus S. epidermidiso pyogenic = produce puso inflammation swelling, pain, rednesso fever if infection has spreado some strains cause toxic shock syndrome- Staphylococci, common skin organisms, are Gram+, aerobic/anaerobic, salt-tolerant (sweat)o some impt Staphylococcus aureus virulence factors Coagulase- is bound tightly to S. aureus surfaces where it stimulates formation of blood fibrin (from fibrinogen) => fibrin “coating” Clumping factor A- helps bacteria colonize fibrin (and plastics) in wound- also coats S. aureus surfaces Protein A- binds (coats) antibody Fc to Staph cell envelope note that all three- protect/‘hide’ (coat) bacteria from immune cells- therefore immunity to Staph infections weak- Staphylococcal Wound Infectionso Staphylococcus epidermidis little or no invasivness, normally stays on skin surface but through a wound- can colonize in-dwelling devices e.g. catheters- biofilm (protects from phagocytosis and antibiotics) - cells from biofilms carried into bloodstream can  subacute bacterial endocarditis or multiple tissue abscesses- generally in immuno-compromised Prevention of infection - cleanse wound- remove dirt and crushed tissue- close promptly- pre-surgical antibioticso lowers infection rateo extensive precautions in hospitals Treatment can be very challenging due to widespread antibioticR- β-lactamaseR penicillins such as methicillin- vancomycin, teicoplanin but vancomycinR (VISA) strain appeared in 1997- newer drugs: linezolid, synercid and daptomycin are effective- several more being testedo Group A Streptococcal Infections- a.k.a. “flesh eating”- primary pathogen is o Streptococcus pyogenes- common cause of wound infections- not alot of antimicrobial resistance => can generally be treated- but if invasive can cause rapidly deteriorating disease and death Severe S. pyogenes infections are invasive- pneumonia, meningitis, Puerperal (childbirth) Fever- Necrotizing fasciitis (fascia = fibrous tissue underlying the skin and surrounding muscles and organs)- Streptococcal toxic shock Two extracellular products important for virulence- Pyrogenic exotoxin A = a superantigen => streptococcal toxic shock- Exotoxin B = tissue-degrading protease helps invasion Epidemiology- “Flesh eating” infections recorded for centuries- usually sporadic but cause public alarm- (USA 2002) ~9,000 cases invasive S .pyogenes infections => 1080 deaths; 135 from necrotizing fasciitis Treatment- urgent surgery (sometimes amputation) due to rapid spread of toxin- Penicillin still usually effectiveo must be given early o little or no effect on bacteria in necrotic tissueso no effect on toxino surgery may still be necessaryo Pseudomonas aeruginosa Infections Pseudomonas aeruginosa- generally aerobic but can grow anaerobically- produces numerous water-soluble pigments- combinations of pigments => tissues often green- opportunistic pathogen- major cause of nosocomial infections – lungs and wounds- wounds – esp. burns- widespread in nature, especially soil, water, plantso enters hospitals on shoes, ornamental plants and flowers, produc- Pseudomonas persist in dampness or standing water- contaminates soaps, cosmetics, contact lens solution, swimming pools, hospital equipment, etc Symptoms- change in tissue color- chills, fever, skin lesions and shock due to bacteria in bloodstream Prevention- eliminate sources of bacteria- prompt wound care- remove dead tissue from burns and applyo silver sulfadiazine (Silverex, etc) o topical sulfonamide/silver antibacterial Treatment- established infections very difficult to treato P. aeruginosa is multi-drug resistant- high dose IV antibioticso Tetanus Early symptoms- restlessness, irritability- difficulty swallowing- contraction of jaw muscles- convulsions, particularly in children Later symptoms- increased muscle involvement and pain- difficulty breathing- deatho pneumoniao regurgitation of stomach contents into lungsClostridium tetani- anaerobic, Gram-positive, spore-former- spherical endospores at tip of rod [instead of oval, centered spores of other Clostridium pathogens- swarming growth on laboratory media- endospores very common in dust and soil Pathogenesis- not invasive: colonization usually confined to wound- toxin does the damage- Tetanus toxin = tetanospasmino toxin = two protein chainso heavy chain binds receptors on motor neuronso lighter chain taken up through endocytosis- Tetanospasmin blocks inhibition of motor neurons, causing spastic paralysiso uncontrolled muscle contraction o usually begins in the jaw, spreads through nervous system, very painful, frequently fatal Epidemiology- C. tetani found in dirt, dust and GI tract of humans and other animals from food carrying C. tetani spores (soil or fecal contamination)- infections in anaerobic locationso puncture wounds: stepping on a nail, body piercing, tattooing, animal bites, dirty needleso incisions: surgical infections- a few dozen cases in US annually - 25% mortality- much more common in poor countries: neonatal tetanus Prevention- immunization- tetanospasmin toxoid- developed in 1924, widely used for WWII wounded- DPT combination vaccine with diphtheria and pertussis Treatment- thoroughly clean wound and remove dead tissue [debridement] => aerobic- metronidazole (IV) to kill multiplying bacteria [but not spores]-