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Dept. Microbiology-PIFM School of Medicine-UAG

Bacterial Infection of the Skin and Soft Tissue. Dept. Microbiology-PIFM School of Medicine-UAG. A.- General Characteristics. 1.- Skin is relatively resistant to infection. 2.- Microflora inhibits harmful organism. 3.- Skin infections occur when protective mechanism fall.

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Dept. Microbiology-PIFM School of Medicine-UAG

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  1. Bacterial Infection of the Skin and Soft Tissue Dept. Microbiology-PIFM School of Medicine-UAG

  2. A.- General Characteristics 1.- Skin is relatively resistant to infection. 2.- Microflora inhibits harmful organism. 3.- Skin infections occur when protective mechanism fall.

  3. A.- General Characteristics Entry 1) Skin (pores, hair follicles). 2) Wounds (scratches, cuts, burns). 3) Insect & animal bites.

  4. A.- General Characteristics Diseases • Localized infections with local and/or systemic effect. • Systemic infections. Multiplication • Extracellular. • Intracellular (??). Damage • Toxin. • Host immune response.

  5. A.- General Characteristics Defense • Dry Usual infection sites are wet areas, skin folds, armpit, groin • Acidic (pH 5.0) • Temperature less than 37oC Some pathogens grow best <37oC • Lysozyme and toxic lipids (pore, hair follicles, sweat gland) • Resident microflora (mainly Gram positives) • Skin-associated lymphoid tissue (SALT)

  6. B.- Skin and Soft Tissue Infections 1.- Impetigo: Initially a vesicular infection that rapidly evolves into pustules that rupture, with the dried discharge forming honey-colored crust on an erythematous base.

  7. 2.- Ecthyma(Pustules): Begin as vesicles that rupture, creating circular erythematous lesions with adherent crusts. 3.- Folliculitis: Inflammation at the opening of the hair follicle that causes erythematous papules and pustules surrounding individual hairs. 4.- Furuncle: Deep-seated inflammatory nodule with a pustular center that develops around a hair follicle. (painful, localized, abscess).

  8. 5.- Carbuncle: Involvement of several adjacent follicles, with pus discharging from multiple follicular orifices. 6.- Cutaneous abscesses: Painful, fluctuant, red, tender swelling, on which may rest a pustule. 7.- Erysipelas: Erythema and swelling of the cutaneous surface, involves the superficial dermis (redness-lymphangitis).

  9. 8.- Cellulitis: Erythematous, hot, swollen skin with irregular edge. (affects the deeper dermis and subcutaneous fat.) 9.- Acne: Infection of sebaceous follicles with plugs of keratin blocking the sebaceous canal, resulting in “blackheads”.

  10. 10.- Necrotizing fasciitis: Rapidly spreading cellulitis with necrosis (skin and deeper fascia; may involve muscle). Begin with fever, systemic toxicity, severe pain in the development of a painful, red swelling that rapidly progress to necrosis of the subcutaneous tissue and overlying skin.

  11. Staphylococcus Dept. Microbiology-PIFM School of Medicine-UAG

  12. Family Micrococcaceae Genera: Micrococcus Planococcus Stomatococcus Staphylococcus Saprophyte

  13. Family Micrococcaceae Genera: Staphylococcus The name staphylococcus is derived from the Greek term sthapylé meaning “ a bunch of grapes”.

  14. Family Micrococcaceae Genera: Staphylococcus May occur singly, in pairs, or clusters, this arrangement is due to tendency of the organism to divide in different planes.

  15. Clinically important species of staphylococci 1.- Staphylococcus aureus 2.- Staphylococcus epidermidis 3.- Staphylococcus saprophyticus

  16. Clinically important species of staphylococci 1.- Staphylococcus aureus (Coagulase +) 2.- Staphylococcus epidermidis 3.- Staphylococcus saprophyticus

  17. Clinically important species of staphylococci S. Aureus classically has a golden or yellow pigmentation, but many clinical isolates have a creamy or white pigmentation.

  18. Morphology and Physiology 1.- Gram positive cocci, usually arranged in clusters. 2.- Non-motile, non-sporeforming. 3.- Grow over a wide temperature range (10-42° C), optimum of 37° C 4.- Aerobic and facultatively anaerobic. 5.- Grow on simple media 6.- Catalase positive.

  19. Morphology and Physiology Gram positive cocci which may lose the ability to retain their gram positive staining characteristics with age. Capsule: a loose – fitting, polysaccharide layer ( slime layer) is only ocasionally found on staphylococci cultured in vitro. Eleven capsular serotypes have been indentified in S. aureus, with serotypes 5 and 7 associated with the mayority of infections. Half of the cell wall by weight is peptidoglycan, a feature common to G+.

  20. Morphology and Physiology The peptidoglycan consists of layers of glycan chains built with 10 to 12 alternting subunits N- acetylmuramic acid and N- acetylglucosamine. The peptidoglycan has endotoxin – like activity, stimulating the production of endogenous pyrogens, activation of complement and the production of IL- 1 from monocytes.

  21. Morphology and Physiology Teichoic Acids are species – specific, ribitol teichoic acid with N- acetylglucosamine residues (polysaccharide A) is present in S. aureus. Glycerol teichoic acid with glucosyl residues (polysaccharide B) is present in S. epidermidis. The outer surface of most strains of S. aureus contains clumping factor ( bound coagulase)

  22. Characteristics of Staphylococcusaureus 1.- Colonial morphology: Colonies are grey to golden yellow and produces hemolysins (beta hemolysis on Blood Agar). 2.- Enzymes: a) Coagulase, which acts on plasma to form a clot. b) Deoxyribonuclease (DNAase) 3.- Protein A, cell-wall antigen 4.- Halophilic (tolerate high concentrations of salt) and ferments mannitol

  23. Epidemiology 1.- Reservoir: Nasal carriage (30-50% of healthy adults), fecal carriage (20%), skin carriage in 5-20% of healthy individuals. 2.- Transmission: a) Via droplets (sneezing) and skin scales (hands) b) Direct contamination of surgical wounds c) Contaminated foods: Ham, canned meats, custard pastries, and potato salad.

  24. Epidemiology Major defenses against S. aureus C3b • Activated by Staph cell wall fragments. • Opsonizes the bacteria. • Enhances phagocytosis. 1) Chemotaxis – attracts neutrophils. 2)Neutrophils – engulf the bacteria. 3) Intracellular killing by O2 radicals.

  25. Epidemiology Conditions predispose to Staph infections 1) C3 hypercatabolism 2) Chemotherapy–induced neutropenia 3) Cyclic neutropenia 4) Chronic granulomatous disease (reduced H2O2 production) 5) “Lazy leukocyte” (chemotaxis deficiency)

  26. 3.- Predisposing Factors: a) Skin trauma: Break or surgery, surgical. packing foreign bodies; e.g. Tampons. b) Neutropenia: < 500/μL Cystic fibrosis. c) IV drug abuse. d) Chronic granulomatous disease.

  27. E.- Virulence Factors: 1) Coagulase: convert fibrinogen to a fibrin deposition which interferes with phagocytosis and increases the invasion of tissue. 2) Hemolysins and Leucocidin: cytolytic exotoxin a) α-Toxin: lyses erythrocytes and damage platelets (pore-forming toxin in cell membrane) b) β-Toxin: degrades sphingomyelin and is toxic for erythrocytes. c) Leucocidin: lyses WBC.

  28. 3) Protein A: inhibit phagocytosis, binds Fc of IgG (prevent Complement activation). 4) Exfoliatins: causes desquamation of the skin (Scalded skin syndrome), formation of bullae.

  29. 5) Toxic shock syndrome toxin(TSST-1): desquamation of skin, shock. Superantigen: activates large numbers of CD4 T cells with induction of cytokines production. 6) Staphylokinase: fibrinolysis 7) Hyaluronidase: dissolves hyaline 8) Lipase: solubilize lipids 9) EnteroToxins: A-E, soluble, heat stable at 60-80 °C for 10min; resistant GI enzymes, acts 2-6 h, vomiting.

  30. F.- Clinical Manifestations: 1)Folliculitis, Furuncles, Carbuncles, Abscess. Mechanism: Coagulase, cytolitic exotoxins.

  31. Suppuration (pus production) is a hallmark of these Infections.

  32. 2) Impetigo: Erythematous papules to bullae. Mechanism: Coagulase, exfoliatins 3) Staphylococcal Scalded Skin Syndrome(SSSS) Mechanism: Exfoliatins *Ritter’s disease: Infants, bullous exfoliative dermatitis. From localized perioral erythema to entire body (2 days). *Bullous impetigo. Negative Nikolsky’s sign. Erythema limited to localized blisters (contains bacteria).

  33. 4) Staphylococcal Food Poisoning: Mechanism: Preformed Enterotoxin A-E Onset is abrupt and rapid (4 h). Severe vomiting, diarrhea, and abdominal pain or nausea. Sweating and headache may occur, but not fever. Watery, non-bloody diarrhea. 5) Toxic Shock Syndrome: Mechanism: TSST-1 Localized growth of toxigenic strains in vagina or wound. Start abruptly, fever, hypotension, and diffuse macular erythematous rash. Multiple organs and systems are involved, entire body skin desquamates.

  34. 6) Bacteremia and Endocarditis: Mechanism: Cytolytic toxins, Fibrin-platele mesh. Nosocomial use of contaminated intravascular catheter or IV drug abusers. Nonspecific influenza-like symptoms, disruption of cardiac output and septic embolization. 7) Pneumonia and Empyema: Mechanism: Cytotoxins and enzymes Aspiration or hematogenous pneumonia: Patchy infiltrates with consolidation or abscesses.

  35. 8) Osteomyelitis and Septic Arthritis: Hematogenous dissemination or secondary infection from trauma. In adults: Vertebral. Intense back pain with Fever. Brodie’s abscess. In children: Metaphyseal area of long bones. Localized pain, fever. Septic arthritis: Young children and adults who are receiving intraarticular injections or have abnormal joints. Painful, erythematous joints, purulent exudates(shoulder, knee, hip).

  36. Laboratory diagnosis 1.- Clinical specimen: Scrapes the base of the abscess with a swabs. Gram stain: Gram (+) cocci in clusters 2.- Culture: Blood Agar, Mannitol Salt Agar Identification: Coagulase (+), heat-stable nuclease (+), and mannitol fermentation On blood agar S. aureus produces beta hemolysis. Other Staph. species produce alpha or gamma hemolysis.

  37. Laboratory diagnosis 2.- Mannitol salts agar (MSA) – high salt(7.5) inhibits the grow most ohtrer organisms, S. aureus ferments mannitol, the acid produce turns the colonies yellow and S. epidermidis does not.

  38. Laboratory diagnosis 2.- Coagulase (+). 2.- Catalasa (+).

  39. Laboratory diagnosis 2.- Novobiocin S. epidermidisis sensitive S. sprophyticus is resistant 2.- Bacitracina (+).

  40. S. Epidermidis 1.- Endocarditis. 2.- Catheter and shunt infections. 3.- Prosthetic Joint Infections. S. Epidermidis Urinary Tract Infections.

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