-
Staphylococcus aureus
coagulase +, b-hemolysis, golden colonies, mannitol +
Direct invasion w/ abscess formation causes folliculitis, furuncles, carbuncles, impetigo. Coagulase and clumping factor convert fibrinogen to a fibrin clot --> abscess formation. Protein A- binds Fc receptor of IgG. Enzymes- Lipases, Cytolytic toxins: alpha toxin pore forming
- Production of exotoxin causes toxin-mediated disease: scalded skin syndrome and toxic shock syndrome
- Scalded skin syndrome: exfoliative Toxins A and B. Proteases- cleave desmoglein on suface of epidermal cells. Involve exfoliative dermatitis. Cutaneus blisters- clear fluid w/ no organisms or leukocytes
- Toxic shock syndrome Toxin 1 (TSST-1): superantigens binds directly to MHCII on macrophages --> nonspecific proliferation of T cells and massive release of cytokines. Sudden onset of fever, vomiting, diarrhea. Red rash resembling a sunburn and desquamation 1-2 wks later. Hypotensive shock, impaired renal and hepatic function, occasional deaths
-
Streptococcus pyogens
- b-hemolytic, Group A strep, bacitracin sensitive
- wound infections, impetigo, erysipelas, cellulitis, necrotizing fasciitis, pharyngitis, scarlet fever, rheumatic fever, glomerulonephritis
- Protection: hyaluronic acid capsule (non-immunogenic), M protein (antiphagocytic), C5a peptidase
- Adhesion: M and F proteins
- Spreading factors and damage: streptolysins (pore forming), streptokinase (lysis of clots and fibrin deposition facilitate spread)
- exo-enzymes: hyaluronidase, DNAase
- Virulence factors: Pyrogenic or erythrogenic exotoxins. Phage coded superantigens --> massive release of cytokines. Scarlet fever (diffuse erythematous rash, strawberry tongue), streptococcal toxic shock syndrome
- Rx: penicillin
-
Vibrio vulnificus
- curved gram - rods, facultative anaerobe, polar flagella, oxidase +
- Halophilic- requires salt for growth
- found in salt water and known for contaminating oysters
- Virulence factors: polysaccharide capsule
- wound infections after exposure to contaminated seawater --> necrotic cellulitis
-
P. aeruginosa
- Hot tub folliculitis: skin rash in healthy persons
- infection of burn wounds: blue green pus, grape-like odor
-
Mycobacterium Leprae
- Acid fast bacillus
- no growth in artificial medium or tissue culture
- Causes Leprosy: chronic granulomatous disease of the peripheral nerves and superficial tissues
- incubation period: 2-7 yrs
- obligate intracellular parasite of macrophages and Schwann cells
- doesn't produce toxins; damage from host response
- Paucibacillary (tuberculoid) leprosy: Macules or large flattened plaques; raised erythematous edges w/ dry, pale, hairless centers (healing). Loss of sensation. low infectivity- few or no acid-fast rods. Dapsone + refampin 6 months
- Multibacillary (lepromatous) leprosy: multiple erythematous nodules, extensive tissue destruction, sensory loss, highly infectious, numerous acid-fast rods in lesions, deficient cell immunity. Dapsone + rifampin + clofazimine. 2 yrs
-
Bacillus anthracis
- gram + in box car chains, polypeptide capsule,
- EF= adenylate cyclase --> inc intracellular cAMP --> inc efflux of fluids and ions --> edema
- LF= mitogen-activated protein kinase kinase (MAPKK) protease --> disrupts cell signaling --> cell death and tissue necrosis
- Cutaneous anthrax:forarm or hands. starts from erythematous papules --> progresses through vesicular and ulcerative stages --> black eschar surrounded by edema
- Rx: fluoroquinolones (ciprofloxacin)
|
|