Lec 6: Agents of Skin Infection II (JERSE) Flashcards
Staphylococcus aureus
Beta hemolytic, Gram (+), Catalase (+), Coagulase (+)
Causes suppurative lesions
S. epidermidis
Gamma hemolytic, Gram (+), Catalase (+), Coagulase (-)
Infectious in hospital setting, immunocompromised patients, and post-surgical patients with indwelling medical devices
S. saprophyticus (sp)
Gram (+), Catalase (+), Coagulase (-)
Catalase Test
Dip small inoculum of bacteria into H2O2, bubbling = positive
Staph = (+)
Strep = (-)
Nosocomial infections
Infections acquired while in the hospital (i.e. MRSA)
S. aureus Virulence Factors
Protein A - “Absorbs” antibodies, binds Fc portion
Catalase - degrades H2O2
Leukocidin - pore forming protein, attacks leukocytes
Ribotechoic Acid, Techoic Acid - Bind fibronectin (in ECM)
Coagulase - Converts fibrinogen to fibrin (clot forming, staph hides in “shell” of clotted blood cells)
Capsule
Hyaluronidase - Breaks down hyaluronic acid, eases movement through subcutaneous tissues
Cytotoxins
S. aureus Cytotoxins
Alpha Hemolysin - toxic pore-former
Beta Toxin - hydrolyzes membrane phospholipids, aka sphingomyelinase C
Delta Toxin - Cytolytic, detergent-like action
Gamma Toxin - Pore-forming toxin, neutrophils and MacPs
Panton-Valentin Leukocidin (PVL) - Pore-forming toxin
S. intermedius
Coagulase (+)
Common flora in dogs, so suspect in dog bites
Exfoliatins
Cause: Bullous impetigo, scalded skin syndrome, staphylococcal scarlet fever
Serine proteases which break down desmosomes in the stratum granulosum of the epidermis
Toxic Shock Syndrome
Clinical Features:
sudden onset of: fever, chills, vomiting, diarrhea, rash, muscle pain
later: hypotension, invasion of mucous membranes and other systems, desquamation
5% fatality
At Risk Persons: Menstruating Women, Women with barrier contraceptive device, people undergoing nasal surgery
Pyoderma
Any skin that is pyogenic, high morbidity in deployed personnel
Bacteriophage Typing
S. aureus strains carry lysogenic viruses (Types I, II, and III) and are immune to infection by their own virus. Placing viruses onto separate S. aureus colonies allows identification of S. aureus strains
Vancomycin
Glycopeptide that binds to D-ala-D-ala residues of peptidoglycan precursors, inhibiting production of future peptidoglycans
Current recommended treatment for MRSA
VRSA
Vancomycin Resistant Staph. Aureus
Strongly resistant to Vancomycin
Due to acquisition of vanA gene (acquired from Enterococcus)
PG precursor now contains D-ala-D-lactate
VISA
Vancomycin Intermediate S. Aureus
Partially resistant to Vancomycin