Gram Pos Cocci Flashcards
Basic characteristics of Staph
-G+
-Nonmotile
-Non-spore-forming
-Spherical in single, pairs, tetrads, or clusters
-Facultative anaerobes (except S. saccharolyticus / S. aureus subsp. anaerobius - SHEEP)
-Cat+
-Grow in 10% NaCl
-Respiratory and fermentative
-Cytochrome ox-
Presumptive ID of Staphs
1) Coagulase Pos = Staph aureus, (sometimes Staph lugdunensis but S. lug is PYR+)
2) Novobiocin S = S.epi group (S. epi, S. capitis, S. haemolyticus, S. hominis, S. lug, S. sacch, S. warneri)
3) Novobiocin R = S. sapro group (S. saprophyticus, S. cohnii, S. kloosii, S. xylosus)
4) Growth / yellow on Mannitol Salt Agar = Staph aureus
S. aureus habitat
Human nasal cavity - 41% carrier state
Can also be carried in other locations - throat, intestine, vagina, skin folds, axillae, perineum
CA-MRSA
-More likely to carry PVL, a pore-forming toxin with cytolytic and inflammatory activities
-Superficial skin and soft tissue infections (rarely pneumonia or necrotizing fasciitis)
CoNS
-S. epi most frequently isolated -> colonies body surface
-S. auricularis -> ear canal
-S. capitis -> forehead / scalp sebaceous glands
-S. haemolyticus / S. hominis -> axillae / pubic apocrine glands
-S. sapro. -> rectum / genital tracts of females
-S. lug -> groin / lower extremeties
S. scuirui / S. xylosus -> animal skin / mucous membranes
Staph causes of HAI
1 = CoNS
#2 = S. aureus
S. aureus #1 in vent-assoc. infections
S. aureus chronic infections
More likely from small-colony variant phenotype -> intracellular
Phenotype switching
Staph toxins: ProteinA
Binds to Fc of IgG to protect from phagocytosis
Staph toxins: Coagulase
Fibrin formation around the bacteria to protect from phagocytosis
Staph toxins: Hemolysins
Alpha, beta, gamma, delta - destroy RBCs and WBCs and platelets
-Alpha = RBC, platelets, Mphage
-Beta = Sphingomyelinase
-Gamma = PVL -> kills PMNs
Staph toxins: Leukocidins
Destroy WBCs
-Ex: PVL of CA-MRSA
Staph toxins: Penicillinase
Beta-lactamase-> secreted
Staph toxins: Novel penicillin binding protein (transpeptidase)
Penicillin / cephalosporin resistance
-Ex: mecA or mecC PBP2A / PBP2C- takes over when transpeptidase is inactive
Staph toxins: Hyaluronidase
Spreading Factor: breaks down peptidoglycans in connective tissue
Staph toxins: Staphylokinase
Lyses fibrin clots
Staph toxins: Lipase
Breaks down fats and oils for colonization in sebaceous glands
Staph toxins: Protease
Destroys proteins
Staph toxins: Exfoliatin (Epidermolytic) toxin A and B
Exotoxin - Scalded Skin Syndrome, Bullous impetigo, Ritter’s disease (>90% body surface)
Staph toxins: Enterotoxins
Heat stable
-A, B, D = Food poisoning
-B, C, G, I = TSS
-B = Pseudomembranous colitis
Staph toxins: TSST-1
Superantigen
Pyrogenic toxins, bind to MHC class II on APCs -> T-cell response (TNF / INL-1) -> cytokines -> toxic shock
Staph aureus infection states
1) Pneumonia - usually after flu in hospital patients -> holes in lungs, pus in pleural spaces
2) Brain - meningitis
3) Osteomyelitis - local infection, fever, chills -> boys <12
4) Acute endocarditis - growth on heart valve -> more sudden onset than VirStrep
5) Septic arthritis - red, swollen joint “closed infection of joint cavity” -> peds & >50
6) Skin - bullous impetigo, cellulitis, abscesses, wounds
7) Blood / Cath
MRSA genomics
SCCmec = staph cassettee chromosome conferring resistance to methicillin -> 12 current variations
HA-MRSA - large SCCmec with lots of resistance genes (types I-IV, VI, VIII)
CA-MRSA - smaller SCCmec with fewer resistance genes (IVa, V, VII)
S. aureus “sister species”
S. argenteus / S. schweitzeri
S. epi pathogenicity
1) Polysaccharide capsule -> biofilm -> implanted devices / shunts / grafts / intravenous lines