Gram Pos Cocci Flashcards

1
Q

Basic characteristics of Staph

A

-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-

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2
Q

Presumptive ID of Staphs

A

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

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3
Q

S. aureus habitat

A

Human nasal cavity - 41% carrier state
Can also be carried in other locations - throat, intestine, vagina, skin folds, axillae, perineum

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4
Q

CA-MRSA

A

-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)

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5
Q

CoNS

A

-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

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6
Q

Staph causes of HAI

A

1 = CoNS

#2 = S. aureus

S. aureus #1 in vent-assoc. infections

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7
Q

S. aureus chronic infections

A

More likely from small-colony variant phenotype -> intracellular
Phenotype switching

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8
Q

Staph toxins: ProteinA

A

Binds to Fc of IgG to protect from phagocytosis

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9
Q

Staph toxins: Coagulase

A

Fibrin formation around the bacteria to protect from phagocytosis

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10
Q

Staph toxins: Hemolysins

A

Alpha, beta, gamma, delta - destroy RBCs and WBCs and platelets
-Alpha = RBC, platelets, Mphage
-Beta = Sphingomyelinase
-Gamma = PVL -> kills PMNs

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11
Q

Staph toxins: Leukocidins

A

Destroy WBCs
-Ex: PVL of CA-MRSA

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12
Q

Staph toxins: Penicillinase

A

Beta-lactamase-> secreted

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13
Q

Staph toxins: Novel penicillin binding protein (transpeptidase)

A

Penicillin / cephalosporin resistance
-Ex: mecA or mecC PBP2A / PBP2C- takes over when transpeptidase is inactive

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14
Q

Staph toxins: Hyaluronidase

A

Spreading Factor: breaks down peptidoglycans in connective tissue

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15
Q

Staph toxins: Staphylokinase

A

Lyses fibrin clots

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16
Q

Staph toxins: Lipase

A

Breaks down fats and oils for colonization in sebaceous glands

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17
Q

Staph toxins: Protease

A

Destroys proteins

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18
Q

Staph toxins: Exfoliatin (Epidermolytic) toxin A and B

A

Exotoxin - Scalded Skin Syndrome, Bullous impetigo, Ritter’s disease (>90% body surface)

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19
Q

Staph toxins: Enterotoxins

A

Heat stable
-A, B, D = Food poisoning
-B, C, G, I = TSS
-B = Pseudomembranous colitis

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20
Q

Staph toxins: TSST-1

A

Superantigen
Pyrogenic toxins, bind to MHC class II on APCs -> T-cell response (TNF / INL-1) -> cytokines -> toxic shock

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21
Q

Staph aureus infection states

A

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

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22
Q

MRSA genomics

A

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)

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23
Q

S. aureus “sister species”

A

S. argenteus / S. schweitzeri

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24
Q

S. epi pathogenicity

A

1) Polysaccharide capsule -> biofilm -> implanted devices / shunts / grafts / intravenous lines

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25
S. lug pathogenicity
-Resembles S. aureus -> skin infections / abscesses (below the waist!!) -Endocarditis (native and prosthetic) -FBRIs
26
S. sapro pathogenicity
-Recurrent UTIs in sexually active women -2nd most common behind E. coli for uUTI -NovobiocinR
27
Molecular detection
mecA / mecC
28
Coagulase test
1) Slide test 2) Tube test -> rabbit plasma 37C 4 hrs, if neg, 18 hrs False neg if: staphylokinase+, SCV
29
Rapid latex agglutination test
-Presumptive ID -Detection of ProteinA, Clumping FactorA, Capsular polysccharides False pos: S. haemo, S. hominis that have type 8 capsular polysacc. or S. sapro w/ cell wall hemmagglutinin
30
Staph Abx resistance
PenR = 75-80% S. aureus / S epi mecA / mecC = R to all pen, ceph, and carbs -cefoxitin / oxacillin R = methicillin R -cefoxitin better surrogate b/c oxacillin requires 2% NaCl w/ 24 hr incubation at no more than 35C --exception = S. pseudintermedius -oxacillin has different breakpoints for different Staph species VISA / VRSA = cell wall alterations (petidoglycan mod) from vanA
31
CoNS HA-sepsis algorithm
-2 pos blood cultures for the same species w/in 5 days OR 1 pos blood culture plus clinical evidence of infection -Same species on intravenous cath tip and blood culture
32
Basic characteristics of Strep
-Cat- -GPC in chains -Intra/interspecies difference due to carbs, surface proteins, teichoic acid -Facultative anaerobes -NO respiratory metabolism b/c no heme -> only fermentative -Adding glucose etc to medium enhances growth but quickly changes pH and then inhibits
33
Strep habitat
-Commensals on mucous membranes -Sometimes transient skin -S. pneumo carriage rate = 30-70% in kids; <5% in adults -GAS carriage rate = 5% of adults -GBS carriage rate = 10-30%
34
GAS disease states
-Most common cause of bacterial pharyngitis (15-30% children/5-10% adults) and impetigo -Scarlet fever (erythematous sandpaper-like rash) -STSS (most often seen if: young child or elderly, diabetes, skin breakdown, cardiac/pulmonary disease, HIV, IV use) -Glomerulonephritis after skin or throat infections -> antibody-mediated inflammatory disease -> puffy face, tea-colored urine -PANDAS -Necrotizing fasciitis (>50% mortality rate) [Fournier's gangrene -> male genitalia] -Rheumatic fever after pharyngitis (antibodies cross-react w/ heart) = fever, myocarditis, arthritis, chorea (uncontrolled dance-like movements), subcutaneous nodules, rash (erythema marginatum)
35
GAS virulence: C carbohydrate
Lancefield antigen
36
GAS virulence: M protein
-80 different types -Inhibits complement -> protects from phagocytosis -Typing used for STSS (M1/M3)
37
GAS virulence: Streptolysin O
-Oxygen labile -Destroys RBCs and WBCs -Antigenic - can order Ab titres against ASO (maximum titre at 3-6 weeks post-infection)
38
GAS virulence: Streptolysin S
-Oxygen stabile -Destroys RBS -NOT antigenic
39
GAS virulence: Pyrogenic exotoxin (erythrogenic toxin)
-Scarlet fever -SUPERANTIGEN -STSS -> superstimulate T cells -> cytokines
40
GAS virulence: Streptokinase, hyaluronidase, anti-C5a-peptidase, DNAases
Break down stuff -Antigen testing against DNaseB (maximum titre 6-8 weeks post-infection)
41
GBS disease states
1) Neonatal sepsis / pneumonia (birth to 7 days) 2) Neonatal meningitis (7 days to 3 months) -> postnatal transmission -> NO stiff neck, instead fever, vomiting, poor feeding, irritability 3) Invasive infection in adults -> elderly, immunocompromised, diabetes, cancer, alcoholism
42
GCS/GGS (S. dysgalactiae) disease states
1) Similar to GAS except no scarlet fever
43
S. pneumo disease states
1) CA-pneumonia (81-87% of cases) 2) Sepsis 3) Meningitis (usually secondary to pneumonia/ear infection) 4) Ear infections (60% of kids < 3 will have an S pneumo ear infection) 5) Sinusitis 6) Peritonitis 7) Endocarditis (rare)
44
S. pneumo virulence: Polysaccharide capsule
-Protect from phagocytosis -Antigenic -84!!! different serotypes -Urine antigen detection is against C-polysaccharide antigen -Bile soluble
45
S. mitis group
-Oral cavity, GI tract, vaginal tract commensals -Transient on skin -Infection of native valves / prosthetic valves (less frequent) -Sepsis after chemo -Increase in PenR
46
S. anginosus group
-Oral cavity, GI tract, urogenital commensals -Abscess formation in brain (S. intermedius), oropharynx, peritoneal cavity -Respiratory infection in cystic fibrosis patients (S. constellatus) -Variable hemolysis (can be any) -Small
47
S. salivarius group
-Oral cavity and blood -Bacteremia, endocarditis, meningitis -S. sal in blood may = neoplasia -Non or alpha -Sucrose-containing agar = large mucoid or hard colonies
48
S. mutans group
-Oral cavity -> dental carries -Bacteremia -Produces extracellular polysaccharide from glucose -Hard, adherent, alpha colonies but can be beta in anaerobic conditions -Sucrose-containing agar = rough frosted glass, heaped colonies surround by liquid
49
S. bovis group
-Bacteremia, sepsis, endocarditis -S. gallolyticus sub gallolyticus = endocarditis and colon cancer/chronic liver disease -S. gallolyticus sub pasteurianus = infant meningitis -Non-enterococcal group D, PYR- -Grow on bile esculin but not in 6.5% NaCl -Non or alpha -Can't ferment sorb
50
Strep collection and transport
-Lose viability quickly -Need moist transport medium except for GAS
51
Strep pneumo urine antigen test
-Against C-polysaccharide antigen -Pos 1-6 months post-infection -BUT also detects carrier states so not useful in children < 6
52
Strep culture conditions
-BAP b/c hemolytic reaction -> growth enhance by external catalase source -35-37C, 5% CO2 or ana conditions enhance growth -S. pneumo / VirStr need 5% CO2 (8% won't grow in ambient air)
53
BHS ID
1) GAS = large hemolysis and PYR+, bacitracinS 2) GBS = soft hemolysis under colony and PYR- and CAMP+ (B is a hipp-ocrit -> hippurate +) 3) S. anginosus = ppt colonies, caramel/butterscotch odor (due to production of diacetyl), VP+
54
GBS screening
-35 - 37 weeks of pregnancy -Vaginal / rectal swab -Transport media (Amies or Stuarts) -> viable up to 4 days at RT or refrigerated -Selective broth -> nalidixic acid + gent or nalidixic acid + colistin
55
BHS Abx resistance
-GAS = PenS -GBS = PBP2x PenR --29% clindamycinR --49.5% erythR -Increasing fluoroquinolone resistance -> do not use as first-line
56
S. pneumo / VirStr Abx resistance
-PenR at higher frequency -Treatment options: Ceph, Macrolides, Fluoro, Vanc -Increasing fluoroR due to mutations in parC (DNA topoisomerase IV) and gyrA -Different B-lactam breakpoints for CSF vs. non-CSF
57
Enterococcus characteristics
-Gram+ -Cat- (can be weak+) -Usually non/alpha-hemolytic but E. faecalis can be beta -Facultative anaerobe -Lactic acid bacteria (lactic acid is end product of fermentation) -Grow in 6.5% NaCl -Bile esculin + (can grow in 40%) -PYR+ -LAP+ -D Lancefield group
58
Enterococcus habitat
-GI tract (they love bile) -Can also be on skin (peritoneum), genitourinary tract, or oral cavity -Super hardy bugs - can tolerate heat, alcohol, and chlorine -> NOSOCOMIAL INFECTIONS
59
Enterococcus disease states
1) Nosocomial infections -> from GI tract to other sites 2) UTIs 3) Wounds 4) Valve endocarditis (native and prosthetic) 5) Bacteremia / sepsis 6) Implants / catheters HIGH RISK: Elderly, immunocompromised, long hospital stay, indwelling devices, recent broad-spectrum antibiotic treatment 2nd or 3rd leading cause of UTIs, wounds, and bacteremia
60
Enterococcus virulence factors
1) Surface adhesin Esp 2) Aggregation substance 3) Secreted cytolysin / hemolysin 4) Secreted protein gelatinase / serine protease 5) Extracellular superoxide 6) Ace -> MSCRAMM (microbial surface components recognizing adhesive matrix molecule) -> adhesin to collagen 7) Capsule and polysaccharide = can make biofilms 8) EfaA -> E. faecalis antigen
61
Enterococcus acquire virulence how?
Large genetic islands or plasmids -> peptidoglycan synthesis pathway alteration to decrease binding affinity - D-Ala-D-Ala -> D-Ala-D-Lac
62
E. faecalis vs E. faecium infection ratio
Was 90%/10% but E. faecium is increasing now
63
Enterococcus culture
-Agar containing blood -Don't require CO2
64
VRE screening
-Needed for hospital surveillance / epidemiology - Enrichment broth: --BHI broth vancomycin concentrations varying from 3 to 30 mg/ml --Bile Esculin-azide broth supplemented with vancomycin at concentrations of 4 to 15 mg/ml (black = Enterococcus -> fast screening tool) --Enterococcosel broth medium supplemented with concentrations of vancomycin varying from 4 to 64 mg/ml --6 mg/ml is most common Vanc conc
65
Enterococcus AST
- Intrinsically resistant to B-lactams and aminoglycosides - Treated with combo agents (synergistic) --B-lactam + aminoglycoside OR --Vanc + aminoglycoside - Acquired R to multiple classes due to genetic islands - Pen can predict Amp/others but Amp can't predict Pen - Amp predicts other -cillins (E. faecalis / faecium) and Imp (E. faecalis)
66
Enterococcus VRE mechinisms
- VanA: inducible HLR to vancomycin as well as to teicoplanin - VanB: variable (moderate to high) levels of inducible resistance to vancomycin only - VanC: low-level resistance to Vanc
67
Staph aureus skin infections
Bullous impetigo -large pustules w/ small zone of erythema Cellulitis without large area of necrosis
68
Staph aureus Scalded Skin Syndrome
Ritter Disease Exfoliative toxin from phage2 -lesion->cutaneous erythema->skin peeling -toxin excreted from kidneys -2-4 days after onset -starts at face, neck, axilla, groin -> trunk, extremities
69
Staph aureus Toxic Shock syndrome
Initiates from tampons, after flu, after surgery -localized infection by systemic toxin -fever, rash, GI symptoms-> hypotensive shock
70
Staph aureus TEN
Toxic Epidermal Necrolysis -Drug-induced hypersensitivity rxn
71
Staph aureus food poisoning
From ingesting toxin Symptoms start 2-8 hours after ingestion and last 24-48 hours
72
GAS Skin infection
1) erysipelas = raised red rash 2) Pyoderma = pustule 3) Necrotizing fasciitis (TYPE II)
73
Scarlet fever
GAS rash trunk & neck -> extremities (NOT face) -Strep Pyrogenic Exotoxin (Spe)
74
Strep Toxic Shock Syndrome
Caused by SpeA Superantigen
75
Rheumatic fever
-only after untreated GAS pharyngitis -fever, myocarditis, arthritis, uncontrolled movements (chorea), subcutaneous nodules, rash -antigen-antibody cross-reaction in heart
76
GAS acute glomerulonephritis
-~1 week after GAS infection (pharyngitis or skin) -Ig-Ag complexes get stuck in kidneys -Puffy face, dark urine
77
Strep pneumo pneumonia
-#1 cause of pneumonia in adults -lobar pneumonia -> chills, dyspnea, cough -lung full of WBCs, bacteria, exudate -high mortality (10% treated, 50% untreated)
78
Most common cause of hospital acquired infection...
Enterococcus! -UTI -Wound infections -Prosthetic valve endocarditis -Bacteremia / sepsis
79
Strep bovis
-if found in blood, high likelihood of colon cancer
80
Aerococcus
-opportunistic pathogen -bacteremia -endocarditis -UTIs -look like virstrep on culture but staph on gram stain
81
Gamella
-colonies like virstrep but decolorize to look like GNC in gram stain -Endocarditis, wounds, abscesses
82
Only B strep that is PYR+ is...
GAS
83
Only B strep that is VP+ is...
S. anginosus group
84
Only B strep that is HIPP+ is...
GBS
85
Optochin S strep is...
S. pneumoniae