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HCLD Micro > Gram Pos Cocci > Flashcards

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
Q

S. lug pathogenicity

A

-Resembles S. aureus -> skin infections / abscesses (below the waist!!)
-Endocarditis (native and prosthetic)
-FBRIs

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26
Q

S. sapro pathogenicity

A

-Recurrent UTIs in sexually active women
-2nd most common behind E. coli for uUTI
-NovobiocinR

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27
Q

Molecular detection

A

mecA / mecC

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28
Q

Coagulase test

A

1) Slide test
2) Tube test -> rabbit plasma 37C 4 hrs, if neg, 18 hrs

False neg if: staphylokinase+, SCV

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29
Q

Rapid latex agglutination test

A

-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

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30
Q

Staph Abx resistance

A

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

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31
Q

CoNS HA-sepsis algorithm

A

-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

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32
Q

Basic characteristics of Strep

A

-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

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33
Q

Strep habitat

A

-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%

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34
Q

GAS disease states

A

-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)

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35
Q

GAS virulence: C carbohydrate

A

Lancefield antigen

36
Q

GAS virulence: M protein

A

-80 different types
-Inhibits complement -> protects from phagocytosis
-Typing used for STSS (M1/M3)

37
Q

GAS virulence: Streptolysin O

A

-Oxygen labile
-Destroys RBCs and WBCs
-Antigenic - can order Ab titres against ASO (maximum titre at 3-6 weeks post-infection)

38
Q

GAS virulence: Streptolysin S

A

-Oxygen stabile
-Destroys RBS
-NOT antigenic

39
Q

GAS virulence: Pyrogenic exotoxin (erythrogenic toxin)

A

-Scarlet fever
-SUPERANTIGEN
-STSS -> superstimulate T cells -> cytokines

40
Q

GAS virulence: Streptokinase, hyaluronidase, anti-C5a-peptidase, DNAases

A

Break down stuff
-Antigen testing against DNaseB (maximum titre 6-8 weeks post-infection)

41
Q

GBS disease states

A

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
Q

GCS/GGS (S. dysgalactiae) disease states

A

1) Similar to GAS except no scarlet fever

43
Q

S. pneumo disease states

A

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
Q

S. pneumo virulence: Polysaccharide capsule

A

-Protect from phagocytosis
-Antigenic
-84!!! different serotypes
-Urine antigen detection is against C-polysaccharide antigen
-Bile soluble

45
Q

S. mitis group

A

-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
Q

S. anginosus group

A

-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
Q

S. salivarius group

A

-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
Q

S. mutans group

A

-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
Q

S. bovis group

A

-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
Q

Strep collection and transport

A

-Lose viability quickly
-Need moist transport medium except for GAS

51
Q

Strep pneumo urine antigen test

A

-Against C-polysaccharide antigen
-Pos 1-6 months post-infection
-BUT also detects carrier states so not useful in children < 6

52
Q

Strep culture conditions

A

-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
Q

BHS ID

A

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
Q

GBS screening

A

-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
Q

BHS Abx resistance

A

-GAS = PenS
-GBS = PBP2x PenR
–29% clindamycinR
–49.5% erythR
-Increasing fluoroquinolone resistance -> do not use as first-line

56
Q

S. pneumo / VirStr Abx resistance

A

-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
Q

Enterococcus characteristics

A

-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
Q

Enterococcus habitat

A

-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
Q

Enterococcus disease states

A

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
Q

Enterococcus virulence factors

A

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
Q

Enterococcus acquire virulence how?

A

Large genetic islands or plasmids -> peptidoglycan synthesis pathway alteration to decrease binding affinity -

D-Ala-D-Ala -> D-Ala-D-Lac

62
Q

E. faecalis vs E. faecium infection ratio

A

Was 90%/10% but E. faecium is increasing now

63
Q

Enterococcus culture

A

-Agar containing blood
-Don’t require CO2

64
Q

VRE screening

A

-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
Q

Enterococcus AST

A
  • 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
Q

Enterococcus VRE mechinisms

A
  • 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
Q

Staph aureus skin infections

A

Bullous impetigo
-large pustules w/ small zone of erythema

Cellulitis without large area of necrosis

68
Q

Staph aureus Scalded Skin Syndrome

A

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
Q

Staph aureus Toxic Shock syndrome

A

Initiates from tampons, after flu, after surgery
-localized infection by systemic toxin
-fever, rash, GI symptoms-> hypotensive shock

70
Q

Staph aureus TEN

A

Toxic Epidermal Necrolysis
-Drug-induced hypersensitivity rxn

71
Q

Staph aureus food poisoning

A

From ingesting toxin
Symptoms start 2-8 hours after ingestion and last 24-48 hours

72
Q

GAS Skin infection

A

1) erysipelas = raised red rash
2) Pyoderma = pustule
3) Necrotizing fasciitis (TYPE II)

73
Q

Scarlet fever

A

GAS rash trunk & neck -> extremities (NOT face)
-Strep Pyrogenic Exotoxin (Spe)

74
Q

Strep Toxic Shock Syndrome

A

Caused by SpeA Superantigen

75
Q

Rheumatic fever

A

-only after untreated GAS pharyngitis
-fever, myocarditis, arthritis, uncontrolled movements (chorea), subcutaneous nodules, rash
-antigen-antibody cross-reaction in heart

76
Q

GAS acute glomerulonephritis

A

-~1 week after GAS infection (pharyngitis or skin)
-Ig-Ag complexes get stuck in kidneys
-Puffy face, dark urine

77
Q

Strep pneumo pneumonia

A

-#1 cause of pneumonia in adults
-lobar pneumonia -> chills, dyspnea, cough
-lung full of WBCs, bacteria, exudate
-high mortality (10% treated, 50% untreated)

78
Q

Most common cause of hospital acquired infection…

A

Enterococcus!
-UTI
-Wound infections
-Prosthetic valve endocarditis
-Bacteremia / sepsis

79
Q

Strep bovis

A

-if found in blood, high likelihood of colon cancer

80
Q

Aerococcus

A

-opportunistic pathogen
-bacteremia
-endocarditis
-UTIs
-look like virstrep on culture but staph on gram stain

81
Q

Gamella

A

-colonies like virstrep but decolorize to look like GNC in gram stain
-Endocarditis, wounds, abscesses

82
Q

Only B strep that is PYR+ is…

A

GAS

83
Q

Only B strep that is VP+ is…

A

S. anginosus group

84
Q

Only B strep that is HIPP+ is…

A

GBS

85
Q

Optochin S strep is…

A

S. pneumoniae

HCLD Micro (13 decks)

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