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Microbiology > Gram Positive and Gram negative Cocci > Flashcards

Gram Positive and Gram negative Cocci Flashcards

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1
Q

What are the three genera of gram positive cocci?

A

Staphylococcus
Streptococcus
Enterococcus

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2
Q

Virulence factors. Examples?

A

Factors that enable an organism to produce disease
Examples: Adhesins/cell surface factors
Secreted enzymes/toxins

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3
Q

Facultative anaerobes

A

Bacteria that can produce ATP aerobically when oxygen is present but can switch to fermentation when oxygen is absent.

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4
Q

Staphylococci

A

Cells in clusters
Facultative anaerobes
Hardy bacteria-persist on fomites
Catalase positive

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5
Q

How do you distinguish staphylococci from streptococci?

A

Staphylococci produce catalase

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6
Q

Which staph is catalase positive? catalase negative?

A

Catalase positive: S. aureus

Catalase negative: S. epidermidis, S. saprophyticus

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7
Q

Staphylococcus aureus

A

Catalase positive
Golden-yellow colonies
Coagulase positive (eco-enzyme that activates blood clotting factors)
Ferments mannitol (detected on mannitol salt sugar)

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8
Q

S. aureus cell surface virulence factors

A

Capsule - antiphagocytic polysaccharide “microcapsule”
Protein A - anti-opsonin effect by binding Fc region of antibodies
Adhesins - facilitate attachment to host cells/connective tissue

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9
Q

S. aureus cytolytic exotoxins

A

They target mammalian cell membranes
Hemolysins: lyse erythrocytes
PVL (Panton-Valentine leukocidin): lyse PMNs

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10
Q

S. aureus invasins

A

Enzymes that facilitate penetration through extracellular tissue

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11
Q

S. aureus superantigen exotoxins

A

Toxic shock syndrome toxin (TSST-1)
Enterotoxins (food poisoning)
Exfoliatin (Scalded skin syndrome)

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12
Q

What is the effect of super antigen toxins?

A

They stimulate T lymphocytes; produce pathology by overproduction of cytokines. They bind TCR to MHC in a relatively non-specific way.

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13
Q

Staphylococcal infections cause skin and soft tissue infections (SSTIs)

A

1) Furuncles: small pus-filled local infections
2) Carbuncles: Larger skin abscesses
3) Impetigo: Spreading, crusting skin infection
4) Cellulitis: Deep skin infection

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14
Q

S. aureus tissue infections

A

1) Osteomyelitis
2) Septic joint/septic arthritis
3) Pneumonia: often follows viral influenza infections
4) Acute endocarditis
5) Bacteremia and Septicemia

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15
Q

What is scalded skin syndrome?

A

Exfoliatin toxin induced bright red flush, blisters (bullae) causing bullous impetigo, then desquamation of the epidermis.

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16
Q

Treatment options for S. aureus?

A
  1. Penicillinase resistant penicillins such as Oxacillin
  2. Clindamycin
  3. If MRSA, vancomycin is SOC antibiotic
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17
Q

Two gram negative staphylococcus

A

S. epidermidis and S. saprophyticus

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18
Q

Virulence of S. epidermidis

A

1) Polysaccharide capsule adheres to prosthetic devices

2) Highly resistant to antibiotics

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19
Q

Clinical manifestation of S. epidermidis

A

Nosocomial infections:

1) Prosthetic joints and heart valves
2) IV lines
3) UTIs

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20
Q

Treatment options for S. epidermidis

A

Vancomycin

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21
Q

Diagnostics for S. epidermidis

A

1) Gram positive cocci
2) Catalase positive
3) Coagulase negative

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22
Q

How is S. saprophyticus distinguished from other CoNS and S. aureus?

A

Resistance to Novobiocin

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23
Q

Clinical manifestation of S. Saprophyticus

A

UTIs and cystitis in women

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24
Q

Treatment options for S. Saprophyticus

A

Penicillin G

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25
Q

Diagnostics for S. Saprophyticus

A

1) Gram positive
2) Catalase positive
3) Coagulase negative
4) Novobiocin resistant

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26
Q

Streptococcus

A 
Gram positive spherical/ovoid cocci arranged in long chains
Catalase negative
Fastidious and require enriched media
Sensitive to drying and heat
Aerotolerant anaerobes
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27
Q

How do you classify different streptococcus?

A

1) hemolysis pattern on blood agar

2) cell wall antigen

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28
Q

Beta-hemolysis

A

Complete erythrocyte destruction

29
Q

Alpha-hemolysis

A

Erythrocytes damaged by peroxide, hemoglobin turns green/brown

30
Q

Gamma-hemolysis

A

No hemolysis

31
Q

Streptococcus Lancefield Groups

A

Classification of streptococcus based on antigenic cell wall polysaccharide. Groups: A, B, D, and none

32
Q

C-Substance

A

Antigenic cell wall polysaccharide on streptococcus

33
Q

Group A streptococci (GAS)

A

S. pyogenes

34
Q

S. pyogenes virulence factors

A

M protein: essential for infection and highly variable antigenic.
Streptolysin O and S: lyse RBCs (ASO titers)
Streptococcal pyrogenic exotoxins (SPE)
Enzymes: streptokinase

35
Q

Clinical Manifestation of GAS infection

A

1) streptococcal pharyngitis
2) Streptococcal skin infections: impetigo or erysipelas which could lead to cellulitis or more severe necrotizing fasciitis.
3) Streptococcal toxic shock syndrome: superantigen pyrogenic toxin mediated shock and multi organ failure
4) Rheumatic fever
5) Acute glomerulonephritis

36
Q

Group B streptococci

A

S. agalactiae

37
Q

S. agalactiae

A

Normal flora of female reproductive tract

38
Q

S. agalactiae is the leading cause of

A

Neonatal sepsis

39
Q

How to distinguish between GAS and GBS?

A

They both follow beta hemolytic. GAS is sensitive to bacitracin while GBS is bacitracin resistant.

40
Q

alpha-hemolytic streptococci

A

S. pneumoniae

Viridans

41
Q

Viridans

A

Large complex group

residents of oral cavity

42
Q

Clinical manifestations of Viridans

A

Dental caries

Subacute endocarditis

43
Q

S. pneumoniae

A

Small “lancet-shaped” cells arranged in pairs and short chains.
Virulence factor: polysaccharide capsule
Antiphagocytic and antigenic

44
Q

Clinical manifestations of S. pneumoniae

A

1) Lobar pneumonia: aspirated into the lungs, multiply and induce overwhelming inflammatory response.
2) Otitis media: gains access to the middle ear
3) Meningitis
4) Bacteremia and sepsis

45
Q

Lab tests for S. pneumoniae

A

1) sensitive to optochin
2) lysis by bile acids
3) Quellung reaction

46
Q

What causes the S. pneumoniae resistance to penicillin?

A

Resistance mediated by altered PBP acquired by genetic transmission from environmental streptococci

47
Q

What is the treatment for penicillin resistant S. pneumoniae

A

3rd generation cephalosporins such as cefotaxime and ceftriaxone

48
Q

Pneumovax

A

23 valente polysaccharide vaccine (PPV) recommended for high risk individuals 2 years and older and adults older than 65 years of age.

49
Q

PCV13 or Prevnar 13

A

Polysaccharide conjugated to protein pneumococcal conjugate vaccine. Given to all children under 5 yrs old and immunocompromised adults.

50
Q

Group D streptococci

A

S. Bovis (Nonenterococcal Group D strep)

51
Q

What hemolysis category is GDS?

A

Non hemolytic or alpha-hemolytic

52
Q

Bacteremia caused by S. bovid associated with ——– and ———.

A

GI malignancy and colon cancer

53
Q

Enterococci

A

Group D antigen
Non hemolytic or alpha-hemolytic
component of GI flora

54
Q

Most clinical relevant enterococcal species

A

E. faecalis and E. faecium

55
Q

Enterococcal epidemiology

A

Not very virulent
Nosocomial pathogens due to multidrug resistant phenotype
Resistant to chemical agents
Cause opportunistic urinary or biliary infections or intra abdominal abscesses in immune compromised individuals
Leads to endocarditis or bacteremia/sepsis

56
Q

Vancomycin resistance is very common in ——-, less so in ——–

A

E. faecium

E. faecalis

57
Q

Lab tests for Enterococci

A

1) Bile Esculin hydrolysis (shared with GDS)
2) Salt resistant so can grow in 6.5% NaCl broth (differentiates GDS from Enterococci)
Nonenterococci grow only in bile

58
Q

Treatment for Enterococci

A

1) Amp + gentamicin or penicillin + streptomycin
2) Vancomycin
3) multidrug resistant: Pristinamycin or Linezolid

59
Q

Gram Negative Cocci

A

Neisseria

60
Q

Two types of Neisseria

A

1) N. gonorrhoeae

2) N. meningitidis

61
Q

Neisseria

A

Gram negative, kidney shaped, diplococci
aerobic
sensitive to heat and drying
Often seen within PMNs upon Gram staining

62
Q

Unlike meningococci, gonococci are ———

A

unencapsulated

63
Q

What are the two mechanism by which gonococci develop heterogeneity of cell surface antigens?

A

Gene conversion and phase variation

64
Q

Gonococci antigens

A

1) pili (facilitate attachment to host)
2) Opa (opacity proteins)
3) LOS (endotoxin similar to LPS)
4) IgA protease (help infect mucosa)

65
Q

Gonococci requires —– for growth and survival

A

IRON

It expresses proteins that can extract iron from host iron proteins such as transferrin and lactoferrin.

66
Q

Gonococci clinical manifestations

A

1) GI tract infections
2) Pharyngitis and rectal infections
3) Ophthalmia neonatorum (passing it on to babies)
4) Bacteremia causing disseminated infection (results in septic arthritis or scattered skin lesions)

67
Q

N. gonorrhoeae is resistant to ——-,——–,——

A

penicillin, tetracycline, quinolones.

68
Q

Treatment for N. gonorrhoeae

A

Ceftriaxone with azithromycin or doxycycline

69
Q

What is the difference in virulence between N. meningitidis and N. gonorrhoeae

A

N. meningitidis has a polysaccharide capsule

Microbiology (5 decks)

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