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Gram + Flashcards

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1
Q

gram + colour?

A

purple/blue

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2
Q

Gram + - subgroups

A
  1. cocci
  2. Robs (bacilli)
  3. branching filaments
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3
Q

gram + branching filaments - bugs (and characteristics)

A
  1. Actinomyces - anaerobe, not acid fast

2. Nocardia - aerobe, acid fast

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4
Q

gram + robs - bugs (and characteristics)

A
  1. Clostiridium - spore forming, anaerobe
  2. Bacillus - spore forming, aerobe
  3. Listeria - no spore forming, tumbling motile, aerobe
  4. corynobacterium - no spore forming, non-motile, aerobe
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5
Q

gram + cocci are divided to (and characteristics)

A
  1. staphylococcus (cat+, clusters)

2. streptococcus (cat-, chains)

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6
Q

staphylococcus - bugs (and characteristics)

A

ALL CAT+, CLUSTERS

  1. S. aureus (coagulase +)
  2. S. epidermidis (novobiosin sensitive)
  3. S. saprophyticus (novobiosin resistant)
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7
Q

streptococci are divided into subgroups according to (and the meaning)

A

hemolysis

  1. partially hemolysis (α)
  2. complete hemolysis (clear) (β)
  3. no hemolysis (γ)
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8
Q

β hemolytic streptococci - bugs (and characteristics)

A
  1. S pyogens (group A, Bacitracin sensitive)

2. S. agalactiae (group B, Bacitracin resistant)

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9
Q

γ hemolytic streptococci - bugs (and characteristics)

A
  1. enterococcus (E. faecalis, E. feacium) - Group D, growth in bile and 6.5% NaCL
  2. Nonenterococcus (Streptococcus bovis) - Group D, Growth in bile, not in 6.5 NaCL
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10
Q

entrococcus - hemolysis?

A

either a- or γ- hemolytic

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11
Q

α hemolytic streptococci - bugs (and characteristics)

A
  1. S. pneumoniae - Capsule, Optichin sensitive, Bile soluble (lysed by bile)
  2. Viridaans streptococci (eg. S. mutans, S. sanguinis, S. mitis) - no capsule, optochin resistant, bile soluble (lysed)
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12
Q

drugs to use to differentiate gram + bugs (and how)

A
  1. novobiocin –> staphyloccous epidermidis is sensitive, but staphylococcus saprophyticus is resistatn
  2. Optichin –> Streptococcus pneumoniae is sensitive but viridans streptococci is resistant
  3. Bcitracin –> S pyogenes (Group A) is sensitive but S. agalactiae (Group B) is resistant
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13
Q

α hemolytic bacteria - appearance and mechanism

A

Partial reduction of Hb causes greenish or broownish color without clear ring around colonies on blood agar

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14
Q

β-hemolytic bacteria - appearance and mechanism

A

complete lysis form clear area of surrounding colony on blood agar

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15
Q

β-hemolytic bacteria - - bugs (and characteristics)?

A
  1. Staphylococcus aureus (cat+, coagulase +)
  2. Streptococcus pyogens (cat- ,group A, Bacitracin sensitive)
  3. Streptococcus agalactiae (cat-, group B, Bacitracin resistant)
  4. Listeria - no spore forming, tumbling motility, aerobe
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16
Q

staphylococcus saprophyticus - characteristics

A

gram +, cat + coag -. UREASE + cocci in clusters, novobiocin resistance

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17
Q

staphylococcus saprophyticus - clinical manifestation

A

Second MCC of UNCOMPLICATED UTI in young women

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18
Q

MCC and 2nd MCC of uncomplicated UTI in young women

A
  1. E. coli

2. staphylococcus saprophyticus

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19
Q

staphylococcus saprophyticus - area of the body

A

Normal flora of female genital tract + perineum

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20
Q

staphylococcus epidermidis - characteristics / area of the body (clinically relevance)

A

gram +, cat+, coag-, UREASE +, novobiocin sensitive

normal skin flora –> contaminates blood cultures

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21
Q

staphylococcus epidermidis - clinical manifestations

A

infects prosthetic valves devises (hip implant, heart valve) and intravenous catheters by producing adherent biofilms

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22
Q

staphylococcus epidermidis infects prosthetic valves devises (hip implant, heart valve) and intravenous catheters by

A

producing adherent biofilms

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23
Q

staphylococcus aureus - characteristics

A

gram +, cat+, coagulase +, β-hemol,

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24
Q

staphylococcus aureus - how to evade immune system

A

Protein A (virulence factor) binds Fc-IgG, inhibiting complement activation and phagocytosis

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25
Q

staphylococcus aureus - area of the body

A

commonly colonizes the nares

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26
Q

Staphylococcus aureus can cause (clinical manifestation) ….. (only the categories)

A

inflammatory disease
Toxin mediated disease
MRSA infection

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27
Q

staphylococcus aureus - inflammatory disease?

A
  1. skin infection
  2. organ abscesses
  3. pneumonia
  4. endocarditis
  5. osteomyelitis
  6. septic arthritis
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28
Q

staphylococcus aureus - pneumonia?

A

often after virus infection

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29
Q

Staphylococcal aureus toxins

A
  1. Toxic shock syndrome toxin (TSST-1)
  2. Exfoliative
  3. enterotoxin
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30
Q

Staphylococcal aureus toxins and manifestations

A
  1. Toxic shock syndrome toxin (TSST-1) –> Toxic shock syndrome: fever, rash, shock, vomiting, desquamation, end-organ failure
  2. Exfoliative –> scalded skin syndrome
  3. enterotoxin –> rapid onset food poisoning
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31
Q

skin infection - staphylococcus aureus can cause

A
  1. impetigo
  2. cellulitis
  3. Abscess
  4. Staphylococcal scalded skin syndrome
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32
Q

cellulitis is caused by

A

usually S. aureus or S. pyogenes

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33
Q

impetigo is caused by

A

usually S. aureus or S. pyogenes

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34
Q

staphylococcal scalded skin syndrome - symptoms

A
  1. fever

2. generalized erythematous rash with sloughing of the upper layers of the epidermis that heals completely

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35
Q

staphylococcal scalded skin syndrome - seen in

A
  1. newborns
  2. children
  3. adults with renal insufficiency
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36
Q

staphylococcal scalded skin syndrome - mechanism

A

exotoxin (exofliative) destroys keratinocytes attachments in stratum granulosum ONLY

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37
Q

staphylococcus aureus - MRSA - infection

A

important cause of serious nosocomial and community-acquired infections

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38
Q

MRSA - mechanism

A

resistant to methicillin and nafcillin because of altered penicillin biding protein

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39
Q

staphylococcus aureus can cause …. (categories and manifestations

A

A. inflammatory disea: 1. skin infection 2. organ abscesses
3. pneumonia 4. endocarditis 5. osteomyelitis
B. Toxin mediated disease: 1. TSST-1 –> Toxic shock syndrome 2. Exfoliative –> scalded skin syndrome
3. enterotoxin –> rapid onset food poisoning
C. MRSA infection: serious nosocomial and community-acquired infections

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40
Q

Toxic shock syndrome toxin (TSST-1) - mechanism of action

A

Binds to MCH II and TCR outside of antigen binding site (polyclonal T-cel activation)to cause overwhelming release of IL-1, IL-2, INF-γ, TNF-α –> shock

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41
Q

Toxic shock syndrome - symptoms / lab

A
  • fever, rash, shock, vomiting, desquamation, end-organ failure
  • increased AST, ALT, blirirubin
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42
Q

Toxic shock syndrome - is associated with (situations)

A
  1. S. aureus –> vaginal tampons, nasal packing

2. S. pyogenes –> painful skin infection

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43
Q

S. aureus - food poisoning is due to

A

ingestion of preformed toxin (enterotoxin)

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44
Q

S. aureus - food poisoning - course

A

short incubation period (2-6h) followed by NON-BLOODY diarrhea and emesis

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45
Q

S. aureus enterotoxin - special feature

A

heat stable –> not destroyed by cooking

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46
Q

S. aureus - coagulase? (relevance in manifestation)

A

coagulase + –> forms fibrins clot around self –> abscess

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47
Q

S. pneumoniae - characteristics

A

gram +, cocci, α hemolytic, Capsule, Optichin sensitive, Bile soluble (lysed by bile)

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48
Q

S. pneumoniae - appearance

A

Lancet-shape, gram + diplococci, encapsuled

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49
Q

S. pneumoniae - clinical manifestation

A

A. MCC OF: 1. Meningitis 2. Otitis media (in children)
3. Pneumonia 4. Sinusitis
B. Sepsis in sickle cell and splenectomy

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50
Q

S. pneumoniae - clinical importance of capsule

A

no virulence without capsule

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51
Q

S. pneumoniae - virulence factor

A
  1. capsule

2. IgA protease

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52
Q

S. pneumoniae - sputum?

A

rusty

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53
Q

S. pneumoniae - sepsis in

A
  1. sickle cell anemia

2. splenectomy

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54
Q

S pneumoniae - vaccines and structure

A

PCV - pneumonococcal congugate vaccine (Prevnar)

PPSV - pneumonococcal polysaccharide vaccine with no congugate protein (Pneumovax)

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55
Q

Viridans group streptococci - hemolysis? / area of the body

A

α / normal flora of the oropharynx

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56
Q

Viridans group streptococci - area of the body

A

normal flora of the oropharynx

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57
Q

Viridans group streptococci - bugs?

A
  1. Streptococcus mutans

2. Streptococcus sanguinis

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58
Q

Viridans group streptococci - clinical manifestation

A
  1. Streptococcus mutans + mitis –> dental carries
  2. Streptococcus sanguinis –> sabacute bacterial endocarditis at damages heart valves
    (It makes dextrans, which bind to fibrin-plaelet aggregates on damaged heart valve)
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59
Q

Viridans group streptococci - characteristics

A

a-hemolytic, no capsule, optochin resistant, bile insoluble (no lysed)

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60
Q

α hemolytic streptococci - bugs (and characteristics)

A
  1. S. pneumoniae - Capsule, Optichin sensitive, Bile soluble (lysed by bile)
  2. Viridaans streptococci (eg. S. mutans, s mutis, S. sanguinis) - no capsule, optochin resistant, bile soluble (lysed)
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61
Q

Streptococcus pyogenes - characteristics

A

cat- ,group A, Bacitracin sensitive, β-hemolytic

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62
Q

Streptococcus pyogenes can cause …… (categories)

A
  1. pyogenic
  2. toxigenic
  3. immunologic
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63
Q

Streptococcus pyogenes - pyogenic

A
  1. pharyngitis
  2. cellulitis
  3. impetigo
  4. erysipellas
64
Q

Streptococcus pyogenes - toxigenic

A
  1. scarlet fever
  2. toxic shock like syndrome
  3. necrotizing fascitis
65
Q

necrotizing fascitis - definition and causes / aka / appearance / sensation

A

deeper tissue injury, usually from anaerobic bacteria or S. pyogenes. aka: flesh eating bacteria

appearance: bullae and purple color to the skin
sensation: crepitus (methane and CO2 production)

66
Q

Streptococcus pyogenes - immunologic

A
  1. rheumatic fever

2. acute glumorelonephritis

67
Q

Scarlet fever - manifestation / caused by

A

blanching, sandpaper-like body rash, strawberry tongue and circumoral pallor in the setting of group A streptococcal pharyngitis (erytrhogenic toxin)

68
Q

how to detect recent Streptococcus pyogenes infection

A

ASO titer

pyrrolidonyl arylamidase +

69
Q

Streptococcus pyogenes - exotixins

A
  1. exotoxin A
  2. Streptolysin O
  3. erythrogenic toxin
70
Q

Streptococcus pyogenes - M antibodies

A

enchance host defence againste S. pyogenes

can give rise to rheumatic fever

71
Q

Streptococcus pyogenes - M antibodies can give rise to

A

rheumatic fever

72
Q

Pyrrolidonyl Arylamidase (PYR) test is / + in

A

a rapid test which is used for the presumptive identification of group A beta-hemolytic Streptococci adn entercocci

73
Q

Major criteria for acute rheumatic fever

A
  1. polyarthritis
  2. carditis
  3. subcutaneous nodules
  4. erythema marginatum
  5. Sydenham chorea
74
Q

streptococcal pharyngitis can result in

streptococcal impetigo can result in

A

Pharyngitis: 1. rheumatic fever 2. glomerulonephritis
Impetigo: glomerulonephritis

75
Q

glomerulonephritis is preceded by

A

streptococcal pharyngitis or impetigo

MORE COMMONLY IMPETIGO

76
Q

Streptococcus agalactiae - characteristics

A

group (-), group B, Bacitracin resistant, β- hemolytic

77
Q

Streptococcus agalactiae colonizes

A

vagina

78
Q

Streptococcus agalactiae causes

A
  1. pneumonia
  2. Meningitis
  3. Sepsis
    MAINLY IN BABIES
79
Q

test to detect Streptococcus pyogenes

A

Pyrrolidonyl Arylamidase (PYR) test

80
Q

test to detect Streptococcus agalactiae

A
  1. Hippurate test
  2. CAMP test
  3. PYR -
81
Q

Streptococcus agalactiae - CAMP test

A

CAMP factor enlarges the area of hemolysis by S. aureus

82
Q

Screen pregnant women for Streptococcus agalactiae at

A

35-37 weeks of gestation

83
Q

patients with + culture of Streptococcus agalactiae –>

A

receive intrapartum penicillin for prophylaxis

84
Q

Enterococci - bugs and characteristics

A

E. faecalis
E. faecium
gram +, cat -, Group D, growth in bile and 6.5% NaCL
α or γ hemolysis

85
Q

Enterococci - area of the body

A

normal flora of the colon

86
Q

Enterococci are resistant to / test to detect

A

penicillin G

PYR +

87
Q

Enterococci can cause

A

I. UTI
2. biliary tract infection
3. sabacute endocarditis
(following GI/GU procedures)

88
Q

Enterococci can cause UTI, biliary tract infection and sabacute endocarditis following

A

GI/GU procedures

89
Q

group D streptococci - bugs (and characteristics)

A
  1. enterococcus (E. faecalis, E. feacium) - Group D, growth in bile and 6.5% NaCL, γ hemolytic
  2. Nonenterococcus (Streptococcus bovis) - Group D, Growth in bile, not in 6.5 NaCL, γ hemolytic
90
Q

Lancefield grouping is based on

A

differences in the C carbohydrate on the bacterial cell wall

91
Q

VRE are important cause of (and means)

A

nosocomial infection (Vancomycin-resistant enterococci)

92
Q

Streptococcus bovis - clonizes the

A

gut

93
Q

Streptococcus bovis biotype 1

A

Streptococcus gallolyticus

94
Q

Streptococcus gallolyticus (Streptococcus bovis biotype 1) can cause

A

bacteremia and sabacute endocarditis and is associated with colon cancer

95
Q

Streptococcus gallolyticus (Streptococcus bovis biotype 1) can cause bacteremia and sabacute endocarditis and is associated with

A

colon cancer (or polyps)

96
Q

Corynobacterium diptheria causes diptheria via exotoxin encoded by

A

β-prophage

97
Q

Diptheria toxin - mechanism of action

A

ADP-ribosilation of E2F –> INACTIVATION OF E2F ELONGATION –> inhibition of tRNA translocation –> inhibition of protein synthesis

98
Q

diptheria - symptoms

A
  1. pseudomembranous pharyngitis (grayish-white membrane)
  2. Lymphadenopathy (bull neck)
  3. myocaridits
  4. arrhythmia
  5. demyelination/paralysis of peripheral nerves
99
Q

diptheria prevention?

A

toxoid vaccine

100
Q

Corynobacterium diptheriae - lab diagnosis

A
  1. gram + rob with metachromatic (blue and red) granules
  2. Elek test for toxin
  3. Black colonies on cystein-tellurite agar
101
Q

test for diptheria toxin

A

Elek test

102
Q

Special culture requirements - Corynebacterium diphtheriae - media ?

A

Tellurite agar and Loffler medium

103
Q

Corynobacterium diptheriae - granules

A

metachromatic (blue and red)

104
Q

spores - bacteria - (when)

A

some bacteria can form spores at the end of the stationary state when nutrients are limited

105
Q

bacterial spore - characteristics / chemical composition

A

resistant to dehydration, heat and chemicals
chemical composotion: 1. keratin like - coat
2. dipicolinic acid
3. peptidoglycan

106
Q

how to kill spores

A

must autoclave to potentially kill spores (as done in surgical equipment) by steaming at 121c for 15 minutes

107
Q

spore forming bacteria - bacteria groups

A
  1. Bacillus
  2. Closturidium
  3. Coxiella burnetti
108
Q

spore forming bacteria - bugs and diseases

A
  1. Bacillus antrhacis –> antrax
  2. Bacillus cereus –> Food poisoning
  3. Clostiridium botulinum –> botulism
  4. Clostiridium difficile –> Antibiotic associated colitis
  5. Clostiridium perfingess –> gas gangrene, food poisoning
  6. Clostiridium tetani –> tetanus
  7. Coxiella burnetii –> Q fever
109
Q

Clostiridia - characteristics

A

gram +, spore forming, anaerobe

110
Q

Clostiridia - bugs and characteristics

A

gram +, spore forming, obligate anaerobe

  1. Clostiridium tetani
  2. Clostiridium botulinum
  3. Clostiridium perfringens
  4. Clostiridium difficile
111
Q

Clostiridia - toxins

A
  1. Clostiridium tetani –> tetanospasmin
  2. Clostiridium botulinum –> Botulinum toxin
  3. Clostiridium perfringens –> Alpha toxin, head labile enterotoxin
  4. Clostiridium difficile –> Toxin A (eneterotoxin), Toxin B (cytotoxin)
112
Q

tetanospasmin blocks release of …(from)

A

inhibitory neurotransmitters, GABA and glycine, from Renshaw cells in spinal cord

113
Q

tetanospasmin - manifestations

A
  1. spasticity
  2. risus sardonicus (raised eyebrows and open grin)
  3. Lockjaw (trismus)
114
Q

tetanus is

A

tetanic paralysis

115
Q

C. tetani - therapy / prevention

A

Prevent with tetanus vaccine

treat with antitoxin +/- vaccine booster and diazepam (for muscle spasms) and wound debridement

116
Q

Botulinum toxin inhibit the releiase of ….(where)

A

ACh at neuromuscular junction (causing botulism)

117
Q

botulism treatment

A

antitoxin

118
Q

Botiulism is caused by ….

A

adults: ingestion of preformed toxin
babies: ingestion of spores in honey (floopy baby syndrome)

119
Q

botulism vs tetanus according paralysis

A

botulism –> flaccid paralysis

tetanus –> spastic paralysis

120
Q

classic symptoms of botulism

A

flaccid paralysis, including diplopia, ptosis, dysphagia, symmetric, descending motor paralysis, death due to respiratry failure

121
Q

MC form of botulism in USA

botulism - death due to

A
  • floopy baby syndrome

- respiratory failure

122
Q

Clostiridium perfringens toxin and its mechanism of action

A

Alpha toxin: Phospholipase (lecithinase) that degrades tissue and cell membranes
enterotixin –> food poisoning

123
Q

Clostiridium perfringens - manifestations

A

A. lalpha TOXIN: 1. myonecrosis (gas gangrene) 2. hemolysis (double zone of hemolyisis on blood agar)
B. spores can survie in undercooked food –> ingested, bacteria can release heat labile enetrotoxin –> food poisoning

124
Q

Clostiridium perfringens - food poisoning

A

spores can survie in undercooked food –> ingested, bacteria can release heat labile enetrotoxin –> food poisoning

125
Q

Clostiridium difficile - toxins and their action

A
  1. Toxin A (eneterotoxin) –> binds to the brush borders of the gut –> diarrhea
  2. Toxin B (cytotoxin) –> causes cytoskeletal disruption via actin depolymerization –> pseudomembranous colitis –> diarrhea
126
Q

pseudomembranous colitis - appearance on endoscopy

A

yellow membrane

127
Q

pseudomembranous colitis is often secondary to

A

antibiotic use, especially clidamycin or ampicillin

associated with PPI use

128
Q

pseudomembranous colitis - diagnosis

A

detection of one or both toxins in stool by PCR

129
Q

pseudomembranous colitis - treatment

A

metronidazole or oral vancomycin

For recurrent cases, consider repeating prior regimen, fidaxomicin, or fecal microbiota transplant

130
Q

Bacillus anthracis - characteristics

A

gram +, spore forming, aerobe

131
Q

Bacillus anthracis produce

A

edema toxin (anthrax toxin)

132
Q

edema toxin - mechanism of action and manifestation

A

mimics the adenylate cyclase enzyme –> increases cAMP –> likely responsible for characteristic edematous borders of black eschar in cutaneous antrhax

133
Q

Bacillus anthracis - unique structural characteristic

A

The only bacterium with a polypeptide capsule (contains D-glutamate)

134
Q

Bacillus anthracis causes

A

Antrhax (cutaneous and pulmonary)

135
Q

cutaneous antrhax?

A

painless, papule surrounded by vesicle –> ulcer with black eschar, (painless, pencrotic) –> uncommonly progress to bactremia and death

136
Q

pulmonary antrhax? / aka?

A

inhalation of spores –> flu like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis and shock. aka: woolsorter’s disease

137
Q

Bacillus - bugs?

A
  1. Bacillus anthracis

2. Bacillus cereus

138
Q

Bacillus cereus causes

A

foot poisoning (reheated rice syndrome)

139
Q

Bacillus cereus poisoning - mechanism

A

Keeping rice warm results in germination of spores and enterotoxin formation

140
Q

Bacillus cereus - types (and causes)

A
  1. emetic type (preoformed heat-labile toxin, cereulide, same mechanism as cholera toxin): nausea and vomiting within 1-5 h
  2. diarrheal type (heat stable toxin): watery, nonbloody diarrhea and GI pain within 8-18
141
Q

Bacillus cereus - emetic type usually seen with

A

pasta and rice

142
Q

Bacillus cereus - emetic type is caused by

A

cereulide, a preformed toxin

143
Q

Bacillus cereus food poisoning - course

A

emetic type –> nausea and vomiting within 1-5 hrs

Diarrheal type –> watery and, nonblody diarrhea and GI pain within 8-18 hrs

144
Q

Listeria monocytogenes - characteristics

A

gram (+) rob, no spore forming, tumbling motile, faculty intracellular

145
Q

Listeria monocytogenes - intra- or extracelullar

A

faculty intracellular

146
Q

Listeria monocytogenes - acquired by

A
  1. ingestion of unpasteurized dairy products
  2. ingestion of cold deli meats
  3. tranplacental transmission
  4. vaginal transmission
147
Q

Listeria monocytogenes is the only gram (+) that

A

produce endotoxin

148
Q

Listeria monocytogenes - mechanism of action

A

Forms rocket tails (via actin polymerization) that allow intracellular movement and cell-to-cell spread accross cell membranes, thereby avoiding antibody –> characteristic tumbling motility in broth

149
Q

Listeria monocytogenes can cause

A
  1. in pregnant –> amnionitis, septicemia, spontaneous abortion
  2. newborns –> granulomatosis infantiseptica, neonatal meningitis
  3. immunocompromised patients –> meningitis
  4. healthy individuals –> mild gastroenteritis
150
Q

Listeria monocytogenes - treatment

A
  1. gastroenteritis is self limited

2. ampicillin in infants, immunocompromised, and the elderly as empirical treatment of meningitis

151
Q

bacteria resembling fungi - bags and characteristics

A
  1. Actinomyces - anaerobe, not acid fast, GRAM +

2. Nocardia - aerobe, acid fast, GRAM +

152
Q

actinomyces vs Nocardia according to location

A

Acinomyces –> normal oral, reproductive, and GI flora

Nocardia –> found in soil

153
Q

actinomyces vs Nocardia according to treatment

A

MNEMONIC: SNAP –> Sulfa - Nocardia / Actinom - Penicillin
Acinomyces –> penicillin
Nocardia –> sulfonamides

154
Q

actinomyces vs Nocardia according to clinical manifestations

A

Acinomyces –> oral/facial abscess that drain through sinus tracts, PID with intrauterine device
Nocardia –> pulmonary infections in immunocompromised and cutaneous infection after trauma in immunocompoment

155
Q

actinomyces vs Nocardia according to pigmented

A

Actinomyces israelli - yellow sulfur granules which are composed of filaments of bacteria

Microbiology (25 decks)

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