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M2.2 Flashcards

1
Q

spore-forming gram positive
rods
aerobic, nonmotile, box-car-shaped

A

Bacillus anthracis

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2
Q

spore-forming gram positive
rods
aerobic, motile,
reheated fried rice

A

Bacillus cereus

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3
Q

Bacillus anthracis

Capsule?
Motility?
Hemolysis?
Sensitivity to Penicillin?

A

Capsule Present
Motility Non-Motile
Hemolysis Non-hemolytic
Sensitivity to Penicillin
Susceptible
String of pearls
reaction on Mueller
Hinton agar with
Penicillin

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4
Q

Bacillus cereus

Capsule?
Motility?
Hemolysis?
Sensitivity to Penicillin?

A

Absent

Motile

Wide zone of beta
hemolysis

Resistant

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5
Q

BACILLUS ANTHRACIS
CHARACTERISTICS

A

• aerobic, gram-positive box-car like rods
• nonmotile
• spore-forming
• Medusa head morphology
o dry “ground glass” surface and irregular edges with
projections along lines of
inoculation

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6
Q

BACILLUS ANTHRACIS

HABITAT AND TRANSMISSION

A

Soil

contact with infected animals or inhalation of
spores from animal hair and wool

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7
Q

BACILLUS ANTHRACIS

PATHOGENESIS: VIRULENCE FACTORS

A

antiphagocytic capsule
Edema factor (EF)
Lethal factor (LF)
Protective antigen (PA)

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8
Q

BACILLUS ANTHRACIS

antiphagocytic capsule

calmodulin-dependent adenylate cyclase

inhibits a signal transduction in cell division

mediates the entry of the other two components into cell

A

poly-D-glutamate
Edema factor (EF)
Lethal factor (LF)
Protective antigen (PA)

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9
Q

BACILLUS ANTHRACIS

SPECTRUM OF DISEASE

A

Cutaneous, Inhalational, Gastrointestinal Anthrax

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10
Q

BACILLUS ANTHRACIS

Cutaneous Anthrax

A

direct epidermal contact with spores causes formation of a
malignant pustule with subsequent eschar and central
necrosis
o 20% mortality rate

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11
Q

BACILLUS ANTHRACIS

Inhalational Anthrax

Chest X-ray?

A

woolsorter’s disease
1. inhaled spores from animals
2. weaponized preparations (bioterrorism)
o prolonged latent period (2 mos) before rapid deterioration

hemorrhagic mediastinitis
-germination of spores in the mediastinal lymph nodes

Mediastinal widening
o pulmonary hemorrhage, pleural effusion, meningeal
symptoms

o 100% mortality rate without immediate treatment

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12
Q

BACILLUS ANTHRACIS

Gastrointestinal Anthrax

A

UGI ulceration, edema and
sepsis (rapidly progressive course)
o mortality rate approaches 100%

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13
Q

cutaneous anthrax

TREATMENT

A

DOC is ciprofloxacin

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14
Q

inhalational/gastrointestinal anthrax

TREATMENT

A

DOC is ciprofloxacin or doxycycline with one or two
additional antibiotics (rifampin, vancomycin, penicillin, imipenem, clindamycin, clarithromycin)

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15
Q

Which of the following is an important virulence factor of Bacillius
anthracis?
A. Calcium dipicolinate
B. Pili
C. Lipopolysaccharide
D. Protective antigen

A

D. Protective antigen

mediates the entry of the other two
components into cell

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16
Q

BACILLUS CEREUS

HABITAT AND TRANSMISSION

A

grains

reheated fried rice

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17
Q

BACILLUS CEREUS

PATHOGENESIS

A

Heat-Labile Enterotoxin
Heat-Stable Enterotoxin

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18
Q

BACILLUS CEREUS

PATHOGENESIS

A

Heat-Labile Enterotoxin
Heat-Stable Enterotoxin

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19
Q

BACILLUS CEREUS

cholera-like enterotoxin causes ADP-ribosylation,
increasing cAMP

A

Heat-Labile Enterotoxin

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20
Q

BACILLUS CEREUS

staphylococcal-like enterotoxin functions as superantigen

A

Heat-Stable Enterotoxin

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21
Q

BACILLUS CEREUS

SPECTRUM OF DISEASE

A

Food poisoning
Emetic form, diarrheal form
Ophthalmitis

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22
Q

BACILLUS CEREUS

EMETIC FORM

Implicated food?
Incubation period (hours)?
Symptoms?
Duration?
Enterotoxin?

A

Implicated food Rice

Incubation period (hours) < 6 (mean, 2)

Symptoms
Vomiting, nausea,
abdominal cramps

Duration
(hours) 8 – 10 (mean, 9)

Enterotoxin Heat-stable

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23
Q

BACILLUS CEREUS

DIARRHEAL FORM

Implicated food?
Incubation period (hours)?
Symptoms?
Duration?
Enterotoxin?

A

Meat, vegetables

> 6 (mean, 9)

Diarrhea, nausea,
abdominal cramps

20 – 36 (mean, 24)

Heat-labile

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24
Q

BACILLUS CEREUS

Ophthalmitis

A

after traumatic penetrating eye injuries with
a soil-contaminated object

complete loss of light perception within 48 hours of injury

vancomycin, clindamycin, ciprofloxacin or gentamicin

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25
Q

spore-forming gram
positive rods

anaerobic,
tennis-racket-like

A

Clostridium tetani

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26
Q

spore-forming gram positive
rods

anaerobic,
bulging cans

A

Clostridium
botulinum

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27
Q

spore-forming gram positive
rods

anaerobic,
bulging cans

A

Clostridium
botulinum

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28
Q

spore-forming gram positive
rods

anaerobic, lecithinase
gas-forming

A

Clostridium
perfringens

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29
Q

spore-forming gram positive
rods

anaerobic,
pseudomembranes

A

Clostridioides
difficile

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30
Q

CLOSTRIDIUM TETANI

CHARACTERISTICS

A

• anaerobic, gram-positive, spore-forming rods
• spore is at one end (terminal spore) so organism looks like a
tennis racket

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31
Q

CLOSTRIDIUM TETANI

HABITAT AND TRANSMISSION

A

soil
• entry through traumatic implantation into tissues with low oxygenation

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32
Q

CLOSTRIDIUM TETANI

PATHOGENESIS

A

tetanus toxin (tetanospasmin)

o Prevents release of GABA from Renshaw cells in spinal cord by cleaving of synaptobrevin

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33
Q

Tetanospasmin

SITE OF
ACTION

A

Presynaptic
terminals

Neuromuscular
junction

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34
Q

Tetanospasmin

SITE OF
ACTION

A

Presynaptic
terminals

Neuromuscular
junction

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35
Q

Tetanospasmin
Presynaptic terminals

MECHANISM OF
ACTION and RESULT?

A

Inhibits release of
GABA by cleavage
of proteins
critical for proper
function of
synaptic vesicle
release

Rigidity: trismus,
risus sardonicus,
opisthotonos,
apnea/laryngospasm,
dysphagia, ↑DTRs

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36
Q

Tetanospasmin

Neuromuscular
junction

MECHANISM OF
ACTION and RESULT?

A

Blocks
neurotransmitter
release

Weakness or
paralysis

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37
Q

Wound infection, multiplication of
Clostridium tetani

A

No symptom

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38
Q

Tetanus toxin uptake into nervous system and
VAMP cleavage in GABA
inhibitory neurons

After how many days?
Initial symptoms?

A

7 - 10 days
Muscle aches, trismus, myslgia

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39
Q

widespread disinhibition of motor and autonomic nervous system of tetanus toxin
After how many hours?
Clinical symptoms?

A

24 - 72 hrs

Muscle spasm: local and generalized

Cardiovascular instability: labile BP, tachy-/bradycardia

Pyrexia, increased respiratory and Gl secretions

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40
Q

TETANUS PROPHYLAXIS

Clean, minor wound

A

Uncertain or <3 doses
Toxoid (TeANA)

> 3 doses
Toxoid (TeANA)
last dose >10 years

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41
Q

TETANUS PROPHYLAXIS

Contaminated wound

A

Uncertain or <3 doses
Toxoid (TeANA)
TIG (ATS)

> 3 doses
Toxoid (TeANA)
last dose >5 years

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42
Q

CLOSTRIDIUM BOTULINUM

CHARACTERISTICS

A

anaerobic, gram-positive, spore-forming rods

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43
Q

CLOSTRIDIUM BOTULINUM

HABITAT AND TRANSMISSION

A

soil

improperly
preserved food
o alkaline vegetables such as green beans, peppers, and
mushrooms
o smoked fish
o canned goods (bulging)
o honey

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44
Q

botulinum toxin

A

(heat-labile neurotoxin) blocks acetylcholine
release causing flaccid paralysis (descending pattern)
• eight immunologic types of toxin

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45
Q

most common in humans among eight immunologic types of botulinum toxin

A

types A, B, and E

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46
Q

a commercial preparation of exotoxin A

uses?

A

Botox

wrinkle removal, torticollis

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47
Q

CLOSTRIDIUM BOTULINUM

SPECTRUM OF DISEASE: TOXIGENIC

A

Food-Borne Botulism

Infant Botulism

Wound Botulism

48
Q

TRIAD OF BOTULISM

A
  1. Symmetric descending flaccid paralysis (with prominent bulbar involvement)
  2. Absence of fever
  3. Intact sensorium
49
Q

CLOSTRIDIUM BOTULINUM

Food-Borne Botulism

symptoms?
bulbar signs?
Sympa/para effects?
paralysis?

A

eye symptoms
§ BOV, diplopia, ptosis, mydriasis

bulbar signs (4 Ds): diplopia, dysphonia, dysarthria,
dysphagia

anticholinergic effects
§ dry mouth, constipation, abdominal pain

bilateral descending flaccid paralysis
respiratory paralysis

50
Q

Infant Botulism

A

Floppy Baby Syndrome

ingest spores found in household dust or honey

51
Q

CLOSTRIDIUM BOTULINUM

TREATMENT

A

TREATMENT
• adequate ventilatory support
• elimination of the organism from GIT
o judicious use of gastric lavage and metronidazole or penicillin
• trivalent botulinum antitoxin (types A, B, E)

52
Q

Contamination of wound
or punctured skin
(common in IV drug
users)

A

C. botulinum

53
Q

CLOSTRIDIUM TETANI

TREATMENT

A

• debridement of primary wound
• Metronidazole (400mg rectally or 500 mg IV every 6 h for 7 days)
is the preferred antibiotic. An alternative is penicillin (100,000–
200,000 IU/kg per day), although this drug theoretically may
exacerbate spasms (Harrisons)
• TIG (at the wound site)
• Vaccination with tetanus toxoid
o given in childhood and every 10 years thereafter

54
Q

CLOSTRIDIUM PERFRINGENS
Hemolysis?
Growth on the?

A

• double hemolysis on blood agar
• growth on egg-yolk agar
o nonmotile but with rapidly spreading growth on culture
media

55
Q

CLOSTRIDIUM PERFRINGENS

HABITAT AND TRANSMISSION

A

soil and human colon

contamination of wound with soil or feces

transmitted by ingestion of contaminated food

56
Q

CLOSTRIDIUM PERFRINGENS

SPECTRUM OF DISEASE: TOXIGENIC

A

Gas Gangrene
Food Poisoning

57
Q

CLOSTRIDIUM PERFRINGENS
Gas Gangrene

Toxin?
Manifestation?

A

alpha toxin, a lecithinase
o pain, edema and cellulitis with crepitation
o hemolysis and jaundice are common

58
Q

CLOSTRIDIUM PERFRINGENS

Food Poisoning

Toxin?

characterized by?

Known as?

A

production of enterotoxin which acts as superantigen

characterized by watery diarrhea with cramps & little
vomiting

Stormy fermentation of milk

59
Q

CLOSTRIDIUM PERFRINGENS

TREATMENT

A

• wound debridement and penicillin for gas gangrene
• supportive management for food poisoning

60
Q

CLOSTRIDIOIDES DIFFICILE

HABITAT AND TRANSMISSION

A

colon
o 3% of the general population
o up to 30% of hospitalized patients

fecal-oral route
hospital personnel

61
Q

CLOSTRIDIOIDES DIFFICILE

HABITAT AND TRANSMISSION

A

colon
o 3% of the general population
o up to 30% of hospitalized patients

fecal-oral route
hospital personnel

62
Q

CLOSTRIDIOIDES DIFFICILE

PATHOGENESIS

A

antibiotics
o clindamycin, 2nd & 3rd gen cephalosporins, ampicillin

exotoxins A (enterotoxin) and B (cytotoxin) inhibit GTPases, leading to apoptosis and death of enterocytes

63
Q

CLOSTRIDIOIDES DIFFICILE

exotoxin in stool detected by what effect where final phase by which viral cells infect cells?
on what diagnostics?

A

cytopathic effect

cultured cells or ELISA

64
Q

pseudomembranes are the visual result of what toxins?

A

exotoxins A (enterotoxin) and B (cytotoxin) inhibit GTPases,
leading to apoptosis and death of enterocytes

65
Q

CLOSTRIDIOIDES DIFFICILE infection can precipitate ____ of ulcerative colitis

A

flare-ups

66
Q

CLOSTRIDIOIDES DIFFICILE

SPECTRUM OF DISEASE: TOXIGENIC

A

Pseudomembranous Colitis

o Non-bloody diarrhea associated with pseudomembranes
(yellow-white plaques) on the colonic mucosa

o toxic megacolon can occur

67
Q

CLOSTRIDIOIDES DIFFICILE

TREATMENT

A

oral metronidazole

oral vancomycin

68
Q

OTHER CLOSTRIDIA
Nontraumatic myonecrosis in immunocompromised patients

A

C. septicum

69
Q

OTHER CLOSTRIDIA
Toxic shock syndrome associated with septic
abortion

A

C. sordellii

70
Q

OTHER CLOSTRIDIA
Traumatic wound infections

A

C. tertium

71
Q

CORYNEBACTERIUM DIPHTHERIAE

Also known as
Motility?
Shape?
Granules?
Culture?

A

Klebs-Loeffler bacillus
non-motile

club or comma-shaped rods arranged in V or L shape looks like Chinese characters

metachromatic granules
Reddish metachromatic (Babes-Ernst / Volutin)

Potassium tellurite: dark black colonies
Loeffler’s medium: after 12 hours of growth, stain with methylene
blue.

72
Q

for detection of toxigenicity
CORYNEBACTERIUM DIPHTHERIAE

A

modified Elek test

73
Q

injection of diphtheria exotoxin into the skin, to determine whether a person is susceptible to infection by diphtheriae

A

Schick test

74
Q

CORYNEBACTERIUM DIPHTHERIAE

HABITAT AND TRANSMISSION

A

• habitat is human throat
• transmission via respiratory droplets

75
Q

CORYNEBACTERIUM DIPHTHERIAE

PATHOGENESIS

A

exotoxin

inhibits protein synthesis by
adding ADP-ribose to elongation factor-2 (EF-2)
o subunit A, has ADP-ribosylating
activity
o subunit B, binds the toxin to cell
surface
o exotoxin encoded by b-prophage

pseudomembranes
death of mucosal epithelial cells

76
Q

CORYNEBACTERIUM DIPHTHERIAE

PATHOGENESIS

A

exotoxin

inhibits protein synthesis by
adding ADP-ribose to elongation factor-2 (EF-2)
o subunit A, has ADP-ribosylating
activity
o subunit B, binds the toxin to cell
surface
o exotoxin encoded by b-prophage

pseudomembranes
death of mucosal epithelial cells

77
Q

ABCDEFG of Diphtheria

A

ADP-ribosylation
Beta-prophage
Corynebacterium
Diphtheriae
Elongation Factor-2
Granules (metachromatic)

78
Q

ABCDE of beta-prophage-
encoded toxins

A

ShigA-like toxin (EHEC)
Botulinum toxin
Cholera toxin
Diphtheria toxin
Erythrogenic toxin
(S. pyogenes)

79
Q

CORYNEBACTERIUM DIPHTHERIAE

SPECTRUM OF DISEASE

A

prominent thick, gray, pseudomembranes over tonsils and throat

80
Q

pseudomembranes

complications

A

o airway obstruction
o Myocarditis - A-V conduction block, dysrhythmia
o Neural involvement: peripheral nerve palsies, GBS, palatal paralysis,
neuropathies, cranial nerve and/or muscle paralysis

81
Q

CORYNEBACTERIUM DIPHTHERIAE

TREATMENT

A

Erythromycin
Macrolides
Penicillin G

82
Q

LISTERIA MONOCYTOGENES

Shape?
Motility?
Hemolysis?
Paradoxical growth in?

A

• aerobic, non-spore-forming, gram-positive rods
• arranged in V- or L-shape
• tumbling motility
• narrow zone of beta-hemolysis
• cold enhancement: paradoxical growth in cold temperature

83
Q

LISTERIA MONOCYTOGENES

HABITAT

A

• colonizes GI and female GUT
• widespread in animals, plants, and soil

84
Q

LISTERIA MONOCYTOGENES

TRANSMISSION

A

• across placenta or by contact during delivery
• ingestion of unpasteurized milk products, e.g., cheese

85
Q

LISTERIA MONOCYTOGENES

PATHOGENESIS

A

• internalin: interacts with E-cadherin on the surface of cells
• Listeriolysin: escape from phagosomes
• actin rockets (actin polymers): propels the bacteria through the
membrane of one human cell and into another

86
Q

LISTERIA MONOCYTOGENES

SPECTRUM OF DISEASE

A

Early-Onset Neonatal Listeriosis

Late-Onset Neonatal Listeriosis

Adult Listeriosis

87
Q

Early-Onset Neonatal Listeriosis

Aka?
Transmission?
Characterized by?
Complicated by?

A

(granulomatosis infantiseptica)
o transplacental transmission
o characterized by late miscarriage or birth complicated by sepsis,
multiorgan abscesses, and disseminated granulomas

88
Q

Late-Onset Neonatal Listeriosis

Transmission?
manifests as?

A

transmitted during childbirth

meningitis or
meningoencephalitis

89
Q

Adult Listeriosis

A

o bacteremia, sepsis, or meningitis in pregnant, elderly, or
immunocompromised individuals

90
Q

LISTERIA MONOCYTOGENES

TREATMENT

PREVENTION

A

ampicillin with or without gentamicin

pregnant women and immunocompromised patients should not ingest
unpasteurized milk products or raw vegetable

91
Q

ERYSIPELOTHRIX RHUSIOPATHIAE

catalase, oxisdase, and indole?

H2S?

A

• gram positive rod
• negative
• H2S producer- unique among gram positive rods

92
Q

ERYSIPELOTHRIX RHUSIOPATHIAE

TRANSMISSION

Highest risk?

A

Distributed in land and sea animals worldwide

Acquired by direct inoculation from a contaminated source

Highest risk : fishermen, handlers, abattoir workers

93
Q

Ersipeloid

Aka?

Pus?

A

ERYSIPELOTHRIX RHUSIOPATHIAE

Seal finger or Whale
finger

Pus is not present (to differentiate
from Staphylococcal/ Streptococcal
infection)

94
Q

Ersipeloid

TREATMENT

A

Penicillin G– drug of choice for severe infections
• Intrinsically resistant to vancomycin

95
Q

ACTINOMYCES ISRAELII

CHARACTERISTICS

A

GRAM POSITIVE BACTERIA WITH BRANCHING
FILAMENTS
anaerobe (normal oral flora)

96
Q

ACTINOMYCES ISRAELII

SPECTRUM OF DISEASE

A

local trauma (broken jaw or dental extraction)

Lumpy Jaw- cervicofacial actinomycosis

Abscesses that drain through sinus tracts

Pelvic inflammatory disease in those with IUDs

Physical exam reveals hard, non-tender swelling with sinus tracts
draining sulfur granules

97
Q

ACTINOMYCES ISRAELII

TREATMENT

A

prolonged treatment with Penicillin G
• consider surgical excision and drainage

98
Q

NOCARDIA ASTEROIDES

CHARACTERISTICS

A

aerobic (normal oral flora)
weakly acid fast
• setting aerobic, filamentous gram-positive rods with aerial hyphae

99
Q

NOCARDIA ASTEROIDES

HABITAT and TRANSMISSION

A

Habitat: soil and water
Transmitted by inhalation of particles from soil

100
Q

NOCARDIA ASTEROIDES

main manifestation

Immunocompromised

Immunocompetent

A

Subacute to chronic pulmonary infection

Pulmonary infection;
Mimics TB with negative
PPD

Cutaneous infection after
trauma; spreads to CNS as
brain abscesses

101
Q

NOCARDIA ASTEROIDES

TREATMENT

A

Cotrimoxazole
Tmpsmx

102
Q

Identified by McFadyean Reaction

A

Bacillus anthracis

103
Q

A 28/M worker has a 2 day history of fever, cough, dyspnea. He
presents in the ER in tripod position, altered sensorium with O2 sat
of 86% at room air. ABG showed metabolic acidosis. Patient was
intubated but still unstable. Patient then expired at the ER. PMHx
(+) DM uncontrolled (+) asthma. Personal Hx: alcoholic drinker,
worker in a factory of linen and fabric from sheep fleece. What is
the most likely diagnosis?
a. CAP
b. Asthma exacerbation
c. Diabetic ketoacidosis
d. Anthrax

A

d. Anthrax

104
Q

Anthrax

In relation to the case above, what is the MOST LIKELY cause of
death?
a. Pulmonary hemorrhage
b. Pleural effusion
c. Hemorrhagic stroke
d. Cardiac tamponade

A

a. Pulmonary hemorrhage

105
Q

Anthrax

What radiologic finding would be compatible with the case above?
a. Meniscus sign
b. Widened mediastinum
c.
“Thumbprint sign”
d. Lemon shaped hyperdensity

A

b. Widened mediastinum

106
Q

T o which of the following clinical entities is the expected cause of
the death of the patient in the above case similar to?
a. Weil’s syndrome
b. Congenital rubella
c. Legionnaires disease
d. All of the above

A

a. Weil’s syndrome

107
Q

Which of the following drugs have coverage for the causative agent
of Woolsorter’s disease?
a. Penicillin and Ciprofloxacin
b. Monoclonal antibody
c. Doxycycline
d. All of the above

A

d. All of the above

108
Q

Muscles affected:
Sardonic smile
Lock jaw
Opisthotonus

A

Orbicularis oris

Muscles of mastic
Lateral pterygoid
Temporalis muscle

Spinalis muscles
Errector spinal

109
Q

Possesses an alpha-toxin (lecithinase)

A

Nagler’s reaction

110
Q

Which of the following drugs can precipitate pseudomembranous
colitis?
a. Clindamycin
b. Cephalexin
c. Amoxicillin
d. All of the above

A

d. All of the above

111
Q

What is the drug of choice in treating pseudomembranous colitis?
a. Vancomycin IV
b. Vancomycin PO
c. Clindamycin
d. All of the above

A

b. Vancomycin PO

112
Q

Causes bull neck diphtheria

A

Corynebacterium

113
Q

Psychrophile

A

LISTERIA

114
Q

Causes of neonatal meningitis

A
  • Group B strep
  • E. coli
  • Listeria
115
Q

Meningitis
- Very young (neonate) and very old:
- Children:
- Adolescent:
- Adult:

A

Meningitis
- Very young (neonate) and very old: E. coli
- Children: Haemophilus influenzae
- Adolescent: Neisseria meningitidis
- Adult: Pneumococci

03 (4 decks)

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