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MICROM 442 > Exam 3 Lecture 24 > Flashcards

Exam 3 Lecture 24 Flashcards

1
Q

Obligate anaerobes are killed by:

A

oxygen

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2
Q

Where are obligate anaerobes found?

A

everywhere: in our mouth, feces, ubiquitous in soil and silt

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3
Q

Clostridium causes 3 classical diseases, which are:

A
  1. gas gangrene
  2. botulism
  3. tetanus
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4
Q

Clostridium causes 2 enteric diseases, which are:

A
  1. food poisoning

2. antibiotic-associated colitis

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5
Q

Cl. perfringens causes:

A
  1. gas gangrene

2. food poisoning

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6
Q

Cl. botulinum causes:

A

botulism

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7
Q

Cl. tetani causes:

A

tetanus

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8
Q

Clostridioides difficile (C. diff) causes:

A

antibiotic-associated colitis

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9
Q

Clostridium natural reservoirs:

A

soil, intestinal tracts, skin of humans and animals

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10
Q

True or false: Clostridium forms endospores

A

True

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11
Q

Gram stain of Clostridium

A

gram positive rods, may see endospores

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12
Q

Why are Clostridium endospores significant?

A

endospores can survive in the presence of oxygen

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13
Q

Clostridial wound infections are caused by:

A

mixed clostridial infection following surgery or trauma (Cl. perfringens, other Cl. species)

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14
Q

Gas gangrene

A

toxins produced by Cl. perfringens causes infection and spreads to healthy muscle tissue; causes myonecrosis

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15
Q

True or false: in gas gangrene, bacteremia is common

A

false - systemic toxemia can result

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16
Q

What toxins does Cl. perfringens produce to cause gas gangrene?

A

exotoxins: alpha toxin and perfringolysin O (PFO)

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17
Q

Cl. perfringens alpha toxin is also called:

A

phospholipase C or lecithinase C

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18
Q

Cl. perfringens alpha toxin function

A

has phospholipase/spingomyelinase activity which leads to cell lysis (broad spectrum)

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19
Q

Cl. perfringens PFO function

A

pore forming toxin similar to streptolysin O/listeriolysin O; lyses cells

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20
Q

Cl. perfringens PFO is toxic specifically to:

A

heart muscle

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21
Q

Cl. perfringens PFO alters ___ ___

A

capillary permeability

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22
Q

True or false: Cl. perfringens PFO is the principal virulence factor for gas gangrene

A

false - alpha toxin is principal

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23
Q

Are there host defenses in gas gangrene?

A

not in necrotic tissues - thus hard to control gas gangrene infection

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24
Q

How is gas gangrene diagnosed?

A

clinically once typical lesions occur

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25
Q

When is gas gangrene treated?

A

as soon as typical lesions are clinically identified - treated before lab results come back

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26
Q

Gas gangrene wound pain evolves to ___ and ___

A

edema and shock

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27
Q

How is gas gangrene treated?

A

antibiotics, surgical removal of necrotic tissue, oxygenating tissue, possible amputation

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28
Q

True or false: Cl. perfringens divides rapidly which contributes to rapid progression of gas gangrene infection

A

true - divides once every ~ 6.3 min (faster than E.coli)

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29
Q

True or false: it is common to see lots of white blood cells and PMNs in a tissue sample for gas gangrene

A

false - altered capillary permeability attributes to no immune cells around infection

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30
Q

True or false: Cl. perfringens often forms spores in gas gangrene infection

A

false - rarely spores are found

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31
Q

Cl. perfringens on blood agar creates a ____ zone of __ hemolysis.

A

double; beta

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32
Q

When Cl. perfringens is plated on blood agar, __ causes ____ hemolysis, which is surrounded by ____ hemolysis caused by ____.

A

PFO causes (beta) complete hemolysis; incomplete hemolysis caused by alpha toxin

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33
Q

Cl. perfringens has ____ activity on egg yolk agar

A

lecithinase (alpha toxin)

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34
Q

True or false: Cl. perfringens is the 3rd most common cause of food poisoning in the US

A

True

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35
Q

Source of Cl. perfringens food poisoning

A

meat products; commercial food preparation

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36
Q

True or false: high inoculum of Cl. perfringens is required to cause food poisoning symptoms

A

true - 10^6-10^7 viable bacterial cells per gram of food

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37
Q

How does Cl. perfringens cause food poisoning? (3 steps)

A
  1. spores germinate during food heating and organisms rapidly increase
  2. organisms ingested
  3. organisms sporulate in small intestine and produce enterotoxin
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38
Q

What does Cl. perfringens enterotoxin do?

A

produces pores in enterocytes, which causes leakage of fluids and ultimately self-limiting diarrhea

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39
Q

Enterocytes

A

Intestinal absorptive cells

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40
Q

When does onset of symptoms occur for Cl. perfringens food poisoning?

A

7-22 hours after ingestion of contaminated food

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41
Q

Common symptoms of Cl. perfringens food poisoning

A

diarrhea, cramps, abdominal pain

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42
Q

True or false: fever, nausea, and vomiting are typically seen in Cl. perfringens food poisoning

A

false - none of these are typically seen

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43
Q

How can we diagnose Cl. perfringens food poisoning?

A
  1. lacks flagella (unlike other clostridia)

2. spores sometimes seen on smears

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44
Q

True or false: regarding Cl. perfringens food poisoning, people rarely seek treatment/care due to quick recovery

A

true (recovery within 24 hours)

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45
Q

What is the difference between infection and intoxication?

A 
infection = ingestion of live bacteria and establish themselves in the intestine and then produce toxin
intoxication = ingestion of preformed toxin in contaminated food
46
Q

True or false: classical botulism is an infection

A

false - intoxication

47
Q

Classical botulism is caused by:

A

ingestion of preformed toxin in food contaminated with spores sealed in anaerobic environment (mainly improperly canned home food)

48
Q

Where is Clostridium botulinum found?

A

soil, silt, vegetation, and intestinal tracts of humans and animals

49
Q

3 types of botulism

A
  1. wound botulism
  2. infant botulism
  3. inhalation botulism (isn’t a thing but is a threat)
50
Q

Wound botulism

A

usually infection of compound fracture, severe laceration, or penetrating wound. organism is contracted from environment

51
Q

Infant botulism

A

caused by germination of spores in intestinal tract of infants 2w-6m of age; adults not affected

52
Q

Infant botulism can be caused by babies ingesting:

A

honey (which can’t be sterilized)

53
Q

Cl. botulinum toxins

A

7 antigenically distinct types (A thru G)

54
Q

True or false: all of the Cl. botulinum toxins induce the same neurological disease in humans

A

True

55
Q

Mechanism of botulinum toxin

A
  1. absorbed in intestine, transported to NMJ via bloodstream
  2. Ach release from synaptic vesicles is blocked, stopping nerve impulses and impairing motor nerve function
  3. Paralysis, respiratory failure and death may ensue
56
Q

Relative toxicity of Cl. botulinum

A

0.1 - 1 microgram is lethal (2.2 pounds can kill the whole world)

57
Q

True or false: Cl. botulinum toxin is heat-labile

A

True - properly cooking food destroys toxin

58
Q

Cl. botulinum incubation period

A

12-96 hours (up to 14 days)

duration is related to dose of toxin ingested

59
Q

Cl. botulinum gastrointestinal symptoms

A

vomiting, constipation

60
Q

Other Cl. botulinum symptoms

A

nervous system-flaccid paralysis

61
Q

Cl. botulinum mortality rate

A

20% (declining)

62
Q

How is Cl. botulinum diagnosed?

A

clinical isolation of organism from contaminated food/stool sample; pt must be treated before lab results come back

63
Q

Treatment of Cl. botulinum

A
  1. eliminate unabsorbed toxin using stomach lavage and enemas
  2. eliminate source of toxin
  3. neutralize unbound toxin using antitoxin
  4. supportive/respiratory care
64
Q

How is antitoxin therapy prepared?

A

7 different antitoxins are made (for each Cl. botulinum toxin); prepared in horses, can result in serum sickness

65
Q

True or false: antibiotics are not important for treatment except in cases of wound botulism

A

True

66
Q

True or false: Cl. tetani produces several different toxins like Cl. botulinum does

A

False - there are dif serotypes of Cl. tetani but all produce identical toxin

67
Q

What type of toxin does Cl. tetani produce?

A

AB toxin

68
Q

Tetanus pathogenesis

A
  1. Cl. tetani spores contaminate penetrating wound
  2. spores germinate to vegetative cells and produce toxin
  3. toxin enters motor neurons and is transported to the CNS interneurons
69
Q

Cl. tetani toxin is transported to the CNS via:

A

retrograde axonal transmission

70
Q

In the USA, Cl. tetani has the highest mortality in:

A

elderly

71
Q

True or false: the tetanus protein toxin is the sole virulence factor in Cl. tetani

A

True

72
Q

Mechanism of tetanus toxin

A

toxin blocks secretion of inhibitory neurotransmitters between CNS interneurons, causes nonstop muscle flexing

73
Q

Relative toxicity of tetanus toxin

A

0.15 to 1 microgram may be lethal for humans

74
Q

Cl. tetani is gram-___, __ shaped, with ___ ___

A

gram-positive; rod; terminal endospore

75
Q

Cl. tetani diagnosis

A

mainly based on clinical findings: cramping, twitching of muscles around wound, then head and neck
- isolation of organism may be done, tetanus spores are presumptively diagnostic

76
Q

True or false: for Cl. tetani, early diagnosis is critical for successful treatment

A

True

77
Q

True or false: for Cl. tetani, definitive diagnosis requires demonstration of toxin and neutralization with antitoxin

A

True

78
Q

Cl. tetani immunity provided by:

A

DTaP toxoid vaccine - boosters required every 10 years

79
Q

Cl. tetani treatment (4)

A

maintenance of airway, Benzodiazepines (GABA antagonists), tetanus immunoglobulin, antibiotics

80
Q

Tetanus and Botulinum toxins are produced as ___ ____ that accumulate in the ___ until the toxin is released via __ ___

A

inactive polypeptide; cytosol; cell autolysis

81
Q

Common mechanism of Tetanus and Botulinum toxin: Active domain transported into ____, specifically cleaves __ of ___ ___, preventing fusion with ___ ___

A

neuron; VAMP; synaptic vesicle; cell membrane (of post-synaptic neuron)

82
Q

___ is required to facilitate synaptic vesivle fusion to axon membrane to release neurotransmitter

A

VAMP (vesicle associated membrane protein)

83
Q

Which toxins cleave VAMP?

A

Tetanus toxin, Botulinum Toxins B, D, F, G

84
Q

C. diff etiology

A
  1. mainly nosocomial in following antibiotic therapy

2. normal microbiota is altered, C. diff spores germinate, overgrow, produce toxins, causing colitis

85
Q

True or false: C. diff is part of the normal microbiota

A

True

86
Q

C. diff morphology

A

slender gram positive rod with large, oval subterminal endospores

87
Q

True or false: C. diff is resistant to many antibiotics

A

True

88
Q

C. diff has _ principal toxins responsible for disease which:

A

2; disrupt cytoskeletal epithelial cells and submucosal tissue

89
Q

C. diff toxin A is an _____ and is specific to ____ ____ ___

A

enterotoxin; intestinal mucosal surface

90
Q

C. diff toxin B is a ___ ___

A

generalized cytotoxin

91
Q

Both C. diff toxins are ___ ____ with __ functional domains

A

large exotoxins; 3

92
Q

What are the functional domains of C. diff exotoxin A and B?

A
  1. receptor binding
  2. membrane translocation
  3. glucosyltransferase activity
93
Q

Regarding C. diff exotoxins, once in the ___, they inactivate __ ___ by transferring ___ onto them, leading to ____ ___, ___ ____ and ____

A

cytoplasm; Rho proteins; glucose; cytoskeletal disruption, cell rounding and retraction

94
Q

C. diff pathogenesis occurs in the ___

A

colon

95
Q

Symptoms of C. diff infection include:

A

abdominal pain, watery diarrhea, mucus or blood may be seen; also red and inflamed colon

96
Q

True or false: C. diff infection may cause formation of pseudomembrane in the colon

A

True

97
Q

C. diff pseudomembrane is characterized as:

A

1-5mm raised white/yellow plaques on mucosa of colon, composed of epithelial debris, fibrin, and PMN leukocytes

98
Q

C. diff diagnosis involves: (2)

A
  1. demonstration of pseudomembrane via sigmoidoscopy

2. fecal filtrate assays for C. diff toxin (rapid)

99
Q

How is C. diff treated?

A

discontinuation of antibiotic therapy, vancomycin or metronidazole, fecal transplant

100
Q

True or false: C. diff relapse infections are not common after treatment

A

False - relapse may occur

101
Q

True or false: C. diff colitis can be spread from person to person

A

True - may result in outbreaks

102
Q

In 2003, a ___ ___ ___ of C. diff was isolated. It had a ___ in ___ ___, causing ____ production of toxin A and B.

A

highly virulent strain; mutation in regulatory gene; increased

103
Q

Bacteroides fragilis is gram-____ ____ and doesn’t form ___

A

Negative rod; spores

104
Q

True or false: there is about 10x as much Bacteroides in the gut as there is E. coli

A

True

105
Q

What diseases does Bacteroides fragilis cause?

A
  1. intra-abdominal abscesses

2. skin and soft tissue infections (cellulitis and fasciitis associated with surgical wound infection)

106
Q

B. fragilis virulence factors

A

has capsular polysaccharides that prevents opsonization, induces abscess formation, promotes adherence to cells

107
Q

True or false: purified capsular material of B. fragilis can alone cause abscess formation

A

True

108
Q

B. fragilis is resistant to:

A

penicillin

109
Q

When B. fragilis causes infection, it is often a ___ infection because other anaerobes and facultative bacteria are present

A

mixed

110
Q

B. fragilis infection diagnosis

A
  1. look for abscesses using radiologic CT and/or aspiration

2. gram stain/culture

111
Q

Treatment for B. fragilis infection

A
  1. 2 antibiotics since most infections and polymicrobial

2. drainage of abscess using CT and needle

MICROM 442 (26 decks)

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