Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Micro Q3 > Clostridia I & II > Flashcards

Clostridia I & II Flashcards

0
Q

Clostridia are: GM (+/-) ______

A

GM + rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Clostridia are: obligate/facultative aerobes/anaerobes

A

Obligate Anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F: Clostridia form spores

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clostridia are: catalase (neg/pos)

A

Catalase Negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clostridia are: Oxidase (pos/neg)

A

Oxidase negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which clostridia species is highly invasive and causes gas gangrene?

A

Clostridium perfringens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which clostridium species is generally non invasive and secretes a toxin that causes pseudommembranous enterocolitis?

A

Clostridium difficle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which clostridium species is generally noninvasive and is the causeitive agent of tetanus?

A

Clostridium tetani

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which clostridium is non invasive and causes botulism

A

C. botulinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which clostridia toxin causes flaccid paralysis?

A

botulism toxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which clostridia toxin causes pseudomembranous colitis?

A

Exotoxin A & B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

this clostridia species is the only one to form terminal spores - “tennis rackets”

A

C. Tetai

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

C. Tetani has ____ serological type(s)

A

ONE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The Tetanus toxin is a ______-toxin that is transported to ________

A

Neurotoxin, transported from infection site to peripheral and CNS nerves (anterior horn cells of S.C. + brain stem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tetanus toxin mechanism of action:

A

inhibits glycine and GABA neurotransmitter release => spastic paralysis + convulsive contractions - lockjaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The tetanus toxin has A and B subunits: one binds ______ _______ and the other _________________

A

binds neuronal ganglioside, the other has neurotoxin activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

C. Tetanus infection clinical syndrome:

  1. Fever?
  2. Spasm?
  3. Sensory?
  4. Complications?
A
  1. NO FEVER
  2. VIOLENT MUSCLE SPASMS
  3. NO SENSORY LOSS
  4. Involvement of respiratory muscles -> failure -> aspiration, dysphagia, pulmonary infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

C. Tetanus diagnosis made based on:

A

Clinical syndrome is the best way to diagnose.

Culture only positive in 39% cases. Organism not usually found in wound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Patient has violent flexor muscle spasms, clenched teeth and jaw, no fever, and no sensory loss. They stepped on a soil-y nail a few days ago. The best treatment is:

A
  1. Human tetanus immunoglobulin
  2. Penicillin + wound debridement
  3. Resp. support
  4. Immunization!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q 
Tetanus fatality rate:
a - 40 %
b - 50 %
c - 60%
d - 70 %
A

C - 60% fatality due to pulmonary complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tetanus immunization accomplished with ____ doses of _____ during the first _______ months/years of life. (Given with the DPT vaccine)

A

3 doses of toxoid (toxin inactivated by formaldehyde) within the first 6 months of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T/F: Tetanus immunization requires a booster every 5 years

A

FALSE. Booster required every 10 years. Also, a booster is often given at 1 year and before entering school.

22
Q

T/F: C. Botulinum spores are heat resistant

A

True

23
Q

T/F: C. Botulinum toxin is heat resistant

A

False. Botulism toxin is HEAT LABILE

24
Q

C. Botulinum spores are often found in:

A

Canned food (anaerobic conditions). Spore grow +germinate, form toxin in 2-3 days

25
Q

T/F: botulism toxin is NOT destroyed by stomach acid

A

True, the toxin is not destroyed by stomach acid, but is heat labile, and thus destroyed by boiling for 10 min.

26
Q

The botulism toxin has ___ types; which are most common??

A

7 types; A thru G.

type A, B, and E are most common

27
Q

Which clostridia toxin is absorbed by the intestine, carried by blood to peripheral nerve synapses, binds to a receptor, and blocks the release of acetylcholine by interfering with proteolytic processing??

a - tetanus toxin
b - botulsim toxin
c - exotoxin A + B
d - Alpha toxin

A

This is the mechanism for Botulism toxin

28
Q

T/F: Botulism toxin exposure will result in fever

A

False.

Botulsim toxin will NOT CAUSE FEVER.

29
Q

T/F: botulism will cause an altered mental status

A

FALSE, botulsim toxin will not have any effect on mental status

30
Q

the incubatio period for botulism toxin is ___ to ____ hours/days/weeks

A

18 to 36 hours

31
Q

T/F: botulsim toxin will result in sesnory deficit

A

False. Botulsim = NO SENSORY DEFICIT

32
Q

Which clostridium syndrome is characterized by flaccid paralysis of peripheral nerves symmetrically, dysphagia, dilated pupils, diplopia, and dry throat?

A

C. Botulinum, botulism

33
Q

T/F: you can diagnose botulism by culturing the microorgannisms

A

FALSE. the preformed toxin is the culprit - better to detect the toxin in feces, vomit, serum, or via serology for diagnosis.

34
Q

Patient has botulism!! - what do you do?

A
  1. Remove toxin from stomach w/ lavage
  2. Treat with Antitoxin (specific) - usually type A, B, + E
  3. May need respiratory support
35
Q

Another clinical variant of botulism with more subtle symptoms and caused by honey as a source of contamination is:

A

Infant Botulism

36
Q

In wound-associated botulism, the contamination comes from:

A

Spores in soil get into wound -> germinate -> toxin

37
Q

A common cause of antibiotic-associated diarrhea is:

A

C. Difficile, due to toxin mediated coloninc inflammation

38
Q

C. Difficle is found in ___% of general population GI tract

A

3%

39
Q

___% of hospitalized patients are colonized vie the shitty-oral route from dirty hospital people

A

30%

40
Q

C. Difficle pathogenesis:

A
  1. Antibiotic suppression of local flora -> C. Difficle proliferation
  2. Exotoxin A produced -> binds to gut receptor
  3. Exotoxin B produced -> cytotoxin -> damages colonic mucosa -> pseudo membrane formation + bloody diarrhea
41
Q

Which clostridium toxin acts by ADP-ribosylating ‘Rho’, a GTP- binding protein?

a - Tetanus toxin
b - Botulism toxin
c - Exotoxin A
d - Exotoxin B
e - Alpha toxin
A

d - Exotoxin B

this causes the bloody diarrhea and pseudomembrane formation associated with C. Difficle infection.

42
Q

Pateint has a hx of antibiotic use, and yellow-white plaque pseudomembrane on colonoscopy; what toxin might you detect in a stool sample to confirm your diagnosis?

A

exotoxin B. ELISA can also be used to detect toxins of C. Difficile.

43
Q

You have diagnosed a pt with a C. Diff infection, you decide to treat by:

A
  1. Stopping any offending antibiotics

2. Treating with metroidazole, vancomycin, or fidaxomicin

44
Q

C. perfringens organisms are primarily found in ______ but also in ________________________

A

Soil, but also in human GI tract + Vaginas

45
Q

Two ‘syndromes’ of C. Perfringens are:

A
  1. Gas Gangrene - invasive and rapidly progressing necrosis

2. Food poisoning - self limiting diarrhea

46
Q

The alpha toxin produced by c. perfringens is a _________, it damages host cell membranes including capillary walls and RBCs

A

Lecithinase.

47
Q

The byproduct(s) of c. perfringens anaerobic growth:

A
  1. H2

2. CO2

48
Q

The enterotoxin associated with C. Perfringens is part of the

A

Spore Coat. It is released into intesting after a large qty (10^8) of spores are consumed.

49
Q

The clinical syndrome of superficial cellulitis, necrotizing cellulitis, necrotizing fasciitis, and myositis/myonecrosis is caused by which Clostridia species?

A

C. Perfringens; this is gas gangrene

50
Q

C. Perfringens diarrhea lasts about _____ hours/days, and is characterize by abdominal cramps ad watery diarrhea.

A

8-22 hours

51
Q

Treatment for gas gangrene would include:

A
  1. Surgical wound debridement
  2. Penicilliin
  3. Hyperbaric O2
52
Q

to diagnose c. perfringens food poisoning you would need to:

A

detect enterotoxin by ELISA of stool or food

53
Q

In addition to the Alpha Toxin - Lecithinase - what other enzymes are involved in the development of gas gangrene by C. Perfringens?

A

Collagenase, Hyaluronidase

Micro Q3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions