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Dent6400 > Exam 2 - (1) Clostridia > Flashcards

Exam 2 - (1) Clostridia Flashcards

1
Q

What type of bacteria are Clostridium in relation to oxygen? What is their shape and membrane (gram) classificaiton?

A
  • Strictly anaerobic

- Gram + rods

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2
Q

Clostridium can produce endo____, making it mostly unique among bacteria.

A

spores

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3
Q

About how many Clostridium(C) species are responsible for human infection?

A

30

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4
Q

How many C. species are found in the environment (water, soil, animal wastes?)

A

> 50

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5
Q

C. can produce _______ toxins that are responsible for disease ______.

A
  • proteinaceous (protein)

- symptoms

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6
Q

What C. species causes pseudomembraneous colitis (PMC)?

A

C. difficile

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7
Q

What C. species is known to cause cellulitis, gas gangrene, and food poisoning?

A

C. perfringens

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8
Q

What C. species causes botulism?

A

C. botulinum

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9
Q

What C. species causes tetanus?

A

C. tetani

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10
Q

Toxin production is linked to all C. diseases save for:

A

Suppurative wounds and abscesses

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11
Q

Most C. diseases are tissue invasive. T or F?

A

True
exception: boutulinum food poisoning, infant botulism
possible exceptions: wound botulism, tetanus, PMC

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12
Q

Describe bacteria in it’s endospore form:

A

metabolically inactive, resistant state in which it can remain for 100s of years.

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13
Q

What conditions are endospores resistant to?

A

extreme heat, drying, radiation, most chemical disinfectins

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14
Q

What causes endospore induction?

A

unfavorable environmental conditions (i.e. nutrient depletion)

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15
Q

When will endospores germinate?

A

when conditions become favorable for vegetative growth

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16
Q

Are C. difficile easy to culture?

A

NO

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17
Q

Describe PMC

A

Yellow plaques containing fibrin and cellular debris in ulcers of colonic mucosa

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18
Q

C. difficile is currently the leading cause of _____ diarrhea.

A

nosocomial (aquired while under medical care/at the hospital)

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19
Q

C. difficile is harbored how?

A

in a dormant state (small amount) within the bowels of a small number of healthy individuals

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20
Q

What is C. difficile’s mode of transportation?

A

endospores! (ex: hands of health care professional)

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21
Q

The disease state caused by C. difficile is usually associated with:

A

antimicrobial drugs (esp. cephalosporins, ampicillin, and clindamycin)

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22
Q

When the normal colonic flora are killed by antibiotics, C. difficile spores can ________ and begin production of _____ resulting in _______. There is no _____ of the bowel wall, however.

A
  • vegetate
  • toxin
  • diarrhea
  • invasion
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23
Q

What are two toxins produced by C. difficile?

A
  • Toxin A

- Toxin B

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24
Q

Describe Toxin A:

A

it is an enterotoxin that causes fluid production and damages mucosa

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25
Q

Describe Toxin B:

A

it is a cytotoxin that causes tissue culture cells to round

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26
Q

What is the mechanism of action for both C. difficile’s toxins?

A

they act in the cytoplasm of the host cell to glycosylate GTP binding proteins (Rho, Rac). As a result, the cells lose their cytoskeletal structure and die.

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27
Q

Name one way to diagnose C. difficile:

A

an ELISA detection of Toxin A

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28
Q

Where can C. perfringens be found?

A

Every soil except sahara desert sand and the intestinal tracts of animals.

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29
Q

C. perfringens is a major pathogen in:

A

wound infections (war wounds 20 - 30%)

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30
Q

C. perfringens has _______ properties which cause ______ damage and ______ effects. This is due to the variety of _______ produced.

A
  • invasive
  • local
  • systemic
  • toxins
31
Q

Damaged tissue has what conditions which cause spores to germinate?

A
  • anaerobic environment
  • compromised blood supply
  • calcium ions
  • availability of peptides and amino acids
32
Q

Toxins produced by C. perfringens typically cause ______ that can lead to _____ _______ which is a necrotizing, gas forming process of muscle, associated with systemic signs of shock/

A
  • cellulitis

- gas gangrene

33
Q

How many toxins can C. perfringens produce?

A

12

34
Q

What is C. perfringen’s main toxin which damages cell membranes and causes gas gangrene?

A

Alpha-toxin (lecithinase)

35
Q

Describe Alpha-toxin’s mode of action:

A

it is a phospholipase type C that hydrolyzes phosphatidylcholine and sphingomyelin that leads to cell death

36
Q

What are the results of Alpha-toxin’s action:

A

Muscle tissue is destroyed (myonecrosis) and becomes reddish blue to black in color with gas bubbles present. Shock and renal failure usually result, and if untreated, has a 100% fatality rate.

37
Q

What are some treatment/prevention strategies for a C. perfringens infection?

A
  • surgical removal of the infected muscle
  • antibiotics to control the infection (amputation still necessary)
  • Antitoxin from horses doesn’t do much
  • exposure to high oxygen concentrations (only a subset of cases responded to)
  • prompt care is IMPERITIVE to restore arterial blood supply
38
Q

What cause the third most common type of food poisoning in the US?

A

C. perfringens

39
Q

Unrealated to gas gangrene, C. perfringens food poisoning is caused by ______ C. perfringens that produce ________ in the intestines of people who have consumed ______ _______ usually ______.

A
  • sporulating
  • enterotoxin
  • contaminated food
  • meat
40
Q

C. perfringens food poisoning causes _______ for ___-___ hours, but is ______ _______ and disappears in ___-___ days.

A
  • diarrhea
  • 12-24
  • self limiting
  • 1-3
41
Q

Where is C. botulinum found?

A

soils and marine sediments

42
Q

C. botulinum’s heat resistant spores often survive _____ _____ and will germinate and grow under _______ conditions (canned foods).

A
  • food processing

- anaerobic

43
Q

What causes botulism?

A

Intoxication from the ingestion of pre-formed C. botulinum toxin (the organism doesn’t need to be present).

44
Q

C. botulinum is considered a _______ and can be used by terrorists i.e. enemies of America.

A

bioweapon

45
Q

How many neurotoxin types does C. botulinum produce?

A

8 serotypes (BoNT) A-G

46
Q

Which serotypes of BoNT are most common in humans?

A

A, B, and E

47
Q

BoNT is one of the most poisonous substances known, what is the lethal dose for humans?

A

> 1 ug (microgram)

48
Q

Purified BoNT is produced as a stable ____ kDa protein complex containing a _____ kDa toxic compontent and a _____ kDa non-toxic component.

A
  • 900
  • 150
  • 750
49
Q

What is BoNT’s mechanism of action?

A

it prevents the release of acetylcholine neurotransmitter by interfering with neurotransmission at peripheral cholinergic synapses.

50
Q

What enzyme is key to BoNT’s action and what does it do?

A

Zinc metalloprotease which cleaves proteins involved with docking at neurotransmitters.

51
Q

Describe the symptoms/effects of BoNT on the body:

A

-Flaccid paralysis within 12-36 hrs:
Cranial nerves first (double vision difficulty swallowing)
then descends to lungs causing respiratory failure

52
Q

What are the 3 types of botulism?

A

1- food borne botulism
2- wound botulism (rare)
3- Infant botulism

53
Q

Briefly describe food borne botulism

A

Ingestion of pre-formed toxin in foods that have not been canned or preserved properly

54
Q

Briefly describe wound botulism:

A

a RARE condition in which C. botulinum inhabits wounds and systematically spreads. This can result from trauma, surgery, heroin injections, nasal cocaine abuse (sinusitis)

55
Q

Briefly describe Infant botulism:

A

Intestinal colonization of organisms in infants younger than 1 yr with a slow onset that results in a hypotonic (floppy) state. There is a favorable outcome

56
Q

What is the mortality rate of botulism with good supportive care?

A

25%

57
Q

How is botulism treated?

A

with a trivalent antitoxin isolated from horses (JRH NBR only) that is administered immediately

58
Q

Even after botulism is treated it may cause some muscles to be permanently damaged. No antibiotics are necessary when treating botulism because:

A

it is caused by a toxin not an infection

59
Q

Clostridium tetani is found:

A
  • GI tract of humans and animals

- soil samples

60
Q

C. tetani spores are resistant to the environment and an infection by it is usually associated with:

A

traumatic wounds

61
Q

Germination of C. tetani’s spores goes hand in hand with:

A

toxin production

62
Q

One common route of C. tetani infection is:

A

neonatal contamination of the umbilical cord at delivery

63
Q

What is C. tetani’s major toxin?

A

tetanospasmin

64
Q

tetanospasmin is responsible for all symptoms of Tetanus, T or F?

A

True

65
Q

tetanospasmin is a ____ kDa Protein with _____ chain and a _____ chain connected by a ______ bridge (like BoNT). Individual chains are _______

A
  • 150
  • heavy
  • light
  • disulfide
  • non-toxic
66
Q

Describe tetnospasmins mechanism of action:

A

it rides peripheral nerves (near a wound site) to the CNS and the cranial nerve nuclei. There it inhibits neurotransmitter release (GABA, an inhibitor). This results in reflex spasms and spastic paralysis.

67
Q

_______ or “lockjaw” is present in ___% of tetanus cases

A
  • Trismus

- 80

68
Q

Trismus is caused by:

A

spastic paralysis of the masseter muscles

69
Q

Once tentanus descends it affects:

A
  • neck and back muscles (opisthontos - bending backwards, spastic paralysis of back extensors)
  • abdomen (rigidity)
  • extremities (stiffness)
70
Q

What are the ultimate effects of advanced tetanus?

A

Tonic seizures and respiratory failure from paralysis of chest muscles

71
Q

how is tetanus pre-emptively treated?

A

-DPT vaccine (formalin-inactivated toxid that retains antigenicity)

72
Q

how is tentanus treated after possible/definite exposure?

A
  • tetanus prone wounds treated with human globulin (passive immunization)
  • antitoxin with penicillin G to prevent further paralysis
  • surgical debridement of the wound to prevent region of bacterial growth
73
Q

What is the mortality rate associated with tetanus?

A

11% usually due to respiratory failure

74
Q

Why aren’t antibodies produced when tetanus is in effect?

A

low amount of toxin present.

Dent6400 (7 decks)

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