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Microbiology & Immunology Unit II > Clostridia > Flashcards

Clostridia Flashcards

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1
Q

shape

A

gram + rods

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2
Q

oxygen requirement

A

strict anaerobe

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3
Q

spore formation?

A

yes

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4
Q

list the species of clostridium

A

dificile
perfringens
botulinum
tetani

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5
Q

how does clostridium cause disease symptoms?

A

produce and release proteinaceous toxin

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6
Q

what induces spore formation?

A

unfavorable conditions (ie nutrient depletion)

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7
Q

when do spores germinate?

A

when conditions become favorable for vegetative growth

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8
Q

Pseudomembranous colitis (PMC) is caused by what strain of clostridium?

A

C. diff

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9
Q

PMC is characterized by:

A

yellow plaques filled with fibrin and cellular debris in ulcers of colonic mucosa

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10
Q

what is leading cause of nosocomial diarrhea?

A

C. diff

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11
Q

C. dificile mode of transmission

A

endospore (hands of healthcare workers)

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12
Q

disease state of C. diff is usually associated with:

A

use of antimicrobial drugs (cephalosporins, ampicillin, clindamycin)

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13
Q

true or false? C. diff is harbored in a dormant state in the small intestine of a small % of healthy people

A

false; harbored in large intestine

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14
Q

how do C. diff spores react to antibiotics?

A

resistant ; antibiotics kill the normal flora

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15
Q

what causes diarrhea in C. diff?

A

vegetative spores begin to produce toxin = diarrhea

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16
Q

does C. diff invade the bowel wall?

A

no, just like E. coli and V. cholera

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17
Q

what are the toxins of C. diff?

A

Toxin A

Toxin B

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18
Q

which C. diff toxin is the enterotoxin?

A

Toxin A

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19
Q

what damage does an enterotoxin do?

A

fluid production and damage to mucosa

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20
Q

which C. diff toxin is the cytotoxin?

A

Toxin B

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21
Q

what does a cytotoxin do?

A

rounding of tissue-culture cells

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22
Q

where do C. diff toxins act?

A

cytoplasm of host cell

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23
Q

how do C. diff toxins act?

A

glycosylate GTP-binding proteins (Rho, Rac)

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24
Q

what happens when GTP-binding proteins are glycosylated by C. diff toxins?

A

cells lose cytoskeletal structure and die

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25
Q

what is standard diagnostic for toxin A of C. diff?

A

ELISA

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26
Q

Where is C. perfringens found?

A

soil and intestinal tract of animals

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27
Q

where is C. perfringens NOT found?

A

Sahara desert sand

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28
Q

what is the major pathogen of wound infections, especially war wounds?

A

C. perfringens

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29
Q

true or false? C. perfringens causes local damage only

A

false, causes local AND systemic damage because of its invasive properties and toxin production

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30
Q

true or false? C. perfringens produces a toxin?

A

true

31
Q

C. perfringens tissue infections caused when:

A

severe trauma introduces spores from environment

32
Q

in C. perfringens, after a severe trauma, environmental spores germinate under what conditions:

A

anaerobic
compromised blood supply
Ca++ ions
Availability of peptides and AAs

33
Q

C. perfringens toxins typically cause:

A

cellulitis

34
Q

cellulitis caused by C. perfringens toxins can lead to:

A

gas gangrene

35
Q

what is gas gangrene:

A

necrotizing
gas-forming
systemic signs of shock

36
Q

how many toxins does C. perfringens produce?

A

12 toxins

37
Q

C. perfringens Alpha-toxin (lecithinase) does what?

A

damages cell membranes

causes gas gangrene

38
Q

how does C. perfringens Alpha-toxin cause its damage?

A

Phospholipase Type C

39
Q

What is Phospholipase Type C and what does it do?

A

produced by Alpha-toxin of C. perfringens

Hydrolyzes phosphatidylcholine and sphingomyelin = cell death

40
Q

what is myonecrosis? symptoms?

A

destruction of muscle tissue
reddish-blue to black in color
gas bubbles present

41
Q

How do you treat a C. perfringens infection?

A

surgery to remove infected muscle
antibiotics for control but still amputation
Antitoxin from horses
High O2
Prompt care to restore arterial blood supply

42
Q

C. perfringens food poisoning results when:

A

sporulating C. perfringens produces enterotoxin in intestine after eating contaminated food

43
Q

At what point is diarrhea is typically seen in C. perfringens food poisoning?

A

12-24 hours

44
Q

True or false? C. perfringens food poisoning is self limiting:

A

true - disappears on its own in 1-3 days

45
Q

C. botulinum is found where?

A

soil and marine sediments

46
Q

C. botulinum spores are unique because they:

A

heat resistant - survive food processing

germinate and grow under anaerobic conditions (cans)

47
Q

causative agent of botulism

A

intoxication by ingestion of preformed toxin

*organism does not need to be present

48
Q

C. botulinum produces how many toxins and what kind?

A

8 neurotoxin (BoNT) serotypes A-G
among most poisonous substances known
pose a bioweapon and bioterrorism threat

49
Q

what are most common BoNT serotypes in humans?

A

A, B, E

50
Q

Purified BoNT is produced as a:

A

900 kDa protein complex with a 150-750 kDa toxic/nontoxic ration
connected by disulfide bridge

51
Q

What is the MOA of C. botulinum neurotoxin?

A

prevents release of acetylcholine NT

zinc metalloprotease

52
Q

C. botulinum neurotoxin prevents release of ACh which leads to:

A

impaired neurotransmission at peripheral cholinergic synapses

53
Q

zinc metalloprotease does what?

A

cleaves proteins involved in NT vesicle docking

54
Q

Symptoms of C. botulinum toxin poisoing

A

Flaccid paralysis in 12-36 hours
Cranial nerves affected first - double vision, difficulty swalling
Paralysis descends = respiratory failure

55
Q

What are the 3 types of botulism?

A

Food-borne
Infant
Wound

56
Q

what causes infant botulism

A

intestinal colonization of organisms in babies <1

honey

57
Q

is infant botulism slow or fast onset?

A

slow

58
Q

infant botulism is characterized by:

A

hypotonic (floppy) baby

59
Q

wound botulism

A

most rare

systemic spread of toxin produced by organisms in wound

60
Q

causes of wound botulism

A

trauma, surgery
subQ heroin injection
sinusitis caused by intranasal cocaine

61
Q

what should be administered immediately to treat C. botulinum?

A

trivalent antitoxin isolated from horses

62
Q

C. tetani is found where?

A

ubiquitous in human and animal GI tracts

soil samples

63
Q

True or false? C. tetani spores are susceptible to the environment

A

false- they are resistant to the environment

64
Q

C. tetani infection is usually associated with:

A

traumatic wounds

65
Q

what is the major toxin of C. tetani:

A

tetanospasmin - responsible for all symptoms

66
Q

size of tetanospasmin:

A

150 kDa

67
Q

Describe makeup of tetanospasmin

A

150 kDa protein

Heavy and light chain (A-B) connected by disulfide bridge)

68
Q

True or false? Individual chains of tetanospasmin are extremely toxic

A

false, individual chains are not toxic

69
Q

tetanospasmin MOA

A

attached to peripheral nerves near wound, transmitted to cranial nerve nuclei

inhibits GABA release and normal inhibitory input

70
Q

result of tetanospasmin actions

A

reflex spasms and spastic paralysis

71
Q

What is trismus?

A

lockjaw

tetanic spasm of masseter mm. that prevent open mouth

72
Q

effects of generalized tetanus

A

trismus (lockjaw)
descends to neck & back = rigid abdomen & stiff extremities
tonic seizures
respiratory failure (chest mm. paralysis)

73
Q

how to prevent tetanus?

A 
DPT vaccine 
tetanus toxoid (inactivated antigenic toxin)
74
Q

treatment of tetanus?

A

human globulin as passive immunization in tetanus prone wounds

immediate antitoxin administration + penicillin G to prevent further paralysis

surgical wound debridement

Microbiology & Immunology Unit II (9 decks)

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