Ex 2- Clostridia- Bailey Flashcards

1
Q

______ is a gram positive rod bacteria that is strictly anaerobic

A

Clostridum

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2
Q

Clostridium produces ______

A

endospores

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3
Q

___ species of clostridium are responsible for human infections

A

30

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4
Q

> 50 species are found in the _______

A

environment (soil,water, animal wastes)

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5
Q

Clostridum produces ________ ______ that re responsible for disease symptoms

A

proteinaceous toxin

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6
Q

Clostridum ______ caues pseudomembraneous colitis (PMC)

A

difficile

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7
Q

Clostridium ____ causes cellulitis, gas gangrene, and food poisoning

A

perfringen

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8
Q

Clostridium _____ causes botulism

A

botulinum

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9
Q

Clostridium _____ causes tetanus

A

tetani

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10
Q

Major clostridial diseases are caused by ____ production

A

toxin

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11
Q

Clostridium and Bacillus can produce ______

A

endospores

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12
Q

_____ are a metabolically inactive state in which organisms can remain viable for hundreds of years

A

spores (virulence factor)

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13
Q

Spores allow bacteria to be resistant to______ conditions (heat, drying (thick peptidoglycan), radiating, most chemical disinfections)

A

adverse

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14
Q

Spore induction is caused by ____ _____ conditions (ie nutrient depletion) and will readily germineate when conditions become favorable for ______ _____

A
  • unfavorable environmental

- vegetative growth

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15
Q

Clostridium _______ is not easy to culture

A

difficile

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16
Q

________ _____ is a yellow plaque containing fibrin and cellular debris in ulcers of colonic mucosa

A

pseudomembraneous colitis (PMC)

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17
Q

Pseudomembraneous colitis is the leading cause of ____ _____

A

nosocomial diarrhea

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18
Q

C. difficile is harbored in the dormant state in the ______ intestine of small percentage of healthy humans in low numbers

A

large

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19
Q

C. difficile is transmitted as an _________

A

endospore via the hands of healthcare personnel

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20
Q

C.difficile is usually associated with ______ drugs, especially cephalosporins, ampicilllin, and clindamycin

A

antimicrobial

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21
Q

C.difficile spores re resistant to _______ bc the normal flora is killed

A

antibiotics

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22
Q

Spores vegetate, _____ production begins resulting in diarrhea but does not invade the bowel wall

A

toxin

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23
Q

Toxin A of C.difficile is an ________

A

enterotoxin

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24
Q

Enterotoxins cause fluid production and damage to the ______

A

mucosa (epithelial cells stop absorbing Na+)

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25
Toxin ___ of C.diffile is a cytotoxin that causes rounding of tissue-cultured cells (cell death)
B
26
Toxin A & B act in the ____ of host cell to _______ GTP-binding proteins (ie Rho, Rac) causing the cells to lose cytoskeletal structure and die
- cytoplasm | - glycosylate
27
Clostridium _______ is found in the soil (except Sahara desert) and intestinal tract of animals
perfringens
28
Clostridium perfringens is a major pathogen of ______ infections (esp war wounds 20-30%)
wound
29
Clostridium perfringens causes _____ damage and _______ effects;
- local | - systemic
30
The invasive properties of clostridium perfringens is due to the variety of _____ produced
toxins
31
Severe trauma introduces C. perfringens spores form the environment that germinate under what conditions?
- Anaerobic - compromised blood supply - calcium ions - availability of peptides + AA
32
Toxins produced by C. perfringens typically cause _____ that can lead to ____ ____, a necrotizing, gas-forming process of muscle associated with systemic signs of shock
- cellulitis | - gas gangrene
33
C. perfringens produces ___ toxins
12
34
C.perfringens produces ______ toxin (lecithinase) damages cell membranes and causes gas gangrene
alpha
35
How does Alpha toxin cause gas gangrene?
phopholipase type C hydrolyzes phosphatidylcholine and sphingomyelin that leads to cell death - muscle tissue is destroyed (myonercrosis) (reddish blue to black w/ gas bubbles)
36
What is usually the result of gas gangrene?
shock and renal failure usually result (untreated = 100% fatality)
37
How is gas gangrene caused by the alpha toxin of c.perfringens treated?
- surgical removal of infected muscle - antibiotics to control infection - antitoxin from horses (little effect) - high O2 concentrations - prompt care imperative (restore arterial blood supply getting rid of anaerobic env.)
38
What is the third most common type of food poisoning in the US?
C. perfringens food poisoning
39
How does C. perfringens cause food poisoning?
sporulating perfringens produces enterotoxin in intestines of ppl who have consumed contaminated food
40
What are the symptoms of C perfringens? How long does it persist?
- Diarrhea in 12-24 hrs | - self limiting 1-3 days
41
Clostridium ______ is found in soils and marine sediments
botulinum
42
The spores of C. botulinum are _____ _____ spores (not toxins) that survive food processing
heat-resistant
43
C. botulinum germinates and grows under ________ conditions
anaerobic (such as in cans)
44
C. botulinum is the causative agent of ______ and is a bioweapon and bioterrorism threat
botulism
45
____ is the intoxication of ingestion of pre-formed toxin (don't need organism to be present)
botulism
46
C. botulinum produces ___ neurotoxins with serotypes __-__
-8 | A-G
47
C. botulinum neurotoxins __, __, __ (fish) are most common in humans
A, B, E
48
C. botulinum neurotoxins are the most _______ substances know
poisonous
49
What is the human lethal dose of C. botulinum neurtoxin?
<1 microgram
50
The 900 kDA protein complex of BoNT is made up of what 2 parts?
150 kDA toxic component | 750 kDA non-toxic component (binding)
51
C. botulinum toxin prevents the release of _________ neurotransmitter that interferes with neurotransmission at peripheral cholinergic synapses (muscles cannot contract)
acetylcholine
52
______ ______ cleaves proteins involved in docking of neurotransmitter vesicles, if you cannot dock you cannot release ACH
zinc metalloprotease
53
What are the symptoms of C. botulinum toxin?
- flaccid paralysis w/in 12-36 hrs - CN affected first - paralysis descends; respiratory failure
54
______ - _____ botulism is the ingestion of preformed toxin in foods that have not been canned or preserved properly
food-borne
55
_______ botulism is the systemic spread of toxin produced by organisms inhabiting wounds (ie trauma, surgery, heroin injection, sinusitis)
wound (rare)
56
_____ botulism is the intestinal colonization of organisms in infants younger than 1 year, slow onset, favorable outcome, hypotonic (floppy state)
infant
57
Currently mortality rate, with good supportive care is ____ % for botulism
25%
58
What is the treatment for botulism?
- trivalent antitoxin, from horse administered ASAP - some muscles perm. damaged and never recover - no antibiotics bc toxin not affected
59
Clostridium _______ is ubiquitious in the GI tract of humans and animals, also in soil samples (spores resistant to env) and infection associated w/ traumatic wounds
tetani
60
What is the major toxin of C. tetani?
tetanospasmin
61
Tetanospasmin is responsible for __ ________ of tetnus
all symptoms of tetanus
62
Tetanospasmin is a ____ kDa proteins that has heavy and light chains connected by disulfide bridge and ind chains are non-toxic
150
63
How does tetnospasmin cause tetanus?
- attaches to peripheral nerves around wound + transmitted to CN nuclei - inhibits neurotransmitter release (GABA) + inhibitory input
64
What are the symptoms of tetanus?
reflex spasms, spastic paralysis, lockjaw (80% cases),rigidity of abdomen and stiffness of extremities, tonic seizures, respiratory failure from paralysis of chest
65
_______ "lockjaw" is the tetanic spasm of masseter muscles that prevents opening of mouth (80% cases)
trismus
66
Advanced tetanus may lead to _____ bending backward of body caused by spastic paralysis of strong extensors of back bc no ____ so cannot turn of muscles contraction
- opisthotonos | - GABA
67
What is used to treat C. tetani?
- DPT vaccine (diptheria pertussis and tetanus) - human globulin as passive immunity to tetanus-prone wounds - antitoxin - penicillin G - surgical debridement to prevent bact. growth
68
What is the mortality rate of tetanus?
11% due to respiratory failure usually
69
_____ are not produced due to low amts of toxin present
antibodies