Brainscape's Knowledge GenomeTM

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


See full index

Micro/Immuno FINAL > Clostridia (G+) > Flashcards

Clostridia (G+) Flashcards

1
Q

are clostridium aerobic or anaerobic?

A

strictly anaerobic

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

what gram classification are clostridium?

A

G+

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

clostridium species produce what?

A

ENDOSPORES and proteinaceous TOXINS that are responsible for disease symptoms

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

about how many species of clostridium are responsible for human infections?

A

~30

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

greater than how many species are found in environment (soil, water, animal wastes)

A

> 50

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

name 4 clostridium species and the disease they cause based on the toxin they produce

A
  • c. difficile: pseudomembranous colitis (PMC)
  • c. perfringens: cellulitis, gas gangrene, food poisoning
  • c. botulinum: botulism
  • c. tetani: tetanus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a spore?

A

form of bacteria that is metabolically inactive & coating that makes them very resistant, can remain viable for hundreds of years

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

which bacteria classes have the ability to produce endospores?

A

bacillus and clostridium

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

what adverse conditions are bacterial endospores resistant to?

A

extreme heat, drying, radiation, most chemical infections

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

what causes a pathogen to release spores?

A

spore induction caused by environmental unfavorable conditions (nutrient depletion)

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

how are spores formed for release?

A

bacteria creates membrane & engulfs

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

describe the structure of an endospore

A

outside surf=protein coat –>lipid mem–>cortex–>inner mem

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

what is the function of the endospore protein coat?

A

helps with heat resistance and drying

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

what is the function of the lipid membrane of the endospore?

A

helps with chemical sensitivity

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

is c.difficile easy to culture?

A

noooo “difficult clostrium”

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

what is pseudomembranous colitis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is c. difficile the leading cause of?

A

nosocomial diarrhea

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

where is c. difficile harbored in the human body?

A

harbored in a dormant state in the large intestine of small percentage of healthy humans in low numbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is c. difficile transmitted?

A

the endospore, hands of health care personnel

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

c. difficile has a disease state that is associated with what?

A

antimicrobial drugs, especially cephalosporins, ampicillin, and clindamycin

*get disease when on high dose of antibiotics

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

are the endospores formed by c. difficile resistant to antibiotics?

A

yes, only normal flora is killed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do the spores infect?

A

spores vegetate, toxin production begins resulting in diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

does invasion of the bowel wall occur with c. difficile?

A

no just like e. coli and v. cholerae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what do the two toxins do?

A
  1. changes function of epithelium cells

2. formation of pseudomembranous colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe toxin A of c. difficile.

A

enterotoxin- fluid production and damage to the mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe toxin B of c. difficile.

A

cytotoxin-rounding of tissue-culture cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

where do both toxins act in the host cell?

A

in the cytoplasm of the host cell to glycosylate GTP-binding proteins (eg Rho, Rac)

  • cell loses cytoskeletal structure and die
  • on dead cell is accumulation of fibrogen and scar tissue
28
Q

how is toxin A found?

A

ELISA detection of toxin A is diagnostic

29
Q

where is c. perfringens found?

A

soil and intestinal tract of animals

environmental pathogen found in every soil except Sahara desert and sand

30
Q

T/F: c. perfringens is a major pathogen of wound infections

A

TRUE; especially prevalent in war wounds

31
Q

what kind of damage does c. perfringens cause?

A

local damage and systemic effects

  • invasive properties
  • due to variety of toxins produced

“spread through spore BUT toxin causes disease”

32
Q

what severe conditions/trauma introduces spores from the environment to germinate?

A

anaerobic
compromised blood supply (main factor)
calcium ions
availability of peptides and amino acids

**all cause tissue damage

33
Q

after the c. perfringen toxins are released what do they typically cause?

A

cellulitis that can lead to gas gangrene, a necrotizing, gas-forming process of muscle associated with systemic signs of shock

34
Q

how many toxins does c. perfringen produce?

A

12

35
Q

describe the alpha toxin (lecithinase) produced by c. perfringens?

A
  • damages cell membranes, and cause gas gangrene
    • phospholipase Type C
    • hydrolyzes phsphatidylcholine and sphingomyelin that leads to cell death = DAMAGES PHOSPHOLIPIDS
  • muscle tissue is destroyed (myonecrosis)
    • reddish blue to black in color
    • gas bubbles present

-shock and renal failure usually result and if untreated 100% fatality rate

36
Q

how is c. perfringens treated and prevented?

A
  • surgical removal of infected muscle
  • antibiotics to control the infection, but surgery (amputation) still necessary
  • antitioxin from horses, relatively little effect
  • high oxygen concentrations: only subset of cases respond to
  • prompt care is imperative: restore arterial blood supply
37
Q

describe the c. perfringens food poisoning?

A
  • 3rd most common type of food poisoning un US
  • unrelated to gas gangrene
  • sporulating c. perfringens that produce ENTEROTOXIN in intestine of people who have consumed contaminated food (usually meat)
  • diarrhea in 12-24 hours
  • self-limiting disappears in 1-3 days
38
Q

where is clostridium botulinum found?

A

soils and marine sediments

39
Q

what type of spores are produced by clostridium botulinum?

A

heat-resistant spores (not toxins) which often survive food processing
-germinate and grow under anaerobic conditions (such as in canned foods)

40
Q

clostridium is the causative agent of what?

A

botulism:

-intoxication of ingestion of pre-formed toxin (don’t need the organisms to be present)

41
Q

which species of clostridium is used as a bioweapon and bioterrorism threat?

A

clostridium botulinum

42
Q

how many toxin serotypes are formed by c. botulinum?

A

8 neurotoxin (BoNT) serotypes A-G

among most poisonous substances know (lethal dose <1 microgram)

43
Q

wish 3 c. botulinum neurotoxins are in fish and humans

A

A, B, E

44
Q

purified BoNT is produced as a stable 900 kDa protein complex containing what?

A
  • a 150 kDa toxic component
  • a 750 kDa non-toxic component

*need both components to cause disease but 1 component is still toxic

45
Q

what does c. botulinum toxin prevent the release of?

A

the release of acetylcholine neurotransmitter therefore interfering with neurotransmission at peripheral cholinergic synapses

46
Q

what component of the c. botulinum toxin cleaves proteins involved in docking of neurotransmitter vesicles?

A

zinc metalloprotease

*NTs in vesicle wait to be released through exocytosis. vesicles have to dock with neuronal membrane and fuse with it then release through exocytosis. this prevents them from docking to synaptic membrane and prevents release of Ach.

47
Q

what does c. botulinum toxin cause clinically?

A

flaccid paralysis within 12 to 36 hours

48
Q

what does c. botulinum affect first?

A
  • cranial nerves affected first
    • double vision, difficulty swallowing
  • paralysis descends to cause respiratory failure
49
Q

name the 3 types of botulinum.

A
  1. food-borne botulism
  2. wound botulism
  3. infant botulism
50
Q

what is food-borne botulism?

A

ingestion of preformed toxin in foods that have not been canned or preserved properly

MOST PREVALENT

51
Q

what is wound botulism?

A
  • systemic spread of toxin produced by organisms inhabiting wounds
  • rare
  • trauma, surgery, subcutaneous heroin injection, and sinusitis from intranasal cocaine abuse
52
Q

what is infant botulism?

A
  • intestinal colonization of organisms in infants younger than 1 year
  • slow onset
  • favorable outcome
  • hypotonic (“floppy”) state

*don’t feed infants honey because of spores

53
Q

how are c. botulinum infections treated?

A
  • current mortality rate with good supportive care is 25%
  • a trivalent antitoxin, isolated from horses, should be administered ASAP
  • some muscles may be permanently damaged, and never recover because trouble releasing Ach
  • no antibiotic necessary because not eating live bacteria, eating toxin
54
Q

where is c. tetani located in humans?

A

ubiquitous in the GI tract of humans and animals

55
Q

where environmentally is c. tetani located?

A

soils

56
Q

T/F: c. tetani spores are not resistant to the environment

A

FALSE

57
Q

what is c. tetani infection normally associated with?

A

traumatic wounds

58
Q

where is a common location for germination of spores and production of c. tetani tetanus toxin?

A

neonatal contamination of umbilical cord at delivery

59
Q

what is the c. tetani major toxin?

A

tetanospasmin

60
Q

describe tetanospasmin.

A
  • responsible for all symptoms
  • 150 kDa protein
  • heavy chain and light chain (A-B) connected by disulfide bridge (just like BoNT)
  • individual chains are non-toxic
61
Q

what is c. tetani tetanospasmin’s mechanism of action?

A
  • attaches to peripheral nerves near wound and is transmitted to cranial nerve nuclei
  • inhibits neurotransmitter release (GABA) and normal input
  • result: reflex spasms, spastic paralysis
62
Q

what is the function of GABA?

A

normally inhibitory, relaxes mm. contraction

63
Q

what is c. tetani generalized tetanus and how can it affect the masseter mm.?

A
  • trismus - “lock jaw” (80% of cases): tetanic spasm of masseter muscles that prevents opening of mouth
  • descends to neck and back muscles and produces rigidity of abdomen and stiffness of extremities
  • respiratory failure from paralysis of chest mm.
64
Q

is c. tetani preventable? if so, then how?

A
  • completely preventable with DPT vaccine
    • diptheria pertussis tetanus vaccine
    • tetanus toxoid (formalin-inactivated toxin that retains antigenicity)
65
Q

how is c. tetani treated?

A
  • human globulin sometimes given as passive immunization in “tetanus-prone wounds”
  • antitoxin should be administered immediately, along with penicillin G to prevent further paralysis
    • antibodies not produced due to low amounts of toxin present
  • surgical debridement of the wound to prevent region of bacterial growth
66
Q

how prevalent is mortality and what is it usually from in c. tetani infection?

A

11% mortality, usually due to respiratory failure

Micro/Immuno FINAL (16 decks)

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