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Microbiology > Bacteria Chapter 20 Clostridium- Bacillus > Flashcards

Bacteria Chapter 20 Clostridium- Bacillus Flashcards

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Biology 101 flashcards
1
Q

what type of microbe is clostridium

A
  • gram positive rods
  • endospore forming
  • obligate anaerobic
  • environment (soil) and intestinal mucus
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2
Q

what color do the endospores in clostridium stain

A

green

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3
Q

what is the virulence factor for clostridium

A
  • spore formation
  • spores are resistance against destruction or sterilization
  • spores are not subject to antibiotics
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4
Q

what does clostridium botulinum cause

A

-botulism
- severe form of food poisoning
- paralysis

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5
Q

what is wound botulism possible from

A

soil or fecal contamination

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6
Q

what is infant botulism and when does it resolve

A
  • occurs in 3-20 week infants without full intestinal flora
  • causes muscle weakness but rarely severe and generally resolves as intestinal flora develops
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7
Q

what are the virulence factors for clostridium botulinum

A
  • botulinum neurotoxin blocks acetylcholine release
  • flaccid muscles including respiratory paralysis -> death
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8
Q

is there tissue invasion in clostridium botulinum

A

no it acts through toxins

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9
Q

while spores are _____, botulinum toxin is _______

A

heat stabile, heat labile

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10
Q

how long does anti toxin neutralization take

A

weeks to months

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11
Q

describe the neurotoxins in clostridium botulinum

A
  • proteolytic and saccharolytic
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12
Q

what is another toxin effect of clostridium botulinum

A

no wrinkles and flaccid paralysis

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13
Q

what are opportunities for anaerobic growth of C. tetani

A

dirty, puncture wounds like knife, bullet, tattoo

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14
Q

what are the virulence factors for clostridium tetani

A
  • tetanospasmin blocks GABA and glycine release -> loss of inhibitory input to motor neuron excitation -> uncontrolled muscle contraction “ spastic paralysis”
  • toxin effect may be localized and one sided ; anti-toxin usually too late
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15
Q

what does tetanus toxin prevent

A

muscle relaxation

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16
Q

tetanus effects can be ____ or _____

A

general or localized

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17
Q

what can prevent neonatal tetanus death by umbilical infection

A

passive immunization of pregnant women

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18
Q

what is the vaccine for tetanus

A

DTP vaccine with tetanus toxoid
- 10 year booster vaccination is standard

19
Q

what is the only clostridium species with tissue invasion

A

clostridium perfringens

20
Q

what are the virulence factors for clostridium perfringens and what do they do

A
  • alpha toxin-> membrane destruction
  • omega toxin -> cytolytic toxin
  • collagenase, hyaluronidase : facilitates tissue invasion from the edges of necrotizing tissues
21
Q

what causes gas gangrene of clostridium perfringens

A
  • anaerobic fermentation of amino acids -> gas increase (H2 and CO2)
22
Q

what is the mortality rate for clostridium perfringens

A

40-100%

23
Q

what causes uterine gangrene

A

puerperal fever

24
Q

is there vaccine for clostridium perfringens

A

no

25
Q

what does antibody do to alpha toxin

A

fails to stop gas gangrene: amputate

26
Q

does clostridium difficile invade tissue

A

acts through toxins

27
Q

what does antibiotic associated pseudomembranous colitis result from

A

broad spectrum antibiotics that kill much of the other normal intestinal bacterial flora, giving resistant species like toxin producing clostridium difficile a chance to take over

28
Q

what is another name for clostridium difficile

A

-hospital diarrhea

29
Q

what are the virulence factors for clostridium difficile and what does each do

A
  • toxin A: inhibits intestinal tight- junctions -> fluid leak
  • toxin B: rounding of epithelial cells -> fluid leak
  • diarrhea results from both
30
Q

what is the treatment and epidemiology for clostridium botulinum

A
  • botulinum antitoxin
  • environment
    and GI tract
31
Q

what is the treatment and epidemiology for c tetani

A
  • toxoid vaccination and anti-tetanus serum
  • environment and GI tract
32
Q

what is the treatment and epidemiology for c. perfringens

A
  • surgery intervention and amputation
  • environment and GI tract
33
Q

what is the epidemiology for C difficile

A
  • colonized intestines, genital tract
  • hospital environment
  • prior antibiotics
34
Q

describe bacillus anthracis

A
  • zoonotic infection “woolsorter’s disease”
  • gram positive rods, facultative anaerobes
35
Q

what are the virulence factors for anthrax toxins and what do each cause

A
  • EF: adenylate cyclase -> cAMP increase -> edema
    -LF: metallo- protease -> cell death with pulmonary edema
  • poly- glutamic acid capsule: inhibition of phagocytosis
36
Q

what is anthrax caused by

A

when spores germinate and produce toxins

37
Q

inhalation anthrax:

A
  • entry lungs, uptake by lung phagocytes - latency of 2 months or more may occur
  • to lymph nodes - pneumonial and meningitis type symptoms are seen
  • bloodstream -> powerful toxins (macrophage TNF alpha: toxic shock death in 1-2 days)
38
Q

gastrointestinal anthrax:

A
  • ulcers in mouth, esophagus -> edema and sepsis
  • lethality if in lower intestines: 100%
39
Q

what does macrophage TNF increase cause

A

toxic shock and death

40
Q

describe skin anthrax and what is the lethality

A
  • redness (inflammatory cytokines)
  • edema with vascular and vesicle rupture
  • lethality - 20%
41
Q

what is the epidemiology for bacillus anthracis

A
  • animal workers
  • microbiological accidents
  • bioterrorism
  • contaminated meat
42
Q

what does bacillus cereus cause

A

-gastroenteritis, ocular infections, bacteremia
- heat stable and heat labile toxins, necrotic toxins

43
Q

what is bacillus sp mostly resistant to

A

penicillin

44
Q

what type of microbe is bacillus

A

-gram positive rods
- strict aerobes or facultative anaerobes

Microbiology (39 decks)

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