Clostridium-Bacillus (EXAM III) Flashcards

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1
Q

Describe the gram stain & shape of Clostridium bacteria:

A

Gram positive; rods

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2
Q

A major virulence factor of Clostridium is that:

A

Endospore forming

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3
Q

Describe the oxygen requirement of Clostridium & spores:

A

Obligate anaerobes; spores are O2 resistant

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4
Q

Where can Clostridium be encountered:

A

Environment (soil) & intestinal mucous

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5
Q

How can we detect spores of Clostridium:

A

Endospores stain hot malachite green

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6
Q

Endospore staining is also used for:

A

Aerobic endospore formers like Gram + bacillus

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7
Q

Describe the virulence factors of Clostridium:

A

Spore formation

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8
Q

The spores of clostridium contribute to virulence because:

A
  1. Resistant to destruction
  2. Resistant to sterilization
  3. Resistant to antibiotics
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9
Q

How might we remove clostridium spores from a medical device?

A

Autoclave (Heat under pressure)

Boiling is NOT effective

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10
Q

When the disease-causing components is solely due to the toxin, this is referred to as:

A

Intoxication

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11
Q

The type of Clostridium that gives rise to severe form of food poisoning leading to paralysis if untreated:

A

Clostridium Bolulinum

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12
Q

In addition to food ingestion, Clostridium Botulinum may cause Botulism by:

A

Soil or fecal contamination

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13
Q

_______ is possible form soil or fecal contamination

A

Wound botulism

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14
Q

Explain how infant botulism occurs:

A

Because of lack of full development of normal intestinal flora, if Clostridium Botulinum is introduced to infant between weeks 30 & 20 it has the capability of rapid overgrowth

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15
Q

Describe the effects of infant botulism:

A

Muscle weakness; rarely paralysis

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16
Q

How does infant botulism resolve?

A

Normally resolves as intestinal flora develops

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17
Q

Describe the virulence factors of Clostridium Botulinum:

A

Botulinum neurotoxin (A-B exotoxin) blocks acetylcholine release

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18
Q

What does botulinum neurotoxin (A-B exotoxin) block & what does this cause?

A

Blocks Acetylcholine release; causes flaccid paralysis - can lead to death

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19
Q

Because Clostridium botulinum does not ______ it acts through _____

A

Invade tissues; toxins

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20
Q

The spores of clostridium botulinum are _____, while the botulinum toxin is _____

A

Heat-stable; heat-labile

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21
Q

How long does anti-toxin neutralization to the botulism toxin take to be effective?

A

Weeks to months

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22
Q

The form of Clostridium that is typically caused by dirty, puncture wounds (knife, bullet, tattoo) that are typically opportunities for the anaerobic growth of this pathogen:

A

Clostridium tetani

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23
Q

Describe the oxygen requirements of Clostridium Tetani:

A

Anaerobic

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24
Q

Bacterial growth of Clostridium Tetani remains _____ but the tetanus toxin _____

A

Localized; spreads

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25
Q

What toxin is responsible for the virulence of Clostridium Tetani?

A

Tetanospasmin

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26
Q

Describe Tetanospasmin:

A

Tetanus A-B exotoxin/neurotoxin; plasmid encoded

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27
Q

Describe the mechanism of action of tetanospasmin:

A

Blocks GABA & Glycine; leads to loss of inhibitory input to motor neuron excitation leading to spastic paralysis

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28
Q

In Clostridium tetani, the spastic paralysis is due to:

A

Uncontrolled muscle contraction caused by Tetanospasmin

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29
Q

The effects of Tetanospasmin may be:

A

Localized & one-sided (on opposite side of infection)

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30
Q

Describe the effects of anti-toxin against tetanospasmin:

A

Usually too late for anti-toxin treatment

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31
Q

Clostridium Tetani does not _____ so it acts through _____

A

Invade tissues; toxins

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32
Q

A dramatically deadly disease characterized by the in ability of muscle relaxation:

A

Tetanus

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33
Q

Tetanus toxin prevents:

A

Muscle relaxation

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34
Q

Infection with tetanus systemically can cause:

A
  1. Cardiac arrythmias
  2. Blood pressure swings
  3. Dehydration
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35
Q

A characteristic symptom of tetanus:

A

Lock jaw

36
Q

Tetanus effects can be _____ or _____

A

General or localized

37
Q

Describe tetanus vaccination of pregnant women:

A

Passive immunization (IgG) of pregnant women can prevent neonatal tetanus death by umbilical infection (250,000 per year worldwide)

38
Q

The ONLY clostridium species with tissue invasion:

A

Clostridium Perfringens

39
Q

Organisms that often cause problems when you have an infection from a dirty wound, as these bacteria can be deep down into a relatively anaerobic environment that allows them to begin growing & invading the tissue:

A

Clostridium Perfringens

40
Q

The tissue invasion seen by Clostridium Perfringens is furthered by:

A

Virulence factors that allow these bacteria to lyse cells & destroy tissue integrity

41
Q

List the virulence factors associated with Clostridium Perfringens:

A
  1. Alpha-toxin
  2. Theta-toxin
  3. Collagenase & Hyaluronidase
42
Q

Describe the mechanism of action of the alpha-toxin in Clostridium perfringens:

A

Hemolytic property resulting in membrane destruction

43
Q

Describe the mechanism of action of the alpha-toxin in Clostridium perfringens:

A

Cytolytic toxin that results in cell killing

44
Q

Describe the mechanism of action of the collagenase & hyaluronidase in Clostridium perfringens:

A

Faciliates tissue invasion from the edges of necrotizing tissues

45
Q

Which virulence factor of Clostridium Perfringens is responsible for its ability to invade tissue:

A

Collagenase & Hyaluronidase

46
Q

Describe the mechanism of reaction seen in Clostridium Perfringens:

A

Anaerobic fermentation of amino acids leads to increased gas production (H2, CO2) resulting in gas gangrene

47
Q

The anaerobic fermentation of amino acids seen in Clostridium Perfringens infections results in:

A

Gas gangrene

48
Q

What childbirth complication has been associated with Clostridium Perfringens:

A

Puerperal “Childbed” fever (Uterine gangrene)

49
Q

Describe the treatment against Clostridium Perfringens:

A

No vaccination possible; antibody against the alpha-toxin but fails to stop gangrene– typically amputation is best option if gangrene occurs

50
Q

List the three types of Clostridium that do NOT invade tissues:

A
  1. C-Diff
  2. Botulism
  3. Tetanus
51
Q

A super infection resulting from broad-spectrum antibiotics that kill much of the other normal intestinal bacterial flora, giving rise to a resistant species of this harmful bacteria:

A

Clostridium Difficile

52
Q

Antibiotic-associated pseudomembrane colitis is caused by:

A

Clostridium Difficile

53
Q

C-Diff may be observed after:

A

Antimicrobial chemotherapy

54
Q

One of the leading causes of hospital-acquired diarrhea:

A

Clostridium Difficile

55
Q

Results from broad-spectrum antibiotics that kill much elf the other normal intestinal bacterial flora, giving species like toxin-producing Clostridium difficile a chance to take over:

A

Antibiotic-associated pseudomembranous colitis

56
Q

List the virulence factors of Clostridium difficile:

A
  1. Toxin A
  2. Toxin B
57
Q

Describe the effects of Toxin A in C-diff:

A

Inhibits intestinal tight-junctions leading to fluid leakage

58
Q

Describe the effects of Toxin B in C-diff:

A

A cytotoxin that functions in actin depolymerization and rounding of epithelial cells leading to fluid leak

59
Q

Both toxin A & toxin B in C-diff cause fluid leak ultimately causing:

A

Diarrhea

60
Q

CDC 2013 report states that _____ is a major threat to antibiotic resistance in the US

A

C-diff

61
Q

What clostridium bacteria is this describing?

Treatment: Botulinum antitoxin

A

C. Botulinum

62
Q

What clostridium bacteria is this describing?

Treatment: Toxoid vaccination

A

C. Tetani

63
Q

What clostridium bacteria is this describing?

Treatment: Anti-tetanus serum (passive immunity)

A

C. Tetani

64
Q

What clostridium bacteria is this describing?

Treatment: Surgery intervention, amputation

A

C. Perfringens

65
Q

What clostridium bacteria is this describing?

Epidemiology: Environment (soil, water, sewage) & GI tract in animals & humans

A

C. Botulinum
C. Tetani
C. Perfringens

66
Q

What clostridium bacteria is this describing?

Epidemiology: Colonized intestines, genital tract, hospital environment, prior antibiotics

A

C. Difficile

67
Q

Describe the shape & gram stain of bacillus:

A

Gram positive; rods

68
Q

B. anthracis gives rise to ______ & is considered a _______infection

A

Woolsorter’s disease; zoonotic infection

69
Q

Describe the oxygen requirements of B. Anthracis:

A

Facultative anaerobe

70
Q

List the virulence factors of B. Anthracis:

A

Anthrax toxins (edema-factor & lethal-factor) & a poly-glutamic acid capsule

71
Q

Describes the difference between the Anthrax toxins Edema-factor & Lethal-factor:

A

The differences lie within the A-component (the B-components are the same)

72
Q

Describe the A-component of Edema-factor (EF) found in bacillus anthracis:

A

EF is an adenylate cyclase that DIRECTLY leads to increased cAMP levels and results in edema

73
Q

Describe the A-component of Lethal-factor (LF) found in bacillus anthracis:

A

LF is a metallo-protease that targets MAP kinase (an important signaling molecule) ultimately leading to cell death

74
Q

Describe the capsule of B. Anthracis:

A

Its a poly-glutamic acid capsule that functions to inhibit phagocytosis

75
Q

Form of anthrax in which spores are uptake by the lungs and then enter lung phagocytes; latency of 2 months or more may occur:

A

Inhalation anthrax

76
Q

Following the entry into lung phagocytes in inhalation anthrax where do the spores travel to?

A

Lymph nodes

77
Q

In anthrax infections if the spores travel to the lymph nodes (from the lungs) the spores germinate causing phagocyte death and ultimately lead to:

A

Pneumonia & meningitis type symptoms

78
Q

In an anthrax infection if spores germinate and produce toxins that enter the bloodstream this can trigger:

A

Macrophage TNF-alpha leading to toxic shock death in 1-2 days

79
Q

In what situation may an anthrax infection lead to toxic shock & death:

A

If toxins enter the bloodstream

80
Q

In what situation may an anthrax infection lead to symptoms of pneumonia & meningitis:

A

If toxins & spores spread to lymph nodes

81
Q

Form of anthrax infection that leads to ulcers in the mouth & esophagus, edema & sepsis:

A

Gastrointestinal anthrax

82
Q

In what case would gastrointestinal anthrax become nearly 100% lethal?

A

In lower intestine

83
Q

Describe skin anthrax infections:

A

Redness & edema with rupturing vesicles

84
Q

What lethality rate of skin anthrax infections:

A

20%

85
Q

List the epidemiology of Bacillus anthracis:

A
  1. Animal workers
  2. Microbiological accidents
  3. Bioterrorism
  4. Contaminated meat