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microbiology > Clostridium-Bacillus - Exam III > Flashcards

Clostridium-Bacillus - Exam III Flashcards

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1
Q

Describe the gram stain and shape of clostridium:

A

Gram positive rods

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2
Q

A major virulence factor of clostridium is that:

A

they are endospore forming

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3
Q

Describe the oxygen requirements of clostridium and spores:

A

obligate anaerobes; spores are O2 resistant

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4
Q

Where can clostridium be encountered?

A

Environment (soil) and intestinal mucus

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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 component 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 a severe form of food poisoning leading to paralysis

A

clostridium botulinum

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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 from 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 intestinal flora, if clostridium botulinum is introduced to infant between 3-20 weeks, 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 (AB-exotoxin) blocks acetylcholine release

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18
Q

What does botulinum neurotoxin (AB-exotoxin) block and what does this cause?

A

acetylcholine; flaccid muscles–> paralysis

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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 botulinum toxin take to work?

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 typical opportunities for the anaerobic growth of this bacteria:

A

Clostridium tetani

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23
Q

Describe the oxygen requirements for 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
What toxin is responsible for the virulence of clostridium tetani:
tetanospasmin
26
Describe tetanospasmin:
tetanus AB-exotoxin neurotoxin; plasmid-encoded
27
Describe the mechanism of action of tetanospasmin:
blocks GABA and glycine release; leads to loss of inhibitory input to motor neuron excitation leading to spastic paralysis
28
In clostridium tetani, the spastic paralysis is due to:
uncontrolled muscle contraction from tetanospasmin
29
The effects of tetanospasmin may be:
localized and one-sided (on opposite side of infection)
30
Describe the effects of anti-toxin on tetanospasmin:
usually too late for anti-toxin treatment
31
clostridium tetani does not ____ so it acts through ____.
invade tissue; toxins
32
A dramatically deadly disease characterized by the inability of muscle relaxation:
tetanus
33
Tetanus toxin prevents:
muscle relaxation
34
Infection with tetanus systemically can cause:
1. cardiac arrhythmias 2. blood pressure swings 3. dehydration
35
A characteristic symptom of tetanus:
lock jaw
36
Tetanus effects can be ___ or ___.
general or localized
37
Describe tetanus vaccination of pregnant women:
Passive immunization (IgG) of pregnant women can prevent neonatal tetanus death by umbilical infection (250,000/year worldwide)
38
The ONLY clostridium species with tissue invasion:
Clostridium perfringens
39
Organisms that often cause problems when you have an infection from a dirty wound, as these bacteria can be deposited deep down into a relatively anaerobic environment that allows them to begin growing and invading the tissue:
clostridium perfringens
40
The tissue invasion seen with clostridium perfringens is furthered by:
virulence factors that allow the bacteria to lyse cells and destroy tissue integrity
41
List the virulence factors associated with clostridium perfringens:
1. alpha-toxin 2. theta-toxin 3. collagenase & hyaluronidase
42
Describe the mechanism of action of the alpha-toxin in clostridium perfringens:
hemolytic property resulting in membrane destruction
43
Describe the mechanism of action of the theta-toxin in clostridium perfringens:
cytolytic toxin that results in cell killing
44
Describe the mechanism of action of the collagenase and hyaluronidase in clostridium perfringens:
facilitates tissue invasion from the edges of necrotizing tissues
45
Which virulence factor of clostridium perfringens is responsible for its ability to invade tissue:
collagenase & hyaluronidase
46
Describe the mechanism of reaction seen in clostridium perfringens:
anaerobic fermentation of amino acids leads to increase gas production (H2 and CO2) leading to gas gangrene
47
The anaerobic fermentation of amino acids seen in clostridium perfringens infections results in:
gas gangrene
48
What childbirth complication is seen with clostridium perfringens?
Puerperal "childbed" fever: uterine gangrene
49
Describe the treatment against clostridium perfringenes:
No vaccination possible; antibody against alpha toxin but fails to stop gas gangrene -- typically amputation is best option if gangrene occurs
50
List the three types of clostridium that do NOT invade tissues:
1. C-diff 2. Botulism 3. Tetanus
51
A super infection resulting from broad spectrum antibiotics that kill much of the other intestinal bacterial normal flora resulting in resistant species of this harmful bacteria:
clostridium difficile
52
Antibiotic-associated psudomembraneous colitis is caused by:
clostridium difficile
53
C-diff may be observed after:
antimicrobial chemotherapy
54
One of the leading causes of hospital acquired diarrhea:
Clostridium difficile
55
Results from broad spectrum antibiotics that kill much of the other normal intestinal bacterial flora, giving resistant species like toxin-producing C. difficile a chance to take over:
Antibiotic-associated pseudomembranous colitis
56
List the virulence factors of clostridium difficile:
Toxin A & Toxin B
57
Describe the effects of toxin A in C. diff:
inhibits intestinal tight-junctions leading to fluid leak
58
Describe the effects of toxin B in C. diff:
A cytotoxin that functions in actin depolymerization and rounding of epithelial cells leading to fluid leak
59
Both toxin A and toxin B in C. diff cause fluid leak ultimately causing:
diarrhea
60
CDC 2013 report states that ____ is a major thereat for antibiotic resistance in the U.S.
C-diff
61
What clostridium bacteria is this describing? Treatment: botulinum antitoxin
c. botulinum
62
What clostridium bacteria is this describing? Treatment: toxoid vaccination
C. Tetani
63
What clostridium bacteria is this describing? Treatment: anti-tetanus serum (passive immunity)
C. Tetani
64
What clostridium bacteria is this describing? Treatment: surgery intervention & amputation
C. Perfringens
65
What clostridium bacteria is this describing? Epidemiology: environment (soil, water, sewage), & GI tract in animals and humans:
C. Botulinum & C. Tetani & C. Perfringens
66
What clostridium bacteria is this describing? Epidemiology: Colonized intestines, genital tract, hospital environments, prior antibiotics
C. Difficile
67
Describe the shape and gram stain of bacillus:
Gram positive; rods
68
B. anthracis gives rise to ____ and is considered a ___ infection
woolsorter's disease; zoonotic infection
69
Describe the oxygen requirements of B. anthracis:
facultative anaerobe
70
List the virulence factors of B. Anthracis:
anthrax toxins (edema factor & lethal factor) & poly-glutamic acid capsule
71
Describe the difference between the anthrax toxins edema factor and lethal factor:
differences lie in the A component (the B component is identical)
72
Describe the A component of edema factor (EF) found in bacillus anthracis:
EF is an adenylate cyclase that DIRECTLY leads to increased cAMP levels and results in edema
73
Describe the A component of lethal factor (LF) found in bacillus anthracis:
LF is a metallo-protease that targets MAP kinase (an important signaling molecule) ultimately leading to cell death
74
Describe the capsule of B. antrhacis:
Its a poly-glutamic acid capsule that functions to inhibit phagocytosis
75
Form of anthrax in which spores are uptaken by the lungs and then enter lung phagocytes; latency of 2 months or more may occur:
inhalation anthrax
76
Following the entry into lung phagocytes in inhalation anthrax where do the spores travel to?
lymph nodes
77
In anthrax infections if the spores travel to lymph nodes (from the lungs), the spores germinate causing phagocyte death and ultimately leading to:
pneumonial and meningitis type symptoms
78
In an anthrax infection if spores germinate and produces toxins that enter the bloodstream, this can trigger:
macrophage TNF-alpha leading to toxic shock death in 1-2 days
79
In what situation may an anthrax infection lead to toxic shock and death:
If toxins enter the bloodstream
80
In what situation may an anthrax infection lead to symptoms of pneumonia and meningitis:
If toxins and spores spread to lymph nodes
81
Type of anthrax infection that leads to ulcers in the mouth and esophagus, edema and sepsis:
Gastrointestinal antrhax
82
In what case would gastrointestinal anthrax become nearly 100% lethal:
in lower intestines
83
Describe skin anthrax infections:
redness and edema with rupturing vesicles
84
What is the lethality of skin anthrax?
20%
85
List the epidemiology of bacillus anthracis:
1. animal workers 2. microbiological accidents 3. bioterrorism 4. contaminated meat

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