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GI Micro > Anaerobes > Flashcards

Anaerobes Flashcards

1
Q

Where are anaerobes found?

A

Gut microbiome (esp. Bacteroides and Clostridia). Also found in oral cavity, skin, colon, female genital tract. Clostridia found in soil and air as spores too.

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2
Q

What 2 enzymes do anaerobes lack?

A
  1. Superoxide Dismutase

2. Catalase

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3
Q

How do anaerobes get their energy?

A

Carbohydrate fermentation or breakdown of amino acids to amines.

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4
Q

Why do anaerobic infections stink?

A

B/c amines stink

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5
Q

Besides smelling awful, what are other characteristics to anaerobic infections?

A

Abscesses and tissue necrosis, smelly pus. Smelly breath. Many are polymicrobial.

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6
Q

What type of pneumonia are you thinking of with an alcoholic?

A

Aspiration of anaerobe

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7
Q

Many anaerobic infections are of what type?

A

Opportunistic: relocalized normal flora to a sterile area.

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8
Q

Why aren’t feces or sputum cultured when anaerobic infection is suspected?

A

B/c it’s just normal flora. Won’t help you any.

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9
Q

Clostridial infections are usually from what?

A

Environmental spores

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10
Q

Shape of Bacteroides fragilis?

A

Gram Negative coccobacillus

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11
Q

What is the major virulence factor of B. fragilis?

A

Anti-phagocytic capsule

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12
Q

B. fragilis is a major component of what?

A

Human GI tract (opportunistic pathogen)

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13
Q

What is the MC anaerobic infection?

A

B. fragilis

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14
Q

What types of dz can B. fragilis cause?

A
  1. Intra-abdominal infections
  2. Abscesses
  3. Pelvic Inflammatory Dz
  4. Pulmonary infections (due to aspiration)
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15
Q

Treatment of B. fragilis abscesses?

A
  1. Surgical drainage

2. DOCs: erythromycin, clindamycin, metronidazole, 3rd gen cephalosporins

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16
Q

What is B. fragilis resistant to?

A

Penicillin

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17
Q

Why aren’t amino glycosides effective against anaerobes?

A

They don’t work under anaerobic conditions.

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18
Q

Shape of Prevotella melaninogenica?

A

Gram Negative coccobacillus

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19
Q

What is the major VF of Prev mel?

A

Anti-phagocytic capsule

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20
Q

Where in the human body can you normally find Prev mel?

A

GI tract, nasopharynx, and vaj

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21
Q

What does Prev mel infection cause?

A

Pulmonary and Periodontal abscesses

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22
Q

What is the reason for Prevotella melaninogenica’s name?

A

When cultured, forms dark black colonies (melanin).

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23
Q

Shape of Clostridium?

A

Gram + spore-forming rods (Note: must be G+ to form spores).

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24
Q

T or F. Clostridium is the only anaerobic endospore-forming bacteria.

A

T

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25
Q

What’s advantageous about the spores of Clostridium?

A

They are resistant to high heat and harsh environments.

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26
Q

What is responsible for Clostridium’s pathogenesis?

A

Exotoxins and secreted hydrolytic enzymes

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27
Q

Where is Clostridium found?

A
  1. Colon

2. Soil as spores

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28
Q

What is the shape of C. perfringens?

A

Large, “boxcar” shaped G+ rods

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29
Q

Where is C. perf found?

A

Soil and intestines of humans and animals

30
Q

Most human C. perf infections are from what?

A

Spores in soil or food

31
Q

What does C. perf cause?

A
  1. Gas gangrene
  2. Cellulitis
  3. Food poisoning
32
Q

Pathogenesis of gas gangrene?

A

Contamination of wound by C. perf spores. Multiple enzymes (phospholipase, collagenase, protease, etc.) facilitate tissue penetration. Necrosis ensues and gas formed.

33
Q

Why is the gas formed in gas gangrene?

A

Carbohydrate fermentation

34
Q

What does untreated gas gangrene lead to?

A

Shock, renal failure, and then death.

35
Q

What is the treatment for gas gangrene?

A
  1. Surgical debridement
  2. Large amounts of Penicillin and protein-inhibiting abx
  3. Hyperbaric oxygen chamber
36
Q

Which strains of C. perf cause food poisoning, the 3rd MC food-borne illness in the US?

A

The enterotoxin-producting strains

37
Q

What allows C. perf to cause food poisoning?

A

Rich meat dishes at low temperatures allow spores to germinate (which allows them to produce the enterotoxins) before consumption.

38
Q

When do symptoms appear after exposure to food contaminated with C. perf?

A

8-24 hours

39
Q

What is the clinical presentation of C. perf food poisoning?

A

Nausea, abdominal pain, diarrhea. NO fever. Vomiting is rare.

40
Q

What is the outcome of C. perf food poisoning?

A

Full recovery w/in 24 hours

41
Q

How does tetanus occur?

A

Spore contamination of wound.

42
Q

What does C. tetani produce that causes the tetanus?

A

Tetanospasmin (aka tetanus toxin)

43
Q

What are the characteristics of tetanospasmin?

A
  1. AB neurotoxin
  2. Enters at NMJ and transported by motor neurons to ganglia (incubation time depends on distance of wound from CNS)
  3. Cuts a V-snare: prevents release of inhibitory NTs (glycine + GABA), blocking postsynaptic inhibition of spinal motor reflexes)
44
Q

Tell me about tetanus.

A
  1. Trismus (lock jaw) occurs first
  2. Risus sardonicus facial feature (in anguish from pain but looks like they’re smiling)
  3. Generalized intermittent spasms
  4. Pt is aware and sensitive to stimuli especially light
45
Q

How can death occur from tetanus?

A

Exhaustion and respiratory failure. Important to keep pt calm.

46
Q

Treatment of tetanus?

A
  1. HTIG antibody to soak up excess toxin
  2. Sedation
  3. Wait for regeneration of axon terminals
    Note: Abx are useless here
47
Q

T or F. Botulism caused by Clostridium botulinum is a true infection.

A

F: it’s an intoxication rather than an infection.

48
Q

How do infants get botulism?

A

The filthy little things eat spores off carpets.

49
Q

What kind of toxin does C. botulinum produce? What does it do?

A

AB toxin. There are 7 antigenic types (A-G). May be the most toxic bacterial exotoxin. 1 gram of this shit could kill a million people! They cleave v- and/or t-snares preventing release of Ach.

50
Q

What’s the most common route of intoxication by botulism toxin?

A

Food poisoning aka Classic Botulism. Don’t buy bulging cans at the grocery store. You will die.

51
Q

What allows C. botulinum spores to be in food?

A

Spores are resistant to heat and then germinate after cooking. They then can release toxin. Note: subsequent heating will inactivate the toxin (heat-labile).

52
Q

What is the clinical presentation of classic botulism?

A
  1. Acute, symmetrical descending flaccid paralysis (note: GBS is ascending)
  2. Symptoms begin 12-36 hours after ingestion
  3. Nauses, dry mouth, diarrhea, then blurred vision
  4. Paralysis descends to respiratory muscles, trunk, and extremities
  5. Death can be caused by respiratory failure
53
Q

Treatment of classic botulism? Prevention?

A

Tx: mechanical ventilation + horse anti-toxin
Prevention: proper cooking/canning (vaccine available for military only)

54
Q

How does infant botulism present?

A

3-8 month old floppyyyyyy babies! Why it’s also called Floppy Baby Syndrome.
Constipation, poor muscle tone, feeding problems.

55
Q

How do infants get botulism?

A

Inhalation or ingestion of spores. Infection occurs first, then intoxication by toxin.

56
Q

What is the MC nosocomial infection?

A

C. difficile. It is the MC diarrheal dz associated with abx use (creates niche). Endogenous or hospital spores are source.

57
Q

T or F. C. difficile is part of the normal GI flora in 5% of the population.

A

T

58
Q

What toxin does C. diff produce?

A

Toxins A and B. Note: this is NOT an AB toxin.

59
Q

C. diff toxins A and B work synergistically to produce dz. What type of toxin is each and what do they cause?

A

Toxin A: enterotoxin- diarrhea
Toxin B: cytotoxin- inflammation
Note: “super strains” are emerging

60
Q

What are the symptoms of a C. diff infection?

A
  1. Pseudomembranous colitis
  2. Fever
  3. Watery diarrhea that can become bloody
61
Q

Diagnosis of C. diff?

A
  1. Detection of Tox B activity from stools on tissue culture cells
  2. RADT detection of Tox A or B in stools
62
Q

Treatment of C. diff?

A
  1. D/C abx
  2. Enema (maybe…if the pt is into that sort of thing)
  3. Metronidazole (if required by acute cases)
63
Q

Watery diarrhea

A
  1. Vibrio cholera
  2. Vibrio parahaemolyticus
  3. Clostridium perfringens
  4. Clostridium difficile
64
Q

Watery > bloody diarrhea

A
  1. Campylobacter jejuni
65
Q

Persistent infection

A
  1. Helicobacter pylori
66
Q

Seasonal infections

A
  1. Vibrio cholera

2. Vibrio parahaemolyticus

67
Q

Food-borne

A
  1. Campylobacter jejuni
  2. Vibrio cholera
  3. Vibrio parahaemolyticus
  4. Clostridium perfringens
68
Q

Normal flora

A
  1. Bacteroides fragilis

2. Clostridium difficile

69
Q

Opportunistic/nosocomial

A
  1. Bacteroides fragilis

2. Clostridium difficile

70
Q

Flaccid paralysis

A
  1. Clostridium botulinum
71
Q

Lock jaw

A
  1. Clostridium tetani

GI Micro (7 decks)

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