Anaerobic Pathogens Flashcards

1
Q

clostridium sp.

A

*OBLIGATE ANAEROBIC
*gram POSITIVE rods
*FORM ENDOSPORES
*part of the normal flora

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

clostridium difficile (C diff) - overview

A

*gram POS anaerobic rod that freely forms spores
*oxygen is toxic
*infection limited to large intestine
*disease is toxin-mediated (not invasive)

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

clostridium difficile - virulence factors

A
  1. Toxin A (enterotoxin) - causes cell death of intestinal mucosa
  2. Toxin B (cytotoxin) - causes actin depolymerization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

C diff - toxin A (enterotoxin)

A

*chemotactic for neutrophils; stimulates infiltration of PMNs
*cytopathic effect: disruption of tight cell-to-cell junction
*increased permeability of intestinal wall and subsequent diarrhea

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

C diff - Toxin B (cytotoxin)

A

*causes actin to depolymerize, with resultant destruction of cellular cytoskeleton

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

3 required events to get C diff infection:

A

hospitalization (usually), followed by:
1) change in normal GI flora (ANTIBIOTICS)
2) acquire C diff spore (usually from environment or another person)
3) inadequate IgG response to toxins A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the name of the disease caused by C diff infection

A

pseudomembranous colitis

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

risk factors for C diff

A

**recent antibiotic exposure
*hospitalization
*recent GI surgery
*recent chemotherapy
*proton pump inhibitors

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

what is the highly virulent strain of C diff in North America

A

BI/NAP1
*more likely to cause death

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

C diff - clinical manifestation

A

*acute onset of severe, watery diarrhea
*fever, toxicity, high WBC count
**COMPLICATION = TOXIC MEGACOLON

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

C diff - treatments

A

*oral vancomycin (recurrences can occur)
*stool transplant is highly effective for recurrent infections

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

C diff - diagnosis

A

*demonstration of Toxin A and B in the stool by ELISA

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

clostridium perfringens - overview

A

*gram positive rod
obligate anaerobe
**
beta (DOUBLE RING) hemolysis

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

what is the pathogen characterized by beta double ring hemolysis

A

clostridium perfringes

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

clostridium perfringens - virulence factors

A

*alpha toxin - lyses erythrocytes and other cells; mediates massive hemolysis
*beta toxin - causes intestinal stasis and necrotic lesions
*enterotoxin - alters membrane permeability and causes diarrhea

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

clostridium perfringens - clinical presentation (in soft tissues)

A

*GAS GANGRENE (characterized by gas formation)
*cellulitis, fasciitis, myositis with myonecrosis
*often follows trauma
*infection leads to muscle necrosis and septic shock
*can cause death within 24 hours

17
Q

clostridium perfringens - clinical presentation (food poisoning)

A

*only in intestine and only making enterotoxin
*causes watery diarrhea, abdominal cramps
*transmitted by poultry

18
Q

clostridium perfringens - diagnosis

A

*gram stain (gram + rods)
*anaerobic culture

19
Q

clostridium perfringens - treatment

A

high dose penicillin & surgical debridement

20
Q

clostridium tetani - overview

A

*anaerobic spore-forming
*gram positive rod
*classic “stepping on a rusty nail”

21
Q

clostridium tetani - virulence factors

A

*tetanus toxin (tetanospasmin)
*taken up by motor neurons (by pinocytosis)
*INHIBITS the INHIBITORY NEURON
*irreversible lack of inhibition of motor neuron produces tetanus (motor neuron is constantly active)

22
Q

primary host defense against clostridium tetani

A

antibodies against the tetanus toxin (this is why we get the vaccine)

23
Q

3 clinical entities of tetanus disease

A

1) generalized tetanus
2) localized tetanus
3) neonatal tetanus

24
Q

generalized tetanus

A

generalized musculature spasms involving the whole body

25
Q

localized tetanus

A

musculature spasms restricted to localized area of primary infection

26
Q

neonatal tetanus

A

neonatal infection primarily involving the umbilical stump; very high mortality
PREVENTION = vaccinate mom before delivery

27
Q

clostridium tetani - diagnosis

A

*clinical presentation (spasmatic paralysis)
*demonstration of seronegative state (no tetanus antibodies)

28
Q

clostridium tetani - treatment

A

*tetanus immunoglobulin (TIG) from CDC
*benzos (relax muscles)
*penicillin (decrease organism number - slowly)

29
Q

clostridium botulinum - virulence factor & its effect

A

*produces botulinum toxin - cleaves SNARE proteins so the Ach vesicle cannot attach to muscle to cause contraction
*causes FLACCID paralysis

30
Q

clostridium botulinum - primary host defense

A

antibody against the toxin (but we do not immunize against it)

31
Q

foodborne botulism

A

*initially - blurred vision, dry mouth, constipation, abdominal pain
*progression to bilateral descending weakness of peripheral muscles with flaccid paralysis

32
Q

other forms of clinical botulism

A

*infant botulism
*wound botulism
*inhalation botulism

33
Q

clostridium botulinum - diagnosis

A

*clinical presentation
*finding the suspected food source

34
Q

clostridium botulinum - treatment

A

*botulinum antitoxin (from CDC)

35
Q

anaerobic colonic gram NEGATIVE rods

A

*NON-spore forming
*LPS is a major virulence factor
*part of the normal flora
*obligate anaerobes
*there are a lot of these

36
Q

actinomyces sp.

A

*BRANCHING gram POSITIVE rods
*obligate anaerobes
*DENTATE appearing colonies on agar
*normal PERIODONTAL flora
*active infections tend to produce and “SPIT OUT” “SULFUR GRANULES” in pus
*tend to cross tissue planes