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2 PID Unit > 20 Anaerobes 1 (Clostridium) > Flashcards

20 Anaerobes 1 (Clostridium) Flashcards

1
Q

T/F

After a stay of two days in a hospital, 10% of patients will develop infection with C. difficile

A

True

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2
Q

What are general characteristics of anaerobes?

A
  • grow better in anaerobic atmosphere
  • lack mechanisms of oxygen metabolism and/or detoxification
  • should be considered when signs of infection but aerobic culture negative
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3
Q

What are general characteristics of anaerobe infections?

A
  • Adjacent to surfaces that normally harbor anaerobes as normal flora (e.g. mucosal surface)
  • Abscess formation or tissue necrosis
  • Putrid odor (fermentation)
  • Gas formation
  • Polymicrobic infection or organisms that look like anaerobes
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4
Q

What level of blood supply promotes anaerobic growth?

A

Poor blood supply > low O2 levels

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5
Q

Basic lab characteristics of genus Clostridium?

A

anaerobic G+ rods

spore formers

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6
Q

Which Clostridium species is non-motile, is a large rectangular rod, and rarely forms spores?

A

Clostridium perfringens

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7
Q 
Which bacterium produces this group of exotoxins?
alpha toxin (lecithinase)
beta toxin
epsilon toxin
iota toxin
heat-labile enterotoxin
collagenase
A

Clostridium perfringens

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8
Q

What characteristic divides Clostridium perfringens into 5 types?

A

exotoxins

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9
Q 
How does each exotoxin secreted by Clostridium perfringens contribute to disease?
alpha toxin (lecithinase)
beta toxin
epsilon toxin
iota toxin
heat-labile enterotoxin
collagenase
A

Alpha toxin (lecithinase) - massive hemolysis, increased vascular permeability, tissue destruction, hepatic toxicity, myocardial dysfuntion
Beta toxin - intestinal stasis, necrotizing enteritis
Epsilon toxin - increased vascular permeability of GI wall
Iota toxin - increased vascular permeability, necrosis
Collagenase - penetration deep into tissues -> fulminating gangrene
Heat-labile enterotoxin - no other info

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10
Q

Where is Clostridium perfringens found in the environment? Is it part of the human microbiome?

A

Spores are in soil and water
Found in the intestinal tract of animals
Yes, found in the intestinal and genito-urinary tracts of humans

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11
Q

What is the cause of Clostridial food poisoning? What form is it ingested in? Symptoms?

A

Clostridium perfringens
Ingestion of preformed toxin, which inserts in membrane of SI altering permeability -> diarrhea
Watery diarrhea and crampy abdominal pain 8-24 hours post ingestion

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12
Q

What infections/diseases are caused by Clostridium perfringens?

A 
Cellulitis
Fasciculitis/suppurative myositis
Myonecrosis
Anaerobic puerperal sepsis
Septic abortions
Clostridial food poisoning
Necrotizing enterocolitis
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13
Q

What is the mode of infection, complications, and death from Clostridium perfringens soft tissue infections?

A
  • spores germinate and vegetative cells grow in traumatized tissue; degradative enzymes ferment carbohydrates and produce gas in tissue
  • bacteria produce necrotizing toxin and hyaluronidase; tissue necrosis extends resulting in incr. bacterial growth, hemolytic anemia, severe toxemia, renal failure, and death
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14
Q

How is a C. perfringens infection diagnosed?

A

appearance and foul smell, smears showing large G+ rods, spores not usually seen, double zone of hemolysis on blood agar

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15
Q

Which exotoxin is most responsible for causing necrotizing enterocolitis?

A

beta toxin

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16
Q 
What infection(s)/disease(s) are caused by C. difficile?
Symptoms?
A
  • pseudomembraneous colitis

- range from non-bloody diarrhea to severe life-threatening pseudomembranous colitis with fever and abdominal cramping

17
Q

Which bacterium produces this group of exotoxins?
enterotoxin (toxin A)
cytotoxin (toxin B)

A

C. difficile

18
Q

How does each exotoxin secreted by Clostridium difficile contribute to disease?

A

Enterotoxin (toxin A) - stimulates infiltration of PMNs into the ileum -> inflammation
Cytotoxin (toxin B) - glycosylates G proteins involved in actin filament polymerization & depolymerization -> loss of cytoskeletal integrity -> death of enterocytes & inflammation

19
Q

What is the cause of increased virulence of the hypervirulent strain of C. difficile?

A

produces increased levels of toxins A & B

20
Q

How is a C. difficile infection diagnosed?

A

Isolation from feces and testing for toxins

21
Q

How is pseudomembranous colitis treated?

A

Metronidazole

may require surgical repair of intestines and stool transplant

22
Q

Which Clostridium species is non-motile, is a large rectangular rod, and produces round terminal spores (drumstick/tennis racket bacilli)?

A

Clostridium tetani

23
Q 
What toxin(s) does C. tetani secrete?
What disease symptoms result?
A

Tetanospasmin (tetanus toxin) - plasmid-encoded heat labile A-B neurotoxin; acts by cleaving neurotransmitter inhibitors resulting in spastic paralysis and muscle spasms

24
Q

What is the mode of infection for neonatal sepsis?

A

Spores enter via contaminated umbilicus/circumcision

25
Q

What is the clinical significance of a C. tetani infection?

Incubation period? Mortality rate?

A

Incubation period 3-21 days (variable)

Death results from compromised breathing (50% mortality)

26
Q

How is a C. tetani infection diagnosed?

A

In most cases diagnosed based on signs, symptoms, and patient history
organism rarely cultured from wounds and antibodies/tetanus toxin are not detected in patients

27
Q

How many doses of vaccine must a patient have received so that no tetanus prophylaxis is not necessary?
What is this prophylaxis

A

3 or more
Clean minor wounds give tetanus toxoid and metronidazole
All other wounds give tetanus toxoid and tetanus immune globulin

28
Q

What bacterium produces the most lethal toxin known?

A

C. botulinum

botulinum neurotoxin

29
Q

What is the incubation period and symptoms of botulinum toxin ingestion?

A

12-36 hours after ingestion begins with nausea, vomiting, and bilateral CN impairment
then drooping eyelids, double/blurred vision, difficulty articulating words & swallowing
then paralysis descends to involve muscles of thorax and extremities leading to death from respiratory and cardiac failure

30
Q

What is the pathogenesis/mode of action of the botulinum neurotoxin?

A

Synthesized during growth as zinc-endopeptidase (an A-B toxin)
Inactivates proteins regulating ACh release from nerve termini, blocking neurotransmission at synapses and resulting in flaccid paralysis

31
Q

What is necessary for recovery after the effects of the botulinum neurotoxin?

A

regeneration of nerve endings (takes months to years)

32
Q

What is the treatment of botulinum neurotoxin ingestion?

A

ventilator support, gastric lavage, metronidazole, and injection of trivalent (A, B, E) botulinum antitoxin

33
Q

How it botulism foodborne intoxication diagnosed?

A

based on symptoms and past history (organism not usually cultured)
confirm diagnosis with mouse protection test

34
Q

What is infant botulism? Age affected? Mode of infection? Signs/symptoms?

A

infected infants 3 weeks-6 months old
preformed toxin not detected in any food - bacterial spores ingested (honey, infant milk powder) and germinate colonizing in intestinal tract
constipation, lethargy with feeding difficulties; followed by marked loss of muscle tone, especially in the head and neck

35
Q

What are the 3 forms of botulism infection/toxin ingestion?

A

Foodborne intoxication
Infant botulism
Wound botulism

36
Q

What is the cosmetic use of a Clostridium species?

A

C. botulinum toxin A used cosmetically (Botox) to remove wrinkles or as muscle relaxant

37
Q

T/F

Botulinum vaccine exists

A

True but immunization of general population not warranted since disease so rare

38
Q

What other Clostridium species is associated with infections in IUDs and cancer patients?

A

C. novyi

2 PID Unit (13 decks)

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