20 Anaerobes 1 (Clostridium) Flashcards

(38 cards)

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)

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
What is the clinical significance of a C. tetani infection? | Incubation period? Mortality rate?
Incubation period 3-21 days (variable) | Death results from compromised breathing (50% mortality)
26
How is a C. tetani infection diagnosed?
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
How many doses of vaccine must a patient have received so that no tetanus prophylaxis is not necessary? What is this prophylaxis
3 or more Clean minor wounds give tetanus toxoid and metronidazole All other wounds give tetanus toxoid and tetanus immune globulin
28
What bacterium produces the most lethal toxin known?
C. botulinum | botulinum neurotoxin
29
What is the incubation period and symptoms of botulinum toxin ingestion?
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
What is the pathogenesis/mode of action of the botulinum neurotoxin?
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
What is necessary for recovery after the effects of the botulinum neurotoxin?
regeneration of nerve endings (takes months to years)
32
What is the treatment of botulinum neurotoxin ingestion?
ventilator support, gastric lavage, metronidazole, and injection of trivalent (A, B, E) botulinum antitoxin
33
How it botulism foodborne intoxication diagnosed?
based on symptoms and past history (organism not usually cultured) confirm diagnosis with mouse protection test
34
What is infant botulism? Age affected? Mode of infection? Signs/symptoms?
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
What are the 3 forms of botulism infection/toxin ingestion?
Foodborne intoxication Infant botulism Wound botulism
36
What is the cosmetic use of a Clostridium species?
C. botulinum toxin A used cosmetically (Botox) to remove wrinkles or as muscle relaxant
37
T/F | Botulinum vaccine exists
True but immunization of general population not warranted since disease so rare
38
What other Clostridium species is associated with infections in IUDs and cancer patients?
C. novyi