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Microm 442 > lecture 18 Anaerobes > Flashcards

lecture 18 Anaerobes Flashcards

1
Q

What are the three classes of disease caused by clostridium?

A
  • gas gang gangrene
  • botulism
  • tetanus
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2
Q

What are two enteric diseases caused by clostridium.

A
  • food poisoning

- antibiotic-associated enterocolitis

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3
Q

What are the characteristics of clostridium?

A

-Anaerobic, gram-positive rods, form endospores, natural reservoirs -soil intestinal tracts and skin of humans and animals

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4
Q

What is the etiology Clostridial wound infections?

A
  • usually mixed clostridial infection in wound following surgery or trauma.
  • By Cl. perfringens, other cl. species
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5
Q

What is the etiology of gangrene?

A

Toxins caused by infection of clostridium spread to healthy muscle tissue and produce myonecrosis; by locally invasive organisms, Bacteremia is not common, but systemic toxemia can occur.

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6
Q

What is the pathogenesis of clostridium wound infections.

A
  • α-toxin, acts on phospholipids and lecithin, causing cell lyses
  • Θ-toxin, pore forming, lyses cell, toxic to heart and alters permeability of capillary
  • No effective host defense in necrotic cells.
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7
Q

How are clostridial wound infections dx clinically?

A
  • Clinical sx:
  • -gas in tissues (crepitus), edema and shock in wound pain.
  • -once a lesion appears, must begin treatment before lab results
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8
Q

How are clostridial wound infection dx in the lab?

A

-Mixed infection, one must be histotoxic (clostridium)
-Exudate smear - Gram positive rods with cellular infiltrate
-bacterial characteristics - “anaerobic growth”
double xone hemolysis (theta toxin)
check lecithinase activity on egg yolk

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9
Q

How are clostridial wound infection prevented/treated?

A
  • surgical debridement and cleansing -antibiotics -Penicillin
  • hyperberic O2
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10
Q

What is the source of clostridium in food?

A
  • Meat prroducts
  • spores germinate when food is heated
  • enterotoxin is produces pores in enterocytes.
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11
Q

How is Cl. perfingens food poisoning dx clinically?

A
  • onset 7-22 hours post ingestion

- diarrhea, cramps, abd pain, possible fever, nausea vomiting.

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12
Q

How is Cl food poisoning dx in the laboratory?

A
  • non-motile (unlike other clostridia)

- spores sometimes seen on smears

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13
Q

Which genus of cl causes food poisoning?

A

Clostridium perfingens

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14
Q

How is Cl food poisoning treated?

A
  • supportive therapy

- mortality near zero

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15
Q

What causes botulism?

A

-Clostridium botulinum

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16
Q

Where can Cl Botulinum be found?

A

-soil, silt, vegetation, intestinal tracts of humans and animals

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17
Q

What is classical botulism?

A

-is an intoxication, not an infection, caused by ingestion of preformed toxin in food contaminated with spores

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18
Q

What causes wound botulism?

A

usually infection of compound fracture, severe laceration or penetrating wound

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19
Q

What causes infant botulism?

A

caused by germination of spores in intestinal tract of infants; most cases in infants 2 weeks - 6 months; adults not affected by this syndrome

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20
Q

What causes inhalation botulism?

A

bioterrorism threat

21
Q

What types of food are incriminated by Clostridium botulinum?

A
  • improperly canned food
  • fish preserved by salting or smoking
  • prepared meats ingested uncooked
22
Q

What is the action of the botulinum toxin?

A
  • 7 distinct type inducing same disease
  • absorbed in intestine, transported to neuromuscular junction.
  • relatively toxic
  • heat-labile
23
Q

How is clostridium botulinum dx clinically?

A
  • 12-96 hours, maybe 14 days
  • GI sx- vomiting, constipation
  • Nervous system- Flaccid paralysis
  • mortality rate about 20% now declining
24
Q

How is clostridium botulinum dx in a lab?

A
  • isolation for organism form contaminated food or stool samples (oval, subterminal spores)
  • Demonstration of toxin in food or patient serum or feces.
25
Q

How is clostridium Botulinum treated?

A

-eliminate unabsorbed toxin; stomach lavage and
enemas
-eliminate source of toxin
-neutralize unbound toxin
-supportive care (especially respiratory support)

26
Q

How is clostridium botulinum treated/prevented?

A
  • antitoxin therapy (passive immunization)
  • antibiotics of questionable value, except in cases of wound botulism
  • Boil raw or fermented native dishes and home canned foods 10 minutes before eating
  • Follow recommended home-canning procedures
27
Q

What is the etiological agent of tetnus?

A

-Cl. tetani toxin, several antigen serotypes, but one toxin

28
Q

What is the pathogenesis of Cl. Tetani?

A
  • spastic paralysis following penetrating wound
  • spores contaminate wounds
  • germination, outgrowth and toxin production
  • toxin enters motor neurons, transported to CNS by retrograde axonal transmission (travels along nerve fibers)
  • highest mortality in elderly: >50% over 60 years
29
Q

What is the action of the tetanus toxin?

A
  • protein toxin is sole virulence factor
  • Spastic paralysis: blocks inhibitory neurotransmitters
  • very toxic like botulism
30
Q

How is clostridium tetani dx clinically?

A

-initial sx- cramping and twitching of muscles around wound, then head and neck (lock jaw)

31
Q

How is Cl Tetani dx in a lab?

A
  • isolation of organism from wound
  • spores
  • demonstration of toxin neutralization with antitoxin
32
Q

How is clostridium treated/prevented?

A
  • maintenance of airway
  • Benzodiazepines - -(GABA* agonists) tetanus immunoglobulin
  • antibiotics to clear infectious focus
33
Q

Does tetanus and botulinum toxins have the same enzymatic effect?

A

-They have the same effects, but in different neurons.
Tetanus attacks interneuron while botulism attacks the neuromuscular junction.
They both cleave the protein VAMP.

34
Q

What causes abx-associated (pseudomembranous) colitis?

A

Clostridium difficile

35
Q

What is the etiology of abx-associated colitis?

A
  • follows antibiotic therapy; normal microbiota altered, spores germinate, overgrow, produce toxins and cause colitis; normal microbiota serve a protective role
  • organism - normal microbiota, slender, gram positive rod with large, oval subterminal spores
36
Q

What is the pathogenesis of Clostridium difficile?

A
  • resistant to may abx
  • two principal toxins cause disease by disrupting cytoskeletal elements of epithelial cells/submucosal tissue, A (enterotoxin) and B (cytotoxin) .
37
Q

How does C. Difficile toxins work?

A
  • large toxin
  • 3 functional domains (receptor, membrane translocation, glucosyltransferase activity)
  • once in cytoplasm, inactivate rho proteins by transferring glucose onto them.
38
Q

What are some sx of C. Diff?

A

-abdominal pain; watery diarrhea, and mucus or blood
may be seen
-Mortality rate; 27-44% in untreated pts

39
Q

How is C. Diff Dx?

A
  • demonstration of pseudomembrane (sigmoidoscopy)

- fecal filtrates can be assayed for toxin

40
Q

How is C. Diff treated?

A

-in most identified cases, symptoms resolve after
antibiotic therapy is discontinued
-Cl. difficile are usually susceptible to vancomycin and metronidazole
-relapse may occur following therapy Fecal Transplants

41
Q

What made a C diff strain more virulent?

A
  • More severe disease, increased complications,
    high mortality rate, increased risk of relapse
  • Has mutation in regulatory gene – makes 16 to 24X as much toxin A&B
42
Q

What are the characteristics of Bacteroides fragilis?

A
  • Gram-negative rods; non-spore forming
  • found primarily in the intestine; relatively O2 tolerant
  • most frequently isolated anaerobe from diseased tissues; usually involved in diseases of the lower 1⁄2 of body
  • bile resistant
43
Q

What diseases are caused by Bacteroides Fragilis?

A
  • intra abd abscess
  • Skin and soft tissue infections
  • secretory diarrhea in children
44
Q

What are sx of intra abdominal abscesses?

A
  • localized infections following compromise of the integrity of the intestine
  • low grade fever abdominal pain
  • can lead to bacteremia with high morality rate
45
Q

What are some sx of skin and soft tissue infections?

A
  • cellulitis, fasciitis associated with surgical wound infections
  • infections of diabetic and decubitus ulcers
46
Q

What is the pathogenesis of bacteroides fragilis?

A
  • capsular polysaccharides, forms abscess
  • mixed infections
  • penicillin resistant
47
Q

How is bacteroides fragilis dx?

A
  • abscesses, Radiologic CT and or aspiration

- gram stain culture

48
Q

How is bacteroides fragilis treated?

A
  • abx, use a couple in case is polymicrobial

- drainage of abcess

Microm 442 (16 decks)

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