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M2 | Microbiolgy > Bacterial Dysentery (Gram Positive) > Flashcards

Bacterial Dysentery (Gram Positive) Flashcards

1
Q

Important properties of Bacillus cereus

A
  • Gram-positive
  • facultative anaerobic
  • sporeforming, large rod
  • Motile & beta hemolytic
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2
Q

Mode of transmission in Bacillus cereus

A
  • Spores on grains such as rice survive steaming & rapid frying

• Spores germinate when rice is kept warm for many hours (e.g. reheated fried rice), then bacteria produce exotoxin, which are ingested steaming

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3
Q

Pathogenesis of B.cereus

A
  • Produces 2 enterotoxins :
    1. Similar to cholera toxin ——> increased cyclic AMP
    2. Similar to staphylococcal enterotoxin —-> superantigen
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4
Q

Clinical findings in B.cereus

A
  1. Vomiting (emetic): short incubation period —-> 4 hours
    * nausea
    * vomiting
  2. Diarrheal: long incubation period ——> 18 hours
    * watery
    * nonbloody diarrhea
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5
Q

Important properties of Clostridium botulinum

A
  • Anaerobic
  • gram positive
  • Spore forming rods
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6
Q

Transmission of C.botulinum

A
  • Spores in soil, contaminate vegetables & meats
  • Canned foods or vacuum-packed without adequate sterilization ———-> spores survive & germinate in anaerobic environment.
  • Toxin is produced within canned food & ingested preformed
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7
Q

Which food/s are the highest risk of C.botulinum infection?

A

(1) Alkaline vegetables (green beans, peppers & mushrooms)
(2) Smoked fish

• Toxin is heat-labile (inactivated by boiling for several minutes)

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8
Q

Pathogenesis of C.botulinum

A

Botulinum toxin is absorbed from gut & carried via blood to

peripheral nerve synapses ——> blocks release of acetylcholine

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9
Q

What is the botulinum toxin ?

A
  • A protease that cleaves proteins involved in Ach release
  • Among the most toxic substances
  • 8 types : type A , B & E are most common
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10
Q

Clinical findings of C.botulinum

A
  1. Descending weakness & paralysis
  2. Diplopia (double vision), blurred vision, slurred speech (difficulty talking), dysphagia & respiratory muscle failure
  3. No fever
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11
Q

What are the 2 special forms that are clinically found in C.botulinum?

A
  1. Wound botulism: spores contaminate wound, germinate & produce toxin at site (drug abuse)
  2. Infant botulism: organisms grow in gut & produce toxin
    * Ingestion of honey containing organism
  • Infants (between 6 weeks & 6 months of age) develop muscular weakness or paralysis, loss of head control & need respiratory
    support (usually recover spontaneously)
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12
Q

Important properties of Clostridium perfringens

A
  • Large Gram postitive rods
  • Anaerobic
  • Spore forming
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13
Q

Laboratory diagnosis of C.botulinum

A
  • Not cultured
    1. Mouse protection tests:
  • Botulinum toxin is found in uneaten food & patient’s serum
  • Mice are inoculated with clinical specimen & will die unless protected by antitoxin
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14
Q

State the diseases that occur from C.perfringens

A
  1. Gas gangrene

2. Food poisoning

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15
Q

Which type of tissue does the C.perfringens grow in ?

A

traumatized tissue (especially muscle)

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16
Q

Which toxin is produced in gas gangrene by c.perfringens ?

A

Alpha toxin (lecithinase)

17
Q

What does the alpha toxin do ?

A

Alpha toxin (lecithinase) ——> damages cell membranes , including those of erythrocytes ——-> hemolysis

18
Q

How production of gas happen in gas gangrene ?

A

Degradative enzymes produce gas in tissues

19
Q

Clinical findings of C.perfringenes

A
  1. Pain,edema, cellulitis & gangrene (necrosis) in wound area
  2. Crepitation indicates presence of gas in tissues
  3. Hemolysis amd jaundice
  4. Shock & death can ensue
20
Q

Laboratory diagnosis of gas gangere due to c.perfringens

A
  1. Smears of tissue & exudate show large gram-positive rods
  2. Cultured anaerobically & colonies exhibit double zone of hemolysis on blood agar
  3. Organisms identified by sugar fermentation reactions &
    organic acid production
  4. Egg yolk agar :
    * demonstrate presence of lecithinase
21
Q

How food poisoning occur by c.perfringens ?

A
  1. Spores are located in soil & contaminate food
  2. Heat-resistant spores survive cooking & germinate
  3. Organisms grow in reheated foods, especially meat dishes
22
Q

Pathogenesis of c.perfringens

A
  • Member of normal flora in colon
  • Enterotoxin acts in small bowel diarrhea
  • Enterotoxin: similar to staphylococcal enterotoxin —-> superantigen
23
Q

Clinical findings of c.perfringens

A

Watery diarrhea with cramps & little vomiting (resolves in 24 hours)

24
Q

What is the incubation period in food poisoning?

25
Laboratory diagnosis of c.perfringens
* Not usually done * No assay for toxin * Organisms isolated from uneaten food
26
Important properties of Clostridium difficile
* gram positive * anaerobic * spore froming rods
27
How is c.difficile transmitted ?
1. Fecal oral route | 2. Ham]nds of hospital personnel
28
Explain the transmission of c.difficile
* Organism is carried in gastrointestinal tract in 3% of general population & 30% of hospitalized patients * Most people are not colonized most people who take antibiotics do not get pseudomembranous colitis
29
Explain the pathogenesis of antibiotics in helping c.difficile
Antibiotics suppress members of normal flora, allowing C. difficile to multiply & produce exotoxin A (enterotoxin) & exotoxin B (cytotoxin)
30
What are the antibiotics used ?
1. Clindamycin : * 1st recognized to cause pesudomembranous colitis 2. Third-generation cephalosporins: * most common used 3. Ampicillin & fluoroquinolones (Gentamicin) * common
31
Whixh chemotherapy is a direct cause if pseudomembranous colitis?
Cancer chemotherapy
32
Explain the pathogenesis of Endotoxin A & B
They are glucosyltransferases (i.e., enzymes that glucosylate [add glucose to] G protein called Rho GTPase) Exotoxin B ——> depolymerization of actin —-> loss of cytoskeletal integrity, apoptosis & death of enterocytes.
33
C. difficile rarely invades______
intestinal mucosa
34
Clinical finding of c.difficile
1. Foul smelling diarrhea + pseudomembranes (yellow-white plaques ) on colonic mucosa 2. Nonbloody diarrhea 3. Neutrophils found in stool 4. Fever and abdominal pain
35
In 2005, new hypervirulent strain of C. difficile emerged & causes:?
- severe disease - recurrences - less responds to metronidazole - resistance to quinolones
36
Laboratory diagnosis of c.difficile
1. Culture stool : * insufficient for presence of C. difficile * because people can be colonized by organism & not have disease 2. Stool isolation: * evidenced by stool toxin test 3. PCR : presence of toxin gene DNA
37
What are the 2 types of tests done to detect c.diificile exotoxins ?
1. ELISA : * using antibody to exotoxins (rapid but less sensitive) 2. Cytotoxic test : * Human cells in culture are exposedto exotoxin in stool filtrate & death if cells is observed * It is more sensetive & specific but requires 24 to 48 hours

M2 | Microbiolgy (17 decks)

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