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MHD #3 > anaerobes > Flashcards

anaerobes Flashcards

1
Q

3 “diseases” associated with Clostridium perfringens

A
  1. gas gangrene (toxin)
  2. intra-abdominal infections (toxin or vegetative)
  3. Food poisoning (toxin)
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2
Q

Clostridium perfringens structure/identifying characteristics

A 
Gram positive
Non-motile
Encapsulated
Forms spores
Double zone hemolysis
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3
Q

Gas Gangrene from Clostridium perfringens

A

• Pathogenesis
- Trauma with devitalized tissue/muscle
 (usually a deep wound like a puncture by farm equipment)
- Spores of C. perfringens, C. novyi, C. septicum, C. ramosum germinate quickly

- Extremities, endometrium, abdominal wall

• Typing A-E – based upon combination of toxins produced by organism
 (type A most common in US)

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4
Q

Clostridium perfringens toxins

A

** α toxin –lecithinase (phospholipase C), lysis of inflammatory cells, tissue destruction (muscle) –keeps the bacteria protected from the immune system (drain the bullae the organism will be present by no WBC)

β-toxin- enteritis necroticans (pig bel)

i – necrosis and vascular permeability

-ε toxin- Systemic, vascular permeability

Θ toxin -Cardiotoxic

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5
Q

clinical presentation of gas gangrene

A 
Rapid onset (6 - 72 hr)
necrosis of muscle (myonecrosis), skin
tense edema
bullae formation
** gas formation (fermentation)
 (=crepitus)

Systemic
shock
hyper or hypothermia

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6
Q

gas gangrene treatment

A
  1. debridement, debridement, debridement
  2. antibiotics (penicillin, B-lactam/inhibitor)
    clindamycin (stops toxin production)

very susceptible to pcn but the devitalized tissue has no blood flow therefore must be amputated

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7
Q

Clostridium perfringens food poisioning

A 
• Heat resistant spores survive 
gravy, soups

• enterotoxin- produced following germination of large numbers of organisms
 (different than toxins involved in gas gangrene) 
• Clinical
8 - 24 hr after ingestion
nausea, abdominal pain, diarrhea
• self-limiting/ usually not treated
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8
Q

Clostridium tetani spread

A

puncture wounds
burns
umbilicus
local germination without necrosis


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9
Q

Tetanospasmin

A

neurotoxin (plasmid borne)
blocks postsynaptic inhibition spinal motor reflexes (GABA)
Spasmotic contractions (uninhibited reflexes)

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10
Q

Clostridium tetani symptoms

A
  • trismus (lockjaw)
  • risus sardonicus (increased tone orbicularis oris)
  • **opisthotonus (arm flexion, leg extension)- classic rigid appearance
  • Respiratory (obstruction, diaphragm)

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11
Q

Treatment of tetnus

A
  • Human tetanus immunoglobulin (HTIG) (will bind any unbound toxin but cannot reverse what has already bound)
  • Sedation
  • Control of spasms
  • supportive (airway)
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12
Q

Clostridium botulinum most commonly comes from

A

Home canning fruits/vegetables, fish
preformed toxin from contaminated food
spores in honey (infants)
12 - 36 hrs after ingestion

spores are very very heat resistant (needs pressure + heat to kill the spores)

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13
Q

Clostridium botulinum toxin

A 
large single polypeptide (150-165 Da)
cleaved by bacterial protease
most potent toxin in nature
blocks acetylcholine
no transmitter release = paralysis 
synapse permanently damaged
can travel axons
heat labile (toxin is killed by boiling 10min)

causes permanent damage therefore synapses must be remade

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14
Q

clinical symptoms of botulism

A

• GI (nausea, dry mouth, diarrhea)

• descending** paralysis (flaccid)
cranial (III, IV, VI) (begins with eyes and moves down the body) 
symmetric neurologic effects
afebrile
patient conscious
heart rate normal
no sensory deficits

• Wound botulism

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15
Q

Prevention/Treatment of botulism

A

avoid contaminated food
heating of food (boiling)
antitoxin (equine serum to A,B,E)
supportive

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16
Q

how is Clostridium difficile aquired

A

Rare normal flora
spores acquired in hospital
antibiotic therapy usually precedes disease

can be spread person to person or environment to person but does not cause illness until something triggers it… often receiving antibiotics

17
Q

Clostridium difficile toxins

A

Toxin A - enterotoxin, inflammatory response, major toxin

Toxin B - cytotoxic

18
Q

Clostridium difficile clinical symptoms

A 
pseudomembranous colitis** classic presentation
diarrhea (watery, severe, bloody)
abdominal pain
leukocytosis**
fever
toxic megacolon
 (risk of perforation)
19
Q

BI (Nap1) strain of Clostridium difficile

A

Increased Toxin A production
Higher mortality, especially elderly
Up to 50% of isolates in the US
- been here for a long time but has some how become more virulent

20
Q

C. difficile diagnosis

A

• Detection of toxin A in stool
- ELISA
85 - 90% sensitivity (single assay)
95% sensitive (two assay)

• *PCR- New standard-amplifies toxin region
90+ % sensitivity, 98% specificity

• Culture
not routinely recommended


• Sigmoidoscopy/colonoscopy (risk of perforating the colon)

21
Q

C. difficile treatment

A

Stop antibiotics if possible

Metronidazole (oral preferred)

** Vancomycin (oral only, expensive)
 main drug
colon resection

Lactobacillus, fecal enema (transplant) - very good success with relapsing C. diff

22
Q

Propionobacterium acnes

A

Slow growing anaerobe
Contaminant in blood cultures

Cause of infection:
Prosthetic devices or hardware
Opportunistic infections
Acne


Treatment – if indicated
Penicillin as well as many other agents except metronidazole!!

23
Q

Peptostreptococcus

A

• Normal flora of mouth, GI tract, pelvis
• Contiguous infections (usually mixed)
Intra-abdominal, endometritis, pulmonary

• Brain abscess

• Diagnosis –culture only gram positive cocci anaerobe

• Treatment – debridement and penicillin, metronidazole, cabapenems, clindamycin

24
Q

B. fragilis group characteristics

A 
mixed infections - usually dominant anaerobe
Non-spore forming, non-motile

Requires enriched media to grow

Normal inhabitant of GI tract (colon)

Provide protection from invasion (?)

25
Q

hallmark of B. fragilis infection

A

abscess formation

  • Inflammatory response to infection
  • Encapsulated “pus”
  • PMN’s
  • Fibrin, fibrinogen
  • Debris, necrotic tissue

Almost always mixed infections (aerobes and anaerobes

26
Q

main virulence factor of B. fragilis

A

polysaccharide capsule

  • adherence to peritoneal cavity
  • Resists phagocytosis
  • Resistance to T cell and humoral immunity
27
Q

virulence factors of B. fragilis

A

Polysaccharide capsule

Oxygen tolerance
Super oxide dismutase
Catalase


Toxins : Defective endotoxin – not associated with sepsis (same toxin as E. coli)

28
Q

Prevotella spp characteristics

A 
Residents of mouth, GI tract, and Pelvis
Gram negative strict anaerobes
Require enriched media (blood containing)
Non-motile
Non-encapsulated
Virulence – unknown
29
Q

Prevotella pathogensis

A

abscess formation

Female genital tract infections
Oral, pleuropulmonary
Oral cavity, urogenital, GI tract

30
Q

most active drugs for bacteroides

A 
metronidazole
chloramphenicol
ampicillin/sulbactam
piperacillin/tazobactam
carbapenems

MHD #3 (11 decks)

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