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Infectious Disease 2 > Anaerobes > Flashcards

Anaerobes Flashcards

1
Q

What is an example of a spore-forming, anaerobic, gram positive rod?

A

Clostridium!!

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2
Q

How does clostridium primarily cause disease?

Subtypes?

A

through the production of numerous exotoxins. They are opportunistic pathogens.

Perfringens, tetani, botulinum, difficile

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3
Q

Where is C. tetani found?

What can it cause?

A

worldwide in soil, occasionally found in intestinal flora of humans and animals

Causes tetanus or lockjaw

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4
Q

C. tetani

  • morphology
  • culture
  • biochemical activities
  • resistance
A
  • morphology: long and slender, flagella, no capsule, *terminal located round spore (drum-stick appearance)
  • culture: obligate anaerobe, gram positive, faint hemolysis
  • biochemical activities: does not ferment any carbs or proteins
  • resistance:live for several years in soil, tolerate boiling for 60 min
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5
Q

C. tetani

-what exotoxins does it produce and what are their actions?

A
  • tetanolysin -dont care
  • tetanospasmin (neurotoxin)
  • -involve 3 components of the nervous system: central motor control, autonomic function, and the neuromuscular junction
  • -retrograde transport to (CNS)
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6
Q

How does tetanospasmin work?

A
  • disseminates quickly
  • binds to ganglioside receptors (inhibitory neurons in CNS)
  • gylcine (neurotransmitter)
  • **spastic paralysis
  • severe muscle contraction and spasms
  • can be fatal
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7
Q

How does C. tetani present?

A

1st- cramping and twitching of muscles around a wound. No fever, sweats profusely and begins to experience pain. Trismus (lock jaw) possible.
2nd- portions of the body become extremely rigid. Opisthotonos (spasm- body bows forward) is common
3rd- complications: fractures, bowel impaction, muscle rupture, pulmonary, renal, and cardiac problems

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8
Q

What type of immunity follows vaccination with tetanus toxoid?

A

active immunity.

there is little, if any, innate immunity and the disease does not produce immunity in the patient.

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9
Q

dx of C. tetani infection

A

dx primarily by the clinical sx, wound may not be obvious.

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10
Q

How to care for a C. tetani infected wound

A
  • offending organism must be removed by debridement
  • toxoid
  • TAT; flagyl
  • AIDs pts may not respond to prophylactic injections of tetanus toxoid
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11
Q

C. perfringens

  • where is it found?
  • what does it cause?
A
  • found in the soil, fecal contamination

- Causes gas gangrene

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12
Q

How does C. perfringens work? (pathogenesis)

A
  • wound contamination
  • tissue degrading enzymes (lecithinase, proteolytic enzymes, saccharolytic enzymes)
  • destruction of blood vessels
  • tissue necrosis
  • anaerobic environment created
  • organism spreads

causes Gas Gangrene

  • as capillary permeability increases, the accumulatoin of fluid increases and venous return is eventually curtailed
  • as more tissue becomes involved, the clostridia multiply with the increasing area of dead tissue, releasing more toxins into the local tissue and the systemic circulation
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13
Q

Gas Gangrene treatment

A
  • abx therapy
  • debridement
  • anti-toxin
  • amputation and death is rare

*without treatment death occurs within two days

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14
Q

What are the initial sx of gas gangrene?

A
  • Fever and pain in the infected tissue; more local tissue necrosis and systemic toxemia.
  • Infected muscle is discolored (purple mottling) and edematous
  • foul odor, gas bubbles form from the products of anaerobic fermentation
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15
Q

C. botulinum

  • morphology
  • found where?
  • transmission
A

morphology- anaerobic, gram positive, rod shaped, sporeformer, produced a protein neurotoxin

-found in soil, sediments of lakes, ponds, decaying vegitation, intestinal tracts of birds, mammals, and fish

Transmission- spores are heat resistant
–often get botulism from canning/eating uncooked foods containing spores

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16
Q

How does the Botulinum toxin work?

A
  • binds to peripheral nerve receptors (ACh)
  • inhibits nerve impulses
  • flaccid paralysis
  • death (resp and cardiac failure)
17
Q

Clincal syndromes of Botulism

A
  • 18-3 hours
  • weakness, dizziness, dryness of the mouth
  • n/v
  • neuro sx: blurred vision, inability to swallow, difficulty in speech, descending weakness of skeletal muscles, respiratory paralysis
18
Q

What can’t babies have honey?

A

They could become infected with C. botulinum

-neonatal botulism is the predominant form of botulism. they get colonization because they have little or no normal flora to compete (unlike adults)

19
Q

How to diagnose Botulism?

A
  • by clinical sx alone
  • most direct and effective: serum or feces
  • most sensitive and widely used: mouse neutralization test 48 hour, culturing of specimens 5-7 days
20
Q

Tx of botulism

A
  • should be treated immediately with antiserum
  • antibiotic therapy (if infection)– vaccination will not protect hosts from botulism, however passive immunization with aby is the treatment of choice for cases of botulism.

*prevent with proper food handling and prep. Spores can survive boiling for 1 hour. Don’t eat food that has spoiled (seal broken)!

21
Q

How does C. difficile (infection) occur?

A

After abx use, normal gut flora is greatly decreased.
colonization occurs
enterotoxin secreted leading to pseudomembranous colitis

22
Q

Sx of pseudomembranous colitis

A

abd pain with watery diarrhea and leukocytosis. “pseudomembranes” consisting of fibrin, mucus, and leukocytes can be observed by colonoscopy.

*untreated can be fatal

23
Q

tx of pseudomembranous colitis

A
  • discontinue abx

- give specific antibiotic therapy (vancomycin)

24
Q

Where do you find anaerobic infection?

A
  • muscle, cutaneous/sub-cutaneous necrosis

- abscesses

25
Q

Why is it difficult to ID an anaerobic infection?

A
  • air in the sample
  • ID takes several days or longer, limiting usefulness
  • often derived from normal flora, sample contamination
26
Q

Characteristics of anaerobic infections

A
  1. usually commensal, originating from our own flora
  2. predisposing conditions such as breaches in mucocutaneous layer, compromised vascular supply, trama with tissue destruction, antecedent infection
  3. Complex flora, multiple species
  4. synergistic mixture of aerobes and anaerobes (E. coli consumes O2, encouraging growth of anaerobes, anaerobes promote growth of other bacteria by being antiphagocytic and producing beta-lactamases)
27
Q

Clues to anaerobic infection

A
  • mucosal surface infection
  • infection with necrosis and abscess formation
  • putrid odor
  • gas in tissues
  • polymicrobial flora
  • failure to grow in lab
28
Q

What is a major cause of infection post abdominal surgery?

A

Bacteroides fragilis

-prominent capsule (anti-phagocytic), endotoxin with low toxicity

Infectious Disease 2 (9 decks)

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