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Nervous System > M- Tetanus & Botulism > Flashcards

M- Tetanus & Botulism Flashcards

1
Q

Describe the microbiological characteristics of clostridium tetani.

A
  1. gram positive bacillus
  2. spore- forming [terminal endospore]
  3. obligate anaerobic
  4. sluggish motility
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2
Q

Who do most of the cases of C. tenani in the US affect? Why?

A

Elderly [especially women] because of:

  1. waning immunity
  2. inadequate immunization
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3
Q

Describe the steps in the pathogenesis of C. tetani.

A
  1. infects a dirty/soiled wound through puncture/laceration
  2. spores germinate in the wound and create the progenitor tetanus neurotoxin
  3. toxin is cleaved into heavy chain [cell receptor specificity] and light chain [toxic moiety] which remain liked via disulfide bonds
  4. toxin circulates locally or in the bloodstream where it binds peripheral nerves
  5. retrograde transport up the axon into the nerve cell body in brainstem/spinal cord
  6. diffuses to the ends of GABA neurons and glycinergic interneurons
  7. the light chain is cleaved from the heavy chain and cleaves synaptobrevin so there cannot be exocytosis of GABA or glycine [inhibitory substances]
  8. LMN are uninhibited and continuously contract antagonist muscles–> muscular rigidity
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4
Q

What are the two ultimate effects of C. tetani on the nervous system?

A
  1. Inhibitory neurons can’t fire –> antagonist contraction–> muscular rigidity

.2. hypersympathetic state by uninhibited release of adrenal catecholamines

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5
Q

What type of toxin are C. tetani and C. botulinum?

A

They are type III toxins [A-B]

B binds to the receptors in the nerves, A acts on the intracellular site

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6
Q

What are the symptoms of generalized tetanus?
What is the patients mental status when they have tetanus?
What is the course of the disease?

A 
1. lockjaw [trismus]
2, sardonic smile [risus sardonicus]
3. abdominal rigidity
4. opisthotonus [flexed arms, extended back/legs] 
5. pain 
6. respiratory compromise

The patient is mentally alert.
The course worsens for 2 weeks and then a slow recovery follows

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7
Q

What is localized tetanus?

A

A patient experiences muscle contractions around the site of inoculation.
This may serve a a prodrome or progress to generalized tetanus

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8
Q

What is cephalic tetanus?

When does it occur?

A

It is tetanus of the CNs due to a head or neck wound.

It presents with facial paralysis followed by generalized tetanus

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9
Q

What causes neonatal tetanus?

A

It is caused by inadequate maternal immunization and follows umbilical cord inoculation

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10
Q

How is C. tetani diagnosed?

A
  1. clinical presentation is key - if it looks like tetanus, start treating so you can take up remaining toxin in the blood stream
  2. “spatula test” - a provacative test where a tongue blade promotes spasm -NOT RECOMMENDED
  3. electromyography in puzzling cases
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11
Q

What is the DDx for a patient who appears to have tetanus?

A
  • strychnine poisoning
  • dental abscesses [trismus]
  • malignant neuroleptic syndrome
  • stiff-person syndrome
  • dystonia due to dopamine blocker/parkinson’s
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12
Q

What is treatment for C. tetani?

How long does rehab take?

A
  1. Maintain the airway, place a feeding tube, and put the patient in a room with minimal stimuli
  2. control spasm with
    - GABA agonists [benzodiazopine] IV
    - NMJ blockers to stop contractions/pain
  3. passive immunization with HTIG [binds up additional unbound toxin], plus active immunization with tetanus toxoid
  4. metronidazole and debridement of the wound
    * no penecillin b/c it is a GABA antagonist
  5. Labetalol [a and b blocker] to damp down hypersympathetic effects
  6. Heparin prophylaxis bc the patient will be bed-bound for weeks [clot formation]

**Rehab lasts 2-6 weeks

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13
Q

How do you prevent the spread of C. tetani?

A
  1. full serious [3 injections] of tetanus toxoid

2. Td booster every 10 years for life

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14
Q

How is neonatal tetanus prevented?

A
  1. maternal immunity should be insured
  2. Tdap booster for pregnant women once during pregnancy
  3. “cocoon” contacts with the baby by giving booster
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15
Q

What should you do to prevent tetanus in a fresh tetanus-prone wound in a person w/o adequate immunization history?

A
  1. HTIG

2. Tetanus toxoid booster

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16
Q

Why doesn’t prior tetanus render a person immune to future insult?

A

The amount of toxin that causes tetanus is insufficient to mount an immune response so you have made no Ab to the toxin

17
Q

Describe the microbiology of C. botulinum.
What agar is required for growth?
How will the colonies appear on the agar?

A
  1. gram positive bacillus
  2. obligate anaerobe
  3. spore-forming with oval “tennis racket” spores
  4. grows on egg agar
  5. lipase-positive [clear halos around colony]
18
Q

Where are spores for C. botulinum found?

A
  1. soil and lake sediment
  2. plants, bees, honey
  3. improper at home canning techniques
  4. black tar heroine [skin popping], pruno in prison

OVERALL it is things that have a pH >4.6

19
Q

What is the most frequently encountered form of botulism in the US? [70 cases a year]

A

Infant botulism.

it does NOT occur in clusters and may be associated with honey ingestions and/or dust-borne spores

20
Q

What are the 4 main forms of botulism seen in the US?

A
  1. Infant botulism and adult intestinal toxemic botulism
  2. wound botulism
  3. food-borne botulism
  4. iatrogenic botulism [from botox that gets into bloodstream instead of concentrating at the nerve]
21
Q

Spore of C. botulinum are heat ______, but the toxin [A-H] are heat __________ and resemble tetanus neurotoxin in that they both have __________________ .

A

spores are heat stable, but toxins are heat labile and resemble tetanus neurotoxin with a heavy and light chain connected by a disulfide bond

22
Q

Which strains of botulinum toxin are chromosomal gene encoded?
Which are on bacteriophage?
Which is on a plasmid?

A 
Chromosome = A,B, F
Bacteriophage = C,D,E
Plasmid = G
23
Q

Which botulinum toxins most frequently affect humans?

Which strains are in food-borne cases?

A

Humans are most affected by A, B, E

Food born is ABEF

24
Q

Which strains of botulinum are associated with wound infection?
Who is most likely to get wound botulism?

A

A and B

Black tar heroine users that do skin-popping are most likely to get would botulism

25
Q

How does infant botulism differ from wound or food-borne botulism in terms of pathogenesis?

A

Infant botulism - the neonatal gut is colonized by C. botulinum due to lack of competing flora or bile acids.
**Pre-formed toxin is NOT ingested, but is produced in the colon by clostridia that are growing

In wound/food-borne, the toxin is ingested not the organism

26
Q

Regardless of the mode of transmission [infant, wound, food-borne, biological warfare, iatrogenic] what is the pathogenesis of C. botulinum toxin in the body?

A
  1. toxin is absorbed into the bloodstream where it circulates
  2. it attaches by heavy chain to the cholinergic ganglionic and parasympathetic synapses at the NMJ
  3. Light chain separates from heavy chain and cleaves SNAP25, synaptobrevin, syntaxin
  4. Ach release is prevented resulting in flaccid paralysis rather than spasm
27
Q

How long after exposure to botulinum toxin do symptoms begin?
What are the symptoms?

A

4-36 hours after exposure to the toxin, the patient will have:

  1. diarrhea, nausea
  2. dry mouth - salivary muscles are paralyzed
  3. slurred speech
  4. blurred vision - pupillary paralysis so no accommodation/ dilated pupils
  5. DESCENDING SYMMETRICAL PARALYSIS
  6. NO fever or sensory deficits
28
Q

A patient presents to you with diarrhea, nausea, dry mouth, blurred vision, and descending symmetrical paralysis with no sensory deficits or fever.
What is your concern?
How long will it take the patient to recover?

A

botulism - it takes weeks to months to recover

29
Q

What is the DDx for botulism?

A
  1. myasthenia gravis
  2. Guillen-Barre
  3. LES
  4. nerve gas/sarin
  5. poliomyelitis [although it is asymmetric and febrile]
30
Q

How is the diagnosis of botulism made?

A
  1. History - if it matches, you need to work fast!
  2. Elecromyogram is supportive
  3. confirm with botulinum toxin assay of serum, stool, gastric content for food-borne
  4. confirm with botulinum toxin assay AND anaerobic culture of stool for infant botulism
31
Q

What does EMG show for botulism?

A
  1. normal nerve conduction
  2. low amplitude motor potentials
  3. facilitation with repeated stimulation
32
Q

What is treatment for botulism?

What are the drawbacks?

A
  1. call CDC and get botulinum antitoxin
    - heptavalent [A-G] equine serum antitoxin for adults [drawback = doesn’t reverse paralysis but stops it from getting worse, serum sickness/anaphylaxis can occur]
    - BIG-IV or BabyBIG for infant botulism
  2. ventilatory support
  3. wound debridement for wound botulism, purgatives for food-borne
33
Q

Why should you not use bactericidal antibiotics for infant botulism?

A

It will kill the bacteria and release whatever toxin was remaining in the bacteria worsening the problem

34
Q

What antibiotics should be used for treatment of wound botulism?

A

penicillin/metronidazole

DO NOT USE clindamycin or aminoglycosides because they will aggravate the NMJ blockade

Nervous System (32 decks)

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