Tetanus and Botulism

Question 1

What’s the causative agent for tetanus

Answer 1

Clostridium tetani

neurotoxin - spastic paralysis
- gram (+), rod shaped, anaerobic, spore-forming bacteria

Question 2

What’s the pathophysiology of tetnaus?

Answer 2

Enter through wounds or bites
- spores
- has 2 to toxins: tetanospasmin and tetanolysin

Tetanolysin - responsible for local tissue damage at the site of penetration to encourage bacterial colonization

Tetanospasmin - lead to the clinical syndrome
1. toxin binds to neuro memebrane
2. internalization
3. transported retrograde (motor neurons first then sensory)
4. intracellular action

Question 3

What are the intracellular actions of tetanospsmin?

Answer 3

mostly effects inhibitory interneurons: prevents release of GABA
- prevents the docking/ export of neurotransmitter
- also promotes cross-linking of vesicles and cytoskeleton

Once neuro binding occurs, it’s irreversible

Question 4

What are the clinical signs of tetanus?

Answer 4

effects sites proximal to the bite
- muscle rigidity, facial muscle spasm
- dogs: carpal extension
- cats: carpal flexion
Generalized signs: increased muscle tone, stiff gait, dyspnea, sawhorse stance
- Severe signs = seizures, opisthotonos, respiratory paralysis

Question 5

How susceptible are cats/ dogs to tetanus?

Answer 5

they are relatively resistant, dogs > cats

Question 6

What are the 4 classes of tetanus severity in dogs?

Answer 6

Class I: facial signs only
Class II: generalized rigidity or dysphagia, +/- facial signs
Class III: recumbent or seizures, plus I or iI
Class IV: abnormal heart rate, respiratory rate, or blood pressure, plus Class I, II, or III

Question 7

What are some differentials for tetanus?

Answer 7

immune-mediated polyarthritis, strychnine intoxication, spinal trauma, hypocalcemia, and meningoencephalitis

Question 8

How is tetanus diagnosed?

Answer 8

serum antibody to tetanospasmin
PCR

Question 9

How is tetanus treated?

Answer 9

main strategies:
1. toxins outside of CNS should be neutralized (anti-serum)
2. organism in body should be destroyed (metronidazole)
3. minimize effects of toxins already in CNS (supportive therapy - dark, quiet environment, benzodiazepine sedation, phenobarbital, propofol CRI, ventilation)

Question 10

What’s the prognosis of tentanus?

Answer 10

Cats have been reported to survive localized tetanus
Dogs with class III+ had 58% survival rate

Question 11

What’s the causative agent of botulism?

Answer 11

Clostridium botulinum
- gram (+), rod shaped, anaerobic, spore-forming bacteria

Question 12

What’s the pathogenesis of botulism?

Answer 12

Similar entrance as tetanus
1. binding with neuronal cell surface receptors
2. endosomal internalization of the toxins
3. membrane translocation

• has affinity for pre synaptic nerve terminals – limbs, trunk, and head muscles
• prevent presynaptic release of acetylcholine in neuromuscular junction – lower motor neuron signs

Question 13

What are the clinical signs of botulism?

Answer 13

flaccid paralysis
- rapid development of clinical signs
- sensory functions, pain perception, and mental alertness = normal
- cholinergic changes: heart rate, pupil size (mydriasis, decreased PLR), KCS, urinary retention, constipation

Question 14

How is botulism diagnosed?

Answer 14

based on history and clinical presentation
- definitive diagnosis = demonstration of botulinum toxin (not from food/ carcass, but from infected patient)

Question 15

What are some differentials for botulism?

Answer 15

• acute polyradiculoneuritis
• tick paralysis
• fulminant myasthenia gravis
• acute polymyositis
• snake envenomation
• lasolocid poisoining
• rabies

Question 16

What’s the treatment for boutlism?

Answer 16

supportive care
- anti-serum is not going to help to decrease the severity or duration of c/s if c/s already set in
- human is type A, B; dog is usually type C – so not the right type of anti-serum that’s available