Tetanus, botulism and LMND Flashcards

1
Q

Which one Is true about Tetanus:

a. Dogs are 10 times more resistant than cats
b. Cats are 20 times more resistant than dogs
c. Cats are more sensitive than horses
d. Dogs are 600 times more resistant than horses

A

d. Dogs are 600 times more resistant than horses

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2
Q

Clostridium tetani is:

a. A static, gram negative , non-encapsulated, anaerobic, spore forming cocci
b. A motile, gram positive, encapsulated, aerobic, rod
c. A motile, gram positive, non-encapsulated, anaerobic, rod.
d. A static, gram negative, encapsulated, aerobic, cocci.

A

c. A motile, gram positive, non-encapsulated, anaerobic, rod.

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3
Q

What is the suitable environment for the Clostridium tetani and its spores?

A

Natural habitat is in moist, fertile soil, however, they can survive indefinitely in dusty indoor environment.
Spores are resistant to boiling water and autoclave temperature of 120degrees 20 min.
Vegetative phase of this bacterium is susceptible to chemical and physical inactivation.

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4
Q

What are the two exotoxins secreted by the tetanus bacillus and what is their pathogenesis?

A

Tetanolysin: locally damaging otherwise viable tissue surrounding the infected area and optimizing the conditions for bacterial multiplication.

Tetanospasmin: leads to clinical signs of tetanus. It has two chains,

The heavy chain is responsible for internalization, cytosolic translocation and fast retrograde axonal transport of the light chain.

The light chain is the neurotoxin and acts pre-synaptically to prevent neurotransmitter release from the neurons by cleaving and inactivating synaptobrevin (“docking” protein necessary for the export of intracellular vesicles containing the neurotransmitter).

The toxin can lead to cross-linking of synaptic vesicles to cytoskeleton, further preventing neurotransmitter release.

The light chain becomes activated after internalization into inhibitory neurons; at this stage the toxin is no longer accessible for neutralisation by the antitoxin.

Toxin affects inhibitory interneurons, inhibitory release of glycine and GABA

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5
Q

How does the parasympathetic and somatic cranial nerve nuclei exacerbate trismus?

A

Increased salivation, increased bronchial secretions and increased respiratory rate.

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6
Q

Why is aspiration pneumonia a main complication of tetanus (additionally to previous mentioned problems?

A

Regurgitation and gastroesophageal reflux can result rarely from oesophageal hiatal hernia and megaesophagus.

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7
Q

What is the mortality rate range for tetanus as per Ettinger/SACCM?

a. 15% - 60%
b. 8% - 50%
c. 5% - 30%
d. 10% - 40%

A

b. 8% - 50%

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8
Q

Describe handling and nursing care needed in a severe case of tetanus

A
Dark quiet environment  
Cotton wool in ear canal  
Ocular care  
Minimal handling (treatment coordinated at same time)  
Feeding tube: Gastrotomy-gastrojejunostomy vs oesophageal vs NG.  
Urinary catheter 
Potential Tracheostomy tube  
Mechanical ventilation
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9
Q

What is the tetanus severity classification proposed in dogs?

A

Class I: only facial signs of tetanus

Class II: generalized rigidity or dysphagia, with or without class I signs

Class III: class I or II signs and are recumbent or have seizures.

Class IV: class I, II, or III as well as abnormal heart rate, respiratory rate or blood pressure measurements.

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10
Q

Mention differential diagnoses of tetanus

A

Immune-mediated polymyositis, strychnine intoxication, spinal trauma, hypocalcemia, meningoencephalitis.

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11
Q

Is there any diagnostic test to achieve definitive diagnosis?

A

Antibodies to tetanospasmin, PCR (not available in vet medicine)

Gram stain from an open wound can identify Gram + rods and dark-staining spheric endospores. (not specific)

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12
Q

What are the three treatment strategies for dogs and cats?

A

Neutralize the toxins present in the body outside the CNS (Antitoxin)

Organisms present in the body should be destroyed to prevent further toxin release.

The effect of the toxin already in the CNS should be minimized

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13
Q

With respect to tetanic antitoxin: (which one is true)

Anti-tetanus equine serum is more likely to cause a reaction than human tetanus immune globulin if given intravenously

There has been no significant benefit in survival, severity of clinical signs or duration of clinical signs shown for dogs treated with antitoxin.

However, the has been demonstrated a benefit of earlier administration on progression of clinical signs

IM administration is preferred due to the high incidence of anaphylaxis (F)

A

There has been no significant benefit in survival, severity of clinical signs or duration of clinical signs shown for dogs treated with antitoxin.

Anti-tetanus equine serum is more likely to cause a reaction than human tetanus immune globulin if given intravenously (F- the other way around)

However, the has been demonstrated a benefit of earlier administration on progression of clinical signs (F)

IM administration is preferred due to the high incidence of anaphylaxis (F)

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14
Q

Which antibiotics are recommended to kill C.tetani? For how long should they be given?

A

Metronidazole is superior. 7-10 mg/kg PO for 10 days

Penicillin G

Also clindamycin, tetracycline or doxycycline

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15
Q

Which drugs are recommended to maintain sedation ?

A

GABA agonists in general: Benzodiazepines, phenobarbital, acepromazine.

If very severe propofol. (mechanical ventilation), neuromuscular blockers

Botulinum toxin has been suggested!

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16
Q

What type of bacteria is clostridium botulinum?

A

Gram positive, anaerobic, spore-forming, rod

17
Q

How many toxins are there? All reported dogs and cats to date have been affected by toxin type__, with the exception of _____.

A

A,B, C1, D, E, F, and G.

By toxin C except 2 in Senegal type D and one in France type B.

18
Q

Explain the pathogenesis of botulism. Extrapoint if you know the 4 phases of neuronal binding.

A

Following cell or spore lysis, the toxin is released and it binds with other protein complexes to form progenitor toxins, which are extremely stables specially at low pH, so they can pass through the stomach into the SI where is released and absorbed by endocytosis.
It enters the lymphatic system and from there the bloodstream.

It binds the presynaptic peripheral nerve terminals affecting limb trunk and head muscles.

a. Binding with neuronal cell surface receptors
b. Endosomal internalization of the toxin
c. Membrane translocation
d. Modification of target SNARE proteines required for exocytosis of acetylcholine at the neuromuscular junction.

Targeting of the SNARE proteins by botulism toxin light chain prevents presynaptic release of acetylcholine at the neuromuscular junction, resulting in flaccid paralysis and evidence of autonomic nervous system dysfunction.

19
Q

Mention 7 differential diagnoses for botulism

A
Acute polyradiculoneuritis,  
Tick paralysis  
Fulminant myasthenia gravis, 
Acute polymyositis  
Coral snake envenomation  
(Lasalocid) poisoning  
Rabies polymyositis
20
Q

How is the definitive diagnosis achieved? Are there any specific recommendations to handle the samples?

A

Botulinum toxin earlier in the course of the disease in blood (10 ml of serum) or intestinal content (faeces, vomitus or food sample) using a mouse protection assay. Other forms (PCR ) still being validated

Samples must be refrigerated but NOT frozen

Strict anaerobic handling

Biohazard-zoonosis

21
Q

Which way of supporting urination in this patients has been associated with the lowest incidence of UTI?

A

1st intermittent catheterisation, then manual expression and finally indwelling catheter.

22
Q

Why is the antitoxin available for botulism not effective in dogs?

A

Human trivalent antitoxin acts against types A,B and E. Would need type C.

23
Q

Which two endocrine disorders you should consider in a patient presenting with a peripheral nerve dysfunction?

A

Diabetes Mellitus and Hypothyroidism

24
Q

What is the mechanism of disease suspected in the case of a paraneoplastic syndrome (not affecting the nerves directly)?

A

Immune mediated, due to antigen mimicry, wherein the immune system generates a response to antigens present within the neoplasm that are shared with the peripheral nerves.

In insulinoma, hypoglycemia might also be a causative role

25
Q

What type of disease is acute polyradiculoneuritis? Do you you know what type of antibodies have been recently detected in a subset of dogs with this disease?

A

Immune mediated, anti-GM2 ganglioside antibodies

26
Q

What is the main treatment for polyradiculoneuritis?

A

Supportive, no steroids as it exacerbate muscle atrophy and predispose to secondary infections.