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LA DX & TX I > Exam 1 - Equine Neurology: Bacterial & Toxic Diseases > Flashcards

Exam 1 - Equine Neurology: Bacterial & Toxic Diseases Flashcards

1
Q

what is a common name for tetanus?

A

lock jaw

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2
Q

what is tetanus?

A

bacterial neurologic disease characterized by extensor muscle rigidity & death

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3
Q

what species is most susceptible to tetanus?

A

horses

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4
Q

what organism causes tetanus?

A

clostridium tetani

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5
Q

what is the etiology of tetanus?

A

common soil inhabitant & strict anaerobe

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6
Q

how does c. tetani commonly gain access to the horse’s body?

A

puncture wound

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7
Q

what is the pathogenesis of the tetanolysin toxin of tetanus?

A

damages tissues & creates an environment favorable for anaerobes & facilitates infection

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8
Q

what 2 toxins are produced/released by clostridium tetani?

A

tetanolysin & tetanospasm

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9
Q

what is the pathogenesis of the tetanospasm toxin in tetanus?

A

diffuses locally & via the bloodstream to peripheral nerve terminals throughout the body

travels retrograde up neurons

into CNS after 1-14 days

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10
Q

how does tetanospasm work?

A

binds irreversibly to pre-synaptic neurons blocking release of inhibitory transmitters causing spastic paralysis

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11
Q

when do clinical signs typically develop in tetanus infections?

A

usually 7-10 days after the wound but can be as short as 1 day or as long as 60 days

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12
Q

what are the main clinical signs of tetanus in the horse?

A

prolapsed 3rd eyelid, generalized whole body rigidity, saw horse stance, elevated tail, hypersensitivity

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13
Q

if an animal presents with a prolapsed eyelid, what 2 differentials immediately come to mind?

A

tetanus & HYPP

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14
Q

what is the saw horse stance characterized by?

A

ears held pricked up

paralysis of breathing muscles

stiff legged gait

tail held out & stiff

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15
Q

what are the advanced clinical signs associated with tetanus?

A

clonic-tonic spasms

severe muscle contractions - rhabdomyolysis

autonomic signs - tachycardia, sweating

recumbency & death

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16
Q

how is tetanus diagnosed?

A

clinical signs, history, & ruling out other diseases

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17
Q

in tetanus, when may you see a patient with a prolapsing nictitating membrane upon stimulation?

A

early in the course of the disease process

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18
Q

what are some differentials for tetanus?

A

myopathy
meningitis
rabies
HYPP
trauma
laminitis
colic

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19
Q

what are the 4 principles of treating tetanus?

A
  1. provide a safe, quiet environment
  2. eliminate organism & unbound toxin
  3. sedation & muscle relaxation
  4. general support
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20
Q

what should the environment be like for a tetanus patient?

A

large, well-bedded stall, padded if possible

minimize light, noise, & other stimuli

cotton in the ears

hang water & feed

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21
Q

how is tetanus eliminated from the body?

A

clean/debride wound

tetanus antitoxin into wound

penicillin

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22
Q

how are the exotoxins eliminated or inactivated in tetanus treatment?

A

use the antitoxin which bounds any residual unbound toxin

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23
Q

T/F: tetanus antitoxin can rarely cause acute hepatic necrosis (theiler’s disease)

A

true

24
Q

what should be included in general support for a tetanus patient?

A

iv fluids, parenteral or enteral nutrition, & pain control

25
Q

what is the prognosis for tetanus?

A

usually poor, fatality >75%

26
Q

what are poor prognostic markers of a tetanus patient?

A

rapid onset/progression of clinical signs & absence of vaccination

27
Q

how is tetanus prevented in the horse?

A

annual vaccine - tetanus toxoid

tetanus antitoxin for non-vaccinated horse with wound or foal from non-vaccinated mare & give toxoid concurrently

28
Q

botulism affects what horses?

A

adults & foals

29
Q

what is botulism called in foals?

A

shaker foal syndrome

30
Q

what age of foals are typically affected by shaker foal syndrome?

A

foals 1-3 months old - can occur in outbreaks

31
Q

what is the etiology of botulism?

A

clostridium botulinum

32
Q

what is the mechanism of infection of botulism?

A

toxins are absorbed into circulation & neuroparalytic botulinum toxins reach presynaptic nerve terminals which blocks exocytosis of acetylcholine at the presynaptic membrane of the neuromuscular junction

33
Q

how do horses get clostridium botulinum?

A

they ingest it or have wound contamination

34
Q

how do horses get botulism from forage toxicity?

A

toxin is in the contaminated feed (decaying vegetable matter, decomposing animal, bird carcass)

hay/silage - anaerobic conditions, pH remains above 4.5

35
Q

T/F: the presence of animal & bird carcasses in processed food materials is incriminating evidence for diagnosing botulism

A

true

36
Q

how do foals get botulism?

A

toxicoinfectious form - associated with type b forms in inflammatory lesions such

-intestinal ingesta
-wounds
-gi ulcers
-liver abscesses

37
Q

what are the common toxic forms of botulism in horses?

A

a, b, c, & d

38
Q

T/F: clinical signs of botulism are acute in onset

A

true

39
Q

what are common clinical signs of botulism in horses?

A

muscle tremors, slow eating, mydriasis (dilated pupil), poor muscle tone, depressed reflexes, weak tongue/eyelid tone, & urine & fecal retention

40
Q

what are the clinical signs of shaker foal syndrome?

A

suckling foals tend to show repeated episodes of trembling just before becoming recumbent - rapidly progressive

41
Q

what are the advanced clinical signs of botulism?

A

recumbency, dyspnea, cyanosis, & death

42
Q

how is botulism diagnosed?

A

typically presumptive based on multiple cases of recumbency/tetra-paresis with evidence of appetence but oral/pharyngeal dysplasia

isolation from feed, patient feces, or wounds

43
Q

what tests detect botulinum toxins?

A

ELISA, PCR, & mouse inoculation assays

44
Q

what is paramount for success in botulism treatment?

A

nursing care!!!

hydration, nutrition, & metabolic support/status

45
Q

what does the prognosis of botulism depend on?

A

amount of toxin affecting the animal & ability of specific antitoxin

46
Q

what are poor prognostic markers of botulism?

A

inability to stand

lower survival rates for adult horses

47
Q

T/F: survival rates for severely affected foals treated with polyvalent antiserum/intensive support can be as high as 50-90%

A

true

48
Q

why is botulism a public safety risk?

A

humans are susceptible - especially infants

don’t take infants to site of outbreak

49
Q

how is botulism prevented in foals?

A

vaccination of mares with clostridium botulinum type b toxoid twice in the last trimester of pregnancy

especially in areas where shaker foal syndrome is common

50
Q

what is the best treatment for botulism for the toxins?

A

IV polyvalent botulism antitoxin

expensive & needs to be administered in the early stages of disease

51
Q

why should tetracyclines & aminoglycosides be avoided when treating botulism?

A

potential exacerbation of neuromuscular blockade

52
Q

what antibiotics should be given IV for a patient with botulism?

A

penicillin or metronidazole

53
Q

when should oxygen be supplemented in a patient with botulism?

A

if PaO2 is low

54
Q

T/F: some foals with shaker foal syndrome require mechanical ventilation

A

true

55
Q

T/F: the survival rate for adult horses with botulism is higher than foals with botulism

A

false - adults have lower survival rates

56
Q

what happens to your botulism patient’s prognosis if you don’t have the specific antitoxin on hand?

A

prognosis is POOR

LA DX & TX I (45 decks)

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