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ZUKU NAVLE PREP > Equine Top 15 Neurologic Diseases - Part 3 > Flashcards

Equine Top 15 Neurologic Diseases - Part 3 Flashcards

1
Q

what is the classic case presentation of rabies in a horse?

A

sudden behavior changes, agitation, aggression, progressive paralysis, rapid breathing, +/- rolling

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2
Q

what is the etiology of rabies?

A

lyssavirus in family rhabdoviridae

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3
Q

how is rabies diagnosed?

A

fresh brain tissue from medulla oblongata or cerebellum is sent to a designated lab - immunofluorescent microscopy diagnoses 98-100% of cases

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4
Q

how is rabies treated? how is rabies prevented?

A

no treatment, always fatal - vaccination to prevent

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5
Q

what are common vectors of rabies?

A

cats, dogs, skunks, raccoons, foxes, & bats

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6
Q

what is the classic case of neuroborreliosis in a horse?

A

ataxia, uveitis, cranial nerve deficits, lethargy, poor tongue tone, muzzle tremors, spinal pain, inappetance/weight loss, spooking, muscle atrophy, & occasionally, lameness, peripheral neuropathy, seizures, & arrhythmias

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7
Q

what is the etiology of neuroborreliosis?

A

borrelia burgdorferi sensu stricto

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8
Q

how is neuroborreliosis diagnosed?

A

CSF to serum ratio using lyme multiplex (detects 3 different antibodies), serology with C6 ELISA test most often used - serology alone isn’t diagnostic because it can indicate infection or exposure

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9
Q

what is the major reservoir host of b. burgdorferi?

A

white footed mouse (p. leucopus)

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10
Q

what is the prognosis of neuroborreliosis?

A

poor even with aggressive therapy

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11
Q

what is the life cycle of b. burgdorferi?

A

vector of ixodes ticks, white tail deer are the tick host, & reservoir hosts are small mammals (white footed mouse), birds, & reptiles

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12
Q

T/F: many horses in the mid-atlantic region have been exposed to b. burgdorferi & most don’t show clinical signs

A

TRUE

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13
Q

how is neuroborreliosis treated?

A

doxycycline or minocycline

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14
Q

what are the diseases included in the alphavirus encephalomyelitidies?

A

EEE/WEE/VEE

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15
Q

what is the classic case presentation of EEE & WEE?

A

fever, depression, altered mentation, head droop, dysphagia, paresis/paralysis, lateral recumbency with paddling, +/- pruritus

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16
Q

what is the incubation period of EEE/WEE?

A

5-14 days

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17
Q

what is the classic case presentation of VEE?

A

may be asymptomatic/mild, similar neuro signs to EEE/WEE, tachycardia, diarrhea, colic, & sudden death

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18
Q

what is the etiology of alphavirus encephalomyelitidies?

A

arboviruses - arthropod borne viruses in the togaviridae family

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19
Q

what are the reservoir hosts of EEE? what kind of hosts are horses? what is the vector?

A

passerines (perching songbirds) +/- rodents, horses are dead end hosts, & culiseta melanura mosquito is the vector

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20
Q

what are the reservoir hosts of WEE? what kind of hosts are horses? what is the vector?

A

passerines (perching songbirds), +/- black tail jack rabbits, horses are dead end hosts, & culex tarsalis mosquito is the primary vector

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21
Q

what are the reservoir hosts of VEE? what kind of hosts are horses? what are the main vectors?

A

wild rodents, horses are important amplifiers for epidemic VEE, & many species of mosquitos, black flies, mites, & ticks are vectors

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22
Q

how are EEE/WEE/VEE diagnosed?

A

serology for IgM antibody capture for EEE/WEE (4 fold elevation in plaque reduction neutralization or high titer in unvaccinated horse), virus isolation only in early febrile stage for antemortem diagnosis, brain tissue for EEE, pancreatic tissue for VEE, IHC or PCR for EEE, lymphopenia often seen with EEE, & azotemia from decreased water consumption is common

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23
Q

what is seen on CSF fluid of a horse with EEE?

A

neutrophilic or mononuclear pleocytosis

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24
Q

how are EEE/WEE/VEE treated?

A

supportive care - pain control, tranquilizers/anticonvulsants, fluids, nutritional support, slings, & broad spectrum antibiotics for bacterial infections due to injuries or pneumonia

25
Q

how are EEE/WEE/VEE prevented?

A

vaccination, mosquito repellants (permethrins), & clearing weeds, feces, & stagnant water from barns/paddocks/pastures

26
Q

what is the mortality rates of EEE/WEE/VEE?

A

EEE, 50-90% sudden death & survivors often have residual neuro deficits, WEE 20-50%, & VEE 50-75%

27
Q

when was the last time VEE was reported in the USA?

A

1971

28
Q

when does human disease from EEE/WEE/VEE occur?

A

approximately 2 weeks after equine cases are reported

29
Q

what is the classic case presentation of a horse with WNV?

A

many are asymptomatic, but mild fever/depression, asymmetric ataxia or paresis involving one or more limbs, cranial nerve VII & XII deficits, behavioral changes, coarse head/neck tremors, & head droop with secondary facial edema

30
Q

what is the etiology of WNV?

A

flavivirus, an arbovirus in flaviviridae family

31
Q

what are the reservoir hosts of WNV?

A

predominantly passernes but also shore birds, raptors, & owls

32
Q

how is WNV diagnosed?

A

elevated IgM antibodies, 4-fold PRN IgG titer elevation - vaccination may complicate serology results (for IgG not IgM), virus isolation, RT-PCR, CSF tap with normal to mononuclear plocytosis with increased protein, lymphopenia, & azotemia from decreased water consumption

33
Q

viral isolation of WNV is best done with what samples?

A

best detected in thalamus, hypothalamus, rostral colliculus, pons, medulla, & spinal cord

34
Q

how is WNV treated?

A

supportive care - pain control, flunixin for tremors/fasciculations), fluids, nutritional support, sling/hoist, broad spectrum antibiotics

35
Q

how is WNV prevented?

A

vaccination, mosquito repellants (permethrins), & clearing weeds, feces, & stagnant water from barns/paddocks/pastures

36
Q

what is the mortality rate of horses with WNV?

A

in symptomatic horses, 35-45%

37
Q

fatal illness from WNV occur in what animals?

A

corvids - crows, ravens, & jays

38
Q

when was WNV first identified in the USA?

A

1999

39
Q

what are the 4 big neurotoxins for horses?

A

fumonisin, hemlock, locoweed, & yellow star thistle

40
Q

what is the classic case presentation of a horse with fumonisin toxicity?

A

apathy/drowsiness, pharyngeal paralysis, central blindness, circling/ataxia, lateral recumbency, icterus, & death

41
Q

what is the classic case presentation of a horse with hemlock toxicity?

A

posion hemlock - weakness/ataxia, ptyalism, colic, bradycardia, irregular respirations/respiratory failure, & death, water hemlock - ptyalism, muscle twitching of lips, ears, & nose, dilated pupils, agitation, bruxism, seizures, coma, & death in less than an hour

42
Q

what is the classic case presentation of a horse with locoweed toxicity?

A

depression, emaciation, ataxia, infertility/abortion, circling, & heart failure

43
Q

what is the classic case presentation of a horse with yellow star thistle toxicity?

A

involuntary chewing, lip twitching, tongue flicking, submerging head into deep water, mouth held open or tightly closed, & death from dehydration/starvation due to inability to eat

44
Q

what Is the etiology of fumonisin toxicity?

A

mycotoxin produced by fusarium verticilliodes & f. proliferatum growing on moldy corn

45
Q

how is fumonisin toxicity diagnosed?

A

history of moldy corn in feed & on necropsy, unilateral or asymmetric malacia (liquefactive necrosis) or leukoencephalomalacia +/- hepatic necrosis

46
Q

what is the etiology of poison hemlock toxicity? how is it diagnosed?

A

alkaloids produced by conium maculatum diagnosed by history/clinical signs

47
Q

what is the etiology of water hemlock toxicity? how is it diagnosed?

A

cicutoxin & cicutol produced by cicuta species diagnosed by history & clinical signs

48
Q

what is the etiology of locoweed toxicity? how is it diagnosed?

A

certain species of astragalus or oxytropis species that produce swainsonine which inhibits golgi aplha-mannosidase II where chronic ingestion causes excess build up of glycoproteins which damage the CNS neurons (metabolic storage disease) - diagnosed by history & clinical signs

49
Q

what is the etiology of yellow star thistle toxicity? how is it diagnosed?

A

toxin produced by centaurea solstitalis which inhibits the brain’s dopamine transporter system - diagnosed by history & clinical signs

50
Q

what treatment is used for fumonisin toxicity in horses?

A

supportive care, no effective treatment - prevent by avoiding moldy corn

51
Q

what treatment is used for poison hemlock toxicity?

A

activated charcoal, saline cathartics, atropine, gastric lavage, stimulants, tannic acid, & prevented with herbicidal treatment of plants (2,4-D plus dicamba)

52
Q

what treatment is used for water hemlock toxicity?

A

sedatives, prevented with herbicidal treatment of plants with 2,4-D plus dicamba or digging up & burning planst

53
Q

what treatment is used for locoweed toxicity?

A

no treatment, prevent via various herbicides

54
Q

what treatment is used for yellow star thistle toxicity?

A

no treatment, euthanasia, prevent with various herbicides

55
Q

how sensitive are horses to fumonisin?

A

very sensitive - can develop signs after chronic ingestion of only 8-10 ppm

56
Q

what are some ways to prevent hemlock toxicity?

A

posion hemlock - hemlock moth defoliates the plant & may help in its control, water hemlock - herbicidal treatment appears to enhance the plant’s palatability before it dies off, so be careful with that

57
Q

how many species of locoweed are there? how many of them are toxic?

A

more than 300 species of astragalus/oxytropis in USA but only 20 or so are toxic locoweeds

58
Q

when do horses eat yellow star thistle?

A

only ingested with no other forage is available!!!!

ZUKU NAVLE PREP (178 decks)

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