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NSB II > LA Spinal Cord Diseases > Flashcards

LA Spinal Cord Diseases Flashcards

1
Q

describe difference in spinal cord exam in large animals

A
  1. muscle tone and reflexes are harder to assess! unless recumbent
  2. no hopping, wheelbarrowing, or hemiwalking (unless small LA)
  3. gait and proprioception:
    try placement tests (could just be a good horse and leave leg where you put it), head elevation, circling, backing, hills, curbs, tail pull
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2
Q

what do LM spinal cord lesions look like in large animals? (5)

A
  1. short strided
  2. trembling
  3. hypotonic
  4. atrophy (unless acute)
  5. weakness progressing to recumbency
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3
Q

what do UMN/GP spinal cord lesions look like in lA?

A
  1. long and lopey (floaty)
  2. stumbling/tripping
  3. truncal sway
  4. traveling on two or more tracks
  5. don’t know where their feet are
    -limb placement
    -circling
    -backing
    -hills/cribs
  6. weakness progressing to recumbency
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4
Q

describe equine protozoal myelitis (EPM)

A
  1. CNS migration of protozoan parasites: sarcocystis neurona!! and also neospore hughesi
  2. exposed via ingestion of opposum feces
    -horses = aberrant, dead end host; does NOT shed oocytes in poop
    -infection is not patent
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5
Q

describe clinical features of EPM

A
  1. high seroprevalence but low clinical disease
    -in some regions 80-90% of horses have been exposed (seropositive) but less than 1% develop neuro disease
  2. means that environmental and host factors are key but clinical signs vary widely!!! protozoan can go anywhere in CNS that it wants to
  3. 3 As:
    -asymmetry: asymmetric spinal cord deficits most common
    -ataxia
    -atrophy
  4. could just be poor performance though! can be acute OR slowly progressive
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6
Q

describe EPM diagnosis

A
  1. gold standard is finding the parasite in the CNS
    -MRI would be helpful bc parasites leave classic regions but most horseys don’t fit so
  2. plan B: consistent clinical signs and prove exposure to organism
    -via serology: antibodies against S. neurona in the blood
    -LOTS of different tests = none are perfect
    –western blot: sucks
    –IFAT: sucks a little less
    –SAG titers: sucks the least
    -these suck because so many horses have been exposed that exposure does not mean disease!!
  3. can look for organism in CSF
    -good but you don’t know where the organism is and PCR only works for spinal cord which you can only get on necropsy

-BEST WAY WE HAVE WHEN ALIVE: antibody titers in CSF: document intrathecal Ab production, looking for a combo on surface antigens in serum AND CSF and calculate a ratio
-if serum:CSF ratio <100 suggests EPM!!!!!
-use equine diagnostic solutions lab in kentucky only!!

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7
Q

describe EPM management and prognosis

A
  1. anti-protozoal
    -3 FDA approved drugs labelled to treat it (you must use them)
    -labelled for 4 week treatment, but usually need to treat for 2-9 months
  2. possum management: good luck charlie

prognosis:
1. most improve or stabilize with treatment BUT
2. some progress despite treatment
3. some relapse or are infected when treatment ends
4. some improve but are never neurologically normal: unsafe/unrideable
be pateint!

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8
Q

describe viral myelo(encephal)itis

A

4 causes:
1. equine herpes virus
2. west nile viru
3. EEE/WEE/VEE
4. rabies

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9
Q

describe equine herpesvirus myeloencephalopathy

A
  1. lots of equine herpesviruses (up to 9 so far)
    -respiratory signs and abortions are more common than CNS disease
  2. only EHV1 and rarely EHV4 cause EHM
    -EHV1 has a neurovirulent form (D752)
    -75% of EHM cases are due to D752
    -25% are wild type (N752)
  3. epidemiology
    -almost all horses infected as foals
    -latent in trigeminal ganglia and lymph nodes
    -in foals: subclinical infection (enough immunity from mom) and shedding leads to spread
    in adults: shedding and clinical disease (usually respiratory)
  4. REPORTABLE
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10
Q

describe EHM pathophysiology

A
  1. respiratory epithelial infection!!
    -to lymph nodes within 24-48 hors
    -shedding for up to 3 weeks
  2. viremia: leukocytes!
    -2 weeks
  3. infection of CNS endothelial cells leads to vasculitis that leads to microthrombi and local hemorrhage that causes ischemic CNS necrosis
    -does not infect neuron!!
  4. only 10% horses in EHM outbreaks develop neuro signs due to
    -virus factors: D752 infection, viremia level
    -host factors: age (>5yrs), big breeds, females?
    -immunity: recently vaccinated horses tend to be at greater risk!
    -environment: season and geography? we don’t rly know
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11
Q

describe clinical signs of EHM (6)

A

1 variable, onset 6-10 days post exposure
2. fever first but we usually miss it (gone by time of neuro signs)
3. +/- respiratory disease (on farm)
4. ataxia (pelvic more than thoracic commonly) progressing to tetraparesis/recumbency
5. back-end signs are common
-incontinence, loss of tail/anal tone, analgesia
6. other variable CNS signs

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12
Q

describe diagnosis of EHM

A
  1. CSF:
    -increased protein
    -+/- mononuclear pleiocytosis
    -not specific for EHM! just mean neuro disease
    -xanthochromia (yellow CSF)
  2. acute and convalescent serum titers
    -too slow for real world use (books say and NAVLE might ask but don’t do it)
  3. signs + shedding/viremia
    -PCR on nasal swabs and/or buffy coat (blood)
    -usually positive at least 10-14 days after infection
    -can shed intermittently; test more than once! (need to test negative at least twice to actually call negative; give at least 12-24 hours between testing)
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13
Q

describe EHM treatment (4) and prognosis

A
  1. SUPPORTIVE CARE
  2. anti-inflammatories:
    -steroids? not for long
    -NSAIDS?
  3. anti-virals!: valacyclovir
  4. anticoagulants (doesn;t attack neuron itself, it causes microthrombi in brain or spinal cord, can slow progression by preventing clotting)

prognosis:
-better if standing and owner has money
-if recumbent, poor

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14
Q

describe EHM prrevention and management

A
  1. vaccination:
    -killed or MLV
    -NEITHER clain to prevent EHM
    -but do limit nasal shedding
    -DONT vaccinate if think exposed bc can increase risk of neuro form
  2. outbreak management
    -early diagnosis: test test test
    -teat clinical cases
    -prevent spread: isolate and quarantine, +/- vaccinate UNEXPOSED only
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15
Q

describe west nile virus

A
  1. flavivirus; not spread horse to horse, spread by mosquitoes
  2. common in summer/early fall
  3. clinical severity varies
    -subclinical to fatal encephalitis
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16
Q

describe clinical signs of WNV

A
  1. fever, depression
  2. ataxia (symmetric, asymmetric)
  3. often muscle fasciculations!! (help rule out other viruses)
  4. +/- other prosencephalon and/or cranial nerve deficits
  5. any age/sex/breed
  6. ACUTE ONSET!!
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17
Q

describe diagnostics and management and treatment of WNV

A
  1. signs, CBC, CSF; not pathognomonic
  2. IgM capture ELISA:
    -serum or CSF: 100% agreement
    -acute infection, even in vaccinated animals
  3. treatment: supportive care
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18
Q

describe prognosis and prevention of WNV

A

prognosis: 28% mortality (less fatal than herpes, even less if vaccinated); but if recumbency = bad

prevention:
1. vaccinate: several available and effective
2. boost 1st year then annually before mosquitoes
-every six months in warm climates
3. improved prognosis in vaccinated
4. try to control mosquitos but good luck charlie

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19
Q

describe equine encephalitis viruses

A
  1. alphaviruses
  2. clinical signs:
    -ataxia/recumbency + prosencephalic signs
    -young or unvaccinated, any breed or sex
    -ACUTE onset, RAPID progression
  3. diagnosis:
    –CSF often has high WBC but not alwyas
    -serology (paired?) IHC on tissue
  4. treatment: supportive
  5. prognosis: POOR
  6. prevention:
    VACCINATE
    every six months in warm climates
20
Q

describe rabies

A
  1. rhabdovirus (lysavirus)
  2. wildlife hosts
  3. signs: days to weeks to months after bite
    -furiouss versus dumb CAN LOOK LIKE ANYTHING
    -progressive an dead in 3-5 days (max 10-14)
  4. signs, bloodwork, CSF, not pathognomonic
  5. diaghosis: IFA on brain
  6. ZOONOTIC AND FATAL AND REPORTABLE
21
Q

describe meningitis

A
  1. uncommon in horses
  2. occurs in:
    -neonatal foals with bacterial sepsis: any organisms
    -0adult horses with immunodeficiencies: any organism
    -adult horses with lyme disease: borrelia bugdorferi
  3. signs:
    -fever, ataxia, NECK PAIN
    -waxing, waning multifocal signs are common
  4. diagnosis by
    -CSF tap: increased WBC (pleiocytosis) and protein, can culture
  5. treatment: antimicrobials: ensure CNS penetration
22
Q

describe discospondylitis

A
  1. UNCOMMON in horses
  2. similar to SA
  3. bacterial:
    -BRIUCELLA, strep, E. coli, fungal
  4. in adults, rule out immunodefiency, recent vaccination (could have stuck needle into disc nad infect)
  5. signs:
    -fever, ataxia, NECK pain, waxing/waning focal signs
  6. diagnosis:
    -imaging +/- sampling if accessible
    -brucellosis testing in adults
  7. treatment: LONGTERM antibiotics
23
Q

describe cervical vertebral stenotic myelopathy

A
  1. also called wobblers
  2. developmental orthopedic disease of the spine
  3. young, big, male horses
    -thoroughbred, warmblood, QH, etc.
    -but not always!
24
Q

describe etiology of CVSM

A

unsure! they outgrew their spine

  1. genetic factors:
    -no clear inheritance pattern
    -genetic predisposition
  2. dietary/environmental factors:
    -too much carbs leading to too rapid growth
    -low copper and high zinc?
  3. trauma: abnormal biomechanics?
25
Q

describe pathogenesis of CVSM

A
  1. developmental abnormalities of the cervical spine lead to spinal cord compression, resulting in neuro deficits at one or multiple sites
  2. can be overt malformation with vertebral canal stenosis OR subtle dynamic instability
26
Q

describe clinical presentation of CVSM

A
  1. ataxia: C1-C5 or C6-T2 signs
    -or both!
    -HALL MARK: often pelvic limbs are worse because the tracts to the pelvic limbs are more superficial so even slight compression causes pelvic limb signs to be worse (true with any compressive myelopathy)
  2. slowly progressive or acute onset when horse had been compensating and then does something dumb
  3. +/- signs of spinal nerve root damage
    -cervical muscle atrophy
    -cervical pain
    -cervical hypalgesia/analgesia
27
Q

describe diagnosis of CVSM

A
  1. radiographs (would want MRI but they can’t fit)
    -suggestive but not definitive
    -facet joint arthritis, collapsed discs, subluxation, narrowed canal
    -sagittal ratios can be helpful to measure canal width (should be a little more than 50% of the body)
  2. cervical myelography
    - greater than 50% reduction of DORSAL dye column is better but up to 25% false negative
28
Q

describe treatment of CVSM

A
  1. surgery:
    -fused +/- dorsal decompression
    -improvement in 44-90% of horses
    –6-12 months of work MINIMUM
    –return to athletic in 12-62% (not great)
  2. dietary restriction: paced diet
    -foals <1 year
    -stall rest
  3. euthanasia often safest/most human
29
Q

describe equine degenerative myelopathy (EDM)/equine neuroaxonal dystrophy (eNAD)

A

diffuse spinal cord degeneration
-eNAD: lesions in specific brainstem nuclei
-EDM: also lesions in cervical cord, grey and white matter (a more severe manifestation of eNAD)

30
Q

describe the pathogenesis of eNAD/EDM

A

unknown cause

genetic predisposition and oxidative damage

-possible vitamin E and/or copper
deficiency
-maybe toxins?

31
Q

describe clinical presentation of eNAD/EDM

A
  1. classic: young horse
    -but could be any age
  2. breed dispostion:
    -but also in any breed (breed might raise higher on list)
    -arab, TB, STDB, paso fino, Qh
  3. C1-C5 ataxia NO FEVER
    -abnormal stance at rest common
    -often mentation/behavior changes, subtle
  4. variable progression but usually on the slower side
32
Q

describe diagnosis and management of eNAD/EDM

A
  1. labwork, CSF, imaging not helpful
  2. serum and CSF pNfh
    -but also increased in CVSM and other neuro disease
  3. no antemortem test and no treatment
33
Q

describe P. tenuis affected species

A
  1. in sheep, goats, llama, alpacas!!
  2. also in cattle, deer, moose, rare in horses (cervical sscoliosis)
34
Q

describe pathogenesis of P. tenuis

A
  1. not a patent infection in domestic ruminants = not in poop!
  2. larvae can go anywhere in the CNS
35
Q

describe clinical presentation of P. tenuis

A
  1. any age (except neonates), sex, breed
  2. classic: asymmetric spinal cord signs
    -asymmetric ataxia
    -recumbency
  3. multifocal localization is common
  4. other sites: prosencephalon, brainstem, less common, not rare
  5. typically acute presentation: ruminants are sneaky and good at hiding more subtle previous clinical signs bc nature says show weakness = dead
36
Q

describe diagnosis, management, and prevention of P. tenuis

A

diagnosis:
1. clinical signs and being a ruminant
2. CSF:
-WBC normal or pleiocytosis
-eosinophilia in 90%
3. +MRI if you like

treatment:
1. anthelmintics that CROSS BBB
-fenbendazole 50mg/kg PO for 5 days
-+/- ivermectin for non-CNS parasitemia
2. anti-inflammatories: NSAIDs or 1-2 doses of steroids

prevention:
1. deer and slug control;
2. +/- monthly ivermectin (resistance an issue)

37
Q

describe thrombotic meningoencephalitis (TME)

A
  1. caused by histophilus somni, a gram negative pleiomorphic coccobacillus
  2. in cattle:
    -recently weaned feeder calves (6-12 months)
    -less often dairy calves
    -often co-infection with other respiratory pathogens
38
Q

describe pathogenesis of TMH (H. somni)

A
  1. commensal on bovine mucous membranes
    -pathogenic and non-pathogenic strains
    -shed in nasal secretions, inhaled, enter bloodstream where it adhere to endothelium, cause thrombi, cause ischemia/necrosis
  2. encephalitis resulting in pleural/lung lesions resulting in myocarditis
39
Q

describe diagnosis, management, and prevention of TME (H. somni)

A

diagnosis:
1. clinical signs and feedlot cattle
-fever/respiratory signs that cause ataxia that lead to recumbency and death
2. lesion culture/PCR at necropsy

treatment:
1. antimicrobials: florfenicol
2. EARLY treatment is needed but is hard- rapidly fatal

prevention:
1. vaccination! in a number of combo cattle vaccines
-variable efficacy if vx AT feedlot arrival (stressed)

40
Q

describe prion diseases

A
  1. transmissible, degenerative, fatal CNS disease in
    -sheep and goats: scrapie
    -cattle: bovine spongiform encephalopathy
    -wildlife: mink, deer/elk (chronic wasting disease)
    -camels, cats
    -people: creutzfeldt-Jakob disease
41
Q

describe pathogenesis of prion disease

A

prions are misfolded cellular prion protein (PRPc): highly conserved protein, expressed in CNS, repro, GI

unsure of function and pathogenesis

42
Q

desribe transmission of prion disease

A
  1. oral exposure to prion
    -eating an infected animal (even processed tissues in feed)
    -contact with an infected animal’s body fluids (esp repro)
    –direct or indirect via contam environment
    -housing with infected animals, mucous membrane contact?
  2. oral cavity to tonsils to GI lymphoid tissue to enteric nerves to autonomic nerves to CNS
  3. neurodegenerative but unknown mechanism
  4. INCUBATION FOR YEARS (wont be young animals)
  5. ZOONOTIC AND FATAL AND REPORTABLE
43
Q

describe clinical signs of prion disease

A
  1. adult animals
  2. progressive over months once start showing signs
  3. vary with stage and species
    -isolation followed by ataxia, pruritis/hyperesthesia, weight loss leading to emaciation, recumbency and then death
44
Q

describe bovine associated lymphoma

A
  1. BLV: bovine leukosis virus
    -oncogenic retrovirus of cattle; infects lymphocytes
    -persistent infection
    -HIGH prevalence in U.S. (almost all cows have)
  2. transmission via blood:
    -handling procedures
    -insects
  3. prevalence of viral infection increases with age
45
Q

describe clinical signs of BLV

A
  1. > 95% asymptomatic
  2. <5% develop lymphosarcoma
    -signs vary with tumor locations
    –juvenile- lymphadenopathy
    -abomasum
    -retrobulbar (behind the eye)
    -uterus
    -heart: right atrium
    -extradural spinal cord (often lumbosacral
    –ataxia, weakness, recumbency
46
Q

describe treatment and prevention of BLV

A

NO treatment

prevention: avoid exposure to blood
-requires eradication from herd, culling

if see a down in the back cow, this is high on you DDx list

NSB II (49 decks)

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