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Smith. Neurolgic DZ > Ruminant neuro > Flashcards

Ruminant neuro Flashcards

1
Q

What is the most common cause of seizures in both goats & sheep?

A

polioencephalomalacia

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2
Q

What are causes of polioencephalomalacia?

A

-excessive sulfur consumption
-altered thiamine metabolism
-salt poisoning or water deprivation
-amprolium admin
-rations of molasses & urea
-Pb intoxication

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3
Q

Thiamine deficiency in PEM is pathologic because important in what cycles?

A

rate limiting enzyme in hexose monophosphate pathway– krebs cycle

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4
Q

What examples of bacteria and plants that produce thiaminases?

A

-bacillus thiaminolyticus, costridium sporogenes

-plants: bracken fern (pteridium aquilinum), horse tail (E. arvense), Nardoo fern (marsilea drummondii)

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5
Q

What is the sulfur role in development of PEM- pathologic mechanism?

A

-INC ruminal sulfide ** overwhelm hepatic index detox capacity
-cattle inhale ruminal gas (bypass hepatic circulation)

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6
Q

PB and sulfur can cause PEM by what mechanism?

A

**impair ATP production
–affect electron transport sim to sulfide

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7
Q

What are clinical signs of subacute PEM polioencephalomalacia?

A

symmetric
-blind
walk with head held erect
slight hyeprmetric gait

progresses to bilat cortical blindness
head pressing
opisthotonos
bilat
dorsomed strabismus
miosis
repetitve chewing
profuse pytalism
defective menace response
variable nystagumus
INC HR, RR

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8
Q

what are clinical signs of acute form of PEM polioencephalomalacia?

A

recumbent
comatose
episodic tonic-clonic convulsions
-recumbent & hypertonic between seizures

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9
Q

What are ddx for PEM polioencephalomalacia?

A

lactic acidosis
carbohydrate engorgement
ruminal tympany
enterotoxemia
salt poisoning/water deprivation
head trauma
bact meningoencephalitis
coccidoiosis w/ NS invovlement
vit A def
ethylene glycol poisoning
locoism
rabies
IBR encephalitis

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10
Q

What does CSF for PEM polioencephalomalacia look like?

A

mild pleocytosis: 5 to 50 WBCs with voaculoation
INC protein concen: >50 mg/dL

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11
Q

what is the treatment of polioencephalomalacia PEM?

A

thiamine
dexamethasone
mannitol
amtimicrobial admin
control convulsions: phenobarb, pentobarb, diazepam

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12
Q

ruminants with PEM secondary to molasses-urea diet don’t respond to what treatmetn?

A

–thiamine administration
** respond to glucose or oral glucose precursor

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13
Q

What are preventative measures to be taken for polioencephalomalacia?

A

-allow appropriate time to adjust to high concen. rations
-feedstuff analysis routinely: ID source too high in sulfur, remove high sulfur hay, ammonium sulfate, molasses
-thiamine supplementation
-brewers yeast
-gypsium
-cobalt

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14
Q

Water intoxication occurs when?

A

concurrent with period of restricted access to water followed by unrestricted access to water

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15
Q

Water intoxication pathogenesis

A

disease occurs once water enters extracellular fluid and moves to brain tissue

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16
Q

What are feedstuffs that are common sources of excess NaCL?

A

whey
saline preserved fish or fish meals
bakery by-products
-milk replacers or oral electroltye solutoins
-brine (flush during teh drilling of oil wells)

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17
Q

Acute salt intoxication occurs when

A

ignestion of large quantity of NaCl

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18
Q

chronic salt intoxication occurs when

A

long periods with decreased water consumption with low-mod salt intake

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19
Q

What is the pathogenesis of hyeprnatremia?

A

imbalance in sodium & water regulation
– INC in sodium plasma concentration
- causes movement of intracellular water into ECF= cellular dehydration

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20
Q

With chronic hypernatremia, when are clinical signs seen?

A

with osmotic adpatation in brain– no C/S seen until treatment with rapidly dec plasma concentraiton Na IVF
or drinking lg quantities of water

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21
Q

When are gastrointestinal signs seen with salt toxicity?

A

-large quantities of salt ingested over short time period
– intestinal lumen hyperosmolarity
(saline catharsis, osmotic diarrhea)

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22
Q

What C/S are seen with salt intoxication?

A

GI and neuro signs
– Stargazing, constant chewing movement, coma, dec milk production, blindness, aggressiveness, hyperexcitability, psychomotor seizures nystagmus vocalization

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23
Q

with salt intoxication, what is seen on serum and CSF?

A

serum/CSF concen: >160 mEq/L
>1:1 CSF: serum ratio
OR
brain NA concen >150 mEq/g or 1800ppm

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24
Q

What is seeing on necropsy with salt intoxication?

A

cerebral edema
softening & flattening of cortical gyri
microscopic lesions: laminar cortical necrosis, poliomalacia, +/- mengineal or perivascular infiltration of eos or monos

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25
Q

Ruminants have a tendency to lick or chew objects that lead to lead poisoning. What are potential sources of Pb?

A

PB arsenate defoliants
PB acid batteries
used motor oils
linoleum
roofing felt
paint
machinery grease
caulking compounds
improperly compounded mineral supplements
foliage- near smelters & battery recycling plants

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26
Q

What are factors that increase likelihood of ingestion?

A

lack of alternative feedstuffs
hunger
phosphorus deficiency

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27
Q

Lead toxicity influenced by what dietary factors?

A

calves on milk– INC correlation with Vit D and enhanced Pb absorption
Copper-pastures fertilized with pig slurry, potentiate accumulation of lead

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28
Q

What are the toxic effects of lead?

A

-inhibition of free sulfhydryl groups in many enzymes
-interference with zinc containing metalloproteins
-steric inhibition of enzyme activity
-enzymes of heme synthesis susceptible to injury– shortens RBC half-life

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29
Q

What are C/S of lead toxicity?

A

-hyperesthesia, muscular fasciculations, rapid fast twitching eyelids/facial mm
-progression: ataxia, CP deficits, cortical blindness, head pressing, ondotprisis, coma, convulsions, bellowing death
-GI signs: bloat, diarrhea, rumen atony, colic
-infertility
-abortions
-fetal malformations

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30
Q

What is the preferred diagnosis of lead toxicosis?

A

blood concen: free RBC porphyrins and RBC concen delta-aminolevulinic acid

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31
Q

When collecting blood for diagnosis of pb levels, what tube should you use?

A

heparin to collect blood b/c does not chelate blood

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32
Q

What can be administered intravenously to in low lead tox poisoning levels?

A

EDTA– solubilizes the bone lead stores adn INC the concen in plasma then excreted in urine

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33
Q

What is seen on radiographs in young animals chronically exposed to lead?

A

“lead lines”–radiopaque transverse bands & metaphyses of long bones

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34
Q

Why is anhydrous ammonia added to poor quality feed?

A

-improves nutrtional density
-dec certain fungal toxic metbaolites
-inc DML
-enhances digestibility
-inc protein value

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35
Q

Cause of cow bonkers

A

overammoniation >3% forage DMI

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36
Q

with lead toxicity, what is the effect on calves

A

toxin concentration in milk– calves show C/S

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37
Q

What C/S are seen with ammoniated forage tox/Cow bonkers?

A

hyperasthetic
ataxia
sawhorse stance- at rest
vocalization
dysphonia
walking/running into objects
when excited: hyperactive, blind (appear), circle propulsively

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38
Q

What is the toxic principle of cow bonkers?

A

diakylimdazoles
r-methylimidazole

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39
Q

ammoniated forage toxicosis/ bovine bonkers is seen at what level?

A

ammoniated >3% of forage on dry matter basis

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40
Q

When are clinical signs of ammoniated forage toxicosis/bovine bonkers worse?

A

worsen with hyperexcitability

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41
Q

Listeriosis can manifest as what forms of disease?

A

neonate septicemia
abortion
neonatal death
ophthalmitis
uveitis
diarrhea
neuro disease

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42
Q

What kind of neurologic disease does listeriosis cause?

A

multifocal brainstem
Diffuse meningoencephalitis

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43
Q

What are possible sources of listeriosis?

A

carrier animals
rottingvegetation pastures
feed bunks

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44
Q

Which species has a higher case fatality rate due to listeriosis than cattle?

A

sheep & goats

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45
Q

What are common sources of contamination with listeriosis?

A

-decaying forage at bottom of feed bunk
-spoiled silage at end of trench silo
-rotting hay at periphery of hay stack

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46
Q

What toxin does listeria monocytogenes produce and what is its MOA?

A

listeriolysin- O- hemolysin

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47
Q

What C/S are seen in listeriosis?

A

asymmetric
-CP deficits
-head pressing
-CN deficits: V-XII

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48
Q

Ocular disease due to listeriosis manifesting as keratitis, conjunctivitis, uveitis manifests in what species?

A

cattle and horses (w/o neuro signs)

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49
Q

Cattle with listeriosis develop metabolic acidosis due to?

A

salivary bicarb losses d/t CN deficits

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50
Q

How is ovine progressive pneumonia (OPP) virus spread?

A

-ingestion of infected colostrum and milk
respiratory transmission
fecal contamination of drinking water
fomite

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51
Q

How is ovine progressive pneumonia (OPP) synergistic with what neoplasm?

A

Adenocarcinoma

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52
Q

What allows for OPP lentivirus to escape elimination by host immune response?

A

mutation of the gene encoding for envelope glycoproteins

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53
Q

ovine progressive pneumonia (OPP) infection establishes in what cell lineage?

A

monocyte or macrophage cell lines

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54
Q

ovine progressive pneumonia (OPP) multi-systemic diseases of adult sheep are characterized by:

A

-chronic progressive, debilitating pneumonia; respiratory failure
-aseptic indurative mastitis (“hard bag”)
-wasting progressive emaciation despite good appetite (“thin ewe syndrome”)
-chronic non-suppurative arthritis

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55
Q

What neurologic deficits are seen with ovine progressive pneumonia (OPP)?

A

weight loss
posterior paresis
hindlimb ataxia
stumbling
proprioceptive deficits
progressing ot paralysis & quadriplegia
**may localize to spinal cord

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56
Q

ovine progressive pneumonia (OPP) diagnosis

A

serology: AGID, ELISA, western blot
**presence of antibodies in serum= evidence of active infection

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57
Q

For testing and culling program for ovine progressive pneumonia (OPP), how often should testing be performed?

A

annual testing should be performed until two consecutive negative test results are obtained to be reasonably confident that the flock is virus free

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58
Q

Caprine arthritis encephalitis virus (CAEV) chronic infection is characterized by

A

demyelinating encephalomyelitis
arthritis
interstitial pneumonia

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59
Q

What are tissues of importance for Caprine arthritis encephalitis virus (CAEV) localization

A

synovium
mammary gland
central nervous system

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60
Q

What is the most common form of Caprine arthritis encephalitis virus (CAEV)?

A

debilitating polysynovitis-arthritis form
**as young as 6 months, but more frequently in mature goats

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61
Q

Caprine arthritis encephalitis virus (CAEV): leukoencaphlomyelitis form is predominately seen in which age

A

predominantly less than 2 year of age (2 -6 months of age especially)

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62
Q

What are differentials for Caprine arthritis encephalitis virus (CAEV) leukoencphalomyelitis form

A

head or spinal trauma
listeriosis
cerebrospinal nedmatodiasis (parelaphostrongylus tenuis)
multisystemic infection with mycoplasma spp

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63
Q

How to ddx Caprine arthritis encephalitis virus (CAEV) from listeriosis?

A

CAEV multifocal CNS lesions
Listeriosis generally restricted to brain stem

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64
Q

Caprine arthritis encephalitis virus (CAEV) differentiating from mycoplasmal infections

A

mycoplasmal infections typically affect kids from 1 to 6 months of age, affected animals are systemically ill and often display septic polyarthritis and polyserositis

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65
Q

how to differentiate Caprine arthritis encephalitis virus (CAEV) from verminous meningoencephalomyelitis?

A

serologic or PCR testing for the virus
CSF analysis
season
geogrpahic disturbtion of white-tailed deer host

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66
Q

What are ddx for Caprine arthritis encephalitis virus (CAEV) chronic interstitial pneumonia form?

A

lung worms, pulmonary abscessation and chronic bronchopneumonia

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67
Q

What is the diagnostic for Caprine arthritis encephalitis virus (CAEV)?

A

ELISA– whole virus, core or enveloped proteins
PCR- milk, tissue blood

AGID– older test, but still official USDA test

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68
Q

Caprine arthritis encephalitis virus (CAEV)L: CSF tap

A

TNCC: 5-1800/uL; predom mononuclear
INC protein: 0-700 mg/dL, and pleocytosis

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69
Q

Caprine arthritis encephalitis virus (CAEV): arthrocentesis

A

brown to red-tinged
inc tnccc, predom mononuclear
dec protein

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70
Q

Which herpesvirus types are seen to cause encephalitis in cattle?

A

BOHV-1 and 5

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71
Q

BOHV-1 typically causes what?

A

infectious bovine rhinotracheitis– fibrinonecrotic plaques upper airway and abortions, epizootic conjunctivitis, infectious balanoposthitis or vulvovaginitis

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72
Q

where does persistently infected with bovine herpesvirus survive?

A

in nasal and tracheal mucosa
trigeminal ganglion

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73
Q

brain involvement seen with bovine herpesvirus is due to

A

centripetal spread along sensory neurons of trigeminal and olfactory nerves

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74
Q

BOHV encephalitis causes a nonsuppurative meningoencephalitis widely distributed in:

A

grey matter of brain
** primarily cerebrum and thalamus

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75
Q

What C/S are seen with BOHV encephalitis?

A

**resp signs proceed or concurrent with neuro C/S
depression
head pressing
aimless circling
paralysis fo tongue
head tilt
nystagmus
convulsions
blindness
coma
death seizures

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76
Q

CSF analysis with BOHV encephalitis

A

mononuclear pleocytosis

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77
Q

ovine encephalomyelitis– louping ill epidemiology

A

ssRNA virus
neurotropic
Flavivrus

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78
Q

How is ovine encephalomyelitis– louping ill transmitted?

A

Ixodes ricrumus, I. persulacatus
Rhipacephalus appendiculatus
fomites (blood contaminated)
blood products

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79
Q

ovine encephalomyelitis– louping ill amplication occurs in what species?

A

wild animals and red grouse (ingesting tick), hare– improtant virus source

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80
Q

ovine encephalomyelitis– louping ill concomittent infection with what increases viremia and mortality

A

anaplasma phagocytophilum

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81
Q

What C/S are seen with ovine encephalomyelitis– louping ill?

A

ataxia, CP deficits, head tremors, hypometria (**characteristic bunny hopping gait), hyperexcitability

**progression to head pressing, recumbency, convulsions, coma, death

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82
Q

Diagnosis of ovine encephalomyelitis– louping ill

A

hemagglutination inhibition
complement fixation
**peak viremia at 7 days
**usu not viremia at time of CNS

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83
Q

What is the cause of hairy shaker lambs?

A

border disease virus
– pestivirus, noncytpathic togavirus

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84
Q

What is the major reservoir for border disease virus?

A

congenitally infected
seronegative animals with no symptoms
–> placenta, infected offspring, saliva, resp secretions, urine & feces

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85
Q

hypomyelination caused by ovine encephalomyelitis– louping ill

A

dyspmelinogenesis: virus induced degenr. of oligodroglial cells

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86
Q

ovine encephalomyelitis– louping ill viral immunosuppression is due to

A

depressed blastogenic activity of lymphs
– dec T helper cell function
– INC T suppressor cell function

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87
Q

ovine encephalomyelitis– louping ill cause of immunosuppression leads to death via

A

parasitism
diarrhea
bronchopneumonia

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88
Q

The worst clinical signs of ovine encephalomyelitis– louping ill are seen in which age lambs?

A

lambs infected in early gestation (<50 days)

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89
Q

ovine encephalomyelitis– louping ill: affected lambs show what C/S

A

short thickened body
shortened legs
smaller orbital size
doming fronta bone
+/- arthrogyropsis
+/- neuro signs

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90
Q

teratogenic effect of ovine encephalomyelitis– louping ill is seen at what days of gestation

A

50 to 90 days

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91
Q

ovine encephalomyelitis– louping ill causes what clinical signs in goats??

A

during pregnancy– fetal mummification and abortion

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92
Q

cattle co-mingling with sheep can contract what disease and develop what clinical signs?

A

ovine encephalomyelitis– louping ill
** abortions in cattle at 50 days gestation

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93
Q

What are differentials for ovine encephalomyelitis– louping ill?

A

other causes of infectious abortion
copper def (sway back)
hydrancephaly: cache valley, blue tongue, schmallenberg virus

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94
Q

Bovine spongiform encephalopathy (“Mad Cow”) disease cause

A

accumulation abnormal prion protein in CNS leading to progressive neuro disease
**altered conformation PrP-BSE

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95
Q

How Bovine spongiform encephalopathy (“Mad Cow”) spread?

A

foodborne disease of cattle
–assoc with ingestoin of meat & bone meal contam with BSE prion

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96
Q

typical Bovine spongiform encephalopathy (“Mad Cow”) is seen in what age cattle?

A

4 to 6 year old

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97
Q

Bovine spongiform encephalopathy (“Mad Cow”) is diagnosed with the startle reaction test with what clinical signs

A

hand test (punching towards animals head)/flash light/ hand clap/ loud “metallic” bang

–> BSE cattle do not habituate to startling

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98
Q

What are C/S seen with Bovine spongiform encephalopathy (“Mad Cow”)

A

inc head rubbing/head tossing
mm fasciculations
excessive vocalization
tremors/ataxia
licking of nostrils
yawning
flehman response
head butting
restlessness

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99
Q

How is Bovine spongiform encephalopathy (“Mad Cow”) diagnosed?

A

PM exam only
rapid prion tests: western blot, paraffin imbedded tissue blot, ELISA
HISTOPATH:t issue of choice: medulla obex
–>intraneuronal vacuolation in sp brain areas accompanied/ preceded by accumulation of Prp-BSE

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100
Q

What are differentials for Bovine spongiform encephalopathy (“Mad Cow”)?

A

viral encephalopathies: pseudorabies/rabies, bronaencephalitis, bovine immunodef virus encephalitis
-listeriosis
-polioencephalomalacia
-lead poisoning
-CNS parasitic migration
-brain tumors/abscesses
-vit A deficiency

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101
Q

Suspected cases of Bovine spongiform encephalopathy (“Mad Cow”) should be disposed of by which methods?

A

alkaline hydrolysis tissue digester

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102
Q

Bovine spongiform encephalopathy (“Mad Cow”) is linked to what human disease?

A

Creutzfeldt Jakob Disease

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103
Q

What is the prion disease of sheep called?

A

Scrapie

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104
Q

When does most scrapie transmission occur?

A

during breeding season
-placentas
-birth fluids

**most likely oral transmission

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105
Q

What are clinical signs of scrapie?

A

ocular lesions
aural hematoms
scratch reflex
bruxism
pytalism
apathy
hypermetria
tremors
ataxia

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106
Q

What are differentials for scrapie?

A

pseudorabies
rabies
borna encephalitis
listeriosis
PEM
Lead poisoning
CSF nematodiasis
bran tumors/abscess
maedivisni
vit A def
metabolic imbalances

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107
Q

What are differentials for pruritis seen?

A

psorptic & sarcoptic mange
ringworm
myiasis
pediculosis
atopy

108
Q

US is free of pseudorabies in the domestic swine, where is pseudorabies present?

A

in feral pigs in the US

109
Q

What is the pathogenesis for pseudorabies?

A

virus spreads centripetally in CBS by axonoplasmic transport–> acute infection: nasal mucosa, secretions and saliva

110
Q

What are the clinical signs of pseudorabies/Aujezkys disease?

A

initial: acute to severe pruritus–alopecia, self-trauma
other signs: twitching, chewing of tongue, ataxia, circling, bloat, nystagmus, strabismus, etc
progression of C/S: hyerpesthesia, continuous mastication, vocalization, coma, opsithotonos, tenesmus, excessive nostril licking, fatal/death

111
Q

what are differentials for pseudorabies/Aujezkys disease?

A

rabies
PEM
salt poisoning
meningitis
Pb poisoning
hypomagnesemia
enerotxemia

112
Q

Where are good places for sampling for testing for pseudorabies/Aujezkys disease?

A

pharyngeal /nasal swabs– cultured from ifnected nervous tissue
-ag distinct from other herpesviruses
-virus culture: sensory ganglia, dorsal horn of sc
-segments serving pruritic areas= highest concen of virus

113
Q

What is pathologic changes are seen indicating pseudorabies/Aujezkys disease on histopathology?

A

eosinophilic intranuclear inclusion bodies
**most pronounced in dorsal nerve rootlets and dorsal horn
-nonsuppurative encephalitis
-neuronal degen.

114
Q

Sporadic bovine encephalitis is caused by what organism?

A

chlamydophila pecorum bioptype 2

115
Q

chlamydophila pecorum bioptype 2 is shed in

A

urine
feces
nasal secretions
milk

116
Q

How is chlamydophila pecorum bioptype 2/sporadic bovine encephalitis transmitted?

A

unknown

117
Q

chlamydophila pecorum bioptype 2/sporadic bovine encephalitis resembles what disease?

A

hardware disease– fibrinous pleuritis/peritonitis– grunt/groan when pressure applied to xiphoid

118
Q

chlamydophila pecorum bioptype 2/sporadic bovine encephalitis what clinical signs are seen?

A

Resp dz: nasal d/c, cough, dyspnea
Polyarthritis/tenosynovitis
meningoencephalitis: ataxia, CP deficits, circling, head tilt, opisthotonos, hyperesthesia, stiff neck, convulsions, coma

119
Q

What diagnostic is highly suggestive of chlamydophila pecorum bioptype 2/sporadic bovine encephalitis?

A

pelural/peritoneal effusion: detection of reticulate bodies
*highly suggestive
PCR/serology

120
Q

What are the most common bacterial isolates from pituitary abscesses?

A

Trueperella pyogenes
corynebacterium pseudotuberculosis

121
Q

What C/S are seen with chlamydophila pecorum bioptype 2/sporadic bovine encephalitis?

A

asymmetric neurologic deficits:
dysphagia
blindness
anisocria
absent PLR
mydriasis
flaccid tongue
facial n paralysis
facial hypalgesia
ventrolat strabismus
head tilt

122
Q

What is that pathologic mechanism that leads to pituitary abscess formatoin?

A

entry via sella turcica hematogenously
–> localizes int eh rete mirable (complex of bv encircling pituitary gland

123
Q

Why is ataxia seen with pituitary abscess?

A

interruption of extrapyramidal motor nuclei in brainstem

124
Q

Why is exophthalmos seen with pituitary abscess?

A

expanding abscess into retroorbital rete

125
Q

Why is the clinical signs of loss of cranial nerve function with pituitary abscess?

A

extradural extension of abscess

126
Q

Why is the clinical signs of bradycardia seen with pituitary abscess?

A

interference with diencephalic cardioaccelatory centers

127
Q

Pituitary abscess formation is commonly seen in bulls that have what?

A

that receive rings and become infected
-why recommend prophylactic admin penicillin
-using aseptic procedure

128
Q

What is the most common organism involved in brain abscesses in horses?

A

strep equi

129
Q

What is the most common organism involved in brain abscesses in cattle?

A

T. pyogenes– extension of sinus infection through calvaria
bacteroides

130
Q

Brain abscesses are difficult to differentiate from what other CNS disorder?

A

septic meningitis

131
Q

Nervous coccidiosis presents with clinical signs similar to what other disease?

A

PEM
ehtylene glycol poisoning
Lead poisoning
clostridial enterotoxemia

132
Q

When is nervous coccidiosis seen?

A

large burden of coccidia oocysts– range 4000 to 4 million/gram feces

133
Q

What is recommended prevention of nervous coccidiosis?

A

ionophores in feed

134
Q

What is the pathogenesis in ruminants with sarcocystis infection?

A

Ruminant ingest sporocysts
– sporocysts hatch in proximal small bowel
– penetrate medium sized mesenteric arterioles
– enter endothelial cells and form sporozoites mature in 3 stages
– total development require 10 weeks, dz at 9-11 wks after infection when sarcocysts encyst in muscle

135
Q

what is the definitive host of sarcocystis?

A

dogs, cats, primates

136
Q

What is the best prevention of sarcocystis infection in cattle?

A

**protect the food supply of ruminants
-prevent savenging of carcasses: deep burial, incineration
-keep feed bunks raised off ground
-prophylactic feeding of monensin
-elimination of predatory/scavenging carnivores

137
Q

When does neospora caninum cause abortion?

A

predom midterm to late-term abortion (3-8 months gestation)

138
Q

Typically fetuses are aborted with infection of neospora caninum, what occurs if the calf is born?

A

Neuro signs: C/S mild at birth then worsen
–unable to stand/suckle
-abnormal spinal refelxes
flexural limb deformities, domed skull, torticullus

139
Q

Babesia is transmitted to cattle via

A

cattle to cattle via
Rhipocephalus (Boophilius) annulatus, microphus, or decloratus spp

140
Q

Babesia causes what forms of diseases?

A

intravascular and extravascular hemolysis
kidney and liver failure
neuro dzes

141
Q

What neurologic signs are seen with babesia infection?

A

Sudden CNS signs: fever, anorexia, depression, ataxia, CP deficits, mania, convulsions, coma +/- sudden death

142
Q

What are causes of babesia encephalitis?

A

capillary thrombosis and infarction
DIC
anoxic encephalopathy
direct invasion of parasite into CNS

143
Q

Heartwater disease is caused by what organism?

A

Ehrlichia ruminantum
**reportable disease in US

144
Q

What is the organism that causes sleeping sickness in cattle?

A

Trypanosoma vivax, congolense, brucei

145
Q

how is trypanosoma spp spread?

A

tsetse fly (glossina spp)

146
Q

Vitamin A deficiency is typically seen in what cattle?

A

feedlots, with growing animals

147
Q

What are diets that are low in vitamin A:

A

cereal grains
beet pulp
cottonseed hulls
sorghum
brewers grain
wheat straw

148
Q

Why are livestock protected from vitamin A deficiency?

A

store Vit A in liver

149
Q

What develops after liver, vitamin A stores are depleted in cattle?

A

adults grow normally
–> pailledema, blindness

150
Q

Primary Vitamin A deficiencies are seen in what livestock?

A

cattle confined to dry lots
pastured on dry grass forage for long periods
fed indoors, unsupplemented
vitamin depleted cereals (dec carotene activity in feed)

151
Q

The destruction of carotene occurs due to what reasons? leading to vitamin A def

A

heat
sunlight
trace mineral supplements
humidity
pelleting
exposure to rancid feed

152
Q

How does secondary vitamin A deficiency occur?

A

interference with absorption
– interference with conversion beta-carotene in SI
–> vitamin A (retinol)

153
Q

What are conditions that require increased intake of vitamin A, in face of decreased intake?

A

fever
lactation
high ambient temperature
inadequate dietary energy

154
Q

Vitamin A is responsible for what in teh retina?

A

rhodopsin

155
Q

Vitamin is responsible in normal function of what cells/tissues

A

osteoclasts/blasts
epithelial tissues
choroid plexus
repro. tissues

156
Q

What are causes of blindness associated with vitamin A deficiency?

A
  1. Nyctalopia (night blinness)– dec vit A aldehyde in regeneration of visual pigment rhodopsin– usu reversible
  2. Degenerative changes in outer retina layer– reversible if txed early
  3. stenosis of optic formen–» compression of optic nerve– irreversible
157
Q

Papilledema, seen with vitamin A deficiency is due to what pathogenesis?

A

due to INC CSF pressure–> INC pressure in optic nerve–> papilledema (swelling of optic disc)

158
Q

What are defects seen in calves born to cattle that are vitamin A deficient?

A

blind
domed foreheads
thickened carpal bones
weak at birth

159
Q

What are optic changes seen with Vitamin A deficiency?

A

pupils dilated & unresponsive
papilledema
optic disk– pale, indistinct borders (inverted heart appearance), swollen disk may cast shadow on adjacent retina)

160
Q

How to differentiate between Vitamin A deficiency from PEM?

A

vit A: no PLR (retina degen, constriction CN 2 @ optic forament)

PB & PEM: intact PLR (normal mesencephalon & optic nerve)

161
Q

What can be performed to diagnose Vitamin A deficiency?

A

assay vit A & beta carotene plasma concentration & feed concentrations

162
Q

treatment of vitamin A deficiency causing acute encephalopathy, simple pappiledema

A

vitamin supplementation (440 IU/kg parenterally, then 6000 IU/kg every 50 yo 60 days
OR
dietary supplementation: leafy, fresh cured hay, green pasture, alfalfa meal
OR
commercial feeds

163
Q

Helichrysum argyrophyllum poisoning Everlasting, Vaal sewejaartjie toxic plant poisoning can cause what clinical signs?

A

blindness/variety of CNS signs
-progressive tetraparesis
-depression
-nystagmus
-mydriasis
-intention head tremor
-stargazing
-older sheep-lens cataracts

164
Q

Helichrysum argyrophyllum poisoning Everlasting, Vaal sewejaartjie toix plant poisoning
–is toxic only in what stage?

A

in flowering stage

165
Q

Helichrysum argyrophyllum poisoning Everlasting, Vaal sewejaartjie toix plant poisoning,
pathogenesis leading to neurologic signs?

A

binds GABA–benzodiazepine receptor

166
Q

What is the toxic principle for flatpea poisoning (lathyrus sylvestris & L collis)?

A

2,4 diaminobutyric acid
– inhibits ornithine transcabamylase– enzyme responsible for urea detoxification

167
Q

latpea poisoning (lathyrus sylvestris & L collis) manifests within how many days of ingestion?

A

within 5 days of consumption

168
Q

latpea poisoning (lathyrus sylvestris & L collis) neurologic signs

A

depression, mm tremors, spasmodic torticollis, recumbency, reluctance to rise
when stim to move: circling, head pressing, odontoprisis

**culminates fatally in seizure

169
Q

Nitrofurazone toxicity is an antimicrobial prohibited use in the US, because it causes neurologic signs through what mechanism?

A

inhibits enzymes of oxidative glycolytic pathways
–> interfere with brain metab. of carbs

170
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) life cycle?

A

adults worms in GIT of dogs/wild carinovres–> shed eggs in feces
–> ruminants ingest on infecte dpastures
–> eggs hatch in SI of ruminant
–>larva travel thorugh blood ot CNS–mature to coenurus cerebralis

**ruminant dies & brain tissue eaten by carnivore

171
Q

Coenursisis or sheep GID is caused by what organism?

A

Taenia multiceps

172
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) occurs in sheep after what epxosure?

A

after 2 weeks of exposure

173
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) pathogenic mechanisms?

A
  1. encephalitis- invasion of CNS from large numbers of larvae
  2. hypertesnive hydrocephalus– interference cNS drainage
  3. large cerebral cysts– INC ICP
174
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) C/s in sheep are dependent on what form develops

A

migratory phase: lambs 6 to 8 weeks: fever, dullness, mild neuro deficits

acute encephalitis– sudden onset of severe neuro signs + death w/in few days

space occupying mass: depression, ataxia, head tild, circling, high estepping forelimb gait, unitl/aymm loss of vision

175
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) treatment

A

praziquantel– tx sheep with neuro signs
NSAID/dex– INC surivval psottreatment
remova cysfs via craniotomy
endemic reas; not feed carcasses to dogs, tx dogs
**appro. mgmt has eliminated dz in N america

176
Q

Coenursisis (sheep GID, coenurus cerebralis infestation, taenia multiceps infestation) diagnosis

A

presumptive dx
rads +/- radiolucent areas in calvaria ((postanerior projection
CT- demonstrate presence of cysts

177
Q

What is the cause of lysosomal storage disease?

A

ceroid lipofuscinosis, an inherited autosomal recessieve disease

178
Q

lysosomal storage disease is reported in what species?

A

SOuth Hampshire
Swedish landrace
Rambouillet sheep
Nubian goats
Devon cattle
horses

179
Q

Ceroid lipofuscinosis is characterized by:

A

intracellular accumulation of abnormal autoflourescent lipopigments in lysosomes of neurons and other cells throughout body
–predom subunit C of mictochondiral synthase

180
Q

Ceroid lipofuscinosis C/S

A

progressive ataxia
postural abnormalities
blindness d/t retinal involvement
sensory depression
terminal stages: coma

181
Q

Ceroid lipofuscinosis CT abnormalities

A

enlargement of lateral ventricles, dec thickness of cerebral cortex

182
Q

ceroid lipofuscinosis treatment?

A

no rpactical method of treatment available

183
Q

What are infectious causes of hydrancephaly?

A

Akabane virus
aino virus
Chuzan virus
Cache Valley virus
Bluetongue virus
BVDV
Schmallenberg virus

184
Q

What serotypes of bluetongue virus infection are most commonly seen in neonatal calves & lambs in epizootics?

A

serotypes 11 & 17

185
Q

Blue tongue virus is spread by what vector?

A

culicodies spp in spring

186
Q

Blue tongue virus is a cause of hydranencephaly is manifested in calves, lambs, kids as what C/S

A

arthrogryposis
brachygnathia
prognathia
excessive gingival tissue

187
Q

Hydrocephalus can be classified into what two categories?

A
  1. normotensive
  2. hypertensive
188
Q

Normotensive hydrocephalus is caused by?

A

failure of cell growth or cellular necrosis
–> loss of fetal neurons inutero

189
Q

Hypertensive hydrocephalus is caused by?

A

INC in CSF vol results in compressive or obstructive lesions in ventricular sys or from dec CSF absorption

190
Q

Obstructive lesions leading to hypertensive hydrocephlus can be caused by congenital or acquired differentials, what is the pathogenesis?

A

trap CSF in ventricles causing inc in CSF vol & pressure–> results in ischemia and CNS degeneration

–> sites of obstruction often: lateral apertures, mesencephalic aqueduct, lateral ventricles, interventricular foramina & 4th ventricle

191
Q

What are causes of acquired hypertensive hydrocephalus?

A

cerebral abscess
cholesteatoma (equines)
EIA
Coenurus cerealis infestation
meningitis
lymphosarcoma
acute inflamm dz: meningities & Vita deficiency

192
Q

What are causes of congenital hypertensive hydrocephalus?

A

hereditary condition in: hereford, charlais, ayrshire, dexter, holstein & Jersey calves
Arabian foals

193
Q

What is the most common congenital brain disease of foals?

A

hydrocephalus

194
Q

Describe dandy walker like syndrome in foals?

A

recurrent violent seizures in foal– agenesis of corpus collosum with cerebellar vermain hypopolasia

195
Q

What clinical signs are seen with hydrocephalus?

A

-skull doming– sign of prematurity/dysmaturity
-slow & somnolent
-cerebral signs: head pressing, aimless & compulsive walking, blindness, seizure activity

196
Q

What is a potential neurologic complication of upper/lower respiratory infection in ruminants?

A

otitis media/interna

bacteria: Mannhemia, hemolytica, pasterurella multocida, C. pseudotuberculosis, H. somni, mycoplasma spp

197
Q

What is the organism that is responsible for the cluster outbreaks on diary farms of otitis media/ interna of ruminants?

A

Mycoplasma spp

**contaminated milk is an important source for young

198
Q

Subclinical otitis is seen in what animals?

A

feedlot reared

199
Q

CNS signs from otitis media/interna in ruminants is caused by what?

A

damage of peripheral vestibular apparatus or extension into the CNS (rare)

200
Q

Neurologic signs seen with otitis media/interna

A

unilateral vestibular disease– more common than bilateral
– head tilt– toward side of the lesion
–continuous horizontal nystagmus– fast away from teh lesion
– imbalance– tendency to stumble, fall or walk toward the side of the lesion

recumbent– lie on side of lesion
ipsilateral facial nerve dysfunction– ptosis, dropped ear, flaccid lips & nostrils

201
Q

What are clinical signs that distinguish peripheral vs central vestibular disease?

A

peripheral: appetant, alert, aware of surroundings, no significant postural deficits, nystagmus constantly horizontal

central: depressed, nystagus varies in direction, mkd CP deficits

202
Q

WhaWhat are antibiotics used in the treatment of otitis media/interna?

A

PPG
mycoplasma– tetracycline, florfenicol, macrolides

**prolonged tx: 3 to 6 weeks, relapses occur

203
Q

What are things to consider if treatment of otitis media/interna does not respond to antimicrobials?

A

-osteomyelitis of petrous temporal bone
-abscess formation in tympanic bulla
-noninfectious cause (ie. neoplasia)

204
Q

What are ear mite species that infest cattle?

A

Rallieta auris

205
Q

What are ear mite species that infest small ruminants?

A

Psoroptes cuniculi

206
Q

Severe ear mite infestations can lead to:

A

perforation of typmanum– vestibular disease, facial paralysis, ataxia

207
Q

What is the ear mite life cycle/how are cattle infected?

A

protonymph, deutonymph (free living life stages)– molt on vegetation and reinfest cattle when grazing/evening bedding

208
Q

What are potential preventative measures/treatment for ear mites (herd level)?

A

till pasture every 14 to 21 days with insecticide (consider for eradication)

209
Q

Describe histophilus somni bacteria

A

pleomorphic
nonencapsulated
gram negative

210
Q

What is the causative organism for thromoboembolic meningoencephalitis?

A

Histophilus somni

211
Q

thromoboembolic meningoencephalitis is a neurologic disease of cattle extending from what?

A

septicemia:
-polenuronpuemonia
-myocarditis
-laryngeal bascess
-polyarthritis
-polyserositis
-infections of ear, eye, udder & urogenital tract

212
Q

thromoboembolic meningoencephalitis is most commonly seen in what cattle?

A

feed lot cattle, less than1 year old

213
Q

H. somni virulence factors that induce apoptosis of enodthelial cells leading to microthrombus formation, what organs are commonly affected?

A

brain stem
spinal cord
synovium
pleura
lungs

214
Q

What neurologic signs are seen with thromoboembolic meningoencephalitis?

A

Cp deficits: knuckling, circumduction, crossing over, interference

Cerebellum & caudal brain stem signs: head tilt, nystagmus, strabismus, blindness, muscular tremors, opisthotonos, coma, convulsions

**death with 36 hours of onset of C/S
**other organ sys typically involved

215
Q

What is seen on CSF analysis with thromoboembolic meningoencephalitis?

A

hemorrahge: high erythrocyte counts, xanthochromia, INC protein concen (>100 mg/dL)
neutrophils: >500 WBCs/uL

216
Q

thromoboembolic meningoencephalitis for post mortem exam, what are hte best tissues with highest concentration of H. somni?

A

kidneys and brain

217
Q

What are ocular lesions caused by histophilus somni?

A

conjunctivitis
multifocal retinal hemorrahges
retinal edema w/ retinal detachment
– primarily seen in fundus
– swollen axos in nerve fiber layer of retina (EOS. cytoid bodies)

218
Q

What are antibiotics used in the treatmnet of histophilus somni?

A

tetracyclines
penicillin
aminoglycosides
ampicillin

219
Q

Extracellular magnesium concentrations are vital for:

A

normal nerve conduction
mm function
bone mineral formation

220
Q

Hypomagnesemia clinical signs

A

nerve hyperexctiability
tetany
convulsions
sudden death

221
Q

hypomagnesemia is typically accompanied by what other electrolyte abnormality?

A

hypocalcemia

222
Q

moderate hypomagnesemia, clinical signs are seen

A

decreased feed intake
nervousness
dec milk fat & milk production

223
Q

What organ mantains magnesium homeostasis?

A

kidney

224
Q

Adult ruminants absorb magnesium from?

A

rumen

225
Q

adult ruminants secret magnesium from what organ?

A

small intestine

226
Q

What electrolyte interferes with absorption of magnesium?

A

K (potassium)

227
Q

Hypomagnesemic tetany is also called

A

grass/spring tetany
grass staggers

228
Q

Hypomagenesemic tetany the seen at what plasma levels?

A

Mg < 0.5 mmol/L or 1.1 mg/dL

229
Q

What C/S are seen in cattle when dec in CSF magnesium?

A

clonic convulsions
chomping jaws
frothing salivation
head arched back
legs paddling
HR >150 bpm
RR> 50/min
Temp> 105 (d/t mm activity)
nystagmus
eyelids flutter

230
Q

Hypomagnesemia is seen in beef & dairy cows and ews grazing lush pastures ebcause of what nutrients involved?

A

INC K, nitrogen
DEC mg, Na

231
Q

Describe magnesiums involvement in PTH?

A

dec PTH secretion from parathyroid gland = DEC blood Ca

OR

DEC tissue response to PTH–> Mg must be present at PTH/PTH receptor complex to activate adenyl cyclase and allow cyclic AMP production

232
Q

Verminous encephalitis can occur in horses caused by what organism?

A

Strongylus vulgaris emoblization to CNS– thrombi to ventricle, proximal aorta, or aortic branches that supply CNS

233
Q

What stage of Strongylus vulgaris is implicated in the verminous thrombI?

A

L4 or L5

234
Q

What are possible outcomes of Storngylus vulagris verminous meningoencephalomyelitis?

A
  1. acute massive infarction
  2. nonlethal or even subclinical
  3. subclinical mebolizaiton & parasite migration
235
Q

The prevalence of strongylus vulagris has decreased with introduction of what anthelmintics?

A

macrocyclic lactones

236
Q

Hypoderma lineatum (common cattle grub) L1 hatch 5 to 7 days, penetrate skin and migrate in dorsal direciton along fascial planes, following BVs or nerves, then what occurs?

A

over 1 year– miraitng larvae moutl once or twice and arrive in SQ along back; direct towards foramen magnum or other foramina of skull to penetrate and meander in brainstem

237
Q

Hypoderma lineatum has decreased in cattle d/t

A

decreased pour-on & injectable systemic organophosphate insecticides

238
Q

Halicephalopbus gingivalis has propensity to invade and proliferate in what organs?

A

kidneys
CNS– brain is usual site of infection, less involvemnt spinal cord and cauda equina
eyes

239
Q

What are characteristic lesions of halicephalobus gingivalis?

A

Renal lesions: multifocal lg nodules in renal parenchyma of 1 or both kidneys

240
Q

halicephalobus gingivalis CSF analysis?

A

normal to xanthochormic with increase dprotein and mild to mod pleocytosis of nucleated cells
differential: mononuclear cells with lesser numbers of neuts & occasional eos

241
Q

What treatment is contraindicated in cerebral nematodiasis (in camelids)?

A

corticosteroids

242
Q

Paralephostrongylus tenuis (meningeal worm) aberrant host

A

horses
lammas
alpacas
ruminants

243
Q

Paralephostrongylus tenuis (meningeal worm) intermediate hosts

A

snales & slugs (ovis aries, occinellidae)
– infective larvae

244
Q

Paralephostrongylus tenuis (meningeal worm) exit through abomasum and migrate to

A

dorsal horn of gray matter of spinal cord– mature into adults before traveling along dorsal nerve roots ot venous sinuses & subarachnoid spaces over cerebral hemispheres

245
Q

What anthelmintics can be used in the treatment of Paralephostrongylus tenuis (meningeal worm)?

A

ivermectin–larval migration **high dose
fenbdendazole– BBB

246
Q

Paralephostrongylus tenuis (meningeal worm) incubation

A

3 to 5 weeks assymetric spinal cord incubation

247
Q

Triaryl phosphate poisoning/chronic organophosphate poisoning/dying back axonopathy common sources

A

motor lubricants
hydraulic oils
industrial solvents
plasticizers
automotive brake fluid

248
Q

Triaryl phosphate poisoning/chronic organophosphate poisoning/dying back axonopathy pathogenesis

A

-effects glial cells
– profound neurotoxic effects on longest axons
–fibers degenerate @ distal, nonterminal areas
- lesions spread proximally from terminal nerve rootlets into spinal cord until cell body dies, dying back axonopathy

249
Q

What are clinical signs of chronic Triaryl phosphate poisoning/chronic organophosphate poisoning/dying back axonopathy?

A

rough hair coat
bloat
dyspnea
mm weakness
incoordination of rear legs

–> slow onset of neuro signs, progress to dog sitting posture, lack of normal CP responses, then become recumbent

250
Q

Triaryl phosphate poisoning/chronic organophosphate poisoning/dying back axonopathy treatment

A

no tx & irreversible
-prevention centered on eliminating access to potential sources

251
Q

What are predisposing factors to the development of spinal abscess?

A

hematogenous spread/bacterial extension from lungs, heart septic inject site
-neonates– secondary septicemia
-lambs– tail docking or ewes chewing ont ail (ascending infection)
-sequestra of vertebral fracture
epizootics d/t inject of contam vx or mineral supplements

252
Q

what are potential infectious agents isolated from spinal abscesses in ruminants?

A

C. pseudotuberculosis
T. pyogenes
M. hemolytica
Staph aureus
Fusobacterum necrophorum

253
Q

what are potential infectious agents isolated from spinal abscesses in foals?

A

Beta-hemolytic streptococci
salmonelal spp
actinobacillus equuli
E. coli
Rhodoccus equi
Klebsiella pneumoniae

254
Q

What are most common sites of spinal abscess formation?

A

costovertebral articulations
intervertebral
vertebral body epiphyses
lumbar vertebrae freq involved

255
Q

What are differentials for ruminants with spinal abscess

A

lymphoma-cattle
trauma– edema/inflammation, fx, hemorrahge, subluxation
parasitic– p. tenus
vit E/selenium– gneralized weakness
Cu def (swaback in lambs)
meningitis
CL (esp sm ruminants)
botulism
neospora
histphalus– TEME
CAE

256
Q

What are ddx in horses for spinal abscess?

A

EPM
EHV-1
viral: West Nile
Halicephalobus, strongylus vulgaris
Wobblers
Trauma
Rabies

257
Q

Ankylosing spondylitis of holstein bulls C/S seen

A

–stilted gait
–reluctance to move
–dragging toes of rear limbs
–slow to mount (bulls)– spine may fx when mounting– causing acute recumbency
–paraperesis & ataxia

258
Q

Pathologic changes seen with Ankylosing spondylitis of holstein bulls

A

calcification of ventral vertebral ligaments T11-L3 vertebrae

259
Q

Ankylosing spondylitis of holstein bulls is hereditary with what genetic association?

A

bulls have class 1 MHC BOLA A*phenotype

260
Q

What are common underlying causes of downer cows (alert downers)?

A

MSK lesions: fracture, torn mm/tendons
–Neuropathies: pelvic trauma, calving paralysis
–Spinal cord compression: lymphosarcoma
–metabolic disease: hypocalemica, hypokalemia, hypohposphatemia, hypomagnesemia

261
Q

Hypocalcemia as a cause of downer cows (alert downers) is seen at what level?

A

Mod: Ca <8 mg/dL
Severe: Ca <5.5 mg/dL

262
Q

Hypomagnesemia as a cause of downer cows (alert downers) is seen at at what level?

A

Mg < 1.9 mg/dL

263
Q

What value on clin path is most predictive of recovery in downer cows (alert downers)?

A

INC AST levels
– AST>171 IU/L- 80% more likley not to recover than AST <171 U/L

264
Q

What values of CSP protein and TNCC are useful in predicting/locating lesion in downer cows (alert downers)?

A

No SC lesion: TP <0.25 g/L, TNCC <4.5

SC lesion: TP >0.39 g/L, TNCC >4.5

265
Q

Prevention of downer cows (alert downers)

A

weakness & unable to rise after calving, INC dietary chloride levels during dry period
– K neg affects absorption of Mg

Smith. Neurolgic DZ (2 decks)

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