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SS - Exam 2 > LA - Brain Diseases > Flashcards

LA - Brain Diseases Flashcards

1
Q

Anatomy involved

A
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2
Q

Key assessment

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3
Q

Cardinal signs

A

Blindness
Mental depression
Seizures
Dementia

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4
Q

Blindness

A

Lesions located in thalamus, occipital cortex or internal capsule. Contralateral loss of menace

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5
Q

Mental depression

A

Dullness, stupor, come, caused by cerebral or serious frontal, temporal lobe lesions

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6
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Seizures

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7
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Dementia

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8
Q

Congenital hydrocephalus

A

Rare in cattle, rare in other species
Lots of pressure on brain or not fully formed brain
Dummy, no maternal bond, secondary septicemia

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9
Q

Cause & lesion of congenital hydrocephalus

A

In utero infection -
Lesion
Diagnosis

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10
Q

Infectious brain diseases

A

Rabies
Bacterial meningitis
Sporadic bovine encephalomyelitis
Thromboembolic meningoencephalitis (sleeper calves)
Brain abscess
Pseudorabies
Malignant catarrhal fever
Bovine herpes encephalomyelitis
Bovine spongiform encephalopathy
Scrapie
Nervous coccidiosis
Coenurosis
Protozoal encephalomyelitis

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11
Q

Rabies clinical signs

A

Excessive salivation
Abnormal behavior
Obtunded
Aggression
Bellowing
Ataxia, convulsions, death within 10 days -48 hrs after recumbancey

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12
Q

Rabies DX

A

CSF - normal
Brain - send section of cerebellum and associated brain stem, Florescent testing, negri bodies less specific (only on 50% of cases) lack of negri bodies doesnt mean its not rabies

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13
Q

Bacterial meningitis

A

Major death cause of neonates
Fever, rigid posture, lack of suckling, hyperesthsia, obtunded, seizures
Signs of sepsis - fever, arthritis, diarrhea, omphalitis
Unilateral forebrain abscess in adult cattle

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14
Q

Cause of BMM

A

Gram neg bacteria - E. coli, salmonella, pasturalla, Mannheima, Trueperella, strep, mycoplasma
Failure of passive transport
Epidural abscess

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15
Q

Lesion and diagnosis of BMM

A

Suppurative meningitis, secondary hydrocephalus
CSF: grossly turbid, neutrophilia,
Serum: culture successful in 50%
Blood & tissues: gram neg sepsis in neonates

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16
Q

Treatment for BMM

A

**high concentrations for long periods of time in infected areas
Ceftiofur, ampicillin trihydrate, florfenicol, oxytetracycline
Optional therapy based on species

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17
Q

Sporadic bovine encephalomyelitis

A

“Buss disease”
Infection of chlamydiophilia percorum (chlamydia)
Young animals are commonly infected
Multisystemic, fever, blindness, ataxia, circling, recumbency, death, lameness, arthitis, nasal discharge

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18
Q

Diagnosis for SBE

A

Lesion: polyserositis, vasculitis
CSF: mononuclear pleocytosis, increased protein
Blood & tissue: elementary bodies in pleural, synovial exudate cells
Treat with Oxytetracycline
Prognosis is 30% mortality

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19
Q

Thromboembolic meningoencephalitis

A

“Sleeper calves”
Caused by histophilus somni

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20
Q

Sleeper calves signalment and signs

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21
Q

Lesion and diagnosis of TEM

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22
Q

Treatment for TEME

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23
Q

prevention for TEME

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24
Q

Brain abscess

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25
Q

Brain abscess

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26
Q

Pseudorabies

A

“Mad itch, aujeskys disease, porcine herpesvirus1”
Main host is pigs and can infect other species, pool is in wild hogs or feral pigs

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27
Q

Signs of pseuorabies

A

High fever, itchy, chewing, rubbing, licking bit area, bellow, maniacal behavior
Opisthotonus, limb ataxia, convulsions, death in 2 d

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28
Q

Lesion and diagnosis for pseudorabies

A

Lesion: mononuclear encephalomyelitis, Intra nuclear inclusions
CSF: moderate mononuclear pleocytosis, ^ protein
Blood & tissue: serology doesn’t work, animals die before developing antibodies
Culture and PCR of secretions or tissue is best bet

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29
Q

Malignant catarrhal fever signs

A

Cattle, bison, elk, farmed deer
Encephalitic variant - head & eye form of MCF
High fever, profound obtunded, mucopurulent nasal discharge = nasal obstruction, ocular discharge, keratoconjuncitivtis, nasal & ocular erosions, lymphadenopathy

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30
Q

Cause of MCF

A
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31
Q

Lesion of MCF

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32
Q

Diagnosing MCF

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33
Q

Bovine herpes encephalomyelitis

A

Complicated rhinotracheitis in cattle
Most cases are calves and most cases are fatal
Necropsy diagnosis is common
Viral latency and persistent infection is a characteristic of these viruses

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34
Q

Bovine spongiform encephalopathy

A

Transmissible
Caused by a prion agent of scrapie, mink encephalopathy, disease of elk, can infect humans
Associated with recycling cattle by feeding muscle and bone meals to cattle

35
Q

Signs of BSE

A
36
Q

Lesion and diagnosis for BSE

A
37
Q

Human transmission & prevention of BSE

A
38
Q

Scrapie signalment

A
39
Q

**scrapie

A
40
Q

Nervous coccidiosis

A

Common in feedlot calves during winters
Sporadic in young ruminants
*heat Labile neurotoxin eimeria

41
Q

Signs of intestinal coccidiosis

A

Muscle tremors, hyperesthsia, seizures, ventroflexion of head, nystagmus, progressing to coma and death

42
Q

Prognosis and treatment for nervous coccidiosis

A
43
Q

Coenurosis

A

Coenuris cerebralis is intermediate (cystic) stage from dog tapeworm
Common in sheep, signs are asymmetric progressive cerebral disease
Treat neuro signs with praziquantel

44
Q

Protozoal encephalomyelitis

A

Cattle - Sarcocystis Cruz
Most infections are in apparent infections of skeletal msucle
Naive animals exposures to high amts are infected w severe systemic disease in brain and spinal cord

45
Q

Nutritional /toxic diseases

A

Salt poisoning
Lead poisoning
Lead intoxication
Vitamin A deficiency
Polioencephalomalacia pem-thiamine deficiency
Non protein nitrogen toxicity

46
Q

Salt poisoning

A

High salt ingestion without adequate water OR water deprivation
Causes hyperOmolality and brain shrinkage
Drinking water after can result in neuronal swelling, brain edema, severe exacerbation

47
Q

Lesion and diagnosing salt poisoning

A

CNS edema and laminar cortical necrosis
Normal to mild mononuclear pleocytosis in cattle
Serum normal, NA may be normal or elevated

48
Q

Lead poisoning - acute

A

Acute - sudden death, bellowing, hyperesthsia, obtunded, tremors, staggering, blindness
Death in 24 hours

49
Q

Lead poisoning - subacute

A

Blindness, absent menace, obtunded, ataxia, staggering, teeth grinding, colic, head pressing
Course of 3 days
Most common toxicosis of cattle
Vitamin D can increase oral availability for lead

50
Q

Mechanism of lead intoxication

A

Ingestion of lead absorbed by GI tract -> lead is irreversibly bound to RBC proteins -> lead inhibits enzymes responsible for synthesis of heme -> lead is released from RBC at the end of life span and deposited into bone -> lead enters brain & alters capillary integrity causing edema & hemorrhage

51
Q

Lesion & diagnosing lead intoxication

A

Minimal changes in acute cases
Cerebral edema, laminar cortical necrosis, cerebral cavitation & yellow discoloration
Mononuclear pleocytosis & increased protein
Blood - anemia w polychromasia, Howell-jolly bodies, basophilic stippling

52
Q

Treating lead poisoning

A

Sedation w Na pentobarbital/diazepam - seizures
Purge rumen
Magnesium sulfate helps precipitates lead
calcium disodium EDTA helps remove lead
Remove source of lead
Prognosis is near 100% mortality w/out treatment, 50% with treatment

53
Q

Vitamin A deficiency

A

Cattle - esp feedlot cattle
Early sign - night blindness, obtunded, true blindness, collapse & convulsions, progressive limb paralysis, dilated unresponsive pupils

54
Q

Cause of vitamin a deficiency

A

Low vitamin A during gestation = numerous brith defects like retinal dysplasia
Signs occur 6-12 months after feeding of deficient diets
Low beta carotene, retinoids in feed
Low amt of green forage & high proportion non-corn
*common animal confined indoors or drought

55
Q

Other causes of vitamin A deficiency

A

Feeds that have been stored in high temps /humidity
Chronically administering with mineral oils
Lack of vitamin a prevents regeneration of visual purple, impaired CSF absorption (hydrocephalus), skull development, vertebral abnormalities, atrophy

56
Q

Lesion, CSF and blood of vitamin A deficiency

A

Lesion - hydrocephalus, CN strangulation, retinal degeneration
CSF - increased opening pressure at AA sight, mild mononuclear pleocytosis & increased protein
Blood - low serum & plasma levels

57
Q

Treating/preventing vitamin A deficiency

A

Parental vitamin A supplementation
Initial supplements should be oral
Acute cases respond rapidly/completely
Chronic cases have irreversible damage & do not respond
Feed green forge
Prognosis - untreated wont recover from retinal degeneration but acute can recover from encephalopathy

58
Q

Polioencephalomalacia pem thiamine deficiency

A

Vitamin B1 deficiency, leads to softening of gray matter
Common in ruminants, sporadic form common in all ages, which is also common in suckling calves/kids
Most common in feedlot weanling (sheep & cattle)

59
Q

Main signs of Polioencephalomalacia

A

Sudden death
Acute onset star gazing, walking aimless, head pressing, blindness, absent menace, Dorso medial strabismus, teeth grinding, recumbency, seizures
Death within 4 days

60
Q

Cause of Polioencephalomalacia

A

Primary thiamine deficiency -
FOOD: sudden change in feed
PLANTS: ruminants bacterial thiaminase = rumen acidosis, plants w thiamine
BYPRODUCTS: High dietary sulfur, ethanol byproducts, molasses
signs occur 10-14 days after sulfide increase in the rumen
Lead & salt poisoning ^ signs of PEM

61
Q

Side effects of Polioencephalomalacia

A

Can cause blind staggers in cases of sulfur associated PEM
Initially interfere with ATP production, dysfunction of membrane ATP dependent Na-K pump, CNS edema, swelling of brain within skull = pressure necrosis

62
Q

Pathogenesis of Polioencephalomalacia PEM

A

Thiamine deficiency -> reduces sodium & water transport into neurons = brain edema

63
Q

Early signs of PEM

A

Dullness, inappetence, blindness, muscle tremors, hyperesthsia

64
Q

Later signs of PEM

A

Ataxia, head pressing, odontoprisis, Dorso-medial strabismus, meiosis

65
Q

latest signs of PEM

A

Recumbency with opisthotonus, coma, seizures

66
Q

Lesion of PEM

A

Cerebral edema, laminar cerebral cortical gray matter necrosis (acute)
Cerebrocoriical spongiosis (chronic)
Lesions fluoresces with UV light
Similar to Na or lead poisoning

67
Q

CSF & Blood of PEM

A

CSF - normal/mild mononuclear pleocytosis, normal to increased protein
Blood - CBC normal, other tests are not reliable, dietary sulfur analysis

68
Q

Diagnosing PEM

A

Recent changes in pasture or feedlot/sudden o sent of neurological signs

69
Q

Treatment / prevention for PEM

A

Thiamine
Supportive care, dexamethasone, mannitol, b complex
Prevent with good food/roughage ratio
Prognosis is >50% complete recovery w treatment
No response to treatment within 8 hrs = poor prognosis

70
Q

Non protein nitrogen toxicity

A

Anhydrous ammonia due to poor feed quality
>3% ammonia get toxicity due to intraruminal formation of 4 methyl imidazole (ammonia/glucose)
Urea can be added to feed = hyper ammonia = depression, ataxia, seizures, death
Treat w oral vinegar

71
Q

Clinical signs of NPNT

A

Typical diffuse cerebral signs of dementia, blinking, ear flicking, blindness, hyperesthsia, compulsive charging/walking, recumbency, seizures
“Bovine bonkers”
Attacks last <30 minutes,

72
Q

Heptoencephlopathy

A

Toxic plants, bovine fatty liver syndromes, pregnancy toxemia can cause signs of dementia & depression due to liver failure / blood ammonia concentrate
Low protein /high carb diet is helpful but prognosis is poor

73
Q

Nervous ketosis

A

Episodes in lactating dairy cows of vestibular signs, vigorous licking/chewing, depraved appetite, blindness
Caused by ketonmeia/hypoglycemia, associated w poor balance in early lactation

74
Q

Treatment/prevention for nervous ketosis

A

Blood findings - ketonemia, ketonuria, blood glucose, fatty infiltration of liver
Treat w dextrose up to 3 days, insulin, vB12 or cobalt
Prognosis is good, prevention in management during pregnancy

75
Q

Pregnancy toxemia

A

Over fat ewe with secondary inadequate feeding +multiple fetuses can present similar to ketosis bc of poor diet
Dull, inappetence, weak, recumbent, blind

76
Q

Diagnostics for pregnancy toxemia

A

Urine - ketonuria
Blood - hyperketonemia, hypoglycemia
CBC - leukopenia, hyperproteinemia
Biochem - Hypocalcemia, hypokalemia, metabolic acidosis

77
Q

treating pregnancy toxemia

A

Reducing fetal drain of energy - abortion w dex or C section
Providing supplementation energy - oral admin of beer (propylene glycol), IV of dextrose
Correction of abnormalities - gastric tube, fluids, mineral/electrolyte, metabolic acidosis corrected

78
Q

Hypoglycemia

A

Metabolic encephalopathy of neonatal calf, lamb or kid caused by inadequate intake of milk or septicemia
Common in neonates w inadequate milk /replacer or with septicemia or concurrent disease
Sudden onset of dullness, weakness, recumbency

79
Q

Diagnostics for hypoglycemia

A

Blood glucose < 30 mg/dl
CBC - leukopenia or leukocytosis
FPT

80
Q

Treating hypoglycemia

A

5% dextrose
Milk/replacement
Antimicrobials if clinical or hematologic evidence of infections
Admin of plasma if hematologic evidence of FPT

81
Q

HypoCalcemia

A

Common in early stages of lactation in dairy cows, goats or late stage gestation in sheep
Early signs - confusion, excitement, hypersensitivity lead to depression & flaccid paralysis
Cows appear drunk - shaky

82
Q

Hypomagnesemia

A

Common in the first 60 days of lactation in beef cattle
Hyper-excitable, aggressive, muscle fasiculations, flashing nicitans, titanic, spasms, convulsions, recumbency

83
Q

Differentials for cerebral disease

A

Polioencephalomalacia
Meningoencephalitis
Lead intoxication
Salt intoxication
Vitamin A deficiency
Pregnancy toxemia
Nervous ketosis
Hypoglycemia
Nervous coccidiosis

SS - Exam 2 (18 decks)

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