LA - Brain Diseases Flashcards
(83 cards)
1
Q
Anatomy involved
A
2
Q
Key assessment
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3
Q
Cardinal signs
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Blindness
Mental depression
Seizures
Dementia
4
Q
Blindness
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Lesions located in thalamus, occipital cortex or internal capsule. Contralateral loss of menace
5
Q
Mental depression
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Dullness, stupor, come, caused by cerebral or serious frontal, temporal lobe lesions
6
Q
Seizures
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7
Q
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
9
Q
Cause & lesion of congenital hydrocephalus
A
In utero infection -
Lesion
Diagnosis
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
11
Q
Rabies clinical signs
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Excessive salivation
Abnormal behavior
Obtunded
Aggression
Bellowing
Ataxia, convulsions, death within 10 days -48 hrs after recumbancey
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
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
14
Q
Cause of BMM
A
Gram neg bacteria - E. coli, salmonella, pasturalla, Mannheima, Trueperella, strep, mycoplasma
Failure of passive transport
Epidural abscess
15
Q
Lesion and diagnosis of BMM
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Suppurative meningitis, secondary hydrocephalus
CSF: grossly turbid, neutrophilia,
Serum: culture successful in 50%
Blood & tissues: gram neg sepsis in neonates
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
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
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
19
Q
Thromboembolic meningoencephalitis
A
“Sleeper calves”
Caused by histophilus somni
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
A
25
Brain abscess
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Pseudorabies
“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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Signs of pseuorabies
High fever, itchy, chewing, rubbing, licking bit area, bellow, maniacal behavior
Opisthotonus, limb ataxia, convulsions, death in 2 d
28
Lesion and diagnosis for pseudorabies
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
29
Malignant catarrhal fever signs
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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Cause of MCF
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Lesion of MCF
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Diagnosing MCF
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Bovine herpes encephalomyelitis
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
34
Bovine spongiform encephalopathy
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
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Signs of BSE
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Lesion and diagnosis for BSE
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Human transmission & prevention of BSE
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Scrapie signalment
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**scrapie
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Nervous coccidiosis
Common in feedlot calves during winters
Sporadic in young ruminants
*heat Labile neurotoxin eimeria
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Signs of intestinal coccidiosis
Muscle tremors, hyperesthsia, seizures, ventroflexion of head, nystagmus, progressing to coma and death
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Prognosis and treatment for nervous coccidiosis
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Coenurosis
Coenuris cerebralis is intermediate (cystic) stage from dog tapeworm
Common in sheep, signs are asymmetric progressive cerebral disease
Treat neuro signs with praziquantel
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Protozoal encephalomyelitis
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
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Nutritional /toxic diseases
Salt poisoning
Lead poisoning
Lead intoxication
Vitamin A deficiency
Polioencephalomalacia pem-thiamine deficiency
Non protein nitrogen toxicity
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Salt poisoning
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
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Lesion and diagnosing salt poisoning
CNS edema and laminar cortical necrosis
Normal to mild mononuclear pleocytosis in cattle
Serum normal, NA may be normal or elevated
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Lead poisoning - acute
Acute - sudden death, bellowing, hyperesthsia, obtunded, tremors, staggering, blindness
Death in 24 hours
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Lead poisoning - subacute
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
Mechanism of lead intoxication
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
Lesion & diagnosing lead intoxication
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
Treating lead poisoning
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
Vitamin A deficiency
Cattle - esp feedlot cattle
Early sign - night blindness, obtunded, true blindness, collapse & convulsions, progressive limb paralysis, dilated unresponsive pupils
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Cause of vitamin a deficiency
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
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Other causes of vitamin A deficiency
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
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Lesion, CSF and blood of vitamin A deficiency
Lesion - hydrocephalus, CN strangulation, retinal degeneration
CSF - increased opening pressure at AA sight, mild mononuclear pleocytosis & increased protein
Blood - low serum & plasma levels
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Treating/preventing vitamin A deficiency
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
Polioencephalomalacia pem thiamine deficiency
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)
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Main signs of Polioencephalomalacia
Sudden death
Acute onset star gazing, walking aimless, head pressing, blindness, absent menace, Dorso medial strabismus, teeth grinding, recumbency, seizures
Death within 4 days
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Cause of Polioencephalomalacia
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
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Side effects of Polioencephalomalacia
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
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Pathogenesis of Polioencephalomalacia PEM
Thiamine deficiency -> reduces sodium & water transport into neurons = brain edema
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Early signs of PEM
Dullness, inappetence, blindness, muscle tremors, hyperesthsia
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Later signs of PEM
Ataxia, head pressing, odontoprisis, Dorso-medial strabismus, meiosis
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latest signs of PEM
Recumbency with opisthotonus, coma, seizures
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Lesion of PEM
Cerebral edema, laminar cerebral cortical gray matter necrosis (acute)
Cerebrocoriical spongiosis (chronic)
Lesions fluoresces with UV light
Similar to Na or lead poisoning
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CSF & Blood of PEM
CSF - normal/mild mononuclear pleocytosis, normal to increased protein
Blood - CBC normal, other tests are not reliable, dietary sulfur analysis
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Diagnosing PEM
Recent changes in pasture or feedlot/sudden o sent of neurological signs
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Treatment / prevention for PEM
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
Non protein nitrogen toxicity
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
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Clinical signs of NPNT
Typical diffuse cerebral signs of dementia, blinking, ear flicking, blindness, hyperesthsia, compulsive charging/walking, recumbency, seizures
“Bovine bonkers”
Attacks last <30 minutes,
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Heptoencephlopathy
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
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Nervous ketosis
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
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Treatment/prevention for nervous ketosis
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
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Pregnancy toxemia
Over fat ewe with secondary inadequate feeding +multiple fetuses can present similar to ketosis bc of poor diet
Dull, inappetence, weak, recumbent, blind
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Diagnostics for pregnancy toxemia
Urine - ketonuria
Blood - hyperketonemia, hypoglycemia
CBC - leukopenia, hyperproteinemia
Biochem - Hypocalcemia, hypokalemia, metabolic acidosis
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treating pregnancy toxemia
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
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Hypoglycemia
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
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Diagnostics for hypoglycemia
Blood glucose < 30 mg/dl
CBC - leukopenia or leukocytosis
FPT
80
Treating hypoglycemia
5% dextrose
Milk/replacement
Antimicrobials if clinical or hematologic evidence of infections
Admin of plasma if hematologic evidence of FPT
81
HypoCalcemia
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
Hypomagnesemia
Common in the first 60 days of lactation in beef cattle
Hyper-excitable, aggressive, muscle fasiculations, flashing nicitans, titanic, spasms, convulsions, recumbency
83
Differentials for cerebral disease
Polioencephalomalacia
Meningoencephalitis
Lead intoxication
Salt intoxication
Vitamin A deficiency
Pregnancy toxemia
Nervous ketosis
Hypoglycemia
Nervous coccidiosis
