general Flashcards

1
Q

Where are the best seen CNS lesions of malignant catarrhal ovine fever?

A

Arteries of the rete mirabile

Malignant catarrhal fever (MCF) is a highly fatal lymphoproliferative

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2
Q

Which virus(es) is(are) implied in malignant catarrhal fever (MCF) in cattle?

A

Alcelaphine herpesvirus type 1 (AlHV-1)

Ovine herpesvirus type 2 (OvHV-2)

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3
Q

What are the difference between goat and sheep with lentivirus infection?

A

Goat (CAEV)
Young kids (1-6 months)
Leukoencephalomyelitis with ascending paresis (short shoppy gait initially)

Sheep (MVV/OPPV)
Adult
Brain form (head tilt & circling toward the affected lateral ventricle ± hindlimb hypermetric ataxia) or spinal form

Irreversible and progressive disease, without treatment in both species
Now believed that ovine & caprine lentivirus form one large group of viruses with strong evidence for cross-species transmission MVV/OPPV and CAEV are taxonomically combined together as the ovine/caprine lentivirus group

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4
Q

Serology conversion usually occurs within .. with lentivirus infection

A

2-12 weeks (up to 8 months)
The clinical condition is slowly progressive and results in paralysis and death over the course of several months.

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5
Q

Positive serologic or PCR test is sufficient for antemortem diagnosis of lentivirus myeloencephalitis in small ruminants?

A

False

High prevalence -> false positive
Postmortem diagnosis is based on demonstration of the characteristic lymphocytic infiltration of the CNS. Virus isolation or additional viral identification is rarely performed.

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6
Q

What is the cause of thrombotic meningoencephalitis in cattle?

A

Histophilus somni

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7
Q

What is the main infectious agent for otitis media in pigs?

A

Streptococcus suis

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8
Q

At which age is menace response present in foals and calves?

A

Several days

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9
Q

What is the most common cause of facial paralysis in cattle?

A

Otitis media

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10
Q

What is the main risk factors for OMI in ruminants?

A

Presence of a coincidental respiratory infection
Many studies document bacterial OM in conjunction with or after respiratory disease, with the same causative pathogens isolated.

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11
Q

Hypovitaminosis A in calves is associated with which abnormality?

A

Dural fibrosis causing hydrocephaly

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12
Q

Ptosis can be caused by

A

Frontalis
levator palpebral superioris muscles
Oculomotor nerve

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13
Q

Which parts of the neurologic system are visible in large animals?

A

Glossopharyngeal nerve, retina, optic disc, optic nerve

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14
Q

Central blindness and opisthotonos are common signs of

A

Polioencephalomalacia

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15
Q

Progressive ataxia of Charolais cattle is due to a defect in:

A

Oligodendrocytes

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16
Q

Which bacteria contain thiaminase?

A

Clostridium thiaminolyticum
Bacillus thiaminolyticus

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17
Q

What is the disease, the gene and the breed associated with congenital hyperammonaemia in cattle?

A

Citrullinemia
Arginosuccinate synthetase (ASS1)
Holstein-Friesian

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18
Q

What is the gene associated with progressive ataxia of Charolais cattle? What pathological changes are found?

A

KIF1C

Leukoencephalomyelopathy: demyelination of the brain and spinal cord; and production of multifocal, acellular, pale, eosinophilic plaques prominent in the cerebellar peduncles and medulla oblongata

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19
Q

What are the 6 entries for pathogens in the CNS?

A

Hematogenous (e.g. thromboemboli)
Penetration of BBB within mononuclear cells (mostly viruses)
Circumventricular organs (e.g. pituitary abscess)
Axons of nerves
CSF (e.g. bacterial)
Direct lesion (e.g. fracture)

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20
Q

What is the most frequent virus implied in bovine herpesvirus encephalitis?

A

BHV-5

Although BoHV-1 rarely causes encephalitis, BoHV-5 demonstrates marked neurotropism and the ability to cause severe and often fatal encephalitis.
Encephalitis caused by BoHV-1 is uncommon compared with the respiratory (infectious bovine rhinotracheitis [IBR]) and genital (IPV and IBP) syndromes.
BHV-5 induced neurologic signs include muscle trembling, circling, ptyalism, jaw chomping, tongue protrusion, head pressing, and ataxia. Absence of blindness.

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21
Q

What are the 2 routes involved in the dissemination of BHV-5 in the CNS?

A

Trigeminal and olfactory pathways

After colonization of the upper respiratory tract, infection of the CNS occurs through neurotropic spread within sensory neurons originating in the nasopharynx.

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22
Q

What is the gene associated with bovine progressive degenerative myeloencephalopathy in Brown Swiss Calves?

A

PNPLA8
Weaver syndrome

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23
Q

In which specie and breed have been described the RELN mutation, similarly to the White Swiss Shepherd?

A

Spanish Churra milking sheep

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24
Q

What are the 2 routes of transmission of Bornavirus to the CNS?

A

Nasal epithelium – olfactory nerve
Pharyngeal epithelium – trigeminal nerve

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25
Q

Give 3 common causes for seizures in cattle

A

HypoMg
HypoCa
Cerebrocortical necrosis
Inflammatory disease
Lead intoxication

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26
Q

Which histopathological finding is pathognomonic to borna disease?

A

Intranuclear eosinophilic inclusion bodies (Joest-Degen bodies)

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27
Q

DDx forebrain

A

Anomalous: congenital malformation

Metabolic: polioencephalomalacia, nervous ketosis, hepatic encephalopathy, hypoglycemia
Toxic: lead, organophosphates, urea/NH3, salt toxicity/water deprivation

Inflammatory:
Bacterial: listeriosis, abscess
Viral: rabies, BHV-5, BHV-1, pseudorabies, malignant catarrhal fever, BSE
(camelid: P tenuis, EEE, WNV, EHV-1)

Traumatic

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28
Q

What are the 3 most common causes of cerebral disease in calves?

A

Polioencephalomalacia:
- Thiamine deficiency
- High-sulfur diet
- Low-roughage diet
- High doses of amprolium
- Cobalt-deficient diet
- Molasses-urea diet
- Ingestion of various toxic plants

Bacterial meningitis (usually in calves less than 2-3 weeks of age)

Hypernatremia (salt poisoning)

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29
Q

Cause and age for meningitis in calves?

A

Cause: sequelae to septicemia: E. coli is the most common pathogen
Others: Salmonella, Campylobacter, Klebsiella, Staphylococcus

Age: before 30 days of age
Colonization of GI tract before establishment of normal flora
Bacterial colonization of another site such as umbilicus (omphalitis)

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30
Q

Which pathogen cause pseudorabies?

A

Suid herpesvirus 1

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31
Q

Congenital abnormalities are seen during in utero infection by bovine diarrhea virus between ____ and ____ days of gestation.

A

125

180

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32
Q

What is the mechanism of maple syrup urine disease (MSUD)?

A

BCKDHA (AR) -> Branched-chain ketoacid dehydrogenase deficiency
Storage disease with elevated concentrations of branched chain alpha-keto acids and their precursors, the branched chain amino acids, valine, leucine and isoleucinein in blood and tissues

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33
Q

What are the lysosomal storage diseases described in ruminants and the breed concerned?

A

Alpha-mannosidosis in Angus, Murray Grey & Galloway: Nonlipid vacuolation of cells in the cerebrum, cerebellum, and spinal nerves

Beta-mannosidosis in Salers: Vacuolation of the Purkinje cells and decreased myelination of the cerebellum

Maple syrup urine disease in poll Herefords & poll shorthorns

GM1 gangliosidosis in Friesian, sheep
Pompe disease (GSD 2) in shorthorn & Brahman

GSD 5 in Charolais
Muscles

Citrullinemia in Holstein-Friesians

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34
Q

What is the gene associated with hemifacial microsomia? In which breed?

A

LAMB1 gene (AR), laminin subunit beta 1
Romagnola calf

Signs: microtia of the left ear, anotia of the right ear, asymmetry of the face, and deafness.

MRI: agenesis of the right pinna and both tympanic bullae, asymmetry of the temporal bones and temporomandibular joints, and right pontine meningocele.

BAER: impaired auditory capacity

Histo: agenesis and hypoplasia of the right and the left external ear, respectively. No histological abnormalities were detected in the inner ears.

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35
Q

What are the typical neuropathologic lesions of bovine spongiform encephalopathy?

A

Bilaterally symmetric intracytoplasmic vacuolation of brainstem gray matter and neurons

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36
Q

Which allele(s) confer resistance to scrapie? Which one(s) confer susceptibility?

A

Resistance: ARR
Note: scrapie is still detected in some sheep that are ARR homozygous
Susceptibility: AHQ, ARH, ARQ, and VRQ

Resistance to scrapie is linked to polymorphisms at codons A136V, R154H, and R171Q of the prion protein gene.

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37
Q

Which clinical and most useful sign is associated with scrapie?

A

Response to scratching or light pressure over the withers causing sheep to raise their head, point their muzzle dorsally, elevate their upper lip and lick their lips and make chewing movements

Clinically, scrapie is a slowly progressive debilitating disease with progression taking from 2 months to as long as a year.
With progression, clinical signs include severe weight loss, poor appetite, pruritis and wool loss, and neurologic signs.
Neurologic signs can include altered mentation, hyperesthesia, head bob, muscle fasciculations, hypermetria, dysphonia, dysphagia, blindness, and uncoordinated muscular movements.

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38
Q

Scrapie is only transmitted horizontally: true or false?

A

False

Horizontal and vertical transmission are reported with scrapie; hence, the prolonged latent period is critically important because ewe’s infected with scrapie will have ample opportunity to transmit the disease to their offspring, and lambs born to other ewes before they themselves manifest with clinical disease.

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39
Q

Which is most frequent clinical profile with BSE?

A

The most frequent clinical profile for a cow with BSE is apprehension or nervousness combined with hyperesthesia and ataxia observed over a 15-day period.
A small proportion of animals may show true “mad cow” syndrome manifest by aggression and manic behavior.

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40
Q

Among calves that have cerebellar hypoplasia and atrophy, what is the proportion of those that have also optic nerve hypoplasia and atrophy?

A

25%

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41
Q

Cerebellar hypoplasia is caused by in-utero infection of bovine viral diarrhea virus at

A

100-200 days of gestation

Congenital abnormalities of BVDV (both cerebellar hypoplasia and ocular abnormalities) occur following infection of the cow at 125 to 180 days in gestation. Administration of a modified live BVDV vaccine induced teratogenesis during 90 to 118 days’ gestation

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42
Q

What are the 4 main causes of cerebellar hypoplasia in ruminants?

A

Inherited: Hereford, Shorthorn, Angus, Holstein, Guernsey, Ayrshire (recessive)

BVD (Pestivirus) in cattle (100-200 d gestation)

Border disease (Pestivirus) in sheep

Bluetongue (Orbivirus) in cattle & sheep

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43
Q

What are the main malformations associated with Schmallenberg virus? In which species?

A

Malformations:
Porencephaly to hydranencephaly
Cerebellar dysplasia (loss of PC and depletion of granular cell layer)
Brainstem dysplasia
Spinal cord dysplasia
Brachygnathia inferior
Arthrogryposis
Vertebral column malformations

Species: calves (45%), lambs (95%), kids

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44
Q

common infectious agent of suppurative otitis media-interna in ruminants kept under intensive stocking conditions?

A

Mycoplasma spp

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45
Q

What are the 2 teratogenic viruses transmitted by Culicoides spp.?

A

Schmallenberg virus
Bluetongue virus

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46
Q

Which cattle breeds are associated with familial cerebellar hypoplasia?

A

Hereford
Shorthorn
Ayrshire

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47
Q

Which cattle breeds are associated with cerebellar abiotrophy?

A

Angus
Poll Hereford
(other breeds: Ayrshires, Charolais, shorthorns, Limousin)

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48
Q

Which plant can induce cerebellar diseases in cattle and goats? Which pathological findings?

A

Solanum spp.

In affected goats, histopathologic lesions were observed throughout the cerebellum consistent with a storage disease; however, the mechanism of the toxicity is unknown. Lesions observed histologically in Solanum toxicities are of wallerian-type degeneration of the cerebellum alone, with loss of Purkinje cells.

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49
Q

Why lead poisoning is more frequent in young animals than adult?

A

Young absorb up to 50% of the lead ingested whereas, older animals absorb 1-3%.

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50
Q

Mechanism of action of strychnine?

A

Inhibit action of glycine in the spinal cord

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51
Q

Which bacteria produce enterotoxemia in cattle? Pig?

A

Clostridium perfringens type D (𝜀/epsilon toxin): sudden death (30-90 minutes) in lambs, kids, and calves, typically in growing animals (the toxin targets the brain, causing liquefactive necrosis, edema, and hemorrhage)
E. coli producing angiotoxin = Shigella (Shiga)-like toxin: brain edema (leakage of protein rich fluid) and symmetrical lesions with vascular hypertrophism, necrosis and hemorragic lesions causing fibrinoid vascular necrosis

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52
Q

Which clinical and pathological findings are associated with C. perfringes type D epsilon intoxination?

A

Clinical signs
Sudden death of well-nourished, growing animals
Abdominal pain, ataxia, trembling, and convulsions may be seen, with death occurring in 30 to 90 minutes

Pathologic findings
Glycosuria in lambs
Encephalomalacia
Large swollen kidneys (pulpy kidney) due to rapid decomposition
Minimal GI lesions in sheep
Catarrhal, necrotic enterocolitis in goats

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53
Q

What is the mechanism for enterotoxemic encephalopathy in cattle?

A

C. Perfringes type D: production of epsilon toxin in the form of a prototoxin with minimal biologic activity: activation by protease or trypsin and chymotrypsin: > 1000 times more toxic than the prototoxin
Action on receptor for epsilon toxin on vascular endothelial cells -> cause degeneration of tight junctions -> influx of protein and fluid -> swelling and rupture of perivascular astrocytes -> elevating ICP

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54
Q

What is the treatment for lead toxicosis in cattle?

A

Calcium versenate (CaEDTA): to chelate lead in bones: Pb binds irreversibly to erythrocytes proteins, When erythrocyte is removed from circulation, most of the lead is deposited in bone as a triphosphate salt

Thiamine: significantly reduce clinical signs

Magnesium laxative: reduce absorption of insoluble lead salts

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55
Q

What are the toxins produced by cyanobacteria, their mechanism of action, and the known antidote?

A

Anatoxin-a: depolarizes nicotinic receptors -> rapid death by respiratory paralysis
Anatoxin-as (Anabaena spp.): blockade of AChE (similar to organophosphate poisoning)

Antidote: atropine, but only for anatoxin-as (muscarinic antagonist)

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56
Q

What is the main physiolopathologic difference between enzootic ataxia and swayback?

A

Swayback: congenital copper deficiency
Enzootic ataxia: postnatal copper deficiency

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57
Q

Which toxicosis can cause alpha-mannosidosis? By which mechanism?

A

Swainsonine poisoning (locoweed)

Swainsonine inhibits lysosomal enzymes (alpha-D-mannosidase and Golgi mannosidase II), resulting in accumulation of their substrates -> lysosomal disease

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58
Q

Most common bacteria responsible for cerebral abcess in ruminants

A

Trueperella pyogenes
(= Actinomyces pyogenes)

Other bacterial species commonly isolated include Staphylococcus sp., Streptococcus sp., Fusobacterium necrophorum, and C pseudotuberculosis.

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59
Q

Give 2 explanations for the preferential location of pituitary gland for abscess in ruminants.

A

Rete mirabile
Absence of BBB

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60
Q

Which non-neurological sign is frequently (>50%) seen with pituitary abscess due to compression of the hypothalamus?

A

Bradycardia

61
Q

What is the most common risk factor for pituitary abscess?

A

Use of nose flaps for weaning calves or the placement of nose rings

62
Q

About 30% of cattle with pituitary abscess can survive with adequate treatment: true or false?

A

False

Pituitary abscess syndrome is consistently fatal. Therefore, treatment is unrewarding and typically not recommended.

63
Q

What are the most common clinical signs associated with pituitary abscess?

A

Brainstem dysfunction associated with cranial nerve deficits:
Depression -> most common sign

Typically asymmetrical
CN II: blindness
CN III: strabismus, PLR
CN V: jaw hypotonia, decreased facial sensation
CN VII: facial paralysis
CN VIII: head tilt, nystagmus
CN IX/X: dysphagia
CN XII: tongue hypotonia
Recumbency, opisthotonus and convulsions may be seen in terminal stages of the disease.

64
Q

What are the causes of thiamine deficiency in cattle?

A

Diet: disruption of the normal ruminal microbial population with decreased thiamine producing bacteria

Bacterial thiaminase (rumen-acidifying high-energy diet -> thiaminase type II)

Thiaminase containing plants (bracken fern, horsetail)

Thiamine antimetabolites (amprolium which is a coccidiostatic)

65
Q

Which CN is often affected in polioencephalomalacia (thiamine deficiency) in cattle?

A

CN IV causing dorsomedial strabismus

66
Q

DDx polioencephalomalacia (cerebrocorticalnecrosis) in ruminants

A

Thiamine deficiency
Sulfur toxicity (High dietary sulfur increased metabolic demand for thiamine )
Lead toxicity
pyrophosphate: high thiamine demand will lead to thiamine deficiency

Salt intoxication/water deprivation
Selenium toxicity
Cerebral anoxia
Mercury toxicity
Copper deficiency in lambs
Molasses and urea diet
Amprolium

67
Q

What is the difference between calves and adult cattle in the metabolism of thiamine?

A

Absorption via food vs. thiamine-producing bacteria in the rumen

68
Q

What are the 3 locations of degenerative lesions in thiamin deficiency?

A

Neocortex
Lateral geniculate nuclei
Caudal colliculi

69
Q

What are the 3 plants that contain thiaminase?

A

Bracken fern
Horsetail
Nardoo fern

They contain thiaminase similar to thiaminase type I.

70
Q

Listeriosis infects the CNS by

A

retrograde axonal transport

71
Q

What is the difference between cattle and small ruminant in CSF evaluation in case of listeriosis?

A

Cattle: mononuclear pleocytosis

Small ruminant: often neutrophilic

72
Q

What are the 4 CN most commonly involved in listeriosis? The less common?​

A

Most common: V > VII, VIII > XII

Less common: VI, IX, X

73
Q

Which test can be used to predict poor prognosis during listeriosis?

A

Creatine phosphokinase level in CSF (studied in sheep)

74
Q

Who has the better prognosis in encephalitic listeriosis, cattle or small ruminants?​

A

Cattle (70% survival) > Small ruminants (26%)

Very acute in SR

(death in 2-4 days in SR vs. 2 weeks in cattle)

75
Q

What are the factors associated with survival in goats with listeriosis?

A

1/ Females: male goats were 14 times more likely to be a nonsurvivor compared to females despite being presented with similar history, clinical signs, and treatments.

2/ Circling: animals presented with circling or a history of circling were 6.24 times more likely to be a survivor than a non-survivor.

Other risk factors evaluated were not significantly associated with outcomes (duration, antimicrobial, anti-inflammatory, CSF)

76
Q

What are the 2 most common Listeria monocytogenes serotypes implied? Which one is the most implied in zoonotic transmission?

A

Serotypes 1/2a

Serotype 4b most often responsible for infections in humans

77
Q

What is the gene/breed associated with spinal dysmyelination ?

A

SPAST (CFA 11, AR)

Congenital recumbency with limb extension, moderate opisthotonos, body tremors
Brown Swiss Cattle

78
Q

DDx spinal cord

A

Degenerative: Brown Swiss myelopathy (NMD/SMA & weaver), Charolais leukodystrophy

Metabolic-toxic: enzootic ataxia (goats), organophosphate toxicity, (hepatic)

Neoplasia: lymphoma (extradural)

Inflammatory: discospondylitis, vertebral abscess, CAEV, rabies, Hypoderma bovis, P tenuis

Traumatic: trauma (risk of fractures in young), (camelid: vertebral malformation)

Vascular: FCEM

79
Q

Spinal lymphoma is more prevalent in small ruminant than in cattle: true or false? Why?​

A

False
Because of Bovine Leukemia Virus

80
Q

What are the causes of nutritionnal myelopathy in pigs?

A

Copper deficiency
Rapidly progressive PL paresis/ataxia in 3.5-6 mo.
Axonal degeneration

Overdose of arsanilic acid
Progressive PL ± TL paresis/ataxia
Axonal and myelin degeneration

81
Q

What neuropathological findings are associated with water deprivation in pigs?

A

Polioencephalomalacia and eosinophils cell infiltrates

82
Q

What is caused by selenium toxicity in pigs?

A

Acute poliomyelomalacia particularly in ventral gray horn at the cervicothoracic and lumbosacral intumescence + lesion in several brain stem nuclei (cuneatus, gracilis, facial, trigeminal, reticular)

83
Q

What is the best diagnostic test for selenium toxicity in pigs?

A

Selenium concentration in the liver
(better than blood)

84
Q

What is the preferential location for lymphosarcoma in cattle?

A

Lymphosarcoma tumors tend to be extradural in nature, causing compression of the spinal cord.

More than half of the cases reported in a recent study affected the lumbar, sacral, and cauda equina regions, leading to clinical signs of hindend ataxia and/or weakness.

85
Q

What is the main risk factor for development of lymphosarcoma in cattle?

A

Bovine leukemia virus

Oncogenic deltaretrovirus that infects lymphocytes

86
Q

What is the most common neoplasia of the bovine spinal cord?

A

Lymphosarcoma

87
Q

Which parasites can induce spinal cord injury due to parasitic migration? Where are they located?

A

Cattle:
Hypoderma bovis
Extradural, in epidural fat, maj LS

Other ruminants:
Parelaphostrongylus tenuis or Elaphostrongylus cervi
Intraspinal (dorsal gray column)

horse
Halicocephalus gingivalis

88
Q

Enzootic ataxia
1/ is caused by
2/ histopathologic lesion
3/ can be caused by high

A

1/Caused by copper deficiency
2/ demyelination in young lambs
3/High molybdenum or sulfur can interfere with absorption of copper

89
Q

Which nutritional deficiency can induce spinal cord disease in kids and lambs? What are pathological findings?

A

Copper deficiency during the prenatal or immediate postnatal period
Enzootic ataxia (postnatal) or swayback (prenatal)
Animals are generally affected between birth and 4 months of age.

Loss of myelin in the spinal cord
Wallerian degeneration
Lesions may also be present in the cerebrum and cerebellum.

90
Q

How to diagnose copper deficiency?

A

Low liver copper levels

91
Q

Treatment of enzootic ataxia with copper is ineffective: true or false?

A

True

Because of impaired fetal development

92
Q

Mechanism of organophosphate and carbamate toxicosis?

A

Block acetylcholinesterase
irreversible bond = organophosphate
reversible = carbamate

-> cholinergic crisis

93
Q

Give 5 infectious agents that spread into nerves in large animals.

A

Bovine herpes virus 5
Listeriosis
Pseudorabies
Rabies
Bornavirus

94
Q

Which mutation cause myotonia congenita in goats (fainting goat)?
+ transmission

A

CLCN1 skeletal muscle chloride channel – autosomal dominant with incomplete penetrance

95
Q

Horner’s syndrome in cattle is characterized by

A

Miosis, ptosis, enophthalmos, anhidrosis

96
Q

Hypocalcemia in cattle manifests:

A

Weakness, cold nose, cold ears, cold extremities, can progress to recumbence

97
Q

What happens with the membrane potential in hypocalcemia?

A

Low Ca2+ => facilitate sodium transport, as the normal inhibition by Ca2+ of sodium movement through voltage-gated sodium channels is lost => increase excitability of excitable cells => discharge spontaneously => tetanic muscle contraction.

98
Q

What are the 2 forms of bovine spastic paresis?

A

Early: < 8 months
Late: 2-6 yo

Progressive hyperextension of hindlimbs and contraction of Achilles tendon caused by persistent spasms of certain muscles

99
Q

Bovine spastic paresis is associated with reversible tonic and clonic muscular cramps: true or false?

A

False

It is bovine spastic syndrome

100
Q

Bovine spastic syndrome has only symptomatic treatment: true or false?

A

False

Surgical treatment is possible

101
Q

Where is the most common location with an hypoderma bovis infection in cattle?

A

Lumbosacral extradural spinal cord epidural fat

102
Q

What are the 3 phases of clinical signs in hypocalcemia?

A

Phase 1: hyper excitability, tetany, hyperaesthesia, tachycardia
Phase 2: non-ambulatory in sternal recumbency with reduced muscle tone; head and neck turned towards the flank
Phase 3: lateral recumbency, progressively reduced mental state, tympany, death within hours

103
Q

What happens with the membrane potential in hypomagnesemia?

A

Low Mg2+
the normal inhibition of Ca2+ movement through voltage-gated Ca2+ channels dissipates, so neurotransmission increases
particularly prominent at the neuromuscular junction
Results in tetany and muscle spasms.

104
Q

Name 4 causes for tetany in large animals

A

Tetanus
Strychnine toxication
Hypocalcemia
Inherited congenital tetany in polled Hereford calves, present at birth (Australia)
Presumptive inherited tetany as myoclonus in Peruvian Pasaos

105
Q

Which gene is implicated in the Hereford calves with congenital tetany and myoclonia?

A

GLRA1
glycine receptor, subunit alpha1

106
Q

What are the most common BoNT in ruminants?

107
Q

What is the main route for botulism in ruminants?

A

Ingestion of the toxin

Botulinum toxin is ingested as a prototoxin that requires activation by endogenous proteases.
The route of infection is in contrast to tetanus, in which spores contaminate a wound, establish an anaerobic environment, and then begin to produce toxin. In cattle, conditions such as phosphorus deficiency may cause pica and result in cattle chewing on the carcasses of dead animals that contain BoNT.

108
Q

What is the most frequent cause of the hypokaliemic myopathy in cattle?

A

Iatrogenic with use of mineralocorticoid drug for treatment of ketosis and clostridial mastitis

109
Q

What are the breeds and the mutation for malignant hyperthermia in pigs?

A

Landrace, Pietrain
RYR-1 (ryanodine receptor)

110
Q

Which nerve is the most commonly affected following dystocia in heifer?

A

Sciatic nerve (peroneal)

Obturator nerve is most commonly damaged secondary to compression following a prolonged dystocia; however, obturator nerve damage is less common than sciatic nerve damage following a dystocia.

Damage to the peroneal nerve following prolonged dystocia can result in the calving paralysis syndrome seen most commonly in first calf heifers.

111
Q

sensitivity of CSF to diagnose lymphocarcoma

112
Q

radial nerve lesion

A

radial nerve : extensor of elbow, carpus and digit + flexor of shoulder
> unable to bear weight or dragging the affected forelimb, with a dropped elbow and partially flexed carpus and fetlock.
distal damage to the radial nerve, the triceps muscle may still be functional

analgesia of the dorsal surface of the foot.

causes: prolonged recumbency leading to a myopathy-compartmentalization syndrome, getting a forelimb trapped, excessive force placed on the distal neck and shoulder in a head catch, or falling on a hard, slick surface, humeral fracture, olecranon fracture, and septic arthritis of the elbow joint.

113
Q

suprascapular nerve lesion

A

C6-C7, innervating the supraspinatus
and infraspinatus muscles.
extension and lateral support of the shoulder joint.

114
Q

most common periferal nerve injury in cattle

A

sciatic (L6-S2) extensors of the hip and hock and flexors of the stifle, ext + flex fetlock
peroneal nerve following prolonged dystocia can result in the calving paralysis syndrome seen most commonly in first calf heifers. Other causes of sciatic nerve dysfunction include injection site abscesses or direct damage to the nerve during an intramuscular injection.

115
Q

obturateur nerve injury

A

L4-L6, adduction of the PL
commonly damaged secondary to compression following a prolonged dystocia; less common than sciatic nerve damage, cattle slipping and abducting their hind limbs.
Animals should be able to walk and bear weight normally once standing.

116
Q

femoral nerve lesion

A

L4-L6, extension of the stifle and flexion of the hip.
most commonly in calves following forced extraction
cannot support the affected limb because of a lack of extensor tone and take on a characteristic crouched posture if the injury is bilateral. Atrophy of the quadriceps femoris muscle may be noted 7 to 10 days after injury and patellar luxation may follow.

117
Q

forms of CAEV and maedi/visna infections

A

CAEV
adult goat: chronic polyarthritis, bilateral mastitis, interst pneumonia, chronic wasting
kids 1-6m : leucoencephalomyelitis

Maedi/visna
kids: paresis
adult sheep: brain (circling) or SC (knuckling 1HL)

118
Q

seroprevalence CEAV

A

widespread (seroprev >65%)
Canada, Norway, France, US

119
Q

retrovirus in small rmnt
% developping disease
where is replication?

A

Caprine Arthritis and Encephalitis
Ovine progressive pneumonia and maedi-visna in North America and Europe, respectively

30% dev disease

replication in monocytes (vs lympho in other retrov), proviral DNA in monocyte for life but lymphoproliferative lesion do not cause immunosuppression
humoral + cell mediated response but do not confer immunity

120
Q

gene confering sensibility to retrovirus in small rumnt

A

specif transmebran protein TMEM154 (3x more likely)

121
Q

transmission lentivirus in small rmnt + favorisant factor

A

ingestion of infected colostrum and/or milk, or through inhalation of respiratory secretions

factor: lenght exposure, animal density, housing type

122
Q

symptoms of listeria infection

A

neurologic (sporadic, higher morbidity and mortality in small rmnt): multifocal assymetric BS, diffuse meningoencephalitis, myelitis
caudal BS, cerebellar peduncle, SC
CN V - XII usually dysfunctional

ocular: keratoconjonct + uveitis +/- hypopyos
septicemia: neonat death
sporadic late abortion
mammitis
diarrhea

123
Q

listeria characteristics, maj serotype

A

gram +, non spore forming, facult anaerobic
persistant years in env, can replicate in refrigerated temp
inhib pH < 5.6
facult intracellular, can replicate in monocytes/macrophages

maj serotype 1/2a and 4b

124
Q

reservoir + transmission of listeriosis

A

soil
digestive tract of human, mamals, bird, fish, crusteacean

infect by ingestion of poorly preserved silage (pH > 5.5 and aerobi c env) during winter or early spring housing

infect sheep and cattle > goat
increase sensib Rambouillet sheep and Angora goat

delay between contamination and clinical signs: 2–6 weeks

125
Q

differential BS disease

A

listeria
otitis media
abcess of BS or pituitary gland (depressed, have a base-wide stance with head and neck extended, bradycardia, or exophthalmia)
tumor
aberent parasit migration
trauma
thrombotic meningoencephalitis (histophilus somni)
bacterial meningitis (young animal)

126
Q

CFS in listeria + prognosis factor

A

increased total protein concentration (usually >40 mg/dL) and nucleated cell count (usually >12 cells/mL), with mononuclear cells predominating
in small ruminants
, neutrophils are often observed in the CSF and, occasionally, predominate

analysis of CSF does not seem to correlate with the severity of the clinical signs or provide information on the outcome of the disease, except for creatinine phosphokinase

Because L monocytogenes rarely reaches the meningoventricular system, detection of the bacteria by culture or polymerase chain reaction in the CSF is frequently negative.

127
Q

most common infected structure in listeria

A

reticular formation
cranial nerves V, VII, and XII nuclei
pons and medulla oblongata

128
Q

macro and microscopic lesion with listeria

A

macro: mild meningeal congestion and increased turbidity of the CSF

micro: multifocal asymmetrical brainstem microabscesses with areas of malacia and intense perivascular cuffing with mononuclear cells, and meningoencephalitis. maj PNN in microabsess, macro in malacia. multifocal
gliosis, axonal swelling, and degeneration and neuronophagia

L monocytogenes was isolated from brain homogenates in approx 50%, best recovered from refrigerated nervous tissues.

129
Q

diagnosis of listeria

A
  1. monocytosis is not observed in ruminants (compared to monosgast)
  2. metabolic acidosis
  3. CSF: increase PT, monocellular cells (sometimes PNN in small rum)
  4. post mortem: multifocal microabscesses in the brainstem and isolation of L monocytogenes from infected brain tissue
  5. combined PCR in milk and ELISA in serum
  6. culturing feed or bedding
130
Q

treatment of listeria

A

penicillin, ampicillin, amoxicillin, aminoglycosides, macrolides (erythromycin), and chloramphenicol

Recomanded: penicillin, ampicillin, and tetracycline 2–4 weeks

proportion of isolates from a dairy environment that were resistant to penicillin, ampicillin, tetracycline, or florfenicol were 40%, 92%, 45%, and 66%, respectively

should penetrate the intracellular space, cross the blood–brain barrier, and be bactericidal.

effective only when instituted early in the disease course

Reported survival rates in small ruminants and cattle with encephalitic listeriosis after treatment are 26% and 70%

131
Q

zoonotic potential of listeria

A

raw or improperly pasteurized milk or milk products (cheese), processed meat products, coleslaw, and contaminated raw produce
including melons.

The 4b serotype of L monocytogenes most often responsible for infections in humans.

Cutaneous listeriosis has been observed as result of handling aborted fetuses and placentas.

132
Q

etiology of otitis media in rmnt

A

Respiratory
tract pathogens including H somni, Mannheimia haemolytica, Mycoplasma bovis, and Pasteurella multocida are often isolated, as is Trueperella
pyogenes (formerly Arcanobacterium pyogenes) in more chronic cases.
M bovis, either alone or in association with other bacteria, is becoming increasingly recognized as the main etiologic agent of OMI in dairy calves

pigs: Streptococcus spp., particularly Streptococcus suis

133
Q

risk factor median otitis

A

young animal
Bottle feeding and feeding contaminated colostrum or milk
presence of a coincidental respiratory infection

OMI is usually unilateral, but at least 25% of cases had bilateral involvement in several reports

134
Q

most common bacterial species isolated from cases of pituitary abscess
+ maj associated infections

A

T. pyogenes

tooth abscess, mastitis, bronchopneumonia, and sinusitis (postdehorning)

135
Q

risk factor for pituitary abcess

A

use of nose flaps for weaning calves
placement of nose rings

136
Q

most common sign with pituitary abcess

A

depression

Signs of brainstem dysfunction and accompanying cranial nerve deficits are typically asymmetrical and include facial paralysis, dysphagia, jaw and tongue hypotonia, decreased facial sensation, and head tilt. Abnormalities found on neuroophthalmologic examination include blindness, abnormal pupillary light reflexes, strabismus, and nystagmus

Bradycardia is reported to occur in up to 50% of cases and is thought to be owing to compression of the hypothalamus

137
Q

breeds predisposed to congenital cerebellar hypoplasia

A

Hereford
Ayrshire
Shorthorn

+ Brown swiss progressive degen myeloencephalopathy (Purkinge C, sc wm, reproductive tract, sq m)

138
Q

viral-induced cerebellar hypoplasia

A
  1. BVD (125-180 d of gestation), BVD vaccine (90-118d)
  2. Sheep pestivirus (Border disease)
  3. Schmallenberg (+ hydranencephaly, porencephaly, dysplasia BS/SC, arthrogryphosis)
  4. Bluetongue
  5. Ainovirus in Japan
139
Q

virus causing polymyositis in gestation

A

Akabane (+ non purulent encephalomyelitis)

140
Q

breeds predisposed to cerebellar abiotrophy

A

Angus
Charolais
Hereford
Shorthorn
Limousin

141
Q

plant causing cerebellar toxicity

A

Solanum: low Purkinge cells, wallerian degen cerebellar wm

Locoweed: mannosidase

142
Q

lysosomal storage disease in rmnt

A

alpha-mannosidosis (cerebellum): Angus, Murray grey, Galloway

beta-mannosidosis (cerebellum): Salers

Mapple syrup urine disease (cerebellum): hereford, Shorthorn

GM1 gang (foreb): Friesian

glycogen storage (muscles): Brahman, Charolais

Citrullinemia (hyperammonemia): Holstein

143
Q

causes of tremors in rmnt

A

grass straggers (hypoMg)
perennial ryegrass (GABA recept, loss Purkinge)
Staggers (phalaris, Dallis, Bermuda)
Penicillum in moldy corn
Aspergillus

144
Q

plants with muscular toxicity

A

White snakeroot:
(Ageratina altissima): toxin tremetone, y reluctance to move and fine muscle tremors. swelling and palor or streaking of many skeletal muscles

Thermopsis spp.:
toxins: quinolizidine alkaloids, anagyrine, thermopsine, cystisine, and N-methylcytisine
muscle weakness often accompanied by recumbency. Microscopically there is prominent skeletal muscle degeneration and necrosis with patchy areas of regenerations

Cassia or Senna spp.: myoglobinuria skeletal muscle
necrosis and degeneration that may be polyphasic making it difficult to differentiate from some
nutritional myopathies.

145
Q

Nutritionnal myelopathy in pigs

A

1/ Copper deficiency: rapidly progressive PL paresis/ataxia in 3.5-6 mo. Axonal degeneration

2/ Overdose of arsanilic acid: Progressive PL+/-TL paresis/ataxia
Axonal and myelin degeneration

146
Q

Infectious agent that spread into nerves in large animals

A

Bovine herpes virus 5
Listeriosis
Pseudorabies
Rabies
Bornavirus

147
Q

Inclusions associated with virus

A

Herpes virus: basophilic, intranuclear in neuron/glial cell

Rabies: negri bodies (eosinophilic inytracytoplasmic in neurons)

Pseudorabies: eosinophilic intranuclear in astrocyte

Distemper: eosinophilic, intranuclear/cytoplasmic

Borna disease: Joesty-Degen inclusion bodies nucleus > cytoplasm neuron in hippocampus

Rubarth’s disease: baso/amphophilic inclusion bodies in nuclei of endothelial cells

148
Q

gram tetanus botulism

A

tetanus gram +
botulism gram -

149
Q

% discharge in non ambulatory adult beef cattle

A

19% were discharged, and the remaining 81% died or were euthanized (69.8%).

The odds of being discharged increased with each additional day of hospitalization and with each additional flotation therapy session.

Down beef cattle with a diagnosis of calving peripheral nerve paralysis and capable of walking out the tank after the first flotation session were 6.66 and 30 times more likely to be discharged