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3. Food Animal 4 > Ruminant Neurology > Flashcards

Ruminant Neurology Flashcards

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1
Q

Otitis Media & Interna
- who gets it? how?
- pathogens

A

 Cattle, sheep (goats)
<><>
 Secondary to respiratory infection:
 Mannheimia hemolytica
 Pasteurella multocida
 Corynebacterium pseudotuberculosis
 Histophilus somni
 Mycoplasma spp.
<><>
 Role of viruses unknown
<><>
- Nasopharynx > auditory tube > middle ear
- external ear > middle ear

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2
Q

Otitis Media & Interna
- signs
- progression
- less common lesions?

A

 Unilateral peripheral vestibular signs
<><>
 Middle ear infection may progress
> Inner ear
> Less common
=> Subdural abscess formation
=> Meningoencephalitis
=> Brain abscess formation

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3
Q

Otitis Media & Interna
- clinical signs

A
  • Head shaking, ear droop
    <><>
  • Vestibular signs:
     Head tilt (towards lesion)
     Continuous horizontal nystagmus (away
    from lesion; “fast away”)
     Imbalance
     Circling (towards lesion)
    <><>
  • Recumbency – tend to lay on side toward
    lesion
    <><>
  • May have facial nerve involvement
     Ear, eyelid, muzzle
    <><>
  • Less common
     Fever
     Purulent exudate
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4
Q

Otitis Media & Interna
 Differential diagnosis

A
  • Central vestibular disease
     Depression, decreased awareness
     Irregular nystagmus (direction varies)
     Marked proprioceptive deficits
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5
Q

Otitis Media & Interna
- treatment

A

 Many antibiotics (penicillin, oxytetracycline,
florphenicol, macrolides, fluoroquinolones (if legal))
 Many need long-term treatment
 Acute has better prognosis than chronic disease

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6
Q

Bacterial Meningitis
- etiology, risk factors
- source

A

 Often result of bacteremia, septicemia
 Often associated with failure of passive transfer of colostral antibodies
 Bacterial source – respiratory, gastrointestinal, umbilicus
 May result from direct extension from trauma
(including iatrogenic), other infections

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7
Q

Bacterial Meningitis
- Bacterial types – many

A

Gram-negative
 Escherichia coli
 Klebsiella pneumoniae
 Salmonella spp.
Histophilus somni
 Actinobacillus equuli
<><>
Gram-positive
 Streptococcus spp.
 Staphyloccus spp.
Listeria monocytogenes

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8
Q

Bacterial Meningitis
- clinical signs

A

 Primary disease site
 Sites of bacterial localization in septicemia
 Fever, depression, decreased suckling
 Hyperesthesia, neck pain
<><>
 Skin stimulation – hyperresponsiveness
> Limb extensor reaction
> Muscle fasciculations
> Generalized frantic motions
<><>
 Cranial nerve signs
 Progressive central signs – compulsive walking, stupor, coma, seizures

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9
Q

Bacterial Meningitis
- Differential diagnoses:

A
  • Viral encephalitidies
    <><>
  • Metabolic encephalosis
     Hypomagnesemia, hypocalcemia, hypoglycemia
     Hepatic encephalopathy
     Renal encephalopathy
    <><>
  • Encephalomalacias
    Salt poisoning
    Polioencephalomalacia
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10
Q

Bacterial Meningitis
 Diagnostic testing

A

 Physical examination
 Complete blood count
 Serum biochemistry profile
 Immunoglobulin level (neonate)
<><>
 Cerebrospinal fluid analysis
> Routine – color, turbidity, nucleated cells, protein
> Gram-stain, bacterial culture
> Glucose level (infection <50% of blood level)

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11
Q

Bacterial Meningitis
- pathophysiology
- necropsy

A

Pathophysiology
 Bacteria, endotoxins, cytokines, other
 Thrombotic or hemorrhagic infarcts
<><>
Necropsy
 Congestion, swelling, inflammation, fibrin, infarcts, hemorrhages

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12
Q

Bacterial Meningitis
 Treatment

A

Antibiotics –
 Identify bacteria – Gram-stain, culture & sensitivity
 Usually aerobic bacteria
 Need to cross the BBB (lipid soluble, small molecule)
 Bactericidal
 Off-label
 Typically: penicillin, ampicillin, trimethoprim sulfa
 Ideally – 3rd or 4th generation cephalosporin (ceftiofur)
<><>
Anti-inflammatory medication
 NSAIDs
 Anti-inflammatory dose corticosteroids
<><>
 Edema control
 Seizure control
 Supportive care: fluids, plasma, nutrition, nursing care

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13
Q

Pituitary Abscesses
- who gets this?
- location?
- pathogenesis
- age

A

 Ruminants (rare in horses)
 Sella turcica
 Seed the rete mirabile (blood vessel
complex encircling the pituitary)
 Expansive mass > brain
 Age: usually 2 – 5 years of age; range 9
mo– 12 yrs

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14
Q

Pituitary Abscesses
 Signs

A
  • Ataxia, head & neck extension, base-wide stance, inappetence, depression, head pressing,
    recumbency
    <><>
  • Cranial nerve signs (may be asymmetric)
     Dysphagia - Flaccid tongue
     Blindness - Nystagmus
     Anisocoria - Facial paralysis
     decreased PLRs - Facial hypalgesia
     Mydriasis - Head tilt
     Strabismus
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15
Q

Nervous Coccidiosis
- pathogen
- who is affected
- when?
- type of disease?
- what causes the problems?
- mortality
- rare associated condition

A

 Eimeria species – E. zuernii, E. bovis (cattle)
 Calves, yearling cattle, sheep, goats
 Winter months, feedlots
 Cerebral cortical disease, encephalopathy
 Heat-labile neurotoxin from parasite
 High mortality (~70%)
 (rarely blind)

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16
Q

Nervous Coccidiosis
 Diagnosis, differentials, PM

A

 Rule out other diseases
 Analyze individual & herd mate feces for Eimeria spp. oocysts
 Differential diagnosis: meningitis, salt poisoning, clostridial enterotoxemia, Vit A deficiency, lead poisoning, polioencephalomalacia, rabies, pseudorabies, ethylene glycol poisoning . . .
 Necropsy – no gross CNS lesions, non-specific histologic findings (edema, congestion, occasional shrunken neuron)

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17
Q

Nervous Coccidiosis
 Treatment

A

 Coccidia – sulfas, amprolium
 Fluids, electrolytes, glucose
 Seizure control – diazepam, phenobarbital

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18
Q

Bovine Herpes Virus
- systems it affects
- strains
- risks
- who is affected

A

 IBR – respiratory, ocular, genital, neuro
 BoHV-1, BoHV-5
 Role of stress?
 Age: < 6 weeks of age but adults too

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19
Q

Bovine Herpes Virus - neurological signs

A
  • encephalitis
     Depression, mild nasal & ocular discharge
     CP deficits, ataxia, vocalization, salivation, bruxism, tongue paralysis, head tilt, nystagmus, convulsions, blindness, coma, death
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20
Q

Bovine Virus Diarrhea Virus
- neurologic lesions, signs, pathogenesis, cells affected

A

 Cerebellar hypoplasia
 Gestational infection – days 90 – 170
 Abortion, hydrancephaly, cerebellar hypoplasia
 Infects developing germinal cells of cerebellum
 Purkinje cell death in granular layer (necrosis & inflammation)

21
Q

Neurologic BVD
 Clinical signs

A

– present at birth
 Inability to stand
 Truncal ataxia
 Base-wide stance
 Falling backward
 Opisthotonus
 Coarse intentional head tremors
 Hypermetria, hyperrelexia
 Nystagmus, strabismus
<><><><>

22
Q

Neurologic BVD
- ocular signs

A

 Lack of vision (hydrancephaly)
 Microophthalmia
 Cataracts, corneal opacities

23
Q

Neurologic BVD diagnosis

A

 Examination findings
 Precolostral antibodies
 (virus isolation)

24
Q

Maedi-Visna Virus
- what is this?
- related viruses, group

A

 Ovine Progressive Pneumonia (OPP)
<><>
Retrovirus (subfamily - Lentivirinae):
 Caprine Arthritis-Encephalitis virus
 Equine Viral Arteritis virus
 Immunodeficiency viruses – human, simian, feline
<><>
 Group – Small Ruminant Lentiviruses

25
Q

Maedi-Visna Virus
- neurological form prevalence
- who is affected
- neurologic signs

A

 Neurologic form – rare
 > 4 months of age
 Neurologic signs (progressive):
- Ataxia - Limb weakness
- CP deficits - Facial twitching
- Circling - Straight, staggering, stumbling
- Hyperesthesia - Blindness
- Coma - Convulsions

26
Q

Maedi-Visna Virus non-neuro signs

A

 Weight loss
 Pneumonia
 Arthritis
 Mammary gland enlargement

27
Q

Maedi-Visna Virus clinical pathology

A

 CSF: pleocytosis, protein may be elevated
 Detect specific antibodies, virus in CSF

28
Q

Maedi-Visna Virus
- pathophysiology
- pathology / lesions
- control

A

Pathophysiology
 Immunosuppressive
 Susceptible to secondary bacterial infections
<><>
Pathology
 May have areas of inflammation & malacia
 White > gray matter lesions
 Diffuse, non-suppurative, peri-vascular inflammation
<><>
 Control – culling, euthanasia

29
Q

Caprine Arthritis Encephalitis
- who gets this
- neuro signs

A

 Leukoencephalomyelitis– usu. < 1 year old
 Neurologic signs highly variable: (spinal)
- Progressive ataxia - hemiparesis
- Paraplegia - tetraplegia
- Tetraparesis - paraparesis
- Hemiplegia
- C1-C2 lesions – recumbent, unable to raise head

30
Q

C.A.E.
 Clinical signs (brain):

A
  • symmetric or asymmetic
  • Head tilt - Nystagmus
  • Tremors - Torticollis
  • Salivation - Depression
  • Coma - Opisthotonus
  • Vision compromise - PLR decreased
     Other signs: fever, joint enlargement, mammary enlargement, shifting lameness, weight loss, tachypnea
31
Q

C. A. E.
 Differential diagnosis:

A

Trauma
Listeriosis
Multi-systemic mycoplasma inf.
Parelophastrongylus tenuis (P. tenuis)

32
Q

C. A. E. diagnosis

A

 Serology (ELISA, AGID), PCR
 CSF – pleocytosis, ↑protein

33
Q

Polioencephalomalacia
- what is this?
- common terms
- causes

A

 Cerebrocortical necrosis (CCN)
 Common terms: polio, sleeper, brainer
 Descriptive term (histological) – softening or
necrosis of the brain, gray matter
 Causes – multiple
> Altered thiamine metabolism
> Excessive sulfas

34
Q

Polioencephalomalacia
 Epidemiology

A

 Worldwide distribution
 Individuals or herd outbreaks
 No gender or breed predilection
 Predominantly in high concentrate diet fed animals but can occur in animals on pasture
 Cattle, sheep, goats, camelids, deer
 Age: 3 weeks to years; peak – 18 months of age or younger; variable depending on system

35
Q

Polioencephalomalacia
 Possible etiologies

A

 Excessive sulfur ingestion
 Altered thiamine metabolism
 Salt poisoning/water deprivation
 Amprolium administration
 Molasses & urea diets
 Lead intoxication

36
Q

Polioencephalomalacia
 Clinical signs

A

 Acute or subacute onset
 Anorexia, separation from group, stagger
 Blindness, slight hypermetric gait, walk with head erect
 Head pressing, opisthotonos, strabismus, miosis,
chewing, ptyalism, odontoprisis
 Other – may have tachycardia, tachypnea, sl.
elevation in temperature (if fasciculations)
 Sulfur smell
 Recumbency, coma, convulsions, death

37
Q

Polioencephalomalacia
 Differential diagnoses:

A

 Grain overload
 Enterotoxemia type D (small ruminants)
 Head trauma
 Bacterial meningoencephalitis
 Nervous coccidiosis
 Vitamin A deficiency
 Ethylene glycol toxicity
 Rabies
 Neurologic IBR

38
Q

Polioencephalomalacia
 Clinical pathology

A

 Diagnosis – hx, exam, response to treatment
 Sulfide concentrations (rumen fluid/gas cap)
 Thiamine concentrations (blood) – several methods
 CSF – increased nucleated cells, increased protein
<><>
 Environmental & feed examination is essential

39
Q

Polioencephalomalacia
- pathgenesis
- end result

A

 Pathogenesis – neuronal edema & necrosis
 Thought to be due to ATP depletion and
malfunction of Na/K pump
 End result– brain swelling in fixed calvarium
 Brain – very high metabolic rate, dependent on high rate of oxygen and glucose delivery (very little glucose stores)

40
Q

Polioencephalomalacia
 What is role of thiamine?

A

 Low thiamine – decreased: intake, production,
absorption, transference
> Thiaminases– bacterial, plant
> Thiamine analogs – amprolium
 High sulfur

41
Q

Polioencephalomalacia
 Necropsy:

A

 H2S smell
 Ruminal, respiratory or coccidial diseases
<><>
Brain:
 Autofluorescense (UV light; Wood’s lamp)
 Swelling, softening, flattening
 Herniation
 Histology: diffuse laminar necrosis

42
Q

Polioencephalomalacia
 Treatment, prognosis

A

 Remove initiating source
 Thiamine HCl– 10 – 20 mg/kg tid, SC or IM (IV first dose – slowly)
 Dexamethasone, mannitol, glucose
 Seizure control
<><>
Prognosis
 Depends on response to therapy, give at least 3 days
 May take weeks to months to recover vision, sensorium
 Subacute cases recovery more favorable than acute cases

43
Q

Listeriosis
- agent
- disease
- who is affected
- forms

A

 Listeria monocytogenes
 Gram-positive organism
 Acute meningoencephalitis
 Ruminants, fowl, humans (rare in horses)
<><>
Neurologic listeriosis– 3 general forms
 Multifocal brainstem disorder
 Diffuse meningoencephalitis
 Myelitis

44
Q

Listeriosis
- clinical signs

A

 Clinical signs – caudal brainstem, cerebellar
peduncles, spinal cord
 Fever, poor appetite, depression > RAS
<><>
Neurologic signs are usually asymmetric
 Conscious proprioceptive deficits – descending motor pathways, ascending proprioceptive fibers
 Head pressing
 Cranial nerve deficits
 Vestibular signs – recumbent, head tilt, torticollis, other

45
Q

Listeriosis - cranial nerves effected?

A

 Cranial nerves – V XII often affected
 Trigeminal (V) > Motor, sensory
 Abducens (VI) – lateral rectus m.
 Facial (VII)
 Vestibulocochlear (VIII)
 Hypoglossal (IX)
 Vagal (X)
 Spinal accessory (XI)
 Hypoglossal (XII)

46
Q

Listeriosis
- clinical pathology, lesions

A

Clinical pathology
 CSF analysis – variable increase protein, nucleated cells monocytes (hence the species
name)
 Adult cattle – metabolic acidosis due to loss of saliva
<><>
Pathology
 Multifocal microabscesses in the brainstem
 Isolate organism

47
Q

Listeriosis pathophysiology, species differences

A

Pathophysiology –
 Trigeminal nerve spread, moves centripedally into CNS
 Bacteremia (?)
 Toxin – role is unknown (hemolysin, listeriolysin-O)
<><>
 Untreated – usually lethal
 Sheep & goats – more acute onset & progression

48
Q

Listeriosis
 Cause

A

 Contaminated feed
 Ensiled feed – improperly cured
> Bacteria proliferates in aerobic conditions, pH >5.3
> Silage, hay, rotten feed,
 Trench silos
 Organism can persist in soil for years

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