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3. Food Animal 4 > Ruminant Neurology > Flashcards

Ruminant Neurology Flashcards

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
Maedi-Visna Virus - neurological form prevalence - who is affected - neurologic signs
 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
Maedi-Visna Virus non-neuro signs
 Weight loss  Pneumonia  Arthritis  Mammary gland enlargement
27
Maedi-Visna Virus clinical pathology
 CSF: pleocytosis, protein may be elevated  Detect specific antibodies, virus in CSF
28
Maedi-Visna Virus - pathophysiology - pathology / lesions - control
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
Caprine Arthritis Encephalitis - who gets this - neuro signs
 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
C.A.E.  Clinical signs (brain):
- 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
C. A. E.  Differential diagnosis:
Trauma Listeriosis Multi-systemic mycoplasma inf. Parelophastrongylus tenuis (P. tenuis)
32
C. A. E. diagnosis
 Serology (ELISA, AGID), PCR  CSF – pleocytosis, ↑protein
33
Polioencephalomalacia - what is this? - common terms - causes
 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
Polioencephalomalacia  Epidemiology
 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
Polioencephalomalacia  Possible etiologies
 Excessive sulfur ingestion  Altered thiamine metabolism  Salt poisoning/water deprivation  Amprolium administration  Molasses & urea diets  Lead intoxication
36
Polioencephalomalacia  Clinical signs
 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
Polioencephalomalacia  Differential diagnoses:
 Grain overload  Enterotoxemia type D (small ruminants)  Head trauma  Bacterial meningoencephalitis  Nervous coccidiosis  Vitamin A deficiency  Ethylene glycol toxicity  Rabies  Neurologic IBR
38
Polioencephalomalacia  Clinical pathology
 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
Polioencephalomalacia - pathgenesis - end result
 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
Polioencephalomalacia  What is role of thiamine?
 Low thiamine – decreased: intake, production, absorption, transference > Thiaminases– bacterial, plant > Thiamine analogs – amprolium  High sulfur
41
Polioencephalomalacia  Necropsy:
 H2S smell  Ruminal, respiratory or coccidial diseases <><> Brain:  Autofluorescense (UV light; Wood’s lamp)  Swelling, softening, flattening  Herniation  Histology: diffuse laminar necrosis
42
Polioencephalomalacia  Treatment, prognosis
 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
Listeriosis - agent - disease - who is affected - forms
 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
Listeriosis - clinical signs
 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
Listeriosis - cranial nerves effected?
 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
Listeriosis - clinical pathology, lesions
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
Listeriosis pathophysiology, species differences
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
Listeriosis  Cause
 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

3. Food Animal 4 (16 decks)

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