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Ruminant clinical medicine > Diseases of the nervous system > Flashcards

Diseases of the nervous system Flashcards

1
Q

NEUROLOGICAL DISORDERS broadly CAUSE what types of signs: (3)

A
  • Abnormal behavior
  • Abnormal motion
  • Neuromuscular abnormalities
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2
Q

Name 4 toxicoses to cause CNS signs in cattle.

A

ammonia
lead
salt
organophophates

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3
Q

Name 8 infectious diseases to cause CNS signs in cattle.

A

Listeriosis
Histophilus somni

Rabies
Aujeszky
BSE

Tetanus
Botulism
Herpes virosis -1

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4
Q

TEME stands for

A

Thromboembolic meningoencephalitis—also called. TEME and “Brainer”—is a severe disease that affects the brain of range and feedlot cattle.

It is caused by the bacteria Histophilus somni, an organism that also can cause pneumonia, arthritis, and abortion in cattle.

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5
Q

Name 2 congenital diseases to cause peripheral NS signs in cattle.

A

Spastic paresis
Spastic syndrome

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6
Q

Name a traumatic cause of peripheral NS signs in cattle.

A

dystocia

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7
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

Evaluate…? (6)

A
  • The mental status of the cow
  • Examination of cranial nerves
  • The gait and posture
  • The postural reactions
  • The spinal reflexes
  • The response to pain
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8
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 1: Mental status – helps you decide

A

Provides the evidence in differentiating intracranial from extracranial lesions.

Abnormalities in brainstem or thalamocortex alter behavior and interaction with the environment.

Is the cow aware of the examiner’s presence or not?

Does the cow act socially with her herd mates?

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9
Q

If brain is infected, the cause is
usually (3)

A

encephalitis, meningitis,
meningoencephalitis

= inflammation of the brain tissues

  • Neural parenchyma is damaged
    by inflammatory mediators, infarctions,
    decreased absorption of CSF which result in
    clinical signs.
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10
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 2 : Cranial nerves – helps you evaluate..

A

which part of the brain is affected.

In cows, CN I and XI are not evaluated.

(XI primarily controls the muscles involved in head and neck movement.)

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11
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 3 : Gait and posture – helps you evaluate…

A

is the problem in the CNS or peripheral nervous system.

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12
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 4 : Postural reactions – helps you evaluate…

A

which part of the spinal cord is affected.

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13
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 5 : Spinal reflexes – helps you evaluate…

A

which part of the spinal cord / which peripheral nerve is affected.

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14
Q

FINDING THE AFFECTED REGION OF THE NERVOUS SYSTEM

STEP 6 : Pain perception – helps you evaluate…

A

gain insight into sensory processing and potential areas of nervous system damage or dysfunction.

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15
Q

TREATMENT OF
MENINGITIS/
MENINGOENCEPHALITIS

A
  • Under normal conditions, antibiotics that reach high plasma concentration, may not
    necessarily reach bactericidal concentrations in the brain.

Under conditions of local inflammation, the (BBB) becomes more permeable and bactericidal concentrations in the brain tissue can be achieved.

  • General rule: use the highest doses recommended to maximize the distribution of antimicrobials across the BBB into the infected neural tissue.
  • Intravenous administration is preferred – to obtain peak blood concentrations and spur greater diffusion of drugs across the BBB.
  • Factors affecting the penetration of drugs into CSF are lipid solubility and molecular size.
  • G-neg: Penicillin G, ampicillin, trimethoprim+sulfa, enrofloxacin, (cephalosporins)
  • G-pos: Penicillin, ampicillin, TMS
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16
Q

”SLEEPER CALVES” are so called due to what disease

A

TROMBOEMBOLIC MENINGOENCEFALITIS
(TEME) – ”SLEEPER CALVES”
HISTOPHILUS SOMNI bacteria

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17
Q

What age calves get TEME?

A

THROMBOEMBOLIC MENINGOENCEFALITIS
(TEME)

weaned calves

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18
Q

How does Histophilus somni cause thromboembolic meningoencephalitis?

A

in the bloodstream, H. somni adheres to and invades the endothelial cells lining blood vessels.

intense inflammatory response damages the vascular endothelium, leading to increased permeability and exposing the subendothelial tissue.

exposure of subendothelial tissue trigger blood clot formation.

these thrombi obstruct blood flow in the capillaries and small blood vessels, especially within the brain, they lead to ischemia and necrosis.

The inflammatory response extends into the meninges (membranes surrounding the brain and spinal cord) and brain tissue, resulting in meningoencephalitis.

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19
Q

Clinical signs of TEME. (6)

A
  • Sudden death
  • Depression
  • Stiffness
  • Muscle weakness
  • Ataxia
  • Hyperesthesia
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20
Q

Treatment & prevention of TEME.

A
  • Oxytetracycline 10-20 mg/kg IV
    Supportive treatment
  • NSAIDS
  • Fluid therapy

Prevention:
* Colostrum = prevention of failure of passive transfer
* Hygiene

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21
Q

What does listeriosis cause?

A

Listeria monocytogenes bacteria cause Encephalitis or meningoencephalitis in adult ruminants.

  • Septicemia in calves
  • Abortions in humans
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22
Q

Listeria is localized to the brainstem and ascends

A

the trigeminal nerve.

23
Q

Cows usually get listeriosis due to:

A

Poorly fermentated silage (less acidic, high pH)

24
Q

Clinical sign of listeriosis in cattle.

A
  • Facial paralysis
  • Somnolence/depression
  • Head pressing
  • Circling
  • Cranial nerve deficits such as lack of menace response, pupillary light
    reflex, palpebral reflex and asymmetric face.
25
Q

Treatment of listeriosis in cattle.

A
  • Penicillin is the drug of choice, when treating listeriosis.
  • The daily dose should be high, 44 000 IU/kg for 1-2 weeks.
  • Double dose!!!

+ Supportive care

26
Q

When brain is affected by poisonings or deficiencies, what occurs

A

polioencephalomalacia occurs.

  • Softening or necrosis of regions of the gray matter of the brain.

Different etiologies – thiamine, B1, deficiency, lead poisoning, salt poisoning,
ammonia poisoning.

27
Q

Who is usually affected by POLIOENCEFALOMALACIA/ CEREBROCORTICAL NECROSIS due to
DEFICIENCY OF VITAMIN B1 (THIAMINE)

A

Young cattle are more frequently affected.

28
Q

Clinical signs of POLIOENCEFALOMALACIA/ CEREBROCORTICAL NECROSIS due to
DEFICIENCY OF VITAMIN B1 (THIAMINE) include:

A
  • blindness, recumbency, tonic-clonic seizures, coma.
  • cortical blindness, absent menace response
  • ataxia and hypermetric gait
  • Also head pressing, opisthotonos and grinding of the teeth may occur.
29
Q

Treatment of B1 deficiency includes:

A

thiamine 10-20 mg/kg IV
or
IM 3 times per day for 3-7
days.

30
Q

AMMONIA TOXICOSIS occurs due to

A
  • Ingestion of excess urea or other
    sources of non-protein nitrogen in
    cows diet.
  • e.g. poisoning by fertilizers
    containing ammonium salts/urea is
    possible.
31
Q

AMMONIA TOXICOSIS * Clinical signs include

A
  • muscle tremors,
  • exophthalmia,
  • frothy salivation,
    bruxism,
  • incoordination and
    weakness.
  • Pulmonary edema leads to
    marked salivation, dyspnea,
    and gasping.
32
Q

Treatment of ammonia toxicosis.

A
  • Supportive care!
  • Ruminal infusion of 5% acetic acid (vinegar 2–8 L in cattle) → NH3 to NH4+.
  • Ruminal infusion of iced (0–4°C) water up to 40 L in adult cattle → Dilution of rumen
    content.
  • IV Ca and Mg to stop seizures
33
Q

LEAD POISONING
* Mainly seen in …

NB can be caused by…

+ Pathogenesis.

A

young animals.

  • Batteries!
  • Cerebellar edema and hemorrhages
    due to capillary damage in the brain
    tissue → cerebral cortex congestion.
34
Q

LEAD POISONING Clinical signs include:

A
  • ataxia,
  • blindness,
  • salivation,
  • convulsions,
  • spastic twitching of eyelids,
  • bruxism,
  • muscle tremors
  • Circling
35
Q

LEAD POISONING treatment methods (4)

A

thiamine 2-4 mg/kg SC

Ca-EDTA 110 mg/kg IV

Magnesium sulfate 400 mg/kg PO

these compounds work together to help reduce lead absorption, enhance its excretion, and mitigate the toxic effects of lead on the nervous system.

Surgery to remove particles
containing lead from the rumen.

36
Q

Salt toxicity / water deprivation / sodium ion toxication Does not occur, if

A

fresh water is always available for the animals!

37
Q

Salt toxicity / water deprivation / sodium ion toxication pathogenesis.

A

Cerebellar edema and inflammation of the meninges→
Na diffuses to CSF and brain by passive diffusion →
hyperosmolarity reduces Na
transport out of neurons →
these neurons are triggered →
animal drinks more and fluids diffuse towards the higher osmolarity in brain causing swelling.

38
Q

Salt toxicity / water deprivation / sodium ion toxication Clinical signs include:

A
  • salivation, increased thirst, diarrhea
  • aggressive behavior, ataxia, circling
  • blindness, seizures and partial paralysis
  • Cow may drag her hind limbs and knuckling of the fetlock joint may occur.
39
Q

Salt toxicity / water deprivation / sodium ion toxication treatment:

A

IV infusion of normal/hypertonic saline in maintainance rate slowly →
idea is to make higher conc of Na in bloodstream →
so that water diffuses from brain to circulation.

  • Give WATER too.
40
Q

Radial nerve innervates

A
  • triceps muscle (flexor of the shoulder)
  • digit, elbow and carpal extensors.
41
Q

Clinical signs of radial nerve paralysis.

A
  • Dropped elbow
  • walking on the dorsal aspect of the fetlock
  • inability to extend the carpus and digit
  • inability to extend the elbow, carpus and fetlock
  • Inability to bear weight
42
Q

In proximal radial paralysis, …

In distal radial paralysis, …

A

In proximal radial paralysis, the elbow drops, the carpus and fetlock are in partial flexion, and the limb is usually dragged.

In distal radial paralysis, because the triceps muscle remains functional, dropping of the elbow is minimal.

43
Q

The femoral nerve innervates

A
  • the flexor muscles of the hips
  • the extensor muscles of the stifle
44
Q

the nerve responsible for weight bearing in
the hind limb

A

The femoral nerve

45
Q

In femoral paralysis:

A
  • paralysis of the quadriceps muscles → flexion the stifle
  • partial paralysis of the psoas major muscle → extension of the hip
46
Q
A

SCIATIC PARALYSIS

47
Q
A

TIBIAL NERVE PARALYSIS
The hock joint is overextended (dropped
hock syndrome) and the fetlock is
partially flexed.

48
Q

ANALYSIS OF CEREBROSPINAL FLUID looks for…

A
  • Protein concentration and cytologic examination are the cornerstones.

these can help to differentiate between infectious, neoplastic, parasitic, metabolic and degenerative disease processes.

+ Culture for identifying bacteria
+ Biochemistry of the csf

49
Q

CSF * Sample is collected from

A

atlanto-occipital space or from lumbosacral
space (not so invasive) – 1-2 ml of CSF.

  • Collection of CSF from lumbosacral space (L6 – S1) in Standing or recumbent animal.
  • 4 inch spinal needle to adult cattle, 1-2 inch spinal needle to calves.
  • Animal is prepared in surgical fashion
  • Local anesthesia can be used
50
Q

CSF samples should be analyzed within

A

2 hours after collection – cells
degenerate rapidly.

  • Protein concentration and cytologic examination are the cornerstones.

+ Culture for identifying bacteria
+ Biochemistry

51
Q

What should CSF look like?

A
  • CSF should be clear and colorless!
  • Turbidity is caused by elevated cell count (extremely high if turbidity is seen
    with naked eye).
  • Reddish tinge may indicate the presence of blood (traumatic puncture or
    previous bleeding).
  • Xanthochromia (yellowing CSF) is caused by the lysis of erythrocytes and is
    evident within 2-6 hours after CNS bleeding (may remain for up to 10 d).
  • Protein concentration increases with infectious diseases.
52
Q

What term describes the presence of yellowish supernatant in the CSF that is caused by the presence of bilirubin.

A

Xanthochromia

53
Q

name 3 main nerves to suffer damage

A

radial
femoral
sciatic

Ruminant clinical medicine (27 decks)

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