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POLIOENCEPHALOMALACIA

Dr. UMESH C G,
Assistant Professor,
Department of Veterinary Clinical
Medicine, Ethics and Jurisprudence,
College of Veterinary and Animal
Sciences, Pookode,
Wayanad, Kerala

Affects

cattle, sheep, and goats.


Affect an individual or appear as a herd problem
Affecting

calves ages 6-12 months and lambs and


kids ages 2-6 months.

Less

common in adults, and it is more sporadic in


small ruminants.

Etiology.
Thiamine

Decreased thiamine synthesis


Increased thiamine destruction by thiaminase

Bracken fern, horsetail

Rumen microbial destruction of thiamine

deficiency

Bacillus thiaminolyricus or Clostridium sporogenes

Thiamine antimetabolites

Amprolium

Predisposing factors.
Feeding

high concentrate, low-roughage diets


High-sulfate dietary or water sources.
Major management changes in feeding

Pathogenesis
Neccessary

for the production of erythrocyte


transketolase enzyme
Increase in blood pyruvate and suppression of
pentose phosphate pathway
Reduction of CHO metabolism of cerebral
cortex and ATP production
Intracellular oedema
Degeneration and necrosis

Clinical finding
Cortical

blindness (i.e., absent menace with intact


palpebral and papillary light reflex) occurs early
in the course of disease.

Dorsomedial

strabismus and nystagmus are also


common findings with PEM.

Clinical signs
Other

neurologic signs

Incoordination
Aimless walking
Circling
Muscle tremors
Head pressing
Convulsions and depression
Hyperexcitability leading to recumbency,
Opisthotonus, and paddling with extensor rigidity.

Clinical signs
Vital

signs can be normal or elevated because of


exertion.

The

rumen usually remains active

Clinical pathology
Low

blood thiamine

(Normal range:75-180 nmol/L; below 50 nmol/L


chance of PEM)

Decreased

erythrocyte transketolase activity.

CSF analysis
The

protein level can be normal to highly elevated

Pleocytosis.

The

CSF pressure is increased to 200-350 mm of


saline (normal pressure is 120-160 mm saline).

Necropsy findings

Diffuse cerebral edema with compression

Yellow discoloration of the dorsal cortical gyri

Laminar necrosis of cerebrocortical grey matter.

Autofluorescence of a freshly cut surface of brain


cortex when placed under ultraviolet light

Laminar necrosis

Gyral contraction

Autofluorescence of a freshly cut surface of


brain cortex

Differential diagnoses.
Lead

toxicity
Pregnancy toxemia in sheep
Nervous ketosis in dairy cattle.

Therapeutic plan
Thiamine

10 mg/kg intravenously early in the course of clinical


signs.
Followed by intramuscular or subcutaneous dosing
every 3 hours for 5 treatments.

Treatment

Corticosteroids, mannitol, or DMSO may be indicated for


animals with possible cerebral edema.
Tranquilizers
Supportive care: Soft, dry bedding while recumbent and
parenteral or oral fluid administration.
Diet: Only roughage for several days before being
reintroduced to concentrates.
Euthanasia. If no response to treatment is seen within 3 days

Prevention.
Thiamine

can be added @ 3mg/kg DM of the

feed.
If

the diets associated with thiamine inadequacy


5-10 mg/kg DM of thiamin can be added.