polioencephalomalacia in goats

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 deficiency Decreased thiamine synthesis Increased thiamine destruction by thiaminase

Bracken fern, horsetail Rumen microbial destruction of thiamine

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.