18/12/2023
Polioencephalomalacia/ Goat polio/ thiamine deficiency/Cerebrocortical Necrosis.
Polioencephalomalacia is a common neurologic disease of ruminants.
The main clinical signs reflect dysfunction of the cerebrum and include wandering, circling, cortical blindness, incoordination, head pressing, recumbency, nystagmus, and seizure activity.
Polioencephalomalacia (PEM) is an important neurologic disease of ruminants that is seen worldwide.
Cattle, sheep, goats, deer, and camelids are affected.
Etiology:
PEM has been associated with altered thiamine status, and high sulfur intake. Other toxic or metabolic diseases (eg, acute lead poisoning, sodium toxicosis/water deprivation) can result in PEM as well.
Risk factors:
1; Polioencephalomalacia is seen sporadically.
2; Younger animals are more frequently affected than adults.
3; Animals on high-concentrate diets are at higher risk.
4; high levels of sulfur, whether in water, feed (rations with byproducts of corn or beets processing), or a combination.
5; altered thiamine status.
Notes:
Preruminant animals depend on dietary thiamine. In adult ruminants, thiamine is produced by rumen microbes. Thiamine inadequacy can be caused by decreased or altered production by rumen microbes (such as high-concentrate feed or factors that interfere with the action of thiamine, eg, plant thiaminases or thiamine analogues. Thiaminases can be produced by gut bacteria or ingested as preformed plant products. They can either destroy thiamine or form antimetabolites that interfere with thiamine function.
Clinical Findings:
Polioencephalomalacia may be occur in acute or subacute form.
1; Acute form often manifest blindness followed by recumbency, tonic-clonic seizures, and coma. Those with a longer duration of acute signs have poorer responses to therapy and higher mortality.
2; subacute form initially separate from the group, stop eating, and display twitches of the ears and face.
The head is held in an elevated position.
There is cortical blindness with absent menace response but normal bilateral pupillary light reflex.
Dorsomedial strabismus may develop.
Animals may show ataxia and sometimes a hypermetric gait.
Head pressing, opisthotonos, and grinding of the teeth may also be seen.
Recumbency and seizures.
Diagnosis:
1; Clinical signs.
2; Response to thiamine.
Differential diagnoses for cattle include.
1; acute lead poisoning
2; water deprivation/sodium toxicosis
3; Histophilus meningoencephalitis
4; rabies
5; coccidiosis with nervous involvement
6; vitamin A deficiency
Differential diagnoses for sheep include:
1; pregnancy toxemia
2; type D clostridial enterotoxemia (focal symmetric encephalomalacia)
3; listeriosis.
Treatment;
1; thiamine at a dosage of 10 mg/kg, three to four times daily, for cattle or small ruminants. The first dose is administered slowly IV; otherwise, the animal may collapse. Subsequent doses are administered IM for 3–5 days.
2; Dexamethasone may help reduce cerebral edema. dexamethasone at a dosage of 1–2 mg/kg, IM or SC.
3; Symptomatic therapy for convulsions may be necessary.
Prevention:
Dietary supplementation of thiamine at 3–10 mg/kg feed has been recommended for prevention.
Key Points
Polioencephalomalacia is a neurologic disease that affects young ruminants and pseudoruminants. It occurs in outbreaks or in individual animals.
Clinical signs include head pressing, blindness, convulsions, nystagmus, dorsomedial strabismus, and recumbency.
Diagnosis is suspected based on signs and response to thiamine administration.
Supplementation with thiamine has been recommended for prevention, but is not fully supported by evidence.
Keep following
Dr Muhammad Saeed Vet