polioencephalomalacia in goats

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Powerpoint presentation about PEM in goats for Undergraduate BVSc students

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  • POLIOENCEPHALOMALACIADr. 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 deficiencyDecreased thiamine synthesis Increased thiamine destruction by thiaminaseBracken fern, horsetail Rumen microbial destruction of thiamineBacillus thiaminolyricus or Clostridium sporogenes Thiamine antimetabolitesAmprolium

  • Predisposing factors. Feeding high concentrate, low-roughage dietsHigh-sulfate dietary or water sources. Major management changes in feeding

  • PathogenesisNeccessary for the production of erythrocyte transketolase enzymeIncrease in blood pyruvate and suppression of pentose phosphate pathwayReduction of CHO metabolism of cerebral cortex and ATP production Intracellular oedemaDegeneration 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 signsOther neurologic signsIncoordinationAimless walkingCirclingMuscle tremorsHead pressingConvulsions and depressionHyperexcitability 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 pathologyLow blood thiamine (Normal range:75-180 nmol/L; below 50 nmol/L chance of PEM)

    Decreased erythrocyte transketolase activity.

  • CSF analysisThe 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 findingsDiffuse 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 toxicityPregnancy toxemia in sheepNervous ketosis in dairy cattle.

  • Therapeutic planThiamine 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.TranquilizersSupportive 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.