Israel Medical Association Journal

Only one case of a cow infected with bovine spongiform encephalopathy has been reported in Israel. Its publication, in 2002, caused both public and professional concern. The inevitable health policy question raised was whether or not to recommend against consuming beef and what public health measures should be taken. In this article we describe the prion diseases among animals and humans, their interaction and the precautionary procedures that were carried out by the state Veterinary Services and the Ministry of Health since 1988. The BSE[1] case (a 10 year old dairy cow) is believed to be the result of local consumption of infected food with mammalian meat and bone meal more than a decade earlier. The risk assessment took into consideration that no cases of vCJD (a new variant of Creutzfeldt-Jacob disease) have ever been diagnosed in Israel, as well as the low risk of contamination of the meat due to the religious method of slaughtering performed in the country. The policy decision was to implement a contingency plan prepared in advance. Israel was reclassified from the level II category of geographic risk where BSE is unlikely but not excluded in the herds, to level III, where BSE is likely but not confirmed, or confirmed at a lower level. No undue damage to the meat industry has occurred. By the end of 2002, despite the examination of more than 3,800 brains from slaughtered cows older than 3 years, no other cases of BSE have been detected.

The addition of methotrexate to treatment protocols in children with acute lymphoblastic leukemia has been found beneficial in preventing central nervous system relapse. However, MTX[1] itself may be associated with neurologic morbidities, the most significant of which is leukoencephalopathy. The present study describes the clinical spectrum of leukoencephalopathy, which ranges from a subclinical disease manifested only radiologically to a progressive, devastating encephalopathy. The interaction of MTX with other components of the treatment protocol is discussed, as is the effect of leucovorin. A summary is presented of the metabolic pathways that may be involved in the development of MTX toxicity. Researchers are still seeking a biochemical marker to aid in the determination of the amount of MTX that may be safely administered.

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