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484 Multiple Sclerosis: A series of patients examined for mycotoxic leukoencephalopathy.
  1. G. J. Ordog
  1. Henry Mayo Hospital, Valencia, CA


Introduction A previous examination of a cluster of patients (42 of 600) working in a mold-infested building confirmed the presence of mycotoxic leukoencephalopathy in these patients as the cause of their multiple sclerosis (MS)-type presentation (AFMR - Monterey, California, February 2005).

Purpose In this current study, the study population consisted of patients previously diagnosed with MS, presenting to a medical toxicology department. This group of patients had no previous toxicological diagnosis and no previous history of mold exposure.

Methodology A history and physical examination, review of previous medical records, diagnostic tests including PET scan of the brain, MRI brain and spinal cord, environmental testing of the home or worksite including airborne mycotoxin levels, serum ELISA mycotoxin levels, hypersensitivity pneumonitis panels for environmental molds; serum ELISA myelin basic protein (MBP), myelin-associated glycoprotein (MAG), crystalline antibodies (CA), glutamate receptor antibodies (GRA), and chondroitin sulfate antibodies (CSA). Other etiologies for leukoencephalopathy were considered. Study period 2004-2005.

Results Six patients completed the study. Six (100%) had positive PET scans of the brain confirming hypometabolism of frontal, parietal, and basal ganglia. Six (100%) had confirmation of demyelination by MRI, with areas of hyperintensity on the T2-weighted images. Six ((100%) had a positive neurological panel, consisting of elevated ELISA testing for MBP, MAG, CA, GRA, and CSA. Results of environmental testing confirmed the presence of pathogenic and toxigenic mold species in either the home or workplace in 6 (100%). Six (100%) had positive airborne mycotoxin levels in the toxic range (nanogram to milligram, per cubic meter) for between 2 and 22 of the possible 40 mycotoxins that could be tested. The presence of 3 groups of mycotoxins in the microgram range (microgram to milligram, per cubic meter air) was consistent with elevated serum ELISA levels for the same groups (100%) for trichothecenes, satratoxins, and aflatoxins. Other causes of leukoencephalopathy were ruled out.

Conclusions The previous study confirmed the cause of a cluster of patients with MS-type presentation to be mycotoxic leukoencephalopathy. The present study confirms a series of patients previously diagnosed with MS had an etiology consistent with environmental mycotoxicosis. The etiology of MS appears to be environmental mycotoxicosis. This is a small study group, with a statistically significant power, but larger studies should be done to confirm this in other geographic areas.

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