Abstract

To the Editor: We saw a 41-year-old man first diagnosed as having multiple sclerosis (MS) in 1993 after complaints of diplopia, hand tremors, and lower extremity ataxia. The diagnosis was confirmed by cerebrospinal fluid analysis and magnetic resonance imaging, He was treated effectively with interferon beta until 1994 at which time it was discontinued for financial reasons. In spring 1996, he had a 3-week episode of dysarthria, but since that time had remained symptom-free. In August 1998, he presented to our clinic with a complaint of paresthesia in the right leg and gluteal region. Two days previous, he had been working in his yard and was stung in the face multiple times by wasps (Vespula), and his symptoms began the next morning. He denied any history of wasp or bee sting allergy. On examination, he had decreased strength throughout in his right lower extremity (4/5), 3+ patellar reflexes bilaterally, and T10 sensory level on the right to all modalities. He was admitted for observation and treatment with intravenous methylprednisolone, had slightly improved symptoms within 24 hours, and was discharged to home. Three weeks later, his lower extremity strength had improved, but he had developed new symptoms in his right arm and was treated again with corticosteroids. In 1960, Goldstein et al1Goldstein NP Rucker CW Woltman HW Neuritis occurring after insect stings.JAMA. 1960; 173: 181-184Google Scholar reported a case of optic neuritis and another with a sensorimotor syndrome consistent with MS, both following bee sting. Means et al,2Means ED Barron KD Van Dyne BJ Nervous system lesions after sting hy yellow jacket: a case report.Neurology. 1973; 23: 881-890Crossref PubMed Google Scholar in 1973, reported a 52-year-old woman with no history of neurologic disease who presented with multiple relapsing-remitting neurologic complaints following a yellow jacket sting. The patient died of a cardiac arrest within 2 months of the sting, and autopsy showed multiple areas of necrosis and demyelination in the brain and spinal cord. Relapses of MS have been reported with other immunologic insults, notably tetanus toxoid, rabies, and other immunizations.3Annunziata P Traversi C Fanctti G Conli T Multiple sclerosis onset after anti-tetanus toxoid immunoglobulin prophylaxis [letter].Ital J Neural Sci. 1993; 14: 270PubMed Google Scholar Bee venom has been studied for its role in inflammatory processes, and bee venom therapy, also known as apitherapy, is being heralded by some as a complementary treatment in MS. There are no reports of MS-like exacerbations resulting from this technique, and while bee sting is common, we found no report of MS exacerbation following single or multiple bee stings. It is interesting to postulate on possible mechanisms that could have occurred, albeit cause and effect have not been proven. The role of interferon gamma has been well established in the pathogenesis of MS.4Panitch HS Interferons in multiple sclerosis: a review of the evidence.Drugs. 1992; 44: 946-962Crossref PubMed Scopus (104) Google Scholar Interestingly, a 1997 study of reaction to wasp stings by Bonay et al5Bonay M Echchakir H Lecossier D et al.Characterization of prolif-erative responses and cytokine mRNA profiles induced by Vespula venom in patients with severe reactions to wasp slings.Clin Exp Immunol. 1997; 109: 342-350Crossref PubMed Scopus (11) Google Scholar showed that even the T cells from nonallergic control patients had a marked increase in production of messenger RNA coding for interferon gamma after exposure to Vespula venom. Is it possible that a wasp sting in a nonatlergic patient could raise serum levels of interferon gamma that might, in turn, lead to a flare of MS symptoms? A search for similar cases, with analyses of symptoms and laboratory data, may help to elucidate possible mechanisms underlying this case and the immunologic pathogenesis of MS.

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