Journal of Neuro-Ophthalmology, June 1983, Volume 3, Issue 2

Beesting papillitis.

A 72-year-old, white male presented with sudden, painless loss of vision bilaterally associated with optic disc swelling. His visual loss occurred within 24 hours of receiving multiple beestings. Clinical examination revealed papillitis. Optic neuritis associated with beestings is a rare complication which is not understood fully.

f. Clin. Neuro-ophthalmol. 3: 97-100,1983. Beesting Papillitis LENORE A. BREEN, M.D. RONALD M. BURDE, M.D. GEORGE E. MENDELSOHN, M.D. Abstract A 72-year-old, white male presented with sudden, painless loss of vision bilaterally associated with optic disc swelling. His visual loss occurred within 24 hours of receiving multiple beestings. Clinical exami­nation revealed papillitis. Optic neuritis associated with beestings is a rare complication which is not understood fully. An estimated 1-2 million Americans have a his­tory of allergic reactions to the stinging insects of the Hymenoptera order. 1 Reactions to the venom include not only anaphylaxis but also a delayed reaction (onset 2 hours-14 days after sting) which can occur in people without any history of Hyme­noptera allergy. These delayed reactions most com­monly affect the immune or nervous systems. In 1960, Goldstein et al. reported the first case of optic neuritis occurring after a beesting.2 Four years later, a patient with papilledema and encephalop­athy associated with a beesting on the vertex of the head was described by Goldstein et al.:l Walsh and Hoyt implicated a similar association in a patient with optic atrophy examined several months after a beesting. 4 To our knowledge, no other case re­ports of optic nerve disease following beestings have appeared in the literature. We present a 72­year- old man with the sudden onset of bilateral visual 1055 within 24 hours of receiving multiple beestings. Case Report A previously healthy 72-year-old, single white male, noted bilateral loss of vision upon awakening on November 9, 1981. The patient had no history of acute or chronic medical illness and did not use medications, tobacco, or ethanol. Dietary and toxin exposure history was unremarkable. The patient had received multiple beestings to his hands, arms, From the Departments of Neurology and Ophthalmology (LAB), West Virginia University School of Medicine, Morgan­town, West Virginia; the Departments of Ophthalmology, Neu­rology and Neurological Surgery (RMB), Washington Univer­sity School of Medicine, St. Louis, Missouri; and the Depart­ment of Neurosurgery (GEM). University of Missouri-Colum­bia, Missouri. June 1983 and neck the day prior to the onset of his visual 1055. He had received multiple bee- and waspstings during the summer but could recall no symptoms of anaphylaxis. The initial ophthalmologic examination on No­vember 11, 1981, revealed a visual acuity of 20/60 in the right eye and finger counting at 2 ft. in the left eye. Confrontation visual fields demonstrated a "right homonymous hemianopsia." "Papill­edema" was noted bilaterally, and the patient was referred for neurosurgical evaluation. The neurologic examination done 1 week after the onset of the illness revealed some subtle changes suggesting a mild right hemiparesis. Skull x-rays and a CT scan with and without contrast enhancement were normal. Opening pressure on lumbar puncture was 130 mm H20. The cerebro­spinal fluid cell count was 1 WBC/mm:l , protein 32 mg%, glucose 74 mg%, and cytologic examina­tion was normal. The patient's complete blood count was normal, and the erythrocyte sedimen­tation rate was 12 mm/hour. The patient was referred to Washington Univer­sity on November 19, 1981. Ophthalmologic ex­amination revealed a visual acuity of 20/60 in the right eye and finger counting at 1 ft. in the left eye. Pupll dIameters measured 4.5 mm (right eye) and 5 mm (left eye) with no increase in the relative difference in light or darkness. The pupillary re­actIon was decreased bilaterally with an afferent pupillary defect in the left eye. Extraocular motility was normal. External and slit lamp examinations were normal. Applanation pressures were 14 mm Hg (right eye) and 16 mm Hg (left eye). Results of kinetic perimetry are shown in Figure 1. The optic discs were bilaterally swollen and hyperemic with associated peripapillary hemor­rhage (Fig. 2). The fundi were otherwise normal. Bilateral papillitis was diagnosed. Additional normal laboratory studies done 10 days after the initial visual 1055 included an antin­uclear antibody, rheumatoid factor, cryoglobulins, complement level, protein electrophoresis, and se­rum immunoelectrophoresis. The patient re­quested discharge before other studies were ob­tained. He was discharged on prednisone, 100 mg daily, with tapering doses over 1 month. Follow-up examination in March 1982 showed significant improvement. Visual acuity was 20/20 97 Beesting Papillitis A.c. 11/19/81 LEFT RIGHT Figure 1. (Right eye) Severe field loss, probably best described in terms of double arcuate bundle defects. (Left eye) Catastrophic visual field loss with small inferior temporal quadrant remaining in the central SO accompamed by a temporal island to large isopters. Figure 2. (alRight disc demonstrating plethora, swelling, and superficial flame­shaped hemorrhages. (bl Left disc demonstrating parallel findings. in the right eye and 20/50 in the left eye. Repeat kinetic visual fields were also improved (Fig. 3). The optic discs were diffusely pale with associated diffuse nerve fiber layer loss. Discussion Apis mellifera (the honeybee), is a member of the Hymenoptera order. This order includes bees, 98 wasps, hornets, yellow jackets, and ants. An esti­mated 50-100 people in the United States die annually from reactions to these insect stings.5 The systemic allergic reaction is initiated by the binding of venom-specific IgE to mast cells and basophils with the attendant release of vasoactive sub­stances. 6 The pathophysiology of the delayed re­action is not understood at this time.6 The majority of patients who have delayed reactions have a Journal of Clinical Neuro-ophthalmology Breen, Burde, Mendelsohn Figure 2 (con!.). A.C. 3/18/82 LEFT RIGHT Figure 3. Bilateral improvement of visual fields with respect to Fig.!. more extensive in the right eye. history of previous Hymenoptera stings. Unusual delayed reactions to beestings primarily have af­fected three systems: immunological, renal, and neurological. Serum sickness, Arthus reaction, he­molytic anemia, and thrombotic thrombocytopenic purpura have all been reported. 7 - 10 Renal compli­cations have included hematuria and proteinuria with or without the nephrotic syndrome. 7. H Both the peripheral and central nervous systems have been affected by nonallergic beesting reac­tions. 2.:J, 9,12-1.5 To date, the underlying pathophys-iology of the neural involvement is poorly under- June 1983 stood. In an effort to find an underlying immune reaction, two patients with Fisher's syndrome, one patient with Guillain-Barre syndrome, and one patient with encephalopathy had myelin antibodies and venom-specific IgG and IgE levels measured.g · 14 The patients with Fisher's syndrome had elevated myelin antibodies but normal immunoglobulin levels. The other two cases had normal myelin antibodies and elevated immunoglobulins. Since the patients with delayed reactions seldom die from the reaction, autopsy studies are rare. Means et al. report a thorough autopsy study of a patient 99 Beesting Papillitis with neurologic sequelae after a yellow jacket sting. 16 They noted changes in the nervous system similar to those seen in experimental allergic en­cephalomyelitis, and propose a possible autoim­mune basis for the lesions. In an experimental model, application of bee venom to peripheral nerves of rats caused local nerve changes, but no distant neurological effects were noted. 17 Several patients allergic to beestings are being treated with immunotherapy6, 7, 18 Increasing doses of venom are given to stimulate production of specific blocking IgG. However, since the delayed reaction is possibly an immune complex reaction, immunotherapy is probably contraindicated.7 Considering this patient's age, our first diagnos­tic consideration was ischemic optic neuropathy. However, our patient clearly did not have pale disc edema. The patient's clinical course and lack of any other underlying disease support the diagnosis of papillitis due to beestings. Unfortunately we were unable to measure myelin antibodies and venom-specific immunoglobulins because of the patient's request to leave the hospital prematurely. References 1. Pence. H.l.: Stinging insect allergy. Prim. Care 6(3): 587-596, 1979. 2. Goldstein, N.P., Rucker, CW., and Woltman, H.W.: Neuritis occurring after insect stings. J,AM.A 173: 1727-1730, 1960. 3. Goldstein, N.P., Rucker, CW., and Klass, D.W.: Encephalopathy and papilledema after bee sting. J.A.M.A 188: 1083-1084, 1964. 4. Walsh, F. B., and Hoyt, W. F.: Clinical Neuro-Oph­thalmology, Vol. 3. Williams & Wilkins, Baltimore, 196~ pp. 2718-2719. 5. Schreiber, R. l.: NIH consensus development con­ference on emergency treatment of insect allergy. Ann. Allergy 42: 109-111, 1979. 6. Yunginger, J.W.: Advances in the diagnosis and treatment of stinging insect allergy. Pediatrics 67: 325-328, 1981. 7. Frankland, A.W., and Lessof, M.H.: Allergy to bee stings: A review. ]. Roy. Soc. Med. 73: 807-810, 1980. 100 8. Wintrobe, M.M., Lee, GR., Boggs, OK, Bithell, T.C, Athens, J. W., and Foerster, J. (Eds.): Clinical Hematology (7th ed.). Lea & Febiger, Philadelphia, 1974, pp. 745-746. 9. Light, W.C, Reisman, R.E., Shimizu, M., and Arbes­man, CE.: Unusual reactions following insect stings. Clinical features and immunologic analysis. ]. Al­lergy Clin. Immunol. 59: 391-397, 1977. 10. Jones, M.B., Armitage, J.O., and Stone, D.B.: Self­limited TTP-like syndrome after bee sting. J.AM.A 242: 2212-2213, 1979. 11. Olivero, J.J., Ayus, J.C, and Eknoyan, G: Nephrotic syndrome developing after bee stings. South. Med. ]. 74: 82-83, 1981. 12. Arne, L., Pautrizel, R., Seilhean, A., Fenelon, J., Bezian, J., and Bargues, J.F.: Etude immunologique apres piqures d'abeilles chez un malade developpant un tableau de sclerose en plaques. Rev. Neurol. (Paris) 116: 345-349, 1967. 13. Bachman, OS, Paulson, GW., and Mendell, J.R.: Acute inflammatory polyradiculoneuropathy fol­lowing hymenoptera stings. ].A.M.A. 247:1443­1445, 1982. 14. Marks, H.G, Augustyn, P., and Allen, R.J.: Fisher's syndrome in children. Pediatrics 60: 726-729, 1977. 15. Ross, AT.: Peripheral neuritis: Allergy to honeybee stings. ]. Allergy 10: 382-384, 1939. 16. Means, ED., Barron, KD., and Van Dyne, B.J.: Nervous system lesions after sting by yellow jacket. Neurology 23: 881-890, 1973. 17. Saida, K., Mendell, J.R., and Sahenk, Z.: Peripheral nerve changes induced by local appliction of bee venom. ]. Neuropathol. Exp. Neurol. 36: 783-796, 1977. 18. Golden, D.B.K., Valentine, M.D., Kagey-Sobotka, A., and Lichtenstein, L.M.: Regimens of hymenop­tera venom immunotherapy. Ann. Intern. Med. 92: 620-624, 1980. Acknowledgment This work is supported in part by a grant from Research to Prevent Blindness, Inc., New York, New York (Department of Ophthalmology). Write for reprints to: Ronald M. Burde, MD., De­partment of Ophthalmology-Box 8096, 660 South Eu­clid Avenue, St. Louis, MIssouri 63110. Journal of Clinical Neuro-ophthalmology