229 J7ournal of Neurology, Neurosurgery,- and Psychiatry 1994;57:229-231 SHORT REPORT Adult Toxocara canis encephalitis C Sommer, E B Ringelstein, R Biniek, W M Glockner Abstract A 48-year-old patient with Toxocara canis infection developed severe ataxia, rigor and neuropsychological disturbances. An aetiology was proven by an indirect immunofluorescence test. CT and MRI revealed both diffuse and circumscribed white matter lesions. Angiography showed multiple occlusion of branches of the middle cerebral artery. Anthelminthic treatment was beneficial in the initial stage of the disease, but had no effect on progression of CNS symptoms. Immunosuppressive therapy with prednisolone and azathioprine yielded partial recovery and stabilisation of the patient. (7 Neurol Neurosurg Psychiatry 1994;57:229-231) The roundworm Toxocara canis is transferred from dog to humans via the eggs of the worm, most commonly to children of dirt- eating age.' After penetrating the small bowel, the larvae may invade any tissue. The typical disease is called 'visceral larva migrans' and can cause hepatomegaly, recurrent bronchitis, splenomegaly, lymphadenopathy, -and subcutaneous granulomas. Adults are rarely affected. Involvement of the CNS has occasionally been described.'- We report the first case of Toxocara canis encephalitis documented over a four-year course by angiography, CT, and MRI. Immunosuppressive treatment was partly successful. Neurologische Klinik und Medizinische Klinik H, Klinikum der RWTH Aachen, Pauwelsstr 30, D-5100 Aachen, Germany C Sommer E B Ringelstein R Biniek W M Glockner Correspondence to: Professor E B Ringelstein Received 18 July 1991 and in final revised form 16 October 1992. Accepted 6 November 1992 Case report A 48-year-old woman, a dog breeder, presented to a small rural hospital in January 1987 with malaise, dizziness, loss of appetite, dysphoria and psychomotor agitation. Her ESR was elevated to 95 mm/hour, she had leukocytosis (22 Giga/l) and eosinophilia of 74%. In March 1987, she was discharged from hospital after her symptoms spontaneously improved but before a diagnosis was made. In July 1987 she was admitted to our hospital because of progressive somnolence. An indirect immuofluorescence test gave a titre of 1:640, which confirmed the diagnosis of Toxocara canis infection. Anthelminthic therapy with thiabendazole (2 x 750 mg daily for 10 days) rapidly improved the patient's condition, and she was discharged in August 1987. She presented again in September, now with rigor, loss of facial expression, brisk tendon jerks and gait ataxia. She had disturbances of memory and concentration. The Toxocara canis antibody titre was unchanged. Eosinophilia amounted to 57%, and IgE was elevated to 3-470 IU/1. The CSF cell count was normal, but eosinophils were present. At that time, CT scan showed cerebral atrophy, diffuse white matter hypodensity, most marked on the left, and a chain of sharply demarcated hypodense lesions with diameters of 4 to 5 mm in the left centrum semiovale. MRI revealed several hyperintense subcortical lesions in the cerebrum and cerebellum (Fig la). Fundoscopy showed occlusion of arterioles and retinal haemorrhages. Visual acuity was considerably decreased (L 0-3, R 0 02). A second treatment with thiabendazole was not effective. The presumptive diagnosis of cerebral vasculitis was made, and the patient was treated with prednisone. This led to a dramatic improvement of her mental state, gait and vision, within 10 days. Her further clinical course, however, was not satisfactory. The prominent recurring symptom was severe ataxia leading to falls. As the Toxocara canis titres remained positive, range between 1:160 and 1:320, two more anthelminthic courses were given (diethylcarbamazine 3 x 150 mg/day for 14 days, fenbendazole 500 mg/day for 10 days) until December 1990. At that time, the titre had decreased to 1:40. A CT scan in June 1990 showed progression of the lesions compared with the initial CT scan, and angiography was performed. Multiple small branches of the middle cerebral artery were occluded (fig lb). Neuropsychological testing at that time revealed a full scale IQ of 55 (WIP, a shortened form of the Wechsler intelligence test'), the premorbid IQ was estimated as 90. Immunosuppression was continued with lowdose prednisone (7 5 mg/day) and azathioprine (3 x 50 mg/day). The clinical course, however, did not parallel laboratory findings. After several weeks of physiotherapy in June and again in December 1990, the patient was able to walk and care for herself, although her IQ had not improved at follow up examination after one year. 230 Sommer, Ringelstein, Biniek, Glkckner Discussion In published reports on Toxocara canis infections in adults, six cases of encephalitis, three with myelitis (such as encephalomyelitis), and !: i,:-.. :::,.:... one case of menftigitis have been reported 2 9 .:;. . i ,5. ;. ,-.o ,- . ,.- . - .."..... ... . 5. '........::,...!:..:..Ii,.-.%-...--.. ....- `....::;: !....1-11 ,"" ,1:%-::..-F On pathological examination, eosinophilic .-.-.-U. -. .::: granulomata and vasculitic lesions have been ::.:: in the found brains of children'O II and of lab .:...%-.-.-.--.-..-. ..J i:::I: oratory animals, 1 2 1 3 predominantly in the .-.%-.--.-.-.-,. . .:.:. and cerebellar white matter. 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".;..... ............-::.......-.: ::. :.... :!-.Q:-.:.:: :-% --........... ....... ....: ....:.%.:::.-:.., :: ::....:..: ':::.: ':". ...:,! ::::.-:.-:- .:, %.....:..::.......:.:.:.:..n:n::. ..:.- -....:: ...:: ...::'.%....... .':'::::% :X .::.:..:.:.....,..::.:.:.:::R:,!:...:,..:::!:..: X: 01 12 3 3 6 9 1 87 6 9 88 12 '!v 3 :::F..:r:: ::.:::: :%:.:.:.V-..!!. X:, ..: 6 9 89 12 3 6 9 90 12 0 191 Eos_nophilia -+-lgE ~m, - *-~oxocaracanis Eosinophilia -+-lgE (lU/ml) Toxocara canis IIFT J Figure 2 Course of laboratory parameters.IIFT: titre of indirect immunofluorescence test. Tisner R, MobiusDtsch W. Akute DA,Toxocara-Larven. Spiekermann 5EngelHi, druch Med ~~~~~~~~~~~~~~~~Meningomyelitis Wschr, 971;96:1498. 6 Muiller-Jensen A, Schall J, Weisner B, et al. Eosinophile Meningo-enzephalo-myelitis und viszerales Syndrom durch Askaridenlarven beim Erwachsenen. Dtsch Med Wschr 1973;98:1175-7. 7 Huismans H. Larva migrans visceralis (Toxocara canis) und zentrales Nervensystem (ZNS). Nervenarzt 1980;51:718-24. Adult Toxocara canis encephalitis 231 8 Wang C, Huang CY, Chan PH, Preston P, Chau PY. Transverse myelitis associated with larva migrans: findings of larva in cerebrospinal fluid. Lancet 1983; 1(8321):423. 9 Ruttinger P, Hadadi H. MRI in cerebral toxocaral disease. J Neurol Neurosurg Psychiatry 199 1;54:361-2. 10 Dent JH, Nichols RL, Beaver PC, Carrera GM, Staggers RJ. Visceral larva migrans. With a case report. Am J Pathol 1956;32:777-803. 11 Hill IR, Denham DA, Scholtz CL. Toxocara canis larvae in the brain of a British child. Trans R Soc Trop Med Hyg 1985;79(3):352-4. 12 Summers B, Cypress RH, Dolinsky ZS, Burright RG, Donovick PJ. Neuropathological studies of experimental toxocariasis in lead exposed mice. Brain Res Bull 1983;19(4):547-50. 13 Glickman LT, Summers BA. Experimental Toxocara canis infection in cynomolgus macaques (Macaca fascicularis). Am J Vet Res 1983;44(12):2347-54. 14 Trelles JO, Trelles L. Cystercercosis of the nervous system. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 35. Amsterdam: North Holland, 291-320. 15 Kramer MD, Aita F. Trichinosis. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol 35. Amsterdam: North Holland, 267-90. A note on heterochromia iridis Pearce, in his short piece on heterochromia iridis,' describes different irides as "harmless but rare". Heterochromia, although rare, is often associated with deafness and is probably a defect of neural crest migration. The London Dysmorphology Database2 lists nine syndromes with iris heterochromia, most of which include deafness as a feature. Chromosomal abnormalities such as triploidy are also associated with heterochromia. Interestingly, asymmetric hypertrophy in Klippel-Trenaunay-Weber syndrome causes iris abnormalities on the affected side of the body. The presence of heterochromia iridis in a patient should alert the clinician to the possible presence of other neurological features. 1 Pearce JMS. A note on heterochromia iridis. J Neurol Neurosurg Psychiany 1992;55:1131. 2 Winter RM, Baraitser M. The London Dysmorphology Database. Oxford: Oxford University Press 1992.