The central nervous system is often affected by gastrointestinal infections caused by Shigella spp, sometimes by Salmonella and Campylobacter spp. 1 Encephalopathy due to Yersinia enterocolitica has not been described. A previously healthy 10-year-old girl presented with a 3-day history of gastroenteritis and fever up to 38· 5ºC. A few hours before admission, she became apathetic and disoriented. She did not recognise her mother and was unable to speak. She had not received any drug treatment. On admission, she was stuporous and responded only to pain by withdrawal. She had normal vital signs, a pulse rate of 80 beats per min, and a normal blood pressure. There were no clinical signs of dehydration. Pupils were dilated and had a delayed reaction to light. Reflexes were normal. On admission her haemoglobin was 14· 3 g/100 mL, platelets 261109/L, leucocytes 13· 4109/L with 16% bands, 64% polymorphonuclear leucocytes, 7% monocytes, 13% lymphocytes. C-reactive protein was raised (2· 3 mg/100 mL), as was her erythrocyte sedimentation rate (35 mm/h). The remainder of her laboratory findings were normal. A urine and serum toxicology screen was negative. Magnetic resonance imaging was done without any abnormal findings. Cerebrospinal fluid (CSF) examination revealed no white blood cells, and a normal protein and glucose concentration. Herpes simplex encephalitis was suspected and treatment with acyclovir was started, but stopped after negative PCR results were obtained. Blood and CSF cultures remained sterile. Stool cultures yielded growth of Y enterocolitica, serotype O: 3. A positive autoagglutination test suggested presence of the pYV-virulence plasmid. No other bacterial, viral, or parasitic pathogen was identified from the patient’s stool samples. Widal serology showed significant antibody titres (1: 80) against both Y enterocolitica O: 3 and OH: 3 antigen in her serum, but not in CSF. Antibody titres against neurotropic pathogens including Borrelia burgdorferi were not raised. Electroencephalogram (EEG) showed a severe and diffuse slowing of background activity. Neurophysiological examination showed a transitory myasthenic reaction. Nerve-conduction velocity was normal. From the fourth hospital day, the girl’s clinical state and EEG abnormalities improved without specific treatment. She was discharged on the seventh hospital day, 3 months later she had no neurological defeat and EEG and neurophysiological tests were normal.

Since no other source was identifiable, enteric infection with Y enterocolitica O: 3 was the most probable cause of encephalopathy in this patient. In shigellosis, neurotoxicity has been attributed to the shiga toxin, the main toxic product of Shigella dysenteriae. 2 However, encephalopathic symptoms are not readily explained by the known properties of the toxin. 3 Brain oedema caused by severe shigellosis has been shown to cause central-nervous-system disease. 4 The