Isolation of influenza virus type AH1 from a child case of acute encephalopathy, December 1999 - Osaka
(IASR 2000; 21:30-30)

On December 28, 1999 our institute isolated influenza A (H1) from a patient with acute encephalopathy from gargling water and cerebrospinal fluid (CSF) collected on December 26. Specimens were inoculated on MDCK cell on December 28. On January 4, 2000, 256HAU of virus multiplication was observed by Hemagglutination reaction using the 0.7% human type O red blood cell. The isolate was identified as influenza A/Beijing/262/95 (H1N1) by the ferret antisera provided by NIID. Homo-antibody titer was as high as 1:1,280 by hemagglutination inhibition test. Virus was not isolated from the CSF. Detection of gene fragment is not conducted yet.

A case report:

Patient; 4 years old boy
Clinical diagnosis; acute encephalopathy
Present illness; the patient developed fever as high as 39C since the morning of December 22, 1999, followed by diarrhea and vomiting. Antipyremic suppository was given and he visited a nearby clinic on 9 o'clock AM. He presented high fever to 40C by 3 o'clock PM, then antipyremic suppository was given. He complained chill in the evening, and fever reached 41C. He vomited once, and slept after taking some juice. He murmured, turn around on the bed, vomited twice, and showed incontinence of urine. He was immediately hospitalized to the Department of Pediatrics, Takatsuki Hospital on 9:50 PM.

Upon admission, his consciousness level deteriorated III-100 to II-30 by the Japanese coma scale (JCS). Cranial computed tomography (CT) revealed that unclear edge image of the narrowed ventricule. He presented frequent watery diarrhea and vomiting after admission. Capillary biochemistry revealed that WBC 12,200/mm3, CRP 0.7mg/dL, GOT 89IU, GPT 56 IU, LDH 686 IU, and NH3 52mg/dL. Acute encephalopathy was suspected, then glycerol was given through IV route. Until the morning of December 23, fever was unstable and diarrhea did not stop. Consciousness level worsened to III-100 to III-200 (JCS) with Babinski reflex positive and talipes equinus CSF was collected with normal pressure, cell count 1 per 3-field, protein 360 mg/dL. Biochemistry of December 23 deteriorated that GOT 1,048 IU, GPT 925 IU, LDH 1,963 IU, and NH3 133 mg/dL. Reye's syndrome or influenza encephalopathy were suspected, then gamma globulin was administered through IV route. In the evening spontaneous respiration weakened and cyanosis was observed. Ventilator was connected around 4 PM. Amantadine was given through gastric tube, glycerol was replaced by manitol, and H2 blocker (Gaster) was given because of gastric bleeding. Additional therapy for disseminated inravascular coagulopathy was given, but consciousness level progressed to III-300 (JCS). On December 24, mydoriasis was observed without light reflex. Electroencephalogram (EEG) showed flat wave and auditory brainstem response (ABR) was negative. On December 25, cranial CT revealed low absorption area in the mid-brain and the brain stem, then inflammation of the brain stem was suspected. Dopamine and dobtamine were given, because of weak peripheral circulation. Although capillary enzyme level improved (GOT 348IU, GPT 446 IU, LDH 1,295 IU on December 25, and GOT 167 IU, GPT 190 IU, LDH 1,604 IU, Na 158 Meq/L, K 3.8 Meq/L, Cl 128 Meq/L on December 28) with intensive therapy, general condition is not improved to date.

As of January 12, 2000, mechanical ventilation was going on, because the patient did not resume voluntary respiration. Gastric tube was not used due to peristalsis arrest. He presented diabetes insipidus, so that desmopression was being given. EEG was examined 3 times on December 24, 28, and January 5, and results were flat. ABR was negative on December 24 and 28, thus, the patients was almost in brain death.

In December 1999, both influenza A (H1) and influenza A (H3) viruses were isolated, however, the former was dominant in Osaka area. Few cases of encephalopathy were reported after influenza A (H1) infection in Osaka area. As influenza A (H3) is getting epidemic, few encephalopathy cases associated with its infection are confirmed due to this.

Reported by Masamitsu Nishino, and Koichi Ando, Dept. of Pediatrics, Takatsuki Hospital; Akiko Maeda, Tetsuo Kase, Saeko Morikawa, and Yoshinobu Okuno, Osaka Prefectural Institute of Public Health.

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