863

ALT data in infant with liver

Fig 2-Amplified HHV-6

DNA in brain

(a) and liver (b).

Positive bands with 776 base-pairs indicated M=molecular weight marker of À.phage DNA.

by square markers.

progression from drowsiness to coma in this patient can be explained by hepatic encephalopathy but HHV-6 invasion of the brain might have contributed. Department of Paediatrics, Fujita Health University School of Medicine, Toyoake, Aichi 470-11, Japan

Department of Virology, Research Institute for Microbial Diseases, Osaka University

YOSHIZO ASANO TETSUSHI YOSHIKAWA SADAO SUGA TAKEHIKO YAZAKI

KAZUHIRO KONDO KOICHI YAMANISHI

K, Okuno T, Shiraki K, et al. Identification of human herpesvirus-6 as a causal agent for exanthem subitum. Lancet 1988; i: 1065-67. 2. Asano Y, Yoshikawa T, Suga S, et al. Viremia and neutralizing antibody response m infants with exanthem subitum. J Pediatr 1989; 114: 535-39. 3 Suga S, Yoshikawa T, Asano Y, Yazaki T, Hirata S. Human herpesvirus-6 infection (exanthem subitum) without rash. Pediatrics 1989; 83: 1003-06. 4. Kondo K, Hayakawa Y, Mori H, et al. Detection of human herpesvirus 6 (HHV-6) DNA in peripheral blood of exanthem subitum patients by polymerase chain reaction DNA amplification. J Clin Microbiol (in press). 5. Downing RG, Sewankambo N, Serwadda D, et al. Isolation of human lymphotropic herpesviruses from Uganda. Lancet 1987; ii: 390 1. Yamanishi

Human

herpesvirus-6 infection with liver injury in neonatal hepatitis

SIR,-We report a case of hepatitis in an infant who had an episode of liver injury associated with human herpesvirus-6 (HHV-6) infection. A 2-month-old baby was referred to this hospital for investigation of cholestasis. Neonatal hepatitis was diagnosed, and giant cell transformation was revealed by needle biopsy at 3 months of age. Hepatitis B surface antigen, hepatitis A virus, Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus were ruled out and his serum oq-antitrypsin was normal. The cholestasis gradually disappeared but alanine aminotransferase activities remained high, with one episode of acute exacerbation of liver dysfunction (figure). He was discharged at 5 months of age on a Chinese herbal medicine (Shosaikoto) alone. At his discharge his serum aspartate aminotransferase was 84 IU/1 and his serum alanine aminotransferase (ALT) was 148 IU/1. He had an uneventful clinical course after discharge, and his serum ALT remained around 148 IU/1 until 7 months of age when liver function deteriorated (figure). An episode of vomiting on Dec 10 was followed by moderate degree of fever lasting 4 days. On Dec 14, red maculopapular eruptions appeared on his back and abdomen, and his serum ALT had risen to 467 IU/1. He was

damage and HHV-6 infection.

admitted for investigation. HHV-6 was isolatedl from peripheral blood mononuclear cells obtained on Dec 14. An HHV-6 antibody test, which had been negative before this episode, was positive on

Jan 10. Roseola infantum due to HHV-6, superimposed upon neonatal hepatitis, exacerbated liver damage in this patient. Although the agent responsible for the initial hepatitis has not been identified, the later exacerbation of hepatitis was probably associated with HHV-6. HHV-6 has a T-cell tropism,2 which might modulate an interaction between host immunity and hepatotropic viruses such as hepatitis B virus.

Department of Paediatrics, Osaka University Hospital, Fukushima 553 Osaka, Japan

H. TAJIRI O. NOSE K. BABA S. OKADA

K, Okuno T, Shiraki K, et al. Identification of human herpesvirus-6 as a causal agent for exanthem subitum. Lancet 1988; i: 1065-67. 2. Takahashi K, Sonoda S, Higashi K, et al. Predominant CD4 T-lymphocyte trophism of human herpesvirus 6-related virus. J Virol 1989; 63: 3161-63. 1. Yamanishi

Meningococci with reduced susceptibility to penicillin SIR,-When we reportedl on the prevalence of meningococci from meningitis or septicaemia with a reduced susceptibility to benzylpenicillin (minimum inhibitory concentration 0 16-1-28 mg/1) it appeared that the incidence of such strains was increasing. However, since 1987, despite an increase in the prevalence of meningococcal infection throughout the UK, the proportion of strains relatively insensitive to penicillin has remained about the same (table). These strains continue to be a mixture of group B and group C serotypes with no particular phenotype predominating. These strains have an altered penicillin-binding protein, the result of the incorporation of genetic material coding for this from a non-pathogenic species, Neisseria flavescens.2 At present, therefore, about 3% of infections may be caused by strains of meningococci showing some diminution in susceptibility to penicillin but we had not heard of any problems arising from the therapeutic use of penicillin until the report by Dr Turner and SUSCEPTIBILITY TO PENICILLIN G OF MENINGOCOCCI FROM CLINICAL CASES IN ENGLAND AND WALES 1985-89

Human herpesvirus-6 infection with liver injury in neonatal hepatitis.

863 ALT data in infant with liver Fig 2-Amplified HHV-6 DNA in brain (a) and liver (b). Positive bands with 776 base-pairs indicated M=molecular...
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