The Topic of This Month Vol.19 No.8(No.222)

Nationwide epidemics of aseptic meningitis due to echovirus 30 (E30) have occurred three times since the start of the National Epidemiological Surveillance of Infectious Diseases (NESID)^*: the first one in 1983 (see IASR, Vol. 4, No. 10), the second one in 1989-1991 (see IASR, Vol. 12, No. 8 and Vol. 13, No. 8), and the third one since 1997. This topic deals with this most recent epidemic.

Reports on the occurrence of aseptic meningitis cases started to increase in June in 1997, attaining the largest number in August-September. Being different from the usual epidemic feature, a considerably large number of reports came out during October-December as was the case in 1991 (Fig. 1). The annual reports of cases in 1997 numbered 3,328 (6.46 cases per sentinel hospital), which was the fourth largest number after 7,672 (14.05 cases) in 1991, 4,753 (9.25 cases) in 1989, and 3,485 (6.66 cases) in 1990. The ages of the cases were 0-4 years accounting for 42%, 5-9 years 39%, 10-14 years 9.8%, and 15 years and older 8.4%. Reports of aseptic meningitis cases suddenly increased in May in 1998 (1.00 case per sentinel hospital), and further increased largely in June (1.88 cases). Both outnumbered those in May 1989 (0.73 cases) and June 1991 (1.50 cases), respectively, and were the largest number in the respective months since 1987 (Fig. 1).

The trend of reports on virus isolation from meningitis cases is shown in Fig. 2. The viral agents of meningitis comprise mainly echoviruses and group B coxsackieviruses, the most important agent being E30 which caused a particularly large-scale epidemic in 1991. During the 1989-1991 epidemic, reports of isolation of E30 started to increase in June, attaining the largest number in July-August. In 1997, such reports started to increase in July, attaining the largest number in October, after which isolation of E30 kept on until it again increased suddenly in May 1998.

To help understand the geographical distribution of the present epidemic, the incidence of aseptic meningitis and isolation of E30 in each prefecture are shown respectively in Figs. 3 and 4. E30 was isolated in June 1997 in Fukushima (see IASR, Vol. 18, No. 9), Osaka, Nara and Hiroshima Prefectures. After July, reports of patients increased in Nara, Okayama, Tottori, and Shimane Prefectures and isolation of E30 kept on increasing until such reports came out from 29 prefectures (34 PHIs) by December (see IASR, Vol. 18, Nos. 11 and 12; Vol. 19, Nos. 1 and 2). Isolation of E30 kept on further after January 1998 in many prefectures, mainly in Chugoku, Shikoku and Kyushu Districts, and has been reported from 20 prefectures (22 PHIs) including Kumamoto, Kagawa, Saga and Kochi Prefectures where reports on patients have increased since April (see IASR, Vol. 19, No. 5 and p. 177-178 of this issue). On the other hand, reports of aseptic meningitis patients increased in Iwate Prefecture in June 1997, but the viruses isolated from them were E9 (see IASR, Vol. 18, No. 8). Isolation of E9 increased in 1997 after three years, attaining the largest number in July (Fig. 2). Few reports on isolation of E9 have so far come out in 1998. Since there is a time-lag from specimen collection to virus isolation, more reports on virus isolation in 1998 may come out from now on. The current trends of case incidence and virus isolation can be found on the home page of IDSC (http://idsc.nih.go.jp/kanja/index-e.html).

E30 was isolated from 1,335 cases during January to December 1997. The clinical diagnoses made were meningitis in 1,128 cases (84%) accounting for a high proportion as was the case in the past epidemics (Table 1) (see IASR, Vol. 13, No. 8). Encephalitis/encephalomyelitis was reported in six cases (aged 2, 4, 7, 7, 12, and 13 years) and encephalopathy in one case (aged 3 years). (In the past reports, encephalitis/encephalomyelitis was reported in 37 of 7,675 cases from which E30 was isolated during 1982-1996).

The age distribution of the cases was very similar to that in the last epidemic (1989-1991) (see IASR, Vol. 13, No. 8); 3-7 years of age with a peak at 5 years accounted for 62% (Fig. 5). It is considered that E30 infection occurs principally in young children born after the last epidemic, but cases of 15 years and older reported accounted for 3.9% and the viruses isolated from adult meningitis cases (37 cases aged 20s-50s) were all E30. Of the cases from which E30 was isolated, 44 were of familial outbreaks and 52 of other outbreaks (IASR, Vol. 18, No. 9, Vol. 19; Nos. 1, 3 and 5; and p. 177 of this issue).

E30 has often been isolated from cerebrospinal fluid, which characterizes the past epidemics. In the present epidemic, E30 was isolated from cerebrospinal fluid of 925 cases (69%), from nasopharyngeal specimens of 544 cases (41%), and from stool specimens of 282 cases (21%) (including isolation from more than one specimens from different sources of the same cases).

E30 has often been isolated with RD-18S cells and also FL and HEp-2 cells as well. Recently, CaCo-2 cells are being used because of their high susceptibility (see IASR, Vol. 19, No. 1 and p. 177 and 179 of this issue). The E30 isolates are serotyped by neutralization with the aid of the antiserum pools "EP95" for echovirus type differentiation (see IASR, Vol. 18, No. 3), but some reports stated that serotyping was difficult with commercially available antisera (see IASR, Vol. 18. No. 9 and Vol. 19, No. 5). Analyses of the currently epidemic strains for the gene nucleotide sequences and the neutralization antigenicities are in progress at PHIs and the National Institute of Infectious Diseases.

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