Early diagnosis of enteroviral meningitis by detection of specific IgM antibodies with a solid‐phase reverse immunosorbent test (SPRIST) and μ‐capture EIA

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Abstract
A solid‐phase reverse immunosorbent test (SPRIST) and a μ‐capture enzyme immunosorbent assay (EIA) for detection of enterovirus‐specific IgM antibodies were evaluated for enterovirus diagnosis of aseptic meningitis in 160 consecutive patients from whom enterovirus (11 different serotypes) were isolated in 64. In patients with an enterovirus isolate and/or four‐fold titre rise in the complement fixation test (CFT) for enterovirus, specific enterovirus IgM antibodies were detected on the day of admission to hospital in 48% by SPRIST and in 50% by EIA and 4‐6 days after onset of symptoms in 71% by SPRIST and 79% by EIA. A significant increase in titre was observed between serum sampled on the day of admission and 2 days later in 38% by SPRIST and in 41% by EIA. These results indicate that the IgM antibody response appears early in the course of aseptic meningitis. Since both SPRIST and EIA provide rapid results the tests may be of differential diagnostic value and the IgM antibody kinetics may be utilized for diagnosis during the acute phase of aseptic meningitis. With optimized serum sampling the positive outcome was 76% in SPRIST and 82% in EIA among patients with positive virus isolation and/or CFT for enterovirus.In 67 patients virus isolation and CFT for en‐terovirus yielded negative results as well as all non‐enteroviral diagnostic tests. Thirty‐eight of these patients were positive by SPRIST and/or EIA and in half of these 38 a significant titre rise and/or fall in SPRIST and/or EIA was recorded. The majority of these IgM‐positive patients became ill in the late summer or autumn, i.e., the “enterovirus season.” These findings indicate that SPRIST and EIA may give additive information about etiology in patients with aseptic meningitis. However, enterovirus IgM responses were seen in 10 cases by SPRIST and in 6 by EIA out of the 25 patients with non‐enterovirus diagnoses. This indicates that the tests may be not only cross‐reacting within the enterovirus group but also, to a smaller extent, be cross‐reacting with sera from patients with non‐enterovirus infections. Dual infections or persistent enterovirus IgM activity after a recent enterovirus infection may be alternative explanations. Thus, additional criteria in support of present enterovirus infection should be sought. In conclusion the detection of enterovirus‐specific IgM has improved the early diagnosis of aseptic meningitis, but rapid enterovirus diagnosis still remains a challenge.