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In the summer of 1978, two children who had recently been swimming in freshwater lakes in Florida died from primary amoebic meningoencephalitis. Despite early and intensive treatment with amphotericin B, both patients died three to five days after the onset of illness. Amoebae were observed in wet preparations of cerebrospinal fluid and in sections of cerebral tissue and were identified as Naegleria fowleri by the indirect immunofluorescent antibody technique. The amoebae were highly virulent in mice. The isolate of N. fowleri was extremely sensitive in vitro to amphotericin B (minimal inhibitory concentration [MIC], 0.15 microgram/ml), somewhat sensitive to miconazole (MIC, 25 micrograms/ml), and resistant to rifampin (MIC, less than or equal to 100 micrograms/ml). Treatment with amphotericin B (7.5 mg/kg of body weight per day) administered intraperitoneally protected 60% of the mice. Lower doses of amphotericin B alone or in combination with miconazole (100 mg/kg) or rifampin (220 mg/kg) were not protective. These results suggest that amphotericin B remains the single effective agent in treatment of primary amoebic meningoencephalitis.

To determine whether artificial heating of water by power plant discharges facilitates proliferation of the pathogenic free-living amoebae that cause primary amoebic meningoencephalitis, water samples (250 ml) were taken from discharges within 3,000 feet (ca. 914.4 m) of power plants and were processed for amoeba culture. Pathogenic Naegleria fowleri grew out of water samples from two of five lakes and rivers in Florida and from one of eight man-made lakes in Texas. Pathogenic N. fowleri did not grow from water samples taken from cooling towers and control lakes, the latter of which had no associated power plants. The identification ofN. fowleri was confirmed by pathogenicity in mice and by indirect immunofluorescence analyses, by using a specific antiserum.

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