PATHOGENIC FREE-LIVING AMOEBAE
AND RECREATIONAL WATERS
S.L. CHANG
Water Hygiene Division, Office of Water programs, Environmental Protection
Agency, Cincinnati, Ohio 45268, U.S.A.
The swimming-associated amoebic meningoencephalitis is a relatively new and
uncommon disease, but has attracted increasing attention of public health workers
because of its extremely high fatality and its occurrence in widely scattered resort areas.
In a very recent report Chang (1971) gathered from the literature and personal
communications a total of 45 cases-22 in the United States, 17 in Czechoslovakia, and 6
in Australia. In addition, five suspected cases were reported in Britain (Symmers, 1969;
Appley et al. y 1970; Warhurst et al y 1970). Two of them were revealed in a retrospective
examination of old pathological specimens and the other three occurred in August 1969
without a history of swimming.
In April 1971 (Hecht et αί, 1971), another case of swimming-associated amoebic
meningoencephalitis occurred near San Bernardino, California, in a different setting. A
girl in a group of about 20 young people was afflicted with the disease after a few days of
swimming in a small, shoulder-deep pool fed by water from a hot spring. The temperature
of the pool water is normally 27.7-39.3°C.
The causative amoeba of this disease is morphologically indistinguishable from the
free-living forms known as Naegleria gruben, which are small (15-18μ in diameter), actively
motile, and capable of transient flagellate transformation, and are commonly found in
sewage effluents from aerobic treatment processes, in fresh surface waters, and in soil
(Singh, 1952; Chang, 1958, 1960, 1971). Cysts of N. gruben have also been found in
municipal water supplies (Chang et al, 1960) and in outdoor swimming pools (Chang,
1971).
The generally accepted belief in the mode of infection of amoebic
meningoencephalitis is that the amoebae gain their entrance into the upper part of
the nasal cavity through diving or swimming activities. From there they work
their way through the nasal mucosa and the cribiform plate into the cranial
cavity. They first attack the meninges; expansion of the lesion into the adjacent
part of the brain results in meningoencephalitis.
To understand the epidemiology of this disease a number of questions must be
answered: (1) Are pathogenic strains of Naegleria fundamentally different from the wild
strains of N. gruben in pathogenicity? (2) Can wild strains of N. gruben become
pathogenic under certain conditions? (3) Can pathogenic strains of Naegleria establish
growth in the midst of wild N. gruben in a natural aquatic environment? (4) Can
pathogenic Naegleria produce asymptomatic infections in man by parasitizing the
nasopharyngeal region and cause the disease only when the amoebae are washed into the
upper nasal cavity? (5) Can wild strains of N gruben parasitize human nasopharyngeal
region and gain pathogenicity through such a parasitism? (6) Do aquatic or terrestrial
85
AND RECREATIONAL WATERS
S.L. CHANG
Water Hygiene Division, Office of Water programs, Environmental Protection
Agency, Cincinnati, Ohio 45268, U.S.A.
The swimming-associated amoebic meningoencephalitis is a relatively new and
uncommon disease, but has attracted increasing attention of public health workers
because of its extremely high fatality and its occurrence in widely scattered resort areas.
In a very recent report Chang (1971) gathered from the literature and personal
communications a total of 45 cases-22 in the United States, 17 in Czechoslovakia, and 6
in Australia. In addition, five suspected cases were reported in Britain (Symmers, 1969;
Appley et al. y 1970; Warhurst et al y 1970). Two of them were revealed in a retrospective
examination of old pathological specimens and the other three occurred in August 1969
without a history of swimming.
In April 1971 (Hecht et αί, 1971), another case of swimming-associated amoebic
meningoencephalitis occurred near San Bernardino, California, in a different setting. A
girl in a group of about 20 young people was afflicted with the disease after a few days of
swimming in a small, shoulder-deep pool fed by water from a hot spring. The temperature
of the pool water is normally 27.7-39.3°C.
The causative amoeba of this disease is morphologically indistinguishable from the
free-living forms known as Naegleria gruben, which are small (15-18μ in diameter), actively
motile, and capable of transient flagellate transformation, and are commonly found in
sewage effluents from aerobic treatment processes, in fresh surface waters, and in soil
(Singh, 1952; Chang, 1958, 1960, 1971). Cysts of N. gruben have also been found in
municipal water supplies (Chang et al, 1960) and in outdoor swimming pools (Chang,
1971).
The generally accepted belief in the mode of infection of amoebic
meningoencephalitis is that the amoebae gain their entrance into the upper part of
the nasal cavity through diving or swimming activities. From there they work
their way through the nasal mucosa and the cribiform plate into the cranial
cavity. They first attack the meninges; expansion of the lesion into the adjacent
part of the brain results in meningoencephalitis.
To understand the epidemiology of this disease a number of questions must be
answered: (1) Are pathogenic strains of Naegleria fundamentally different from the wild
strains of N. gruben in pathogenicity? (2) Can wild strains of N. gruben become
pathogenic under certain conditions? (3) Can pathogenic strains of Naegleria establish
growth in the midst of wild N. gruben in a natural aquatic environment? (4) Can
pathogenic Naegleria produce asymptomatic infections in man by parasitizing the
nasopharyngeal region and cause the disease only when the amoebae are washed into the
upper nasal cavity? (5) Can wild strains of N gruben parasitize human nasopharyngeal
region and gain pathogenicity through such a parasitism? (6) Do aquatic or terrestrial
85