In sum, the researchers determined that, "There are strong indications that the isolation of nonpathogenic seropositive strains from water is an indication for the occurrence of pathogenic N. fowleri" (de Jonckheere & Voorde, 1977, p.12).

A seminal study by de Jonckheere, Van Dijcka and van de Voorde (1975) investigated the distribution of N. fowleri to determine its role as the causal agent of primary amoebic meningoencephalitis. For this study, the principal researchers isolated N. fowleri from water taken from a thermally polluted canal (de Jonckheere et al., 1977). According to de Jonckheere and his associates, "These amoeboflagellates were not isolated from another thermally polluted canal in the neighbourhood indicating that, apart from high temperature, other factors are involved in the selective proliferation of N. fowleri" (p. 8). This study determined that N. fowleri was not present in the other samples taken from two canals, a stream, two lakes, several reservoirs and slow sandfilters of a water supply service and also a water distribution network (de Jonckheere et al., 1977). Although the majority of the N. fowleri strains isolated from these water sources were not virulent for mice, they all demonstrated the characteristics of the pathogenic strains (de Jonckheere et al., 1977).


Infection results from water containing N. fowleri entering the nose, followed by the movement of the amoeba into the brain through the olfactory nerve (Paracer & Ahmadjian, (2000). Although the condition has been treated successfully with amphotericin B, victims can die within 24 hours following first appearance of the symptoms; however, the process can take as long as 2 weeks (Bakalar, 2003). Diagnosis of N. Fowleri infection is accomplished by performing a lumbar puncture and analyzing the cerebrospinal fluid; however, since the condition advances so quickly, there is rarely time for this diagnostic step (Bakalar, 2003, p. 184). Interestingly, electron microscopy of trophozoites of N. fowleri has identified so-called "feed cups" or amoebostomes that are employed in the consumption of host cells (Marciano-Cabral, 1988).

Effects on Humans

According to Visvesvara, Moura and Schuster (2007), of the vast majority of the numerous genera of free-living amoebae that exist naturally, just four genera have been associated with disease in humans: Acanthamoeba spp., Balamuthia mandrillaris, Naegleria fowleri and Sappinia diploidea. These researchers report that, "Of more than 30 species of Naegleria, only one species, N. fowleri, causes an acute and fulminating meningoencephalitis in immunocompetent children and young adults" (Visversvara et al., 2007). Following approximately one week of incubation, symptoms from N. fowleri infections can develop rapidly, including: headaches, vomiting, fever, lethargy, nausea, inflammation of the pharynx, confusion, stiff neck, convulsions, coma or death (Bakalar, 2003).

Although just 112 cases of PAM have been reported in the United States since 1937, six cases of PAM in the United States were reported to the Centers for Disease Control in 2007, and all six of these cases resulted in death (Matthews et al., 2008). In response to these and others deaths from PAM, federal and state health authorities have sought to educate the public concerning the risk posed by N. fowleri, but improved diagnosis, treatment, case reporting, and environmental sampling are still required (Matthews et al., 2008). Although most infections of this type are fatal, the eyes can also become infected by N. Fowleri-tainted water which can result in blindness (Bakalar, 2003).

N. Fowleri in Florida

There were three cases of N. fowleri infection reported in Florida in 2007 (Matthews et al., 2008). The first case of N. Fowleri infection took place on June 8, 2007 and involved a 14-year-old boy being admitted to an emergency room with complaints of symptoms that began 2 days previously (Matthews et al., 2007). Upon admission, the victim was unable to walk and was determined to be apneic and without a pulse (Matthews et al., 2008).The symptoms in this first episode of N. Fowleri infection included a sensation of ear pressure which expanded to include a severe headache and periodic vomiting on June 9, 2007. The youth expired shortly thereafter and following an autopsy, the victim was diagnosed with PAM. According to Matthews and his associates, "The youth had access to multiple drainage ditches and canals and to an apartment swimming pool during the 2 weeks before onset of symptoms; no location was conclusively identified as the source of exposure" (2008, p. 576).

The second case of N. Fowleri infection in Florida occurred on August 6, 2007 when an 11-year-old boy was admitted to a tertiary healthcare facility with complaints of a headache, fever, nausea, vomiting, and confusion, with a possible diagnosis of bacterial meningitis (Matthews et al., 2007). This victim's symptoms started 4 days earlier and consisted of a headache and a mild rash (Matthews et al., 2007). According to Matthews et al., "Motile amoebe, later identified as N. fowleri, were found in CSF samples collected August 7. The same day, the patient was treated with amphotericin B, epinephrine, mannitol, fluconazole, ceftriaxone, azithromycin, and rifampin; however, the boy died August 8" (p. 577). The young victim had been wakeboarding and swimming in a local lake about a week-and-a-half prior to admission, and these episodes were deemed the source of exposure to the N. fowleri.

The final case of N. Fowleri infection in Florida took place on September 2, 2007 when an emergency room examined a 10-year-old boy complaining of headache, body aches, high fever, nausea, vomiting, and fainting (Matthews et al., 2007). The onset of this victim's symptoms was 3 days earlier when he reported a headache and was observed lethargic (Matthews et al., 2008). Following admission to a tertiary healthcare facility, the 10-year-old's symptoms included a high fever (104.0°F), confusion, as well as abdominal pain. According to Matthews et al., "Motile amoeba, later identified as N. fowleri, were found in CSF on September 3 and 4, 2007. Amphotericin B, rifampin, azithromycin, and fluconazole were administered; however, the boy died September 4" (2008, p. 577). The potential source of the infection for this victim included a history of wakeboarding and swimming at water sports facility twice on hot days (Matthews et al., 2008).


The research showed that the Naegleria fowleri amoeba is a free-living ubiquitous amoeba that parasitizes humans and can result in serious injury or even death when the N. fowleri infection enters the brain through the nasal passages. Although there have been just 121 cases of N. Fowleri infection since 1935, the historical record shows that there have been several spikes, including one in 2007 when there were seven fatalities reported. The research also showed that people are typically exposed to N. Fowleri when bathing or swimming in untreated warm freshwater, and most of the cases occur within Arizona, Arkansas, California, Florida, Georgia, Louisiana, Mississippi, Missouri, Nevada, New Mexico, North Carolina, Oklahoma, South Carolina, Texas, and Virginia. Finally, the research showed that most of the infections by N. fowleri to date have occurred during the warmer months of the year.


Abraham, S.N. & Lawande, R.V. (1982, October). Incidence of free-living amoebae in the nasal passages of local population in Zaria, Nigeria. The Journal of Tropical Medicine And

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Bakalar, N. (2003). Where the germs are: A scientific safari. Hoboken, NJ: Wiley.

Chang, S.L. (1978, February). Resistance of pathogenic Naegleria to some common physical and chemical agents. Applied Environmental Microbiology, 35(2), 368 -- 375.

de Jonckheere, J., Van Dijcka, P. & van de Voorde, H. (1975). The effect of thermal pollution on the distribution of Naegleria fowleri. Journal of Hygiene, 75(1), 7-13.

de Jonckheere, J. & Voorde, H. (1977). The distribution of Naegleria fowleri in man-made thermal waters. The American Journal of Tropical Medicine and Hygiene, 26(1), 10-15.

Ferrante, A. (1986). Discovery and control of primary amoebic meningoencephalitis (PAM).

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