Nigeria Fowleri in Florida Pathways and Consequences

Naegleria Fowleri in Florida: Pathways and Consequences Life Cycle Pathways Effects on Humans N. Fowleri in Florida Naegleria fowleri in Florida: Pathways and Consequences Complex Life Cycle This section describes the life cycle of N. fowleri and describes the results of representative studies to date. Ferrante (1986); Chang (1978); Fowler & Carter (1965); John (1982); Abraham & Lawande (1982); de Jonckheere & Voorde (1977); Jonckheere, Van Dijcka and van de Voorde (1975); Ugonabo & Gugnani (1989); and, Lawande (1983). Pathways This section describes the pathways by which humans can become infected by the N. fowleri amoeba.

Paracer & Ahmadjian (2000); Bakalar (2003); Fowler & Carter (1965); and, Marciano-Cabral (1988). Effects on Humans A description of the N. fowleri's effect on humans is provided in this section. Visvesvara, Moura and Schuster (2007); Matthews, S., Ginzl, D., Walsh, D. et al. (2008); 3. Bakalar (2003); N. Fowleri in Florida Finally, a description of the three most recent deaths in Florida that were attributable to N. fowleri is presented in this section. Matthews, S., Ginzl, D., Walsh, D. et al. (2008).

Abstract The Naegleria fowleri amoeba is a ubiquitous and free-living creature that parasitizes humans and can result in encephalitis when the pathogen penetrates the brain through the nasal passages. In most cases, eye infections by the N. fowleri amoeba can cause blindness and other infections are typically fatal. Although cases of N. fowleri infection are relatively rare, there have been a dozen or so cases in recent years that concern healthcare authorities. Exposure to N.

fowleri generally takes place in warm freshwater lakes or rivers that are untreated, with the majority of cases occurring in 15 southern tier states (Arizona, Arkansas, California, Florida, Georgia, Louisiana, Mississippi, Missouri, Nevada, New Mexico, North Carolina, Oklahoma, South Carolina, Texas, and Virginia). Although infections from N. Fowleri can occur at any time, the months of July through September account for the vast majority of the infections to date. This paper examines the pathways, complex life cycle and the effects that N.

fowleri can have on humans, followed by a discussion concerning its economic impact and specific cases of N. Fowleri in Florida. A summary of the research and important findings are presented in the conclusion. Naegleria fowleri in Florida: Pathways and Consequences Introduction Many Americans have heard horror stories about brain-eating pathogens that inhabit the nation's freshwater lakes, rivers and streams, and the popular press is replete with vivid tales of human encounters with these types of pathogens.

Unfortunately, the stories about Naegleria fowleri are true, and although infections caused by this amoeba are rare, when they do occur they typically leave humans blinded or the microbe kills them outright. This paper provides a review of the relevant peer-reviewed and scholarly literature concerning the pathways to infection used by Naegleria fowleri, the effects that infections can have on humans, and its economic impact. Finally, an analysis of Naegleria fowleri in Florida is followed by a summary of the research and important findings in the conclusion.

Review and Discussion Complex Life Cycle Naegleria fowleri is a ubiquitous, free-living amoeba that parasitizes humans that can cause encephalitis when it enters the brain through the nasal passages (Ferrante, 1986). In 1966, researchers termed the infection caused by the N. fowleri primary amoebic meningoencephalitis (PAM) to differentiate the central nervous system (CNS) invasion from other secondary invasions caused by other true amoebas such as Entamoeba histolytica (Fowler & Carter, 1965; John, 1982). According to Matthews, Ginzl, Walsh et al.

(2008), "Primary amebic meningoencephalitis (PAM) is a rare but nearly always fatal disease caused by infection with Naegleria fowleri, a thermophilic, free-living amoeba found in freshwater environments" (p. 573). Generally, exposure to N. Fowleri takes place in warm, freshwater lakes or rivers within untreated water in 15 southern tier states: Arizona, Arkansas, California, Florida, Georgia, Louisiana, Mississippi, Missouri, Nevada, New Mexico, North Carolina, Oklahoma, South Carolina, Texas, and Virginia; however, it remained unknown what state was involved in the exposure in four cases of infection in 2007 (Matthews et al., 2008).

The overwhelming majority of the 121 infections (see Figure 1 below) that have taken place since 1937 occurred between July and September (Matthews et al., 2008). Figure 1. Number of identified cases of PAM: 1937-2007 Source: Matthews et al., 2008, p. 577 The N. fowleri organism has a protective cyst which is broken through in order for reproduction to take place within the victim (Bakalar, 2003). Resistance of pathogenic N.

fowleri to drying, low and high temperature, and two halogens was studied by Chang (1978) who determined that dying immediately made the trophozoites nonviable and cysts nonviable in less than 5 minutes. According to Chang, "Trophozoites degenerated in hours at temperatures below 10 degrees C. And in minutes when frozen; cysts survived according to the equation th - t0/theta 1,440/1.122T (t0 is survival at 0 degrees C; Tis temperature between 0 and 10 degrees C), but 1.5 h at --10 degrees C. To 1 h at --30 degrees C." (1978, p. 368).

Subsequent evaluation by the principal researcher at 51, 55, 58, 63, and 65 degrees C, indicated that the trophozoites were capable of surviving approximately 30, 10, 5, 1 and less than 0.5 min, respectively; by contrast, the cysts survived three to four times longer at 51 degrees C. And six to seven times longer at 55 to 65 degrees C (Chang, 1978). Based on these findings, Chang (1978) reports that, "Cyst destruction rates by heat indicated first-order kinetics with 25,400 cal/1 degree C. For energy of activation. Cyst destruction rates by free chlorine and I2 also conformed to first-order kinetics" (p. 369).

In addition, Chang (1978) also analyzed concentration-contact times and found that concentration coefficient values of 1.05 for free chlorine and 1.4 for I2 and indicates that superchlorination may represent an effective way of killing the cysts when free residuals are used as a guide and allowance is made for high pH waters and/or low temperature. Likewise, the presence of free living N. fowleri amoebae in the nasal passages of 50 healthy children and in environmental sources in Maiduguri, Borno State of Nigeria was investigated by Ugonabo and Gugnani (1989).

In this region of Africa, the pathogen is truly ubiquitous. For instance, according to the findings from this study, "Three of the children yielded positive cultures of Naegleria fowleri. All the five water samples and two of the nine soil samples examined from different localities were positive for N. fowleri. The isolates proved pathogenic for laboratory mice causing a fatal meningoencephalitis" (Ugonabo & Gugnani, 1989). A study by Lawande (1983) recovered soil amoebae from the air during the dry and dusty trade wind season in Zaria, Nigeria.

For this study, Lawande seeded non-nutrient agar plates with Escherichia coli, which is known to be a food source for the amoeba, which were used as settle plates. These plates were subsequently air-exposed for 30 minutes-4 hours, following which the plates were incubated at 27 degrees C. Or 37 degrees C; all told, 38 strains of amoeba were cultured (21 of the genus Hartmannella, eight Naegleria, four Schizopyrenus, three Didascalus and two Tetramitus) (Lawande, 1983). In addition, three pathogenic species, H. culbertsoni, N. fowleri and H.

rhysodes, were also cultured and all three of these strains were shown to kill mice. Based on these findings, the principal researcher concluded that, "These results suggest the possibility of airborne primary amoebic meningoencephalitis infections in Nigeria" (Lawande, 1983, p. 45). A similar study by Abraham and Lawande (1982) also identified three species that were pathogenic for mice: H. culbertsoni, H. rhysodes and N. fowleri.

According to these researchers, "It was observed from this study that a significant percentage of the Zaria population carry free-living amoebae in the nasal passages" (Abraham & Lawande, 1982, p. 218). The monthly incidence rate for this population, though, was shown to vary dramatically from 1.8 to 3.1% during the rainy season compared to the dry trade wind season when it varies from 4.2 to 7.9% (Abraham & Lawande, 1982).

Because the highest monthly incidence rates correspond to the peaks of the dry season, these researchers speculate that the dry trade winds have an effect on the nasal carriage that facilitates infection (Abraham & Lawande, 1982). A study by de Jonckheere and Voorde (1977) investigated the effluent discharges of 16 thermal polluting factories for the occurrence of Naegleria fowleri, the causative agent of primary amebic meningoencephalitis. Nearly half (7) of the waters that were tested were identified as containing N. fowleri (de Jonckheere & Voorde, 1977). All told, 22 N.

fowleri isolates were identified and of these, three were found to be highly virulent for mice when they were inoculated intranasally (de Jonckheere & Voorde, 1977). According to these researchers, "The three pathogenic strains were isolated from three different places during summer. More N. fowleri were found during summer than in winter, which could be attributed to the lower temperature during winter" (de Jonckheere & Voorde, 1977, p. 11).

Although there was no connection identified between the type of factories that were involved in the study and the level of contamination, the older factories discharged cooler water compared to their newer counterparts, accounting for the difference in water temperatures (de Jonckheere & Voorde, 1977). 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). Pathways 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.