Free-living amoeba (FLA) is unicellular protozoa widely distributed throughout world-wide that can survive and replicate in the environment without a host. FLA feed on microorganism as a food source. FLA are present in a large variety of natural habitats, including lake, river, swimming pool, thermal bath, tap water, sources of running water which receive industrial refuse, sewage, humid soil, and dust.(1) Pathogenic and opportunistic FLA such as Naegleria fowleri, Balamuthia mandrillaris and several species of Acanthamoeba that can potentially cause infections in humans. All three amoebae can cause fatal central nervous system (CNS) infections. Naegleria fowleri causes acute necrotizing and hemorrhagic meningoencephalitis, known as primary amoebic meningoencephalitis (PAM), while Acanthamoeba and Balamuthia cause the insidious, chronic and mostly fatal disease granulomatous amoebic encephalitis (GAE), leading to death in healthy children and adult with history of recent contact with fresh water. In addition to causing CNS infections, Acanthamoeba also causes a vision threatening disease (Acanthamoeba keratitis). Both Acanthamoeba and Balamuthia also can cause infections of the lungs and skin.(2)
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Pathogenic and nonpathogenic species of Naegleria have been isolated from environmental sources and more than 35 species that have been identified which N. fowleri only is caused in human disease.(3book) Two other species, N. australiensis and N. italic have been shown pathogenic for experimental animals.(4) N. fowleri can causes PAM that a rapidly fatal disease of CNS. Human disease caused by FLA was first reported in 1965 by Fowler and Carter. The first successful isolation and culture of N. fowleri from cerebrospinal cord fluid and infected brain tissue in1968 by Butt.(5) and later Carter designated the amoeba was N. fowleri.(6) The term of primary amoebic menigoencephalitis was used first by Butt.(7) At the present time, PAM in human have been reported from worldwide. The majority of PAM cases were reported with a history of swimming and diving and other recreational activities in fresh water and chlorinate not adequately swimming pools.(8)
N. fowleri are distributed increasing number in the United States (fig.1) and worldwide due to combination of factors including increased freshwater recreational activities during heat waves, cases more than 180 have been identified in worldwide.(9) In Thailand, the first case of Naegleria infection was found at Si Sa Ket in 1983, was published by Jariya and colleagues.(10) Since the first case report, there have been at least 12 reports of PAM in Thailand.(11)
Figure 1: Number of conï¬rmed cases of primary amebic meningoencephalitis (PAM), US, 1937-2007. Source: US Centers for Disease Control and Prevention (CDC), available at www.dpd.cdc.gov/mmwr/preview/mmwrhtml/mm5721a1.htm.
N. fowleri in nature has three morphological forms, an amoeba or trophozoite stage, a flagellate stage, and a cyst (fig. 2). A trophozoite stage that feeds and divides, flagellate form that swimming and look for a new food source, and the resistant cyst that protects the amoeba from environmental stress conditions.(12morpho)
Figure 2: Naegleria fowleri: (a) trophozoite, (b) a ï¬‚agellate, and (c) a cyst. All images at x 1000 (2)
1. Trophozoite stage
The trophozoite of Naegleria is the vegetative or feeding stage, which can moves rapidly by producing hemispherical bulge, lobopodia, at the anterior end and exhibits active sinusoid locomotion and food cups or amoebastomes which are cytoplasmic extensions of the surface used to ingest bacteria or yeast in the environment or erythrocyte and brain tissue in the infected host. It measures approximately 10 to 25 µm and reproduces by binary ï¬ssion. Naegleria trophozoite exhibits typical features of a eukaryotic cell. It has a single vesicular nucleus with a prominent, centrally placed nucleolus that stains densely with chromatic dyes. The cytoplasm shows a sharp distinction between ectoplasm and endoplasm that contain numerous mitochondria, ribosomes, food vacuoles, and the contractile vacuole and protoplasmic ï¬laments. The trophozoite transforms into a ï¬‚agellate stage when the ionic concentration of the environment change. (2, 3book, morpho)
2. Flagellate stage
The flagellate stage of N. fowleri is the pear-shaped, ranges in length from 10 to 16 µm, but neither divides nor feeds and usually turns back to the amoeboid form within an hour or less. The flagellate stage is transient and can differentiate into this stage involves a change in cell shape and change in synthesis of all organelles of the flagellar apparatus. In this process, cytoplasmic vacuoles decreased and basal bodies and flagella are formed. Flagella exhibit the typical arrangement of filaments (9+2) surrounded by a sheath which is continuous with the cytoplasmic membrane. The mature flagellar apparatus usually consists of two flagella, two basal bodies, microtubules and a single striated rootlet.(2,3book,13)
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3. Cyst stage
The cyst of N. fowleri usually spherical, approximately 8 to 12 µm in diameter,(14) which consists of double walled with a thick endocyst and a closely appose thin ectocyst.(15) The cyst wall has pores sealed with a mucoid plug. The cyst provides protection from non-suitable environmental conditions. Factors that induce cyst information include food lacking, crowd, drought, accumulation of waste products, pH changes, and slats.(2,3book,)
N. fowleri in nature has three forms, the resistant cyst, the actively feeding trophozoite that replicates by promitosis with an intact nuclear membrane and a transient flagellate stage. Infection with N. fowleri occurs mainly during swimming by flagellate stage. N. fowleri penetrates the nasal mucosa and moves via the olfactory nerves to the brain (fig. 3). The life-cycle depends on temperature, salt concentrations and nutrients in the environment of the amoeba. N. fowleri usually is much more sensitive to environmental conditions, for example pH or desiccation than other amoebae. (Schuster and Visvesvara, 2004, 2)
Figure 3: Life cycle of N. fowleri (Cited from http://www.dpd.cdc.gov/dpdx)
Pathogenesis and symptomatology
The pathogenesis of PAM caused by N. fowleri is an acute, suppurating infection of the brain and meninges which the portal of entry into the human host is the nasal cavity. After entry, the trophozoite penetrates the nasal mucosa and migrates along mesaxonal spaces of unmyelinated olfactory nerves terminating at the olfactory bulb in the subarachniod space. This space is quite vascularized and is a route of dissemination of trophozoites to other areas of the brain such as brainstem and cerebellum.(16,17)
This disease shows bad prognosis in humans; the time between contact with the amoebae and the onset of symptoms may vary from 2 to 15 days. Early symptoms are thoracic pain, headache, lethargy and alteration of sense of smell. Progressive symptoms like fever, vomiting, neck rigidity, mental confusion and lung edema may occur, usually 3 to 5 days before death. Amoeba invasion causes ulcers in the nasal pharyngeal mucosa and neuritis and necrosis of the olfactory nerves. PAM can be misdiagnosed as acute suppurating bacterial meningitis. The cause of death is often respiratory arrest.(18,19)
10. Jariya P, Jaroomvasama N, Kunaratanapruk S, Lawhanuwat C, Pongchaikul P. Primary amoebic meningoencephalitis: a first reported case in Thailand. Southeast Asian J Trop Med Pub Health 1983;14:525-7.
11. Wiwanitkit V. Review of clinical presentations in Thai patients with primary amoebic meningoencephalitis. MedGenMed 2004;6(1):2.
19. Sparagano O. Detection of Naegleria fowleri cysts in environmental samples by using a DNA probe. FEMS Microbiology Letters 1993;112:349-51.