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Naegleria fowleri, colloquially known as the "brain-eating amoeba", is a species of

the genus Naegleria, belonging to the phylumPercolozoa.[1] It is a free-living, bacteria-eating


amoeba that can be pathogenic, causing a fulminant (sudden and severe) brain infection
callednaegleriasis, also known as primary amoebic meningoencephalitis (PAM).
This microorganism is typically found in bodies of warm freshwater, such as ponds, lakes,
rivers, and hot springs. It is also found in the soil near warm-water discharges of industrial
plants, and in unchlorinated or minimally-chlorinated swimming pools. It can be seen in
either an amoeboid or temporary flagellate stage.[2] Naegleria infection does not respond to
any known treatment and is lethal.
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1Life cycle
1.1Cyst stage
1.2Trophozoite stage
1.3Flagellate
1.4Ecology
2Pathogenicity
3See also
4References
5External links

Life cycle[edit]
Naegleria fowleri is a thermophilic (heat-loving), free-living amoeba. It is found in warm and
hot freshwater ponds, lakes and rivers, and in the very warm water of hot springs. As the
water temperature rises, its numbers increase. It was first discovered in 1965, and first
identified in Australia.[3] N. fowleri occurs in three forms as a cyst, a trophozoite (ameboid),
and a biflagellate (it has two flagella). It does not form a cyst in human tissue, where only
the amoeboid trophozoite stage exists. The flagellate form can exist in the cerebrospinal
fluid.

Biotic phases: cyst, trophozoite, flagellate

Cyst stage[edit]
The cyst form is spherical and about 7-15 m in diameter. They are smooth, and have a
single-layered wall with a single nucleus. Cysts are naturally resistant to environmental
factors, so as to increase the chances of survival until better conditions occur. Trophozoites
encyst due to unfavorable conditions. Factors that induce cyst formation include a lack of
food, overcrowding, desiccation, accumulation of waste products, and cold temperatures.
[4]
When conditions improve, the amoeba can escape through the pore, or ostiole, seen in the
middle of the cyst. N. fowleri has been found to encyst at temperatures below 10 C (50 F).[5]

Trophozoite stage[edit]

The trophozoite is the feeding, dividing, and infective stage for humans. The trophozoite
attaches to olfactory epithelium, where it follows the olfactory cell axon through thecribriform
plate (in the nasal cavity) to the brain. This reproductive stage of the protozoan organism,
which transforms near 25 C (77 F) and grows fastest around 42 C (106.7 F), proliferates
by binary fission. The trophozoites are characterized by a nucleus and a surrounding halo.
They travel by pseudopodia, which means that they extend parts of their body's cell
membrane (the pseudopods) and then fill them with plasma to force locomotion. The
pseudopods form at different points along the cell, thus allowing the trophozoite to change
directions. In their free-living state, trophozoites feed on bacteria. In tissues,
they phagocytize (consume by enclosing and then digesting prey) red blood cells and white
blood cells, destroying tissue.[4]

Flagellate[edit]
The flagellate is pear-shaped and biflagellate: this means that it has two flagella. This stage
can be inhaled into the nasal cavity during swimming or diving. This biflagellate form occurs
when trophozoites are exposed to a change in ionic concentration, such as placement in
distilled water. The flagellate form does not exist in human tissue, but can exist in
the cerebrospinal fluid. Once inside the nasal cavity, the flagellated form transforms into a
trophozoite. The transformation of trophozoite to flagellate occurs within a few hours.[4]

Ecology[edit]
Naegleria fowleri are amoeboflagellates that inhabit soil and water. Naegleria fowleri is more
sensitive to drying and pH (acid levels) than other amoeboflagellates. It cannot survive in sea
water. This amoeba is able to grow best at moderately elevated temperatures making
summer month cases more likely. N. fowleri is thermotolerant and able to survive 45 C (113
F). Warm, fresh water with a sufficient supply of bacterial food provide a habitat for
amoebae. Man-made bodies of water, disturbed natural habitats, or areas with soil and
unchlorinated/unfiltered water are locations where many amoebic infections have happened.
N. fowleri seems to thrive during periods of disturbance; the flagellate-empty hypothesis
explains that Naglerias success may be due to decreased competition from decreased
amount of the normal, thermosensitive protozoal fauna. In other words, N. fowleri thrives in
the absence of other predators consuming its food supply. This hypothesis suggests that
human disturbances such as thermal pollution increase N. fowleri abundance by removing
their resource competitors. Ameoboflagellates have a motile flagellate stage that is designed
for dispersal which is advantageous if an environment has been cleared out of competing
organisms.

Pathogenicity[edit]
Main article: Naegleriasis
N. fowleri can cause a lethal infection of the brain called naegleriasis (also known as primary
amoebic meningoencephalitis (PAM), amebic encephalitis, or Naegleria infection). Infections
can occur when water containing N. fowleri is inhaled through the nose, where it then enters
the nasal and olfactory nerve tissue, travelling to the brain through thecribriform plate.[6] N.
fowleri normally eat bacteria, but when it enters humans, it uses the brain as a food source. It
takes up to 5 days(112 days average) for symptoms to appear after N. fowleri amoebas
enter the nose. Initial symptoms may include headache, fever, nausea, or vomiting. Later
symptoms can include stiff neck, confusion, lack of attention, loss of balance, seizures, and
hallucinations. Once the trophozoites ingest brain tissue and symptoms begin to appear,
death will usually occur within two weeks. A person infected with N. fowleri cannot spread the
infection to another person.

The core antimicrobial treatment consists of antifungal drug amphotericin B,[7] but the fatality
rate even with this treatment is greater than 95%. [8] New treatments are being sought. [9].
Miltefosine, an antiparasitic, has been used by the CDC in a few cases, with mixed results.
However, a private pharmaceutical company is offering to stock this drug on consignment at
US hospitals.[10]

See also[edit]

Toxoplasma gondii - pet-carried protozoan that causes the disease toxoplasmosis


Necrotizing fasciitis - the "flesh-eating bacteria"
Vibrio vulnificus - warm saltwater infectious bacteria
Methicillin-resistant Staphylococcus aureus (MRSA)
Acanthamoeba - an amoeba that can cause amoebic keratitis and encephalitis in
humans
Entamoeba histolytica - an amoeba that is the cause of amoebiasis, or amoebic
dysentery
Balamuthia mandrillaris - an amoeba that is the cause of (often fatal) granulomatous
amoebic meningoencephalitis

References[edit]
1.

Jump up^ Schuster, Frederick L., and Govinda S. Visvesvara. "Free-living Amoebae
as Opportunistic and Non-opportunistic Pathogens of Humans and Animals." International
Journal for Parasitology 34.9 (2004): 1001-027. Web.
2.
Jump up^ "General Information | Naegleria fowleri | CDC". www.cdc.gov.
Retrieved 2015-12-14.
3.
Jump up^ "Brain-eating-amoeba". WebMD. Retrieved 1 July 2015.
4.
^ Jump up to:a b c Marciano-Cabral, F (1988). "Biology of Naegleria
spp". Microbiological reviews. 52 (1): 11433. PMC 372708 . PMID 3280964.
5.
Jump up^ Chang, SL (1978). "Resistance of pathogenic Naegleria to some common
physical and chemical agents". Applied and Environmental Microbiology. 35 (2): 368
75. PMC 242840 .PMID 637538.
6.
Jump up^ Baig, AM (Aug 2015). "Pathogenesis of amoebic encephalitis: Are the
amoebae being credited to an 'inside job' done by the host immune response?". Acta
Trop. 148: 726.doi:10.1016/j.actatropica.2015.04.022. PMID 25930186.
7.
Jump up^ Subhash Chandra Parija (Nov 23, 2015). "Naegleria Infection Treatment &
Management". Medscape.
8.
Jump up^ Cetin N, Blackall D.Naegleria fowleri meningoencephalitis.Blood 2012 Apr
19;119(16):3658.PMID 22645743
9.
Jump up^ https://www.statnews.com/2016/07/22/brain-eating-amoeba/
10.
Jump up^ http://www.businessinsider.com/why-brain-eating-amoeba-miltefosinemedicine-is-hard-to-find-2016-9?amp

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