Naegleria fowleri

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Naegleria fowleri
Different stages of Naegleria fowleri
Scientific classification
Domain:	Eukaryota
(unranked):	Excavata
Phylum:	Percolozoa
Class:	Heterolobosea
Order:	Schizopyrenida
Family:	Vahlkampfiidae
Genus:	Naegleria
Species:	N. fowleri
Binomial name
Naegleria fowleri Carter (1970)

Naegleria fowleri (pronounced /nəˈɡlɪəriə/, also known as "the brain-eating amoeba") is a free-living excavate form of protist typically found in warm fresh water, from 25–35 °C (77–95 °F) in an amoeboid or temporary flagellate stage. It belongs to a group called the Percolozoa or Heterolobosea.

N. fowleri can invade and attack the human nervous system; although this occurs rarely,^[1] such an infection will nearly always result in the death of the victim.^[2]

Lifecycle

Life Cycle Stages: Cyst, Trophozoite, & Flagellate.

Naegleria fowleri exists in nature in three forms: a flagellate, a trophozoite and a cyst.

Flagellate stage: Occurs when the trophozites are exposed to a change in ionic concentration such as placement in distilled water, they transform into bi-flagellated cells. The transformation of trophozoites converts to flagellated form within a few minutes.^[3]

Trophozoite stage: The reproductive stage of the protozoan organism which grows fastest at around 42°C and proliferates by binary fission. The trophozoite’s are characterized by a nucleus and a surrounding halo. The trophozoite’s travel by lobopodia, which are the round surrounding processes, filled with granular cytoplasm. The lobopodia 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, trophozoites phagocytize RBCs, WBCs, and destroy tissue.^[3]

Cyst Stage: Trophozoites encyst due to unfavorable conditions. Factors that induce cyst formation can include food deprivation, crowding, desiccation, acclamation of waste products, and cold temperatures.^[3] N. Fowleri has been found to encyst at temperatures below 10°C. ^[4]

Infection

Life cycle of N. fowleri and other free-living Amebae. Click to enlarge and view caption.

In humans, N. fowleri can invade the central nervous system via the nose, more specifically the olfactory mucosa and cribriform plate of the nasal tissues. The penetration initially results in significant necrosis of and hemorrhaging in the olfactory bulbs. From there, amoebae climb along nerve fibers through the floor of the cranium via the cribriform plate and into the brain. The amoebae begin to consume the cells of the brain piecemeal by means of a unique sucker apparatus extended from their cell surface.^[5] It then becomes pathogenic, causing primary amoebic meningoencephalitis (PAM or PAME). PAM is a syndrome affecting the central nervous system, characterized by changes in olfactory perception (taste and smell), followed by vomiting, nausea, fever, headache, and the rapid onset of coma and death in two weeks.

PAM usually occurs in healthy children or young adults with no prior history of immune compromise who have recently been exposed to bodies of fresh water.^[6]

Amphotericin B is effective against N. fowleri in vitro, but the prognosis remains bleak for those that contract PAM, and survival remains less than 1%.^[6] On the basis of the in vitro evidence alone, the CDC currently recommend treatment with Amphotericin B for primary amebic meningoencephalitis, but there is no evidence that this treatment affects outcome.^[6]

Timely diagnosis remains a very significant impediment to the successful treatment of infection, as most cases have only been appreciated post-mortem. It killed 121 people in the U.S. from 1937 through 2007, including six in 2007 (three in Florida, two in Texas, and one in Arizona);^[6] it killed one in 2008 (California) and one in 2009 in Florida.^[7]

Detection

N. fowleri can be grown in several kinds of liquid axenic media or on non-nutrient agar plates coated with bacteria. Escherichia coli can be used to overlay the non-nutrient agar plate and a drop of CSF sediment added to it. Plates are then incubated at 37 degrees and checked daily for clearing of the agar in thin tracks, which indicate that the trophozoites have fed on the bacteria.^[8] Detection in water is performed by centrifuging a water sample with Escherichia coli added, and then applying the pellet to a non-nutrient agar plate. After several days the plate is microscopically inspected and Naegleria cysts are identified by their morphology. Final confirmation of the species' identity can be performed by various molecular or biochemical methods.^[9] Confirmation of Naegleria presence can be done by so called flagellation test, when amoeba is exposed to hypotonic environment (distilled water). Naegleria in contrast to other amoebae differentiates within two hours into flagellar state. Pathogenicity can be further confirmed by exposition to high temperature (42°C): Naegleria fowleri is able to grow at this temperature, but the non-pathogenic Naegleria gruberi is not.

Incidents and outbreaks

Czech Republic

Histopathology of amoebic meningoencephalitis

• Between years 1962–1965, 16 young people died of acute meningoencephalitides in Ústí nad Labem as a consequence of bathing in an indoor swimming pool.^[10]

New Zealand

• Between years 1968–78, eight fatal cases have been confirmed from primary amoebic meningoencephalitis. All occurred in the Waikato area, and all victims had been swimming in the Waikato River, between Taupo and Matamata.^[11]

United States

According to the Centers for Disease Control and Prevention, the amoeba killed 23 people between 1995 and 2004.

• In August 2005, two Oklahoma boys, ages 7 and 9 were killed by N. fowleri after swimming in hot stagnant water of the lakes in the Tulsa area.^[12]
• In 2007, six cases were reported in the U.S., all fatal:^[6]
  • In July, the amoeba caused the deaths of three boys in lakes around Orlando, Florida. Possible causes of the infections include higher temperature and droughts in that area of Florida.^[13]
  • N. fowleri can be found in all bodies of water in Texas (even pools) except colder water, typically spring fed. In late summer, the amoeba caused the death of a 12-year-old boy and a 22-year-old young man in Lake LBJ in Texas.^[14][1]
  • In September, a 14-year-old boy was killed by the amoeba after likely having caught it while swimming in Lake Havasu in Arizona. The doctors suspected meningitis before the boy died, but did not know the etiology until the CDC confirmed it as N. fowleri.^[15][16]
• In August 2008, a 9-year-old boy was killed after having been exposed to the amoeba while swimming several times in Lake Elsinore in California. The boy was the first ever confirmed case in Riverside County.^[7]
• On September 23, 2009, a 22-year-old man hospitalized in Florida died from a confirmed case of n. fowleri after having contracted it at the Orlando Watersports Complex.^[17]
• There was also a reported case of a 10-year-old child on August, 2009, who died from a confirmed case of "PAM" after having contracted it from a lake in Polk County, Florida.

See also

List of parasites (human)

References

External links

• Naegleria Infection fact sheet from the website of the Centers for Disease Control and Prevention
• Tree of Life: Naegleria