Naegleria fowleri : Causes, Symptoms & Treatment

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Naegleria fowleri colloquially known as a “brain-eating amoeba” is most commonly found in warm bodies of water, such as lakes, streams, ponds, and swimming pools. The prevalence is highest during the summer months. In addition to contaminated water sources, there have been reports of contaminated dust. One such incident occurred in Nigeria, a country with a hot climate.

Naegleria fowleri ameboid trophozoites enter the human body through the nasal mucosa. Other infections have been linked to inhaling contaminated dust. Sniffing contaminated water may also transmit this ameba, according to some evidence.

Common associated disease or condition name: Primary amebic meningoencephalitis (PAM)

Morphology of Naegleria fowleri

Naegleria fowleri is the only ameba known to have three morphologic forms: ameboid trophozoites, flagellate (protozoa that move with flagella) forms, and cysts.

Naegleria fowleri Ameboid trophozoites

Naegleria fowleri’s typical ameboid trophozoite is elongate, measuring 8 to 22 m in length. The front end is usually broad, while the back end is usually tapered. Naegleria fowleri ameboid trophozoite sluglike motility is accomplished by blunt pseudopodia. A large karyosome is found in the single nucleus and is generally located in the center. There is no peripheral chromatin. The cytoplasm of the ameboid trophozoite Naegleria fowleri is granular and frequently contains vacuoles.

Flagellate forms

Naegleria fowleri is a pear-shaped flagellate that ranges in size from 7 to 15 m. Flagella are two whip-like structures that extend from the broad end of the organism and aid select parasites in locomotion. Jerky movements or spinning are used to achieve the typical motility seen. The nucleus is essentially identical to that of an ameboid trophozoite, consisting of a large central karyosome devoid of peripheral chromatin. Flagellate trophozoites typically have granular cytoplasms with vacuoles.


The cysts, which range in size from 9 to 12 m, are generally round and have thick cell walls. The Naegleria fowleri cyst, like both corresponding trophozoite stages, has only one nucleus, which consists of a large, centrally located karyosome devoid of peripheral chromatin. The cytoplasm is typically granular, with vacuoles present.

  Naegleria fowleri  Ameboid trophozoites ,cyst and flagellated stage
Naegleria fowleri Ameboid trophozoites ,cyst and flagellated stage

Life Cycle of Naegleria fowleri

  • Naegleria fowleri ameboid trophozoites are the only type known to exist in humans.
  • Ameboid trophozoite replication is accomplished through simple binary fission.
  • After being transferred to water from a tissue or culture, ameboid trophozoites transform into flagellate trophozoites in vitro.
  • Flagellate trophozoites do not divide, but instead lose their flagella and revert to ameboid form, where reproduction resumes.
  • Only in the external environment is the cyst form known to exist.
  • The entire life cycle of Naegleria fowleri, which appears to consist of amebic trophozoites converting to cysts and flagellates and then back to amebic trophozoites, appears to occur in the external environment.
  • Swimming in contaminated water is the most common way for humans to become infected with this ameba. Ameboid trophozoites enter the human body via the nasal mucosa and frequently migrate to the brain, where they cause rapid tissue destruction.
  • Inhaling dust contaminated with Naegleria fowleri may result in some infections.
naegleria fowleri life cycle
naegleria fowleri life cycle

Clinical Symptoms of Primary amebic meningoencephalitis


Patients with Naegleria fowleri colonization of the nasal passages are usually asymptomatic.

Primary amebic meningoencephalitis

Primary amebic meningoencephalitis (PAM) occurs when N. fowleri ameboid trophozoites invade the brain, causing rapid tissue destruction. Initially, patients may experience fever, headache, sore throat, nausea, and vomiting. Meningitis symptoms, such as stiff neck and seizures, appear quickly. In addition, the patient will frequently experience changes in smell and taste, a blocked nose, and Kernig’s sign (defined as a diagnostic sign for meningitis, where the patient is unable to fully straighten his or her leg when the hip is flexed at 90 degrees because of hamstring stiffness). Death usually occurs 3 to 6 days after onset in untreated patients. These patients’ postmortem brain tissue samples reveal the typical ameboid trophozoites of Naegleria fowleri.

Laboratory Diagnosis of Naegleria fowleri

  • The method of choice for recovering Naegleria fowleri ameboid trophozoites is microscopic examination of cerebrospinal fluid (CSF).
  • It is recommended to prepare and scan saline and iodine wet CSF preparations.
  • Tissue and nasal discharge samples may also be examined.
  • Cultures of clinical specimens are possible.
  • When ameboid trophozoites of Naegleria fowleri are placed on agar plates previously inoculated with gram-negative bacilli, they exhibit a distinct trailing effect.

Prevention and Control of Primary amebic meningoencephalitis

  • Because there are so many bodies of water that could be infected, total eradication of N. fowleri is highly unlikely.
  • Posting no-entry signs near known sources of contamination, as well as educating the medical community and the general public, may help reduce infection rates.
  • It is also critical that swimming pools and hot tubs are properly chlorinated.
  • Cracks in the walls of pools, hot tubs, and baths should be repaired as soon as possible to avoid the creation of a potential source of contamination.

Treatment of Primary amebic meningoencephalitis

Unfortunately, meningitis and amebic infection medications are ineffective against N. fowleri. Despite its known toxicity, there is evidence that prompt and aggressive treatment with amphotericin B may benefit patients with N. fowleri infections. Amphotericin B in combination with rifampin or miconazole has also been shown to be effective in rare cases. Amphotericin B and miconazole damage the cell wall of Naegleria, inhibiting ergosterol biosynthesis and increasing membrane permeability, allowing nutrients to leak out of the cells. Rifampicin inhibits RNA synthesis in amoebas by binding to the beta subunits of DNAdependent RNA polymerase, which then prevents RNA transcription. If symptoms are detected early, a person can survive; otherwise, PAM almost always results in death.

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About the Author: Labweeks

KEUMENI DEFFE Arthur luciano is a medical laboratory technologist, community health advocate and currently a master student in tropical medicine and infectious disease.

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