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Brains Eating Amoeba

"Brain-eating amoeba" is a species of the genus Naegleria is Naegleria fowleri. It is classified as a shape-shifting ameboflagellate excavate and is a member of the Percolozoa phylum. Most of the time, this free-living organism feeds on bacteria, but it has the potential to turn pathogenic and cause naegleriasis or Primary Amoebic Meningoencephalitis (PAM), a highly uncommon, sudden, severe, and typically fatal brain illness. It is a substance that is frequently discovered in warm freshwater bodies of water, such as ponds, lakes, rivers, hot springs, warm water discharge from industrial or power plants, geothermal well water, poorly maintained or sparsely chlorinated swimming pools (with residual chlorine levels less than 0.5 mg/m3), soil, and pipes that are connected to tap water. It can exist as a transitory flagellate or as an amoeboid.

Brains Eating Amoeba


Malcolm Fowler, an Australian pathologist at Adelaide Children's Hospital and the original writer of the PAM case reports, was honoured by having the organism named in his honour.

The Life Cycle

The lifecycle stages of N. fowleri can be observed under a light microscope in the following order: cyst, trophozoite, and flagellate.

Naegleria fowleri is a thermophilic, free-living amoeba that lives in warm, hot freshwater areas like ponds, lakes, rivers, and hot springs. Its population tends to grow as temperatures rise. Although it is believed that the United States is where the amoeba evolved, it was first detected in Australia in the 1960s. In solid human tissue, the amoeboid trophozoite stage does not produce cysts, but the flagellate form has been found in cerebrospinal fluid.

Cyst Stage

To survive in harsh environments, trophozoites change into microbial cysts. The cyst's nucleus measures 7-15 mm in diameter and it has a single, spherical layer. The cyst serves as a strong coating that protects the amoeba from harsh environments. Cyst formation is influenced by several circumstances, including a lack of food, crowding, desiccation, waste buildup, and cold temperatures. The amoeba may pass via the cyst's pore or ostiole when the situation gets better. At temperatures lower than 10 degrees Celsius (50 degrees Fahrenheit), N. fowleri has been observed to encyst.

Trophozoite Stage

The infective phase of an organism that can actively feed and multiply in humans is known as the trophozoite stage. Before passing through the cribriform plate of the nasal canal and entering the brain on the axons of olfactory receptor neurons, the trophozoite clings to the olfactory epithelium. The reproductive stage of this protozoan organism changes at around 25 °C (77 °F), and it grows best at 42 °C (108 °F), replicating via binary fission.

Trophozoites have a flexible membrane covering their nucleus. They move by extending pseudopod-like extensions of their cell membrane that are filled with protoplasm to facilitate mobility. Pseudopods develop in the direction of movement. Trophozoites are free-living organisms that eat bacteria. They appear to encapsulate and digest red blood cells in tissues, a process known as phagocytization. This process damages tissues by either producing cytolytic chemicals or by coming into direct contact with cytolytic membrane proteins on neighbouring cells.

The trophozoites of Naegleria fowleri can produce one to twelve amoebastomes (amorphous cytostomes), also called "suckers" or "food cups," on their membrane, which they employ for feeding in a manner like trogocytosis.

Flagellation Stage

Naegleria fowleri's flagellate stage is pear-shaped and biflagellate, meaning it has two flagella. Inhaling this stage into the nasal cavity is possible, for instance, during swimming or scuba diving. Trophozoites turn into flagellates when their fluid undergoes an ionic strength change, such as when they are placed in distilled water. Cerebrospinal fluid contains the flagellate form, even though human tissue does not contain it. When the flagellated form enters the nasal canal, it changes into a trophozoite. This changeover only takes a few hours.


Naegleria fowleri excavata thrives in soil and water. It is incapable of surviving in seawater because it is sensitive to dry and acidic surroundings. Infections are more likely in the summer because the amoeba thrives at slightly higher temperatures. Considering that N. fowleri is a facultative thermophile, it can survive in environments with temperatures as high as 46 °C (115 °F). Amoebae thrive in warm freshwater environments with an abundance of bacteria for feeding. Amoebic infections have been recorded in soil, unchlorinated or unfiltered water sources, altered natural ecosystems, and manmade water bodies.

When there is unrest, N. fowleri seems to flourish. The "flagellate-empty" hypothesis states that when thermosensitive protozoal fauna cannot withstand temperature changes, Naegleria may be more successful since there is less competition. N. fowleri hence thrives in the absence of other predators that deplete its food supply. Theoretically, human interferences such thermal pollution led to an increase in N. fowleri abundance by eliminating its resource rivals. Ameboflagellate can disperse in the absence of competing organisms thanks to their motile flagellate stage.


Due of N. fowleri, Bath's Roman Baths have been off-limits to bathers since 1978. Naegleriasis, often referred to as Primary Amoebic Meningoencephalitis (PAM), amoebic encephalitis/meningitis, or simply naegleria infection, is a disease that is typically fatal and is brought on by N. fowleri. Inhaled N. fowleri reaches the nasal and olfactory nerve tissue and goes through the cribriform plate to the brain, where it most usually causes infections. N. fowleri infection cannot be brought simply by drinking polluted water. While cases have been observed in cooler climates like Minnesota, USA, most illnesses start after swimming in warm-climate freshwater. In very rare cases, using polluted water to rinse the nose or sinuses with a device like a neti pot has led to illnesses.

Normally, N. fowleri feeds on bacteria, but when it infects people, the trophozoites eat neurons and astrocytes. Although the neurotransmitter acetylcholine has been suggested as a stimulus since Naegleria and Acanthamoeba have been found to have structural homologs of mammalian CHRM1, the exact cause of N. fowleri crossing the cribriform plate is still unknown. One to nine days (on average five) after nasal exposure to N. fowleri flagellates, symptoms appear. Headache, fever, nausea, vomiting, lack of appetite, altered mental status, coma, drooping eyelid, blurred vision, and loss of taste are typical symptoms. Subsequent symptoms could include neck stiffness, confusion, inattentiveness, loss of balance, convulsions, and hallucinations. Within two weeks of the onset of symptoms, death typically occurs. Because N. fowleri is not contagious, an infected person cannot spread the virus to another person. Between 2009 and 2017, 34 diseases were identified in the US.

Animals can contract Naegleria fowleri infection, albeit it is not common. In studies, mice, guinea pigs, and sheep have all contracted PAM. Tapirs and cattle from South America have also reportedly contracted the disease. Most usually, animal disease goes unnoticed.


The death rate is greater than 95% even with current treatment. Amphotericin B, an antifungal medication, kills the infection by binding to the sterols in its cell membrane and suppressing it. Researchers are looking for novel therapies. Miltefosine, an antiparasitic medication that inhibits the pathogen by blocking the PI3K/Akt/mTOR signalling pathway, has been utilised in a few cases with unpredictable outcomes.

Effective therapy depends on a diagnosis being obtained as soon as possible. Naegleriasis is a rare condition that is frequently misdiagnosed; as a result, the discovery of the microbe in the clinical laboratory may mark the beginning of research into the amoebic aetiology. Delays in diagnosis and treatment can often be avoided with quick detection.

PAM can be diagnosed with amoeba cultures and real-time polymerase chain reaction (PCR) tests for N. fowleri, but these tests must be done at a reference lab because they are not commonly accessible. The time of the patient's presentation may also have an impact on the bacterium's identification because PAM has a varied incubation period that can last anywhere between 1 and 7 days. PAM symptoms are similar to those of bacterial and viral meningitis and include fever, stiff neck, and excruciating headaches. Seizures, chronic nausea, and vomiting are also potential symptoms. Acute hemorrhagic necrotizing meningoencephalitis, which can be lethal in 7-10 days, can develop from the condition. Time intervals between different stages of care, such as exposure to symptom emergence, arrival for treatment at a medical facility, workup of the diagnosis (initial diagnosis of likely bacterial meningitis), and finally, from diagnosis to start of recommended therapy, can cause a variable delay in treatment. Successful PAM therapy is rare and only possible following a precise diagnosis, which is reliant on medical technologists and pathologists swiftly identifying the bacterium. Particularly during the summer, medical technologists must continuously perform quick CSF testing, look for PAM diagnosis, and look for amoebae in the context of meningitis.

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