Naegleria fowleri

The organism was named after Malcolm Fowler, an Australian pathologist at Adelaide Children's Hospital, who was the first author of the original series of case reports of primary amoebic meningoencephalitis.[12][13]

Biotic phases: cyst, trophozoite, flagellate

Naegleria fowleri is a thermophilic, free-living amoeba. It is found in warm and hot freshwater ponds, lakes and rivers, and in the very warm water of hot springs.[14] As the water temperature rises, its numbers increase. The amoeba was identified in the 1960s in Australia but appears to have evolved in the United States.[15] N. fowleri occurs in three forms – as a cyst, a trophozoite (ameboid), and a biflagellate. It does not form a cyst in solid human tissue, where only the amoeboid trophozoite stage exists, however the flagellate form has been found in cerebrospinal fluid.

Roman Baths in Bath, Somerset, closed for bathing since 1978 due to presence of N. fowleri

N. fowleri can cause an often fatal infection of the brain called naegleriasis (also known as primary amoebic meningoencephalitis, amoebic encephalitis/meningitis, or simply Naegleria infection). Infections most often 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 the cribriform plate.[19] N. fowleri cannot cause infection by swallowing contaminated water.[20] Infections typically occur after swimming in warm-climate freshwater, although there have been cases in cooler climates such as Minnesota, USA.[21] In rare cases, infection has been caused by nasal or sinus rinsing with contaminated water in a nasal rinsing device such as a neti pot.[10]

N. fowleri normally eat bacteria, but during human infections, the trophozoites consume astrocytes and neurons. The reason why N. fowleri prefers to pass across the cribriform plate has remained unknown, but the neurotransmitter acetylcholine has been suggested to act as a stimulus, as a structural homolog of animal CHRM1 has been shown to be present in Naegleria and Acanthamoeba.[22]

It takes one to nine days (average five) for symptoms to appear after nasal exposure to N. fowleri flagellates.[23] Symptoms may include headache, fever, nausea, vomiting, loss of appetite, altered mental state, coma, drooping eyelid, blurred vision, and loss of the sense of taste.[24] Later symptoms can include stiff neck, confusion, lack of attention, loss of balance, seizures, and hallucinations. Once symptoms begin to appear, death will usually occur within two weeks. A person infected with N. fowleri cannot spread the infection to another person. From 2009 to 2017, 34 infections were reported in the United States.[25]

Though rarely observed, infection by Naegleria fowleri can occur in animals. Experimentally, mice, guinea pigs, and sheep have been infected, and there have been reports of South American tapirs and cattle contracting PAM. Animal infection is likely quite overlooked.[26]

The core antimicrobial treatment consists of the antifungal drug amphotericin B,[27] which inhibits the pathogen by binding to its cell membrane sterols, thus leading to cell membrane disruption and pathogen death;[28] however, even with this treatment, the fatality rate is greater than 95%.[29] New treatments are being sought.[30] Miltefosine, an antiparasitic drug that inhibits the pathogen via disrupting its cell survival signal pathway PI3K/Akt/mTOR,[28] has been used in a few cases with mixed results.[31]

A key factor to effective treatment is the speed of diagnosis. PAM is a rare occurrence and is not often considered as a likely diagnosis; therefore, the clinical laboratory’s identification of the microorganism may be the first time an amoebic etiology is considered. The rapid identification can help to avoid delays in diagnosis and therapy. Amoeba cultures and real-time PCR studies for N. fowleri are diagnostic of PAM, however, they are not readily available at most institutions and would require being performed at a reference laboratory. The time of presentation of the patient can also affect the identification of the microorganism as PAM has a variable incubation time, ranging from 1 to 7 days. The clinical signs of PAM are similar to bacterial and viral meningitis, including fever, neck stiffness, and severe headaches. Symptoms can progress to prolonged nausea, vomiting, and even seizures. The disease can progress to acute hemorrhagic necrotizing meningoencephalitis, which can lead to death in as soon as 7–10 days. A variable delay in treatment can be secondary to time intervals in multiple stages of care, including exposure to exhibition of symptoms; arrival for treatment at a health care facility; workup of the diagnosis (initial diagnosis of likely bacterial meningitis); and finally, from diagnosis to initiation of recommended therapy. Successful treatment of PAM is a rare occurrence and can only be attempted after correct diagnosis, which relies on rapid recognition of the microorganism by medical technologists and pathologists. It is critical that medical technologists consistently provide timely CSF evaluation, explore the diagnosis of PAM, and look for amoebae in the setting of meningitis, especially in the summertime.[32]

• Acanthamoeba – an amoeba that can cause amoebic keratitis and encephalitis in humans
• Balamuthia mandrillaris – an amoeba that is the cause of (often fatal) granulomatous amoebic meningoencephalitis
• Entamoeba histolytica – an amoeba that is the cause of amoebiasis, or amoebic dysentery
• Leptospira – a zoonotic bacteria that causes leptospirosis
• Methicillin-resistant Staphylococcus aureus (MRSA)
• Necrotizing fasciitis – the "flesh-eating disease", caused by certain types of bacteria
• Toxoplasma gondii – cat-carried protozoan that causes the disease toxoplasmosis
• Vibrio vulnificus – warm saltwater infectious bacteria

Wikimedia Commons has media related to Naegleria fowleri.

• Naegleria information site from the Centers for Disease Control and Prevention
• Naegleria from The Tree of Life Web Project