Naegleria Fowleri - Infection

Infection

In humans, N. fowleri can invade the central nervous system via the nose (specifically through 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, the amoeba climbs along nerve fibers through the floor of the cranium via the cribriform plate and into the brain. The organism begins to consume cells of the brain piecemeal by means of a unique sucking apparatus extended from its cell surface. It then becomes pathogenic, causing primary amoebic meningoencephalitis (PAM or PAME). PAM is a syndrome affecting the central nervous system. 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.

Amphotericin B is effective against N. fowleri in vitro, but the prognosis remains bleak for those who contract PAM, and survival remains less than 1%. On the basis of the in vitro evidence alone, the CDC currently recommends treatment with amphotericin B for primary amoebic meningoencephalitis, but no evidence supports this treatment affecting outcome. Treatment combining miconazole, sulfadiazine, and tetracycline has shown limited success only when administered early in the course of an infection.

While miltefosine had therapeutic effects during an in vivo study in mice, chlorpromazine (Thorazine) showed to be the most effective substance - the authors concluded: "Chlorpromazine had the best therapeutic activity against N. fowleri in vitro and in vivo. Therefore, it may be a more useful therapeutic agent for the treatment of PAME than amphotericin B."

Untimely diagnoses remain a very significant impediment to the successful treatment of infection, as most cases have only been discovered post mortem. Infection killed 121 people in the United States from 1937 through 2007, including six in 2007 (three in Florida, two in Texas, and one in Arizona).