Pediatric Naegleria Medication

Updated: Oct 14, 2021
  • Author: Nicholas John Bennett, MBBCh, PhD, FAAP, MA(Cantab); Chief Editor: Russell W Steele, MD  more...
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Medication Summary

To date, the most effective proven therapy remains amphotericin B (intravenous and intrathecal). Eight patients have survived PAM, and nearly all of them received amphotericin B with or without additional agents. One survivor was treated with intravenous and intrathecal miconazole plus rifampin and sulfisoxazole.

One report has described highly effective and selective in vitro activity of voriconazole (Vfend) against N fowleri. [12] It showed lasting inhibition from concentrations of more than 1 µg/mL. The antiprotozoal drug miltefosine (Miltex) was also tested and found to be amebicidal in serum concentrations of more than 55 µmol. Neither drug is currently recommended in the treatment of PAM, but these preliminary data may lead to in vivo studies or case reports of empirical use.

In conjunction with the FDA, the CDC has an expanded access investigational new drug (IND) protocol in effect with the FDA to make miltefosine available directly from the CDC for treatment of free-living amebae (FLA) in the United States. These infections include primary amebic meningoencephalitis (PAM) caused by Naegleria fowleri and granulomatous amebic encephalitis caused by Balamuthia mandrillaris and Acanthamoeba species. [11]


Polyene antibiotics

Class Summary

Amphotericin B is the most effective drug against N fowleri.

Amphotericin B desoxycholate (Fungizone)

Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.


Antibiotic agents

Class Summary

Antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Rifampin (Rifadin, Rimactane)

Inhibits RNA synthesis in bacteria by binding to beta subunit of DNA-dependent RNA polymerase, which in turn blocks RNA transcription.