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Acute PAM presents 1 to 12 days (median 5 days) after exposure. The most common early symptoms are headache, fever, nausea, and vomiting. Later symptoms include neck stiffness, lethargy, confusion/disorientation, photophobia, seizures, and cranial nerve abnormalities. Findings on exam may include meningeal signs and focal neurologic deficits. Signs and symptoms mimic those of bacterial meningitis, especially in the early stages. Rarely, abnormalities in taste or smell, nasal obstruction, and nasal discharge have been observed.
PAM progresses rapidly and frequently leads to coma and death in 1 to 18 days (median 5 days) after symptom onset. The infection destroys brain tissue and causes cerebral edema, which is often the cause of death. Autopsy findings include hemorrhagic necrosis of the olfactory bulbs and cerebral cortex.
In contrast, other free-living amebae (Acanthamoeba spp. and Balamuthia) cause mostly sub-acute or chronic granulomatous amebic encephalitis (GAE), with a clinical picture that can include headaches, altered mental status, and focal neurologic deficits. GAE generally progresses more slowly than PAM and death usually occurs several weeks to months after symptom onset.
- Capewell LG, Harris AM, Yoder JS, Cope JR, Eddy BA, Roy SL, Visvesvara GS, Fox LM, Beach MJ. Diagnosis, clinical course, and treatment of primary amoebic meningoencephalitis in the United States, 1937–2013.J Pediatric Infect Dis Soc. 2014;Epub:1–8.
- Visvesvara GS. Free-living amebae as opportunistic agents of human disease.J Neuroparasitol. 2010;1.
- Gharpure R, Bliton J, Goodman A, Ali IKM, Yoder J, Cope JR. Epidemiology and clinical characteristics of primary amebic meningoencephalitis caused by Naegleria fowleri: a global review. Clin Infect Dis. 2021 Jul 1;73(1):e19-e27.