|
Free-living amebas are protozoa that live independently in soil or water and do not require a human or an animal host. They rarely cause disease, unlike the parasitic ameba Entamoeba
histolytica, which is a common cause of intestinal infection (see Intestinal Protozoa: Amebiasis). Pathogenic free-living amebas are of the genera Naegleria
, Acanthamoeba, and Balamuthia.
Three major syndromes occur, primary amebic meningoencephalitis, granulomatous amebic encephalitis, and amebic keratitis. Acanthamoeba can also cause skin lesions.
Primary
Amebic Meningoencephalitis
Primary amebic
meningoencephalitis is a generally fatal, acute CNS infection caused
by Naegleria fowleri.
N. fowleri inhabits fresh water worldwide. Swimming in contaminated water exposes nasal mucosa to the organism, which can enter the CNS via olfactory neuroepithelium and the cribriform plate. Most patients are healthy children or young adults.
Symptoms begin within 1 to 2 wk of exposure, sometimes with alteration of smell and taste. Fulminant meningoencephalitis ensues with headache, meningismus, and mental status change, progressing to death within 10 days, usually from cerebral herniation.
Diagnosis is suspected by history of swimming in fresh water, but confirmation is difficult because CT and routine CSF tests, although necessary to exclude other causes, are nonspecific. Wet mount of CSF should be performed, which may demonstrate motile amebic trophozoites (which are destroyed by Gram stain techniques).
Only a few patients have survived, so optimal treatment is unclear. A reasonable regimen uses amphotericin B intravenously and intrathecally; effective doses are unclear. Some have added oral rifampin , oral and intrathecal miconazole , and oral sulfisoxazole . Experimental evidence suggests azithromycin might be of benefit.
Granulomatous
Amebic Encephalitis
Granulomatous
amebic encephalitis is a generally fatal subacute CNS infection
in immunocompromised or debilitated hosts caused by Acanthamoeba sp or Balamuthia mandrillaris.
Acanthamoeba sp and Balamuthia mandrillaris are present worldwide in water, soil, and dust. Human exposure is common, but infection is rare. Acanthamoeba infection occurs almost entirely in immunocompromised or otherwise debilitated patients, but B. mandrillaris may also infect healthy hosts; manifestations are otherwise similar. The entry portal is thought to be the skin or lower respiratory tract, with subsequent hematogenous dissemination to the CNS.
Onset is insidious, often with focal neurologic manifestations. Mental status change, seizures, and headache are common. Survival is highly unlikely (and only in immunocompetent patients), death occurring between 7 and 120 days after onset (average, 39 days).
Diagnosis is often postmortem. CT and routine CSF tests are obtained but are nonspecific. CT may show multiple nonenhancing lucent areas, and CSF shows elevated WBC count (predominantly lymphocytes), but trophozoites are rarely demonstrated in the CSF. Visible skin lesions often show amebas and should be biopsied; if detected, amebas may be cultured and tested for drug sensitivity. Brain biopsy is often positive.
Against Acanthamoeba, the diamidine derivatives (propamidine, pentamidine , dibromopropamidine) appear to have the greatest activity in vitro. Other agents include trimethoprim-sulfamethoxazole , ketoconazole , itraconazole , miconazole , paromomycin , neomycin , 5-fluorocytosine, and, to a lesser extent, amphotericin B . Recent studies suggest that B. mandrillaris is sensitive to pentamidine in vitro, and this drug may be beneficial in treatment of CNS infections.
Amebic
Keratitis
Amebic keratitis
is corneal infection by Acanthamoeba sp,
typically occurring in contact lens wearers.
Acanthamoeba sp can cause chronic and progressively destructive keratitis. The main risk factor (85% of cases) is contact lens use, particularly if lenses are worn while swimming or if unsterile lens cleaning solution is used. Some infections follow corneal abrasion.
Lesions are typically very painful with foreign body sensation. Initially, lesions have a dendriform appearance resembling herpes simplex keratitis. Later there are patchy stromal infiltrates, and sometimes a characteristic ring-shaped lesion. Most have an associated anterior uveitis. Vision is diminished.
Diagnosis is confirmed by examining Giemsa- or trichrome-stained corneal scrapings and by culture on special media. Viral culture is obtained if herpes is considered.
Early, superficial infection responds better to treatment. The encysted stage of the life cycle appears to cause most problems. Epithelial lesions are debrided, and intensive drug therapy is applied. Combination therapy with ≥ 2 antimicrobials works best. Polyhexamethylene biguanide 0.02% and propamidine isethionate 0.1% have been applied hourly for the first 3 days. Other topical agents, such as clotrimazole 1%, chlorhexidine, fluconazole , natamycin , or neomycin - polymyxin B -gramicidin, are sometimes added. Systemic treatment with fluconazole or itraconazole has also been used, particularly in patients with anterior uveitis or involvement of the sclera. Early recognition and treatment have eliminated the need for therapeutic keratoplasty in most instances, but it remains an option in cases in which pharmacologic therapy fails. Intensive treatment is required for the 1st month, being tapered per clinical response, but often continuing for 6 to 12 mo. Recurrence is common if treatment is stopped prematurely.
Last full review/revision November 2005
Content last modified November 2005
| 
