Acanthamoeba Infection Clinical Presentation

Updated: Jul 06, 2021
  • Author: Theresa M Fiorito, MD, MS, FAAP, CTH®; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Presentation

History

Acanthamoeba keratitis usually is associated with a history of excessively long lens wear and/or contamination of the lens with unsterile water. Typical sources include swimming, showering, using nonsterile lens cleaners, contaminating lenses and cases by "topping off" or other unhygienic practices, and handling lenses with wet hands. [18, 19] The incubation period for Acanthamoeba keratitis is unknown but thought to range from several days to several weeks. [5] Keratitis typically begins with a unilateral foreign-body sensation followed by pain, tearing, photophobia, blepharospasm, and blurred vision. [18, 17] . Although pain out of proportion to inflammation in early keratitis has been observed, it can present as a painless keratitis, so lack of pain should not be used to rule out this disease process. [16]  Bilateral involvement has been described in up to 11% of cases. [20]

Granulomatous amebic encephalitis (GAE) is a subacute to chronic meningoencephalitis. The incubation period is unknown but is probably weeks to months. The duration of illness until death ranges from 7-120 days (average, 39 days). Patients with GAE may have concurrent sinus, lung, or skin disease. Most patients present with focal neurologic deficits coupled with signs of increased intracranial pressure; other symptoms may include confusion, seizures, headache, focal weakness or ataxia, visual disturbances, and fever.

Skin disease may precede the onset of CNS manifestations by weeks to months and may include ulcers, nodules, or subcutaneous abscesses. Disseminated disease without CNS involvement may manifest as skin lesions, sinusitis, and/or pneumonitis. Other unusual manifestations of Acanthamoeba infection include osteomyelitis, adrenalitis, and vasculitis.

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Physical

Early physical findings in amebic keratitis include punctate keratopathy, pseudodendrites, epithelial or subepithelial infiltrates, and perineural infiltrates. [17] Confocal microscopy assists in identifying 5 stages of keratopathy, as described by Tu [21] : epitheliitis, epitheliitis with radial neuritis, anterior stromal disease, deep stromal keratitis, and ring infiltrates. Ring infiltrates are characteristic, but are found in only 50% of cases. Early infection can mimic herpes keratitis, and late infection can mimic fungal keratitis. Perineural infiltrates are also highly suggestive of amebic keratitis.

The physical findings of GAE are highly dependent on location of lesions and result from increased intracranial pressure and focal neurological damage. These include abnormal mental status examination results, focal weakness or ataxia, and papilledema.

Disseminated disease without GAE may manifest as skin lesions that are typically hard, erythematous nodules or skin ulcers.

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