GENERAL CHARACTERISTICS Unlike

 N. fowleri, Acanthamoeba spp. do not have a flagellate stage in the life cycle, only the trophozoite and cyst. Several species of Acanthamoeba cause granulomatous amebic encephalitis (GAE), primarily in immunosuppressed, chronically ill, or otherwise debilitated individuals. These patients usually have no relevant history involving freshwater exposure. Acanthamoeba spp. also cause amebic keratitis, and it is estimated that the incidence in the United States may be one to two cases per million contact lens users. Apparently, the incidence of Acanthamoeba keratitis in the United Kingdom is 15 times higher than that in the United States and 7 times higher than that in Holland.

Motile organisms have spine-like pseudopods; there is a wide organism size range (25 to 40 µm), with the average diameter of the trophozoites being 30 µm. The nucleus has the typical large karyosome, similar to that found in N. fowleri. This morphologic characteristic can be seen on a wet preparation.

The cysts are usually round with a single nucleus, also having the large karyosome as in the trophozoite nucleus. The double wall is usually visible, with the slightly wrinkled outer cyst wall and what has been described as a polyhedral inner cyst wall. This cyst morphology is identifiable in organisms cultured on agar plates.

PATHOGENESIS AND SPECTRUM OF DISEASE

 GAE

 Meningoencephalitis caused by Acanthamoeba spp. may present as an acute suppurative inflammation of the brain and meninges similar to N. fowleri infection. The incubation period of GAE is unknown; several weeks or months are probably necessary to establish disease. The clinical course tends to be subacute or chronic and is usually associated with trauma or underlying disease, not as a result of swimming. GAE may present with symptoms of confusion, dizziness, drowsiness, nausea, vomiting, headache, lethargy, stiff neck, seizures, and sometimes hemiparesis. Unlike PAM caused by N. fowleri, both trophozoites and cysts are found throughout the tissue. Also, dissemination to other tissues such as the liver, kidneys, trachea, and adrenals can occur in immunocompromised individuals; or additional unusual sites also include the ear and necrotic bone from a bone graft of the mandible. Some patients, especially those with AIDS, can develop erythematous nodules, chronic ulcerative skin lesions, or abscesses.

 Keratitis

 Acanthamoeba spp. also cause keratitis and corneal ulceration. Clinicians need to consider acanthamoebic infection in the differential diagnosis of eye infections that are not responding to bacterial, fungal, or viral therapy. These infections are often due to direct exposure of the eyes to contaminated materials or solutions. Use of contact lenses is the leading risk factor for keratitis. Conditions that are linked with disease include the use of home-made saline solutions, poor contact lens hygiene, and corneal abrasions. A contact lens can act as a mechanical vector for transport of amebae present in the storage case onto the cornea. Subsequent multiplication and invasion of the tissue may occur. Decreased corneal sensation has contributed to the misdiagnosis of Acanthamoeba keratitis as herpes simplex keratitis. Acanthamoeba keratitis may be present as a secondary or opportunistic infection in patients with herpes simplex keratitis. Unfortunately, as a result, treatment can be delayed for 2 weeks to 3 months.

LABORATORY DIAGNOSIS

Routine Methods

 The most effective culture approach uses non-nutrient agar plates with Page’s saline and an overlay growth of Escherichia coli on which the amebae feed. Tissue stains are also effective, and cysts isolated from cultures can be stained with Gomori’s silver methenamine, periodic acid-Schiff, and calcofluor white. Identification of Acanthamoebae in ocular samples and other tissues can be difficult, even for trained laboratory professionals; in histologic preparations, the organisms appear similar to keratoplasts, as well as neutrophils and monocytes. It has been estimated that up to 70% of clinical Acanthamoeba keratitis cases are misdiagnosed as viral keratitis. Also, the average time to diagnosis of keratitis attributable to Acanthamoeba infection can average 2.5 weeks longer for non–contact lens wearers than for contact lens users.

Other Methods

 CSF or bronchoalveolar lavage fluid cytospin preparations can be used to look for amebae in patients with GAE or respiratory symptoms. The characteristic morphology of the Acanthamoeba trophozoites, such as the prominent nucleolus, contractile vacuole, and cytoplasmic vacuoles, can be seen more easily using trichrome or hematoxylin and eosin stains on fixed preparations after cytocentrifugation.

In the differential diagnosis of GAE, other space occupying lesions of the central nervous system (CNS) (e.g., tumor, abscess, fungal infection) must also be considered. Predisposing conditions include Hodgkin’s disease, diabetes, alcoholism, pregnancy, and corticosteroid therapy. Organisms have also been found in the adrenal gland, brain, eyes, kidneys, liver, pancreas, skin, spleen, thyroid gland, and uterus.

In infections caused by Acanthamoeba spp., periodic acid-Schiff stains the cyst wall red and methenamine silver stains the cyst black. Normally, Naegleria and Acanthamoeba isolates are identified to the species level by a reference laboratory, such as the Centers for Disease Control and Prevention, using indirect fluorescent antibody procedures with a monoclonal or polyclonal antibody.

THERAPY

 Disseminated Infections Trophozoites and cysts of Acanthamoeba isolates vary in their sensitivity to antimicrobial agents. They are sensitive in vitro to ketoconazole, pentamidine, hydroxystilb amidine, paromomycin, 5-fluorocytosine, polymyxin, sulfadiazine, trimethoprim-sulfamethoxazole, azithromycin, and extracts of medicinal plants, especially, to combinations of these drugs. In vitro testing confirms strain and species differences in sensitivity.

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