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Clinical Features

Clinicians: For 24/7 diagnostic assistance, specimen collection guidance, shipping instructions, and treatment recommendations, please contact the CDC Emergency Operations Center at 770-488-7100.

The incubation period of Balamuthia granulomatous amebic encephalitis (GAE) is unknown although, in disseminated infections with preceding cutaneous involvement, a few weeks to about 2 years may elapse between the appearance of skin lesions and the recognition of central nervous system (CNS) disease 1,2. Patients exposed through solid organ transplantation can develop symptoms of Balamuthia GAE more quickly, within a few days to weeks (range 12–24 days), possibly because of direct inoculation and immunosuppression 3–5. GAE symptoms can appear mild at first but can progress over weeks to months. Early symptoms might include personality and mental status abnormalities alone or in combination with headache, stiff neck, photophobia, nausea, vomiting, lethargy, fever, ataxia, diplopia, impaired speech, focal neurologic deficit, and seizures 6,7. Delayed diagnosis of Balamuthia GAE is not uncommon, as it may be easily confused with other neurologic diseases, even non-infectious ones, like stroke. The disease is most often fatal once it spreads to the brain.

Some patients with Balamuthia GAE have presented with rhinitis with sinus infections, otitis media, and/or skin lesions, often on the face (particularly involving the nose or cheek) but also on the torso or limbs 1,2. In patients with cutaneous involvement, most generally have a single lesion, but multiple lesions are also seen 1. These lesions are chronic and granulomatous in nature, beginning as papulonodular, erythematous, plate-like areas that enlarge over time. The lesions are typically painless but can ulcerate and cause tissue destruction. Involvement of the oral cavity, especially of the palate, may also be present. Most patients with Balamuthia skin lesions later develop GAE 1. However, many people with Balamuthia GAE (including most cases identified in the U.S.) never develop preceding skin lesions (CDC unpublished data).

Initially, magnetic resonance imaging (MRI) shows one or a few lesions, even when computed tomography (CT) scans of the brain are unremarkable. Lesions typically are of low density with peripheral ring enhancement and mass effect. Over time, lesions increase in size and number to involve the cerebral hemispheres, cerebellum, brainstem, and thalamus. CT and MRI may indicate hemorrhage within lesions, and angiography may demonstrate occluded blood vessels corresponding to areas of infarction 8. Space-occupying masses and unifocal or multifocal ring-enhancing lesions up to 3–4 cm in diameter might be evident, and hydrocephalus and/or edema might also be present 9,10.

  1. Bravo FG, Cabrera J, Gottuzo E, Visvesvara GS. Cutaneous manifestations of infection by free-living amebas. Tropical Dermatology. Tyring SK, Lupi O, Hengge UR, editors. Philadelphia: Elsevier. 2006. pp. 49–55.
  2. Visvesvara GS, Moura H, Schuster FL. Pathogenic and opportunistic free-living amoeba; Acanthamoeba spp., Balamuthia mandrillaris, Naegleria fowleria and Sappinia diploidea. FEMS Immunol Med Microbiol. 2007;50(1):1–26.
  3. CDC. Balamuthia mandrillaris transmitted through organ transplantation—Mississippi, 2009. MMWR Morb Mortal Wkly Rep. 2010;59:1165–70.
  4. CDC. Notes from the field: transplant-transmitted Balamuthia mandrillaris — Arizona, 2010. MMWR Morb Mortal Wkly Rep. 2010;59:1182.
  5. Gupte AA, Hocevar SN, Lea AS, Kulkarni RD, Schain DC, Casey MJ, Zendejas-Ruiz IR, Chung WK, Mbaeyi C, Roy SL, Visvesvara GS, da Silva AJ, Tallaj J, Eckhoff D, Baddley JW. Transmission of Balamuthia mandrillaris through solid organ transplantation: utility of organ recipient serology for guide clinical management. Am J Transplant. 2014;14:1417–24.
  6. Schuster FL, Visvesvara GS. Free-living amoebae as opportunistic and non-opportunistic pathogens of humans and animals. Int J Parasitol. 2004;34:1001–27.
  7. Martinez AJ, Visvesvara GS. Balamuthia mandrillaris infection. J Med Microbiol. 2001;50:205–7.
  8. Visvesvara GS, Roy SL, Maguire JH. Pathogenic and Opportunistic Free-Living Amebae: Acanthamoeba spp., Balamuthia mandrillaris, Naegleria fowleri, and Sappinia pedata. Tropical Infectious Diseases—Principles, Pathogens, & Practice, 3rd ed. Guerrant RL, Walker DH, Weller PF, editors. Philadelphia, PA: Elsevier Churchill Livingstone. 2001. p. 707–13.
  9. Healy JF. Balamuthia amebic encephalitis: radiographic and pathologic findings. AJNR Am J Neuroradiol. 2002;23:486-9.
  10. Duke BJ, Tyson RW, DeBiasi R, Freeman JE, Winston KR. Balamuthia mandrillaris meningoencephalitis presenting with acute hydrocephalus. Pediatr Neurosurg. 1997;26:107–11.