J Neurocrit Care.  2024 Dec;17(2):88-93. 10.18700/jnc.240032.

Granulomatous amebic encephalitis in a patient treated with chemotherapy: a case report and literature review

Affiliations
  • 1Department of Clinical Sciences, University of Medicine and Health Sciences, Basseterre, Saint Kitts and Nevis
  • 2Department of Clinical Sciences, Ross University School of Medicine, Bridgetown, Barbados
  • 3Department of Clinical Sciences, St. George’s University, School of Medicine, True Blue, Grenada
  • 4Division of Neurocritical Care, Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA

Abstract

Background
Granulomatous amebic encephalitis (GAE) is caused by Acanthamoeba species or Balamuthia mandrillaris, which are microscopic, free-living amoebas found worldwide. People with compromised immune systems are at an increased risk of fatal cerebral infection caused by Acanthamoeba species, whereas B. mandrillaris can affect both immunocompromised and immunocompetent patients. Infections can involve the central nervous system causing GAE.
Case Report
A 71-year-old Caucasian woman, previously diagnosed with chronic lymphocytic leukemia and undergoing chemotherapy, arrived at the emergency department exhibiting seizure-like symptoms. Brain imaging revealed bilateral cerebral masses with central necrosis and hemorrhage, among other findings. The patient underwent a biopsy and was diagnosed with GAE.
Conclusion
Unfortunately, even with the correct diagnosis, GAE leads to rapid deterioration and a higher risk of mortality. This case demonstrates the rapid and severe nature of GAE and emphasizes the need for ongoing studies and better treatment options to improve GAE outcomes.

Keyword

Immunocompromised; Amoeba; Central nervous system infection; Encephalitis; Neurocritical care; Granulomatous amebic encephalitis

Figure

  • Fig. 1. Brain magnetic resonance imaging with T2 fluid-attenuated inversion recovery. (A) A lesion with central necrosis, where the ameba is located, surrounded by vasogenic edema (arrow). (B) Vasogenic edema causing a compression of the left lateral ventricle (arrow). (C) A parenchymal lesion (arrow).

  • Fig. 2. Brain magnetic resonance imaging with T2 fluid-attenuated inversion recovery following the treatment protocol. (A) The necrotizing lesion with an improved surrounding vasogenic edema (arrow). (B, C) Improved vasogenic edema based on the size and mass effect decreased (arrows) when compared to Fig. 1.


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