Granulomatous Amoebic Encephalitis: Clinical Diagnosis and Management

Abstract

Granulomatous amoebic encephalitis (GAE) is a serious human disease with fatal consequences. With the mortality rate of more than 90%, it is not surprising that the majority of GAE infections are identified at the post-mortem stage. The most distressing aspect is that the high level of mortality is attributed to lack of awareness. Early diagnosis with aggressive treatment can lead to successful prognosis for the patient. Here, we describe a brief overview of the current understanding of the pathophysiology of GAE, available diagnostic methods, possible therapeutic interventions and the causative agents.

Amebic encephalitis

“…Acanthamoeba and Balamuthia both can cause the syndrome of GAE, which our patient had, an insidious and almost uniformly fatal encephalitic process. [ 5 6 ] Acanthamoeba is also associated with keratitis in otherwise healthy individuals, typically contact lens wearers who use homemade solutions to clean lenses or wear lenses while swimming in fresh water, and with chronic skin ulcers. [ 5 6 ]…”

Isolates from ancient permafrost help to elucidate species boundaries in Acanthamoeba castellanii complex (Amoebozoa: Discosea)

“…It is common in soils and aquatic environments all around the world (Geisen et al , 2014). The genus is also known as an opportunistic pathogen causing amoebic keratitis and encephalitis in humans (Khan, 2005;Maycock & Jayaswal, 2016). Due to a well-established method of axenic cultivation, it has become a popular model in biochemical and cell structure studies (Siddiqui & Khan, 2012).…”

Autoimmunity in the Mediation of Granulomatous Amoebic Encephalitis: Implications for Therapy

“…However, the mechanism by which amoebae actually enter the CNS is not clearly elucidated. Although it is postulated that they enter through the cerebral capillary endothelium or choroid plexus, the former being the more widely accepted mechanism (Khan, 2003, Marciano-Cabral & Cabral, 2003, Khan, 2005b, Khan, 2006, da Rocha-Azevedo, et al, 2009. These two modes of entry lead to the localization of amoebae in the cerebrum and cerebrospinal fluid (CSF) respectively (Elsheikha & Khan, 2010).…”

“…Acanthamoeba-induced encephalitis is not routinely suspected, the disease can be misdiagnosed as neurocysticercosis; viral, rickettsial, fungal, and bacterial meningitis; toxoplasmosis; and brain tumors (Schuster & Visvesvara, 2004, khan, 2005b. Serologically, detection of Acanthamoeba-reactive antibodies gives an indication of amoebic exposure at a population level (Cursons, et al, 1980, Cerva, 1989, Khan, 2006.…”

“…To identify structural brain lesions, computed tomography and magnetic resonance imaging are widely used (Sell, et al, 1997, Kidney & Kim, 1998. These evaluations can reveal changes such as multifocal areas of signal intensities or ring-like lesions or low-density areas indicating occupying mass of tumor or abscess (Martinez, et al, 1977, Martinez, et al, 1980, OforiKwakye, et al, 1986, Matson, et al, 1988, khan, 2005b, Khan, 2008, da Rocha-Azevedo, et al, 2009. The regions of the brain that are usually affected are midbrain, basal areas of the temporal and occipital lobes, and the posterior fossa (Seijo Martinez, et al, 2000, MarcianoCabral & Cabral, 2003, Khan, 2006.…”