This composite educational graphic illustrates the macroscopic and microscopic pathology of Granulomatous Amoebic Encephalitis (GAE) and systemic dissemination caused by Acanthamoeba culbertsoni in a murine model. Panels A through C display the progression of neuroanatomical damage: Panel A (4 days post-infection) shows early inflammation with loss of central sulcus integrity and incipient hemorrhage. Panel B shows hyperemic meninges and severe congestion. Panel C demonstrates advanced encephalomalacia, characterized by total loss of brain tissue integrity, extensive bleeding, and edema. Panel D depicts secondary pulmonary involvement, showing a hyperemic lung with peripheral hemorrhage and granular lesions suggestive of granulomatous inflammation. Panels E and F provide microscopic confirmation: Panel E (40x optical microscopy) reveals rounded amoebic trophozoites embedded within brain tissue imprints. Panel F (10x inverted microscopy) shows trophozoites migrating from brain tissue explants onto Non-Nutrient Agar (NNA). This series serves as a clinical reference for understanding the fulminant pathophysiology of opportunistic free-living amoebic infections, highlighting tissue necrosis, vascular congestion, and morphological identification of the pathogen.

This diagnostic imaging composite displays a series of brain MRI scans illustrating the longitudinal progression of granulomatous amoebic encephalitis (GAE) caused by Balamuthia mandrillaris. The image is organized into two panels (A and B) across three imaging modalities: T2-weighted (T2W2), Diffusion-Weighted Imaging (DWI), and Gadolinium-enhanced T1-weighted (Gd-T1WI). Panel A (A1–A4) follows a right parietal lobe lesion from initial presentation through post-surgical follow-up. The lesion shows high T2 signal intensity and restricted diffusion on DWI, with peripheral enhancement on Gd-T1WI. Over time (Nov 2020 to Apr 2021), the lesion and associated perilesional edema significantly decrease in size. Panel B (B1–B3) tracks a subsequent left occipital lobe lesion. Key features include high T2 and DWI signal intensity, marked contrast enhancement, and evidence of a left cerebral subfalcine herniation (indicated by white arrows). Follow-up scans after a second surgery and combined antimicrobial therapy (sulfamethoxazole/trimethoprim, azithromycin, flucytosine, and fluconazole) show gradual stabilization of the lesion and slight improvement of the midline shift. This series demonstrates the characteristic multifocal, infiltrating, and necrotic nature of GAE and its response to intensive medical and surgical management.

This diagnostic image pair displays axial T2-weighted magnetic resonance imaging (MRI) of the brain, comparing a pathological state with post-treatment resolution. Figure (a) illustrates multiple intracranial lesions consistent with granulomatous amoebic encephalitis, specifically Balamuthia mandrillaris. Key findings include an area of biopsy-related signal change in the left frontal region, extensive hyperintense perilesional oedema associated with a mass in the right temporal lobe, and hyperintense satellite lesions within the left frontal and parietal lobes. These lesions demonstrate characteristic T2-hyperintensity and mass effect. Figure (b) shows a follow-up MRI of the same patient taken two years into treatment, demonstrating significant clinical improvement. There is a complete resolution of the previously observed central nervous system (CNS) lesions, disappearance of the associated vasogenic oedema, and restoration of normal ventricular and sulcal anatomy. This comparison serves as a clinical timeline for the radiological monitoring of rare parasitic encephalitis under intensive therapy.