Polymicrobial brain abscesses: A complex condition with diagnostic and therapeutic challenges

Abstract

Brain abscesses (BA) are focal parenchymal infections that remain life-threatening conditions. Polymicrobial BAs (PBAs) are complex coinfections of bacteria or bacterial and nonbacterial pathogens such as fungi or parasites, with diagnostic and therapeutic challenges. In this article, we comprehensively review the prevalence, pathogenesis, clinical manifestations, and microbiological, histopathological, and radiological features of PBAs, as well as treatment and prognosis. While PBAs and monomicrobial BAs have some similarities such as nonspecific clinical presentations, PBAs are more complex in their pathogenesis, pathological, and imaging presentations. The diagnostic challenges of PBAs include nonspecific imaging features at early stages and difficulties in identification of some pathogens by routine techniques without the use of molecular analysis. Imaging of late-stage PBAs demonstrates increased heterogeneity within lesions, which corresponds to variable histopathological features depending on the dominant pathogen-induced changes in different areas. This heterogeneity is particularly marked in cases of coinfections with nonbacterial pathogens such as Toxoplasma gondii. Therapeutic challenges in the management of PBAs include initial medical therapy for possibly underrecognized coinfections prior to identification of multiple pathogens and subsequent broad-spectrum antimicrobial therapy to eradicate identified pathogens. PBAs deserve more awareness to facilitate prompt and appropriate treatment.

Keywords: abscess stage; brain abscess; coinfection; lesion heterogeneity; pathogen; pathogenic complexity; polymicrobial.

Figure 1.

MRI of brain abscess with Nocardia and Toxoplasma coinfection. (A) Axial T1-weighted image demonstrates a peripherally enhancing left parietal lesion with central T1 hypointense complex fluid contents (arrow). (B) On diffusion-weighted imaging (left) and the corresponding apparent diffusion coefficient map (right), the lesion exhibits central diffusion restriction extending into the ventricle (arrowhead) indicating internal pus and pyogenic ventriculitis. (C) Sagittal FLAIR acquisitions confirm communication between 2 multilobulated components (arrows). (D) There is substantial hypointense signal dropout on susceptibility-weighted imaging, indicating intralesional hemorrhage (arrowhead).

Figure 2.

Pathology of concurrent brain Toxoplasmosis and Nocardiosis. (A, B) Microphotographs of the left parietal lesion show an abscess with necrosis (A, hematoxylin & eosin; *necrotic focus) surrounded by inflammatory cell infiltrates and other reactive changes such as gliosis/fibrosis forming a capsule highlighted by abundant Reticulin staining (B). (C) Nonnecrotic foci exhibit vasculitic changes with transmural inflammatory cell infiltration and some destruction of the vessel wall (arrows, elastic lamina breakdown). (D) Multinucleated giant cells are focally identified (arrows). (E-H) Immunohistochemistry reveals abundant CD68+ macrophages (E) and frequent CD8+ T-cells (F), and CD138+ plasma cells (G), as well as Toxoplasma+ tachyzoites (H, arrows; an inset of higher magnification). (I) Grocott-Gomori methenamine silver staining shows focally scattered filamentous branching, beaded bacteria (arrows; an inset of higher magnification). Scale bars: A-C = 20 µm, D-I = 10 µm.