This is a photomicrograph of a splenic parenchyma section from a splenectomy specimen, prepared for light microscopy and stained with hematoxylin and eosin. The specimen shows multiple subcentimeter nodules within the splenic parenchyma, with well-formed, non-caseating granulomas composed of tightly arranged epithelioid macrophages and multinucleated giant cells surrounded by a lymphocytic rim. The granulomas lack central necrosis, which, along with histiocytic microarchitecture, is highly suggestive of granulomatous inflammation due to Toxoplasma gondii infection. Serologic tests confirmed toxoplasmosis in this patient, correlating with disseminated disease or focal splenic involvement associated with lymphadenopathy and splenomegaly. In the spleen, toxoplasmosis can produce discrete nodules or focal granulomatous lesions that may mimic lymphoma or other granulomatous diseases on imaging or gross examination. Key differential diagnoses include sarcoidosis, fungal infections such as histoplasmosis, mycobacterial infections, and other parasitic infestations; clinical correlation with serology and immune status is essential. This image is relevant for teaching granulomatous splenitis due to toxoplasmosis, assessing granuloma morphology, distinguishing non-caseating from caseating granulomas, and correlating histology with systemic infection. Appropriate clinical scenarios include immunocompromised patients with fever, cytopenias, or organomegaly and routine pathology review in splenectomy specimens. This image exemplifies infectious granulomatous disease companion to serology and morphology in clinical practice.

This is a low-magnification brightfield histology image of a tissue section stained with Hematoxylin and Eosin (H&E). The specimen shows granulomatous inflammation with aggregates of epithelioid macrophages forming a rounded granuloma, often with multinucleated giant cells, surrounded by a lymphocytic cuff. The central focus is well circumscribed within native parenchyma, suggesting a chronic, organized immune response to a persistent antigen. Necrosis is not clearly evident at this magnification, though subtle caseation cannot be excluded. Morphology is compatible with tuberculoid or non-caseating granulomas, and infectious versus noninfectious etiologies must be distinguished with ancillary studies. This pattern can occur in lymph nodes or solid organs and prompts a differential that includes tuberculous lymphadenitis, sarcoidosis, fungal granulomatous infections (Histoplasma, Coccidioides), and foreign-body reaction. Clinically, recognition of granulomas guides testing: acid-fast bacilli staining (Ziehl-Neelsen), fungal stains (GMS/PAS), cultures, PCR panels, and radiologic correlation. The image is educational for medical trainees, illustrating granuloma architecture, macrophage differentiation, and the spectrum of chronic inflammatory responses. Educational context.

Pulmonary tissue from a wedge resection stained with Hematoxylin and Eosin, analyzed by brightfield light microscopy. The specimen shows robust granulomatous inflammation within the lung parenchyma consistent with a granulomatous infectious process. Nodular aggregates of epithelioid histiocytes are surrounded by a rim of lymphocytes and scattered plasma cells; multinucleated Langhans-type giant cells are present, producing a palisading appearance. The granulomas appear well circumscribed within the interstitium and may encroach upon adjacent alveolar spaces. Central necrosis is variably present and not conspicuously predominant in this field, a feature compatible with coccidioidal granulomatous reaction (coccidioidomycosis) that may display BCG-like granulomas in tissue specimens. The background alveolar architecture is preserved in portions, with mild interstitial inflammation and occasional eosinophils. Although fungal organisms are not definitively visualized in this image, the histology is compatible with fungal infection of the lung in the clinical context of pulmonary coccidioidomycosis, potentially associated with chronic granulomatous response. This image emphasizes characteristic granuloma morphology useful for differential diagnosis from mycobacterial tuberculosis or sarcoidosis, and provides histopathologic confirmation to guide clinical management, including antifungal therapy decisions and serology correlation. It is suitable for education on pulmonary granulomatous disease and wedge resection pathology.

Histology, light microscopy of cardiac tissue, reveals classic non-caseating granulomatous inflammation characteristic of cardiac sarcoidosis within the full thickness of the myocardium. The predominant architectural feature is well-demarcated granulomas composed of epithelioid histiocytes with multinucleated giant cells, embedded in a mononuclear lymphocytic infiltrate. Rare eosinophils may be present, but necrosis is minimal or absent. Granulomas are distributed along lymphatic channels and are frequently associated with the cardiac conduction system tracts, explaining potential electrical disturbances. The surrounding myocytes show preserved morphology with only focal interstitial fibrosis in many areas, reflecting chronicity and prior inflammatory injury. This histologic pattern differentiates sarcoid granulomas from other granulomatous myocarditis such as tuberculosis or hypersensitivity reactions, where caseation or different inflammatory profiles may occur. The tissue shows extensive lymphatic involvement and perivascular localization, contributing to impaired conduction and remodeling. The specimen, stained with Hematoxylin and Eosin, highlights the pink cytoplasm of myocardium and the dark nuclei of inflammatory cells, facilitating recognition of granulomatous foci, giant cells, and fibrotic change. Clinically, these findings support a diagnosis of cardiac sarcoidosis and carry implications for prognosis, arrhythmia risk, and indications for immunosuppressive therapy and device management. This description enhances searchability for cardiac pathology, granulomatous myocarditis, and sarcoid research applications.