A granuloma forms when macrophages cannot fully clear a persistent pathogen (e.g. M. tuberculosis, fungi, foreign material) and instead wall it off. The core dynamics are modelled as coupled rate equations, integrated forward in time each frame:
dB/dt = r·B·(1 − B/K) − k·M·B/(B + h)
dM/dt = ρ·B/(B + 20) − δ·M
B = bacterial burden M = activated macrophages
r = replication rate (↑ with virulence)
k = kill rate, ρ = recruitment gain (↑ with immune competence)
K = 200 (carrying capacity), h = 15, δ = 0.05 (macrophage turnover)
The first term is logistic pathogen growth; the second is saturating macrophage-mediated killing (Michaelis–Menten form — killing plateaus as burden rises). Macrophage recruitment saturates similarly with antigen load.
- Epithelioid transformation / Langhans giant cells — sustained macrophage activation around a stable core fuses macrophages into multinucleated giant cells at the granuloma rim, shown as orange spheres replacing green ones.
- Caseous necrosis — when the bacterial:macrophage ratio stays high (macrophages overwhelmed), central tissue dies from a mix of cytotoxic T-cell activity and ischemia, forming the cheese-like (caseous) core.
- Fibrous capsule — if containment holds (low, stable burden) long enough, fibroblasts lay down collagen around the granuloma — the latent, walled-off state seen in healed TB.
- Dissemination — if burden overwhelms capacity (low immune competence, high virulence), the granuloma ruptures and pathogens spread — miliary/disseminated disease.
This is the general pathology pattern behind chronic granulomatous inflammation (TB, sarcoidosis, foreign-body reactions, fungal infections) — persistence, containment or breakdown, not a single named disease.