Granulomas are organized immune cell aggregates that form in response to persistent infections and are traditionally viewed as host-protective structures that contain tuberculosis (TB) bacteria. However, recent studies in zebrafish infected with *Mycobacterium marinum* (Mm) challenge this view, showing that granulomas may actually facilitate early bacterial growth. Using quantitative intravital microscopy, researchers observed that intracellular mycobacteria use the ESX-1/RD1 virulence locus to recruit and move new macrophages into nascent granulomas. This motility allows multiple macrophages to efficiently find and phagocytose infected macrophages undergoing apoptosis, leading to rapid bacterial expansion. The primary granuloma then seeds secondary granulomas via egress of infected macrophages. These findings suggest that pathogenic mycobacteria exploit granulomas during the innate immune phase for local expansion and systemic dissemination. The study highlights the role of the ESX-1/RD1 system in enhancing macrophage recruitment and infection, as well as in promoting rapid motility and phagocytosis of dead infected macrophages. The results indicate that granuloma formation is not solely a host-protective mechanism but can be manipulated by bacteria to enhance their spread. The study also shows that infected macrophages can egress from the primary granuloma to initiate secondary granulomas, contributing to the dissemination of TB. Overall, the findings reveal that granulomas play a complex role in TB pathogenesis, with both host and bacterial factors influencing their formation and function.Granulomas are organized immune cell aggregates that form in response to persistent infections and are traditionally viewed as host-protective structures that contain tuberculosis (TB) bacteria. However, recent studies in zebrafish infected with *Mycobacterium marinum* (Mm) challenge this view, showing that granulomas may actually facilitate early bacterial growth. Using quantitative intravital microscopy, researchers observed that intracellular mycobacteria use the ESX-1/RD1 virulence locus to recruit and move new macrophages into nascent granulomas. This motility allows multiple macrophages to efficiently find and phagocytose infected macrophages undergoing apoptosis, leading to rapid bacterial expansion. The primary granuloma then seeds secondary granulomas via egress of infected macrophages. These findings suggest that pathogenic mycobacteria exploit granulomas during the innate immune phase for local expansion and systemic dissemination. The study highlights the role of the ESX-1/RD1 system in enhancing macrophage recruitment and infection, as well as in promoting rapid motility and phagocytosis of dead infected macrophages. The results indicate that granuloma formation is not solely a host-protective mechanism but can be manipulated by bacteria to enhance their spread. The study also shows that infected macrophages can egress from the primary granuloma to initiate secondary granulomas, contributing to the dissemination of TB. Overall, the findings reveal that granulomas play a complex role in TB pathogenesis, with both host and bacterial factors influencing their formation and function.