Granulomas, organized aggregates of immune cells, are hallmarks of tuberculosis. Traditionally, granulomas were thought to be host-protective structures that contain and restrict mycobacteria. However, recent studies using zebrafish infected with *Mycobacterium marinum* (Mm) have challenged this view. In these studies, granulomas formed within days of infection, coinciding with rapid bacterial expansion. The presence of the ESX-1/RD1 virulence locus in Mm is crucial for granuloma formation and bacterial growth. Virulent Mm uses the ESX-1/RD1 locus to enhance macrophage recruitment and motility within nascent granulomas. This motility enables multiple arriving macrophages to efficiently find and phagocytose infected macrophages undergoing apoptosis, leading to rapid expansion of infected macrophages and bacteria. The primary granuloma then seeds secondary granulomas by the egress of infected macrophages. These findings provide new insights into how pathogenic mycobacteria exploit granulomas during the innate immune phase for local expansion and systemic dissemination.Granulomas, organized aggregates of immune cells, are hallmarks of tuberculosis. Traditionally, granulomas were thought to be host-protective structures that contain and restrict mycobacteria. However, recent studies using zebrafish infected with *Mycobacterium marinum* (Mm) have challenged this view. In these studies, granulomas formed within days of infection, coinciding with rapid bacterial expansion. The presence of the ESX-1/RD1 virulence locus in Mm is crucial for granuloma formation and bacterial growth. Virulent Mm uses the ESX-1/RD1 locus to enhance macrophage recruitment and motility within nascent granulomas. This motility enables multiple arriving macrophages to efficiently find and phagocytose infected macrophages undergoing apoptosis, leading to rapid expansion of infected macrophages and bacteria. The primary granuloma then seeds secondary granulomas by the egress of infected macrophages. These findings provide new insights into how pathogenic mycobacteria exploit granulomas during the innate immune phase for local expansion and systemic dissemination.