When the tubercle bacilli infect a susceptible host, the initial reaction is a polymorphonuclear inflammatory exudate. Within 48 hours, this is replaced by mononuclear cells, which become the prime sites for intracellular tubercle replication. As cellular immunity develops, destruction of tubercle bacilli takes place and caseation necrosis occurs. Later reactivation of a focus of infection results in proliferative granulomatous lesion, classically with central caseation necrosis surrounded by concentric layers of epithelial and giant cells, with peripheral lymphocytes, monocytes, and fibroblasts.