Abstract
Chronic cervical lymphadenopathy (CCL) presents a familiar diagnostic challenge to pediatricians and adult physicians [1]. Its importance lies not only in the local symptoms and disfigurement that may result; it is often a sign of multifocal disease requiring systemic management. Infectious agents—chief among them the mycobacteria—account for most cases of CCL worldwide. Historically, tuberculous lymphadenitis due to Mycobacterium tuberculosis and Mycobacterium bovis was predominant, typically arising during youth as a metastatic manifestation of uncontrolled primary infection acquired by the respiratory or oral rout. After 1950, as tuberculosis (TB) waned and M. bovis disease virtually disappeared from “developed” countries, nontuberculous mycobacteria (NTM) emerged as major agents of CCL, mainly in young children [2–5].