Various studies have reported 5 year survival rates of 50-60% for children with HLH, including familial and acquired forms [2, 3] . The diagnosis of familial HLH is often based on the age of onset, family history including a history of consanguinity, the clinical profile and/or co-existence of inherited immune deficiencies. Frequent relapses are common and these patients are usually candidates for BMT [4] . However, differentiation from early onset acquired HLH can be difficult. Absence of markers of immune deficiency (CHS, GS or XLP) or genetic perforin-granyzyme mutations does not rule out familial HLH. Acquired HLH has been described in association with collagen vascular disease (macrophage activation syndrome), post-transplant, malignancies especially T-cell lymphomas (lymphoma associated HLH) and infections (infection associated HLH). [5] . Both familial and secondary HLH are usually precipitated by an immunological trigger which may be an infectious agent or a drug. Among the infectious agents viruses especially Ebstein-Barr virus and Cytomegalovirus (virus associated HLH) are most commonly implicated, but bacterial, fungal and parasitic infections have also been described [6, 7] . With the possible exception of visceral leishmaniasis, immunomodulation is indicated in most cases [8] . Mycobacterium tuberculosis has been related to haemophagocytic syndrome in case reports from the Indian subcontinent, often with high mortality despite aggressive immunosuppressive therapy [1, [9] [10] [11] . We report a case of haemophagocytic syndrome related to mycobacterial infection which was managed with steroids and IVIG with complete clinical and haematological response.