Consider susceptibility to the following pulmonary pathogens- 1. M. tuberculosis 2. P. aeruginosa 3. S. aureus 4. Nocardia sp. Which of the above is/are associated with long-term glucocoicoid therapy?

Pathology and pathogenesis M. bovis infection arises mainly drinking non-sterilised milk from infected cows. M. tuberculosis is spread by the inhalation of aerosolised droplet nuclei from other infected patients. Once inhaled, the organisms lodge in the alveoli and initiate the recruitment of macrophages and lymphocytes. Macrophages undergo transformation into epithelioid and Langhans cells, which aggregate with the lymphocytes to form the classical tuberculous granuloma . Numerous granulomas aggregate to form a primary lesion or 'Ghon focus' (a pale yellow, caseous nodule, usually a few millimetres to 1-2 cm in diameter), which is characteristically situated in the periphery of the lung. Spreadof organisms to the hilar lymph nodes is followed by a similar pathological reaction, and the combination of the primary lesion and regional lymph nodes is referred to as the 'primary complex of Ranke'. Reparative processes encase the primary complex in a fibrous capsule, limiting the spread of bacilli. If no fuher complications ensue, this lesion eventually calcifies and is clearly seen on a chest X-ray. Lymphatic or haematogenous spread may occur before immunity is established, however, seeding secondary foci in other organs, including lymph nodes, serous membranes, meninges, bones, liver, kidneys and lungs, which may lie dormant for years. The only clue that infection has occurred may be the appearance of a cell-mediated, delayed-type hypersensitivity reaction to tuberculin, demonstrated by tuberculin skin testing or an interferon gamma release assay (IGRA): so-called latent TB . If these reparative processes fail, primary progressive disease ensues . The estimated lifetime risk of developing disease after primary infection is 10%, with roughly half of this risk occurring in the first 2 years after infection. Glucocoicoids reduce inflammation and limit tissue damage; they are currently recommended when treating pericardial or meningeal disease, and in children with endobronchial disease. They may confer benefit in TB of the ureter, pleural effusions and extensive pulmonary disease, and can suppress hypersensitivity drug reactions. Surgery should be considered in cases complicated by massive haemoptysis, loculated empyema, constrictive pericarditis, lymph node suppuration, and spinal disease with cord compression, but usually only after a full p aregenosa,s aureus, Nocardia sps course of antituberculosis treatment. Ref Harrison20th edition pg 1078