The upper respiratory tract is constantly bombarded with infectious agents and has a resident microbial community. The lower respiratory tract is essentially sterile unless it is infected with a pathogen. Infections in the upper tract are usually mild and self-limiting, infections of the lower tract are serious and can be life threatening. As we need to breathe continuously, the upper respiratory tract is a popular portal of entry for microbes. Both parts of the respiratory tract have significant defences. The mucocilliary escalator of the upper tract moves pathogens up and out, aided by coughing and sneezing; this makes the tract a good portal of exit. Most respiratory infections are viral, meaning they cannot be treated by antibiotics.
Influenza is subject to numerous mutations. Over the course of a year the infecting influenza virus might be different enough from the antibody response you raised in the previous year that you are susceptible. Since you work in a hospital many of your patients are liable to enter it with influenza and your risk of being infected is higher than most others in the population.
The main impact of these viruses is to destroy the mucociliary escalator. Other organisms which are normally cleared from the lower respiratory tract then have an increased chance of entering it and retaining their positions.
For most healthy people, tuberculosis is a self-limiting disease that will be dealt with by the host defence. However, if cell-mediated immunity is in some way compromised or inefficient, tuberculosis can be serious. Mycobacterium is a problem for the host defence because of its unique cell wall, which interferes with macrophage function and with T cell activation. In point of fact, when Mycobacterium is ingested by macrophages, it inhibits the formation of the phagolysosome and eventually escapes into the cytoplasm of the macrophage. Here the bacterium will increase in number and eventually spread to the lymph nodes, where it will enter the blood and distribute throughout the body. The cell wall components of Mycobacterium attract T cells and macrophages to the site of the infection, and there is an uncontrollable release of enzymes and metabolites that destroy tissues, leading to necrosis. Necrosis in the lung liquefies and spreads to adjacent areas of the lung, a migration that causes the cycle to continue. If host defence does not contain the primary lesion, tubercles will form. A tubercle is composed of aggregates of enlarged macrophages filled with bacteria. This tubercle can be surrounded by fibroblasts and lymphocytes. Frequently, the center of the tubercle will undergo gaseous necrosis, which may later calcify. When this occurs, these calcifications are referred to as Ghon complexes; they are readily seen on X-ray.