**2. Pathophysiology**

Pneumonia is an inflammatory process in lung parenchyma most commonly caused by bacteria and viruses. Less common etiologies include mycoplasma, fungi and parasites. Organisms spread to the lungs through aerosolization, aspiration, or hematogenous spread due to inhalation of droplet or by aspiration of fluids in the oropharynx [8] Pneumonia results if host defense mechanisms are unable to keep the respiratory network infection free. The pathophysiology varies depending on etiology. In the case of bacterial pneumonia there is an intraalveolar suppurative exudate with consolidation [9].

In the case of viral pneumonia there is an inflammatory interstitial inflammation with infiltrate in the alveolar, causing damage to ciliated epithelium surfaces. The lungs become congested, hemorrhagic and Intracellular viral inclusions may form. Local host defenses, such as mucociliary clearance, or secretion of specific secretory IgA antibodies can remove some of the virus particles. However, if mucociliary clearance is impaired or secretory anti-influenza IgA antibodies are absent, infection continues to spread. Respiratory epithelial cells are invaded, and viral replication occurs. Newer viruses then infect larger numbers of epithelial cells, shut off the synthesis of critical proteins, and ultimately lead to host cell death [10].

There can be numerous types of immune response depending on how cytokine is produced. For example, cell-mediated immunity is initiated in type 1, while type 2 cytokines are responsible for allergic responses. Children infected with respiratory syncytial virus (RSV) with more serious acute bronchiolitis often have impaired type 1 immunity or augmented type 2 immunity [11].

Respiratory viruses such as RSV or rhinovirus that damage the respiratory tract cause release of multiple humoral factors, including leukotriene C4, and histamine. In the case of RSV virusspecific immunoglobulin E is released. Rhinovirus infections can cause release of bradykinin, interleukin 1, interleukin 6, and interleukin 8. A further complication of RSV infections is that they can increase bacterial adherence to respiratory epithelium, impair mucociliary clearance, and cause changes in bacterial phagocytosis by host cells [12].

In co infections, secondary bacterial superinfection makes for a poor prognosis of the original viral infection [13]. Interleukin-10, is purported to attract large numbers of macrophages and neutrophils to the lung. The presence of these cytokines increases the immune response, causing inflammatory damage and preventing the proper removal of bacteria.
