1. Pneumonia is an infection of the pulmonary parenchyma, defined as lung inflammation in which air sacs are filled with inflammatory cells, resulting in consolidation. It results from the proliferation of microbial pathogens at the alveolar level and the host's response to those pathogens.

2. as seen here, it is imperative to describe the pneumonia in

terms of etiology, morphology, duration, and its clinical manifestations.

3. Pneumonia, in terms of mode of acquisition, is classified as

community-acquired, hospital-acquired, or atypical. The most common of these is community-acquired.

4. In terms of etiologic agent, pneumonia may arise from

bacterial, viral, protozoal, or fungal infection. They differ from one another in terms of clinical and laboratory presentation.

5. In terms of morphology, pneumonia may be lobar,

broncho, or interstitial pneumonia. As will be discussed later on, the case at hand presents with manifestations of the lobar type.

6. lobar pneumonia evolves in four stages : Congestion (first

2 days), Red hepatisation (fibrinous alveolitis) (2nd to 4th day), Grey hepatisation (leukocytic alveolitis) (4th to 8th day), Resolution (after 8th day)

7. First, microorganisms gain access to the lower respiratory

tract, the most common of which is by aspiration from the oropharynx. Normally, the branching architecture of the tracheobronchial tree traps particles on the airway lining, where mucus and local antibacterial factors prevent entry. Resident alveolar macrophages are also extremely efficient at clearing and killing pathogens. When the microbes bypass the mechanical barriers and exceed the capacity of the alveolar macrophages to ingest or kill, clinical pneumonia becomes manifest. In that situation, the alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses. The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia.

8. This inflammatory response presents in the patient as

fever, an increase in mucus production, and airway constriction resulting in wheezes. It also triggers the release and accumulation of macrophages and neutrophils. The initial phase is, thus, one of edema, with the presence of a proteinaceous exudateand often of bacteriain the alveoli. Consequent leukocytosis and capillary leak cause both a decrease in compliance and the ability of gas to diffuse, leading to hypoxemia. Hypoxemia presents as increased respiratory rate, intercostal retractions, and increased PR. The resulting manifestation of these is dyspnea.

9. The occurrence of pleurisy also arises dues to the invading

inflammatory exudates coating the pleural surfaces causing three Rs: roughening, rubbing, and receptor irritation.

10. The congestion phase is rapidly followed by a red hepatization phase. The presence of erythrocytes in the cellular intraalveolar exudate gives this second stage its name. Bacteria are occasionally seen in pathologic specimens collected during this phase. Indicated here are the findings associated with this stage.

11. Seen here is the histology of the congestion and red

hepatization phase.

12. In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with successful containment of the infection and improvement in gas exchange.

13. Seen here is the gray hepatization stage, evidencing the

continuous predominance of neutrophils and the fibrin deposition mentioned earlier.

14. In the final phase, resolution, the macrophage reappears

as the dominant cell type in the alveolar space. Enzymatic digestion may eliminate the debris of neutrophils and bacteria, or reabsorb certain components, or may lead to fibrosis.

15. Seen here is the resolution stage.