Bacterial pneumonia

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Bacterial invasion of the lung parenchyma evokes exudative solidification (consolidation) of the pulmonary tissue known as bacterial pneumonia. Many variables, such as the specific etiologic agent, the host reaction, and the extent of involvement, determine the precise form of pneumonia. Thus, classification may be made according to etiologic agent (e.g., pneumococcal or staphylococcal pneumonia), the nature of the host reaction (e.g., suppurative, fibrinous), or the gross anatomic distribution of the disease ( lobular bronchopneumonia versus lobar pneumonia)

Patchy consolidation of the lung is the dominant characteristic of bronchopneumonia. This parenchymal infection usually represents an extension of a preexisting bronchitis or bronchiolitis. It is an extremely common disease that tends to occur in the more vulnerable two extremes of life – (infancy and old age. In the young there is little previous experience with pathogenic organisms rendering these patients suceptible to organisms of even low virulence. Resistance likewise falls in the aged, particularly in those already suffering from some serious disorder. Bronchopneumonia, a common finding on postmortem examinations, frequently terminates a long course of progressive heart failure or disseminated tumor

Lobar pneumonia is an acute bacterial infection of a large portion of a lobe or of an entire lobe. Classic lobar pneumonia is now infrequent, owing to the overlap. The lobular involvement may become confluent producing virtually total lobar consolidation; in contrast effective antibiotic therapy for any form of pneumonia may limit involvement to a subtotal consolidation. Moreover the same organisms may produce lobular pneumonia in one patient, whereas in the more vulnerable individual a full blown lobar involvement develops. Most important from the clinical standpoint are identification of the causative agent and determination of the extent of disease.

Each day the respiratory airways and alveoli are exposed to more than 10,000 liters of air containing hazardous dusts, chemicals and microorganisms. The fates of inhaled particles depend on their sizes. Thus particles larger than 10mm are deposited largely in the turbulent airflow of the nose and upper airways; particles of 3 to 10 mm lodge in the trachea and bronchi by impaction; and smaller particles and the size of most bacteria, 1 to 5 mm are deposited in the terminal airways and alveoli Smaller particles (<1 mm) may remain suspended in the inspired air and can be exhaled.

Nasal clearance

Particles, including aerosolized droplets carrying microorganisms deposited near the front of the airway on the nincliated epithelium, are norkmally removed by sneezing and blowing whereas those deposited posteriorly are swept over the mucus lined cliated epithelium to the nasopharynx, where they are swallowed

Tracheobronchial clearance

This is accomplished by mucociliary action: The beating motion of cilia moves a film of mucus continiously from the lung toward the oropharynx; particles deposited on this film are eventually either swallowed or expectorated.

Alveolar clearance

Bacteria or solid particles deposited in the alveoli are phagocytosed by alveolar macrophages. A particle is either digested or carried to the ciliated bronchioles. From here, the macrophage is propelled to the oropharynx and then swallowed. Alternatively the particle- laden macrophage may move through the interstitial space and either reente the broncholes or enter lymphatic capillaries. If the particle load is heavy and macrophage transport to the surface and alveolar pathways is overwhelmed, some particles may eventually reach the regional lymph nodes and via the blood stream be carried elsewhere in the body.

Pneumonia can result whenever these defense mechanisms are impaired or whenever the resistance of the host in general is lowered. Factors that affect resistance in general is include chronic disease, immunologic deficiency, treatment with immunosuppressive agents, leukopenia and unusually virulent infections. The clearing mechanisms can be interfered with by many factors wuch as the following:

Loss or suppression of the cough reflex, as a result of coma, anesthesia, neuromuscular disorder, drugs, or chest pain.

Injury to the mucociliary appparatus by either impartment of ciliary function of destruction of ciliated epithelium, owing to cigarette smoke, inhalation of hot or corrosive gases, viral disease, or genetic disturbances (e.g., immotile cilia syndrome)

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