Porth's Essentials of Pathophysiology, 4e

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Respiratory Function

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Most hospital-acquired infections are bacterial. The organisms differ from those responsible for community- acquired pneumonias, and reflect those present in the hospital environment. Gram-negative rods ( Entero­ bacteriaceae and Pseudomonas species) and S. aureus are the most common isolates. 14 Many of these organ- isms have acquired antibiotic resistance and are thus difficult to treat. Pneumonia in Immunocompromised Persons. Pneu­ monia in immunocompromised persons remains a major source of morbidity and mortality. Although almost all types of microorganisms can cause pulmonary infection in immunocompromised persons, certain types of immu- nologic defects tend to favor certain types of infections. 14 Defects in humoral immunity predispose to bacterial infec- tions against which antibodies play an important role, whereas defects in cellular immunity predispose to infec- tions caused by viruses, fungi, mycobacteria, and protozoa. Neutropenia and impaired granulocyte function, as occur in persons with leukemia or bone marrow depression as well as persons undergoing chemotherapy, predispose to infections caused by S. aureus, Aspergillus, gram-negative bacilli, and Candida. The time course of infection often provides a hint to the type of agent involved. A fulmi- nant pneumonia usually is caused by bacterial infection, whereas an insidious onset usually is indicative of a viral, fungal, protozoal, or mycobacterial infection. Acute Bacterial (Typical) Pneumonia Bacterial pneumonias remain an important cause of mortality among the elderly and debilitated. The lung below the main bronchi is normally sterile despite fre- quent entry of microorganisms into the air passages by inhalation during ventilation or aspiration of nasopha- ryngeal secretions. Most people unknowingly aspirate small amounts of organisms that have colonized their upper airways, particularly during sleep. These organ- isms do not normally cause infection because of the small number that are aspirated and because the respi- ratory tract’s defense mechanisms prevent them from entering the distal air passages (Table 22-1). Loss of the

cough reflex, damage to the ciliated endothelium that lines the respiratory tract, or impaired immune defenses predispose to colonization and infection of the lower respiratory system. Bacterial adherence also plays a role in colonization of the lower airways. The epithelial cells of critically and chronically ill persons are more receptive to binding microorganisms that cause pneu- monia. Other clinical risk factors favoring colonization of the tracheobronchial tree include antibiotic therapy that alters the normal bacterial flora, diabetes, smoking, chronic bronchitis, and viral infection. Bacterial pneumonias are commonly classified accord- ing to etiologic agent. This is because the clinical and morphologic features, and thus the therapeutic implica- tions, often vary with the causative agent. The discussion in this section focuses on two types of bacterial pneumo- nia: pneumococcal pneumonia and Legionnaires’ disease. Pneumococcal Pneumonia. S. pneumoniae (pneumo- coccus) causes pyogenic (pus-forming) infections, pri- marily of the lungs, ears, sinuses, and meninges. It is one of the most common bacterial pathogens and the most common cause of bacterial pneumonia. 14,26,27 S. pneumoniae is an aerobic, gram-positive diplococ- cus. There are over 80 antigenically distinct serotypes of pneumococci; antibody to one serotype does not protect against infection with another. 26 The virulence of S. pneumoniae is a function of its polysaccharide capsule, which prevents or delays digestion by phago- cytes. The polysaccharide is an antigen that primarily elicits a B-cell response with antibody production. In the absence of antibody, clearance of the pneumococci from the body relies on the reticuloendothelial system, with the macrophages in the spleen playing a major role in elimination of the organism. This, along with the spleen’s role in antibody generation, increases the risk for pneumococcal bacteremia in persons who are ana- tomically or functionally asplenic, such as children with sickle cell disease. The initial step in the pathogenesis of pneumococ- cal infection is the attachment and colonization of the organism to the mucus and cells of the nasopharynx. Colonization does not equate with signs of infection.

TABLE 22-1 Respiratory Defense Mechanisms and ConditionsThat Impair Their Effectiveness Defense Mechanism Function FactorsThat Impair Effectiveness

Glottic and cough reflexes

Protect against aspiration into tracheobronchial tree

Loss of cough reflex due to stroke or neural lesion, neuromuscular disease, abdominal or chest surgery, depression of the cough reflex due to sedation or anesthesia, presence of a nasogastric tube (tends to cause adaptation of afferent receptors) Smoking, viral diseases, chilling, inhalation of irritating gases Tobacco smoke, chilling, alcohol, oxygen intoxication Congenital and acquired immunodeficiency states

Mucociliary blanket

Removes secretions, microorganisms, and particles from the respiratory tract Removes microorganisms and foreign particles from the lung

Phagocytic and bactericidal action of alveolar macrophages Immune defenses (IgA and IgG and cell-mediated immunity)

Destroy microorganisms