Alcohol and bacterial pneumonia

Alcohol Health & Research World, Wntr, 1992 by Steve Nelson, Judd Shellito, Carol Mason, Warren R. Summer

An alcohol-impaired pulmonary immune system is no defense against pneumonia-producing bacteria.

At least one-half of the adult U.S. population consumes alcohol. Among these consumers, approximately 15.2 million abuse or depend upon alcohol, making alcoholism the leading form of drug abuse in the United States. Because alcohol can exert potent suppressive effects on the immune system, the susceptibility of alcohol users to a variety of infections is significant. Among these infections, bacterial pneumonia has the strongest and best documented association with alcohol abuse.

One of the earliest reports to link alcohol consumption and pulmonary infections was published in 1785 by Benjamin Rush. In An Inquiry Into the Effects of Ardent Spirits Upon the Human Body and Mind, Rush listed tuberculosis and pneumonia as "infectious sequelae" (aftereffects) of alcoholism. Sir William Osler, in his Principles and Practice of Medicine (1909), stated that alcoholism was "perhaps the most potent predisposing factor" to pneumonia. Indeed, the frequency and severity of pneumonia are so pronounced among alcohol abusers that physicians have historically been convinced that the alcohol-consuming patient is, in fact, an immunocompromised host. However, while the relationship between alcohol abuse and pulmonary infection has been noted, an understanding of the basic mechanisms by which alcohol suppresses the immune system of the host remains unclear and continues to evolve. Further progress in reducing disease and death among alcohol abusers who contract pneumonia will depend upon increased understanding of the means by which alcohol depresses host defenses against invading disease-causing pathogens. New counteractive treatment strategies will result from increased research and understanding.

NORMAL LUNG HOST DEFENSES

Bacterial pneumonia is the clinical manifestation of infection caused by multiple host and pathogen interactions involving characteristics of the invading microorganism, immunologic defenses, nutrition, metabolism, and environmental exposure. As most patients with pneumonia do not have a clinically recognized genetic defect in their host defense system, their disease is typically the outcome of an acquired imbalance resulting from a failure of the immune system to destroy or rid itself of invading pathogens. To understand the sequence of events leading to this acquired state of immune deficiency in alcohol-abusing patients, it is necessary to review the means by which the lungs maintain sterility in the airways of normal hosts (also, see sidebar).

The lower respiratory tract is the largest internal surface of the body exposed to the external environment. Air breathed in normally through the nose and mouth exposes the tract not only to oxygen but also to various particles, noxious gases, and microorganisms. The lungs, therefore, are repeatedly exposed to infectious microorganisms. To defend against exposure, essential mechanical and immunologic components of the pulmonary defense system are distributed throughout the respiratory tract from the point of air entry in the upper tract to the site of gas exchange in the lower tract. Another essential component, inflammatory response, augments this standard apparatus. Because the invading pathogens encounter a highly integrated system of defense mechanisms, which comprises both mechanical components and immunologic components, infectious challenges to the lower respiratory tract rarely cause pneumonia in healthy people under normal circumstances.

Mechanical Components

The pulmonary defense system includes five major mechanisms: aerodynamic filtration in the nose; airway reflexes that cause cough and bronchospasm (spasm in the airways to and from the lungs); the mucociliary transport system, or "mucociliary escalator"; soluble factors in airway secretions; and phagocytic, or scavenger, cells(1) that engulf particulate matter.

The conducting airways of the lung extend from the upper portion of the throat (nasopharynx) to the lower portion of the lungs, to the bronchioles that make up the final portion of the purely conducting airways. The surfaces of these airways are lined with mucosa composed of a specialized fluid layer; ciliated cells (hair-covered epithelial cells that line the conducting airways); a basement, or foundation, membrane; and a submucosa containing organized structures including secretory glands and aggregates of plasma cells and lymphocytes (white blood cells formed in lymphoid tissue throughout the body).

Approximately 100 to 200 cilia per cell beat up to 1,000 times each minute in a coordinated, sequential, wavelike motion with a rapid-action stroke directed toward the throat (i.e., the glottis) and a slower, oppositely directed recovery stroke. Mucus is produced by specialized cells in the respiratory epithelium and the submucosal glands. It is composed of substances that coalesce and float on the fluid layer that bathes the ciliated epithelial cells, thereby trapping particles and microorganisms. Mucus has viscoelastic properties, allowing it to stretch and contract as it is moved up the airway surface by ciliary action. Because the ciliated epithelium ends near the terminal bronchioles, mucociliary clearance is of importance for particles that are deposited in the airways. Mucociliary clearance has no role, however, in the removal of organisms from the surfaces of air sacs (alveoli) at the base of the bronchioles, which is the site of air exchange.