Viral Infections Followed by Bacterial Pneumonia

In the clinical course of this syndrome, patients typically report that after beginning to feel better, they experienced a return of symptoms, a worsening of cough. and production of purulent sputum. When this occurs, one should identify the responsible bacterial pathogen (pneumococcus, Staphylococcus, and Hemophilus influenzae are common causes) and initiate appropriate antibiotic therapy promptly.

This syndrome's pathophysiology is relatively simple. Following flu-induced destruction of the epithelium, the tracheal toilet is severely compromised, and bacteria are retained in the lower respiratory tract. Bacterial seeding of the injured respiratory tract, however, is not the only factor in post-influenza bacterial pneumonia. Gareth Green, of the Johns Hopkins School of Hygiene and Public Health, has shown that the phagocytic function of alveolar macrophages is severely compromised after the flu. Thus, not only are bacteria more likely to get into the lungs, but the host is less capable of destroying them.

Influenza Viral Pneumonia

The clinical course of influenza viral pneumonia progresses rapidly. It can lead to hypoxemia and death within a few days of onset. Understanding the pathophysiology of this disease is aided by review of microscopic anatomy. Figure 3 shows schematically that two very thin cells, the alveolar epithelial cell and the capillary endothelial cell, maintain a tenuous interface between gas in the alveolar airspace and fluid in the capillary lumen. If the influenza virus destroys alveolar epithelial cells, plasma leaks from the capillary, filling the airspace. If enough alveoli are involved, patients drown in their own plasma. This is especially true of patients with increased pulmonary capillary pressure (e.g., those with mitral stenosis), because destruction of alveolar epithelial cells will lead to greater extravasation of plasma and more pulmonary edema than in otherwise healthy people.

An important question is whether both alveolar type I and type Il cells have receptors for the virus. If influenza virus attacks only the type I cell, new alveolar epithelium could regenerate from the type II cell, just as ciliated epithelium regenerates from basal cells in the trachea. If alveolar regeneration is possible, maintaining patients with extracorporeal membrane oxygenation (ECMO) might be lifesaving. However, if both alveolar cell types have virus receptors, both could be killed by the virus, recovery would be impossible, and ECMO would be futile.