Fig. 13.32 Viralpneumonia.Thethickenedalveolarwallsareinfiltratedwithlymphocytesandsomeplasmacells,whicharespillingoverintoalveolarspaces.Notethefocalalveolaredema(center) andearlyfibrosis(upper right).
The clinical course of viral pneumonia is extremely varied. It may masquerade as a severe upper-respiratory tract infection or “chest cold” that goes undiagnosed, or manifest as a fulminant, life-threatening infection in immunocompromised patients. The initial presentation usually is that of an acute, nonspecific febrile illness characterized by fever, headache, and malaise and, later, cough with minimal sputum. The localization of the inflammatory exudate to the alveolar walls, prevents oxygenation of blood flowing through the affected air spaces which in turn causes mismatch of ventilation and perfusion. As a result, the degree of respiratory distress often seems out of proportion to the physical and radiographic findings. Identifying the causative agent can be difficult.
Perhaps no other communicable disorder causes as much public concern in the developed world as the threat of an influenza epidemic. The influenza virus is a single-stranded RNA virus, bound by a nucleoprotein that determines the virus type—A, B, or C. The viral surface has a lipid bilayer containing the viral hemagglutinin and neuraminidase, which determine the subtype (e.g., H1N1, H3N2). Host antibodies to the hemagglutinin and neuraminidase prevent and ameliorate, respectively, future infection with the influenza virus. The type A viruses infect humans, pigs, horses, and birds and are the major cause of pandemic and epidemic influenza infections. Epidemics of influenza occur through mutations of the hemagglutinin and neuraminidase antigens that allow the virus to escape most host antibodies (antigenic drift). Pandemics, which last longer and are more widespread than epidemics, may occur when both the hemagglutinin and neuraminidase are replaced through recombination of RNA segments with those of animal viruses, making all animals susceptible to the new influenza virus (antigenic shift). Commercially available influenza vaccines provide reasonable protection against the disease, especially in vulnerable infants and in older adults.
Insight into future pandemics has come from studying those past. DNA analysis of viral genomes retrieved from the lungs of a soldier who died in the great 1918 influenza pandemic that killed 20 million to 40 million individuals worldwide identified swine influenza sequences, consistent with this virus having its origin in an antigenic shift. The first flu pandemic of this century, in 2009, also resulted from an antigenic shift involving a virus of swine origin. It caused particularly severe infections in young adults, apparently because older adults had antibodies against past influenza strains that conveyed partial protection. Comorbidities such as diabetes, heart disease, lung disease, and immunosuppression also were associated with a higher risk for severe infection.
What then might be the source of the next great pandemic? One concern is centered on avian influenza, which normally infects birds. One avian strain, type H5N1, has spread throughout the world in wild and domestic birds. As of September 2015, approximately 700 H5N1 influenza virus infections and 400 deaths in humans (from 15 countries) have been reported to the World Health Organization (WHO). Nearly all cases have been acquired by close contact with domestic birds; most deaths resulted from pneumonia. Fortunately, the transmission of the current H5N1 avian virus is inefficient. However, if H5N1 influenza recombines with an influenza that is highly infectious for humans, a strain might emerge that is capable of sustained human-to-human transmission (and, thus, of causing the next great pandemic).
S. pneumoniae (thepneumococcus)isthemostcommoncauseofcommunity-acquiredbacterialpneumoniaandusuallyhasalobarpatternofinvolvement.