Viral Pneumonia

Bao Q. Luu

Viruses are recognized increasingly as a primary cause of pneumonia and also as coinfection with bacterial pneumonia. Interest in viral pneumonia has increased in recent years because of several factors: (a) the increasing number of immunosuppressed patients resulting from hematologic stem cell and solid organ transplants; (b) the availability of new molecular diagnostic techniques such as nucleic acid amplification (i.e., polymerase chain reaction [PCR]); and (c) the development of new, effective antiviral therapies as well as preventive measures (i.e., immunization as well as chemoprophylaxis). In addition, interest has been heightened by recent epidemics of respiratory illness caused by novel strains of viruses such as severe acute respiratory syndrome (SARS) in 2003, avian flu (H5N1) from 2006 to 2008, swine flu (H1N1) in 2009, and, most recently, the H7N9 reassortment of influenza A causing severe flu with high mortality rate among rural Chinese exposed to infected poultry.

This chapter reviews several of the most common viral pneumonias in immune-competent hosts. In such individuals, most viral respiratory infections have similar clinical presentations. Diagnosis, therefore, depends heavily on a high index of suspicion based on the epidemiologic context and confirmation by diagnostic tools such as serologic and immunohistochemical data as well as molecular diagnostic techniques such as PCR.

Influenza viruses remain the most common cause of pulmonary viral infections. These are RNA-containing viruses in the myxovirus family. They are divided into three groups (A, B, and C) on the basis of internal membrane (M) and nucleoprotein (NP) antigens. Group A is further divided into a variety of antigenic subtypes based on two distinct surface glycoproteins: hemagglutinin (H) and neuraminidase (N). Hemagglutinin is necessary for binding and penetrating the host cell membrane. Neuraminidase aids in the release and spread of replicated viral particles. Influenza A viruses can mutate spontaneously, producing new strains with changes in the H and N glycoproteins. The complete nomenclature of a strain of influenza virus includes the viral type (A, B, or C), geographic location of discovery, strain number, year, and H and N numbers (e.g., A/California/7/2009[H1N1]). All three types (A, B, and C) can undergo minor structural changes; however, only type A produces serologically distinct strains designated by numerical subscripts in the H and N loci. Immunity to influenza infection depends on the host’s production of antibodies to these glycoproteins. When a small antigenic change (antigenic drift) occurs, the effect on immunity is relatively minor. However, with a major antigenic change (antigenic shift) most people are not immune to the new (e.g., novel) virus resulting in a pandemic. The swine flu (H1N1) virus responsible for the 2009 pandemic is an example of such an antigenic shift. The WHO estimated that 16,226 deaths were attributed to H1N1 from April 2009 to January 2010. A growing body of literature supports the theory that aquatic birds and other animals (e.g., pigs) serve as important reservoirs of influenza virus, allowing genetic recombination leading to new, antigenically distinct, and, thus, more virulent strains of virus.

Influenza A is the most virulent subtype and the cause of the annual epidemics. Influenza B usually causes disease in populations confined to closed spaces such as daycare centers and boarding schools. Influenza C is the least virulent and found in sporadic cases. Typically, patients present with fever, cough, myalgia, headache, conjunctivitis, and prostration. Significant gastrointestinal symptoms, rhinorrhea, and pharyngitis are uncommon. Infections often exacerbate chronic illnesses such as chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, and congestive heart failure. Chest radiographs are often negative. However, in cases of pneumonia, infiltrates are usually patchy and bilateral. Infiltrates are generally self-limited and resolve within 3 weeks. Occasionally, influenza pneumonia evolves into diffuse pneumonia with bilateral infiltrates, severe hypoxemia, and acute respiratory distress syndrome (ARDS).

Coinfection with bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenza can occur within days and up to 2 weeks of influenza infection. Bacterial coinfection is a significant factor in the high mortality rate seen during epidemics and pandemics. The clinical course is determined in part by the specific bacterial pneumonia. However, complications such as abscess formation (especially with S. aureus), septic shock, empyema, and Reye syndrome are common.

Neurological sequelae of influenza, including Guillan-Barre syndrome, seizures, and transverse myelitis, have been reported. Severe myositis with elevated serum creatinine and phosphokinase levels also have been reported. Other rare complications include myoglobinuria, thrombocytopenia, renal failure, myocarditis, and disseminated intravascular coagulation.

Vaccination remains the most important preventive measure against the epidemic of influenza A. The Centers for Disease Control and Prevention (CDC) recommends that vaccination efforts be directed toward at-risk populations including children aged 6 months to 4 years; adults aged 50 and older; persons with chronic pulmonary, cardiovascular (except hypertension alone), renal, hepatic, neurologic, hematologic, or metabolic disorders (including diabetes mellitus); and immunosuppressed patients, and women who are pregnant or will be pregnant during the influenza season. Vaccination is also recommended for residents of nursing homes and chronic care facilities, healthcare workers, household contacts, caregivers of children younger than 5 years and adults 50 years and older, and household contacts and caregivers of persons with medical conditions that put them at higher risk for severe complications from influenza.

Amantadine and rimantadine have been approved for prevention and treatment of influenza A but are not effective against influenza B. However, many influenza A strains are now resistant to these drugs; thus, they are no longer recommended for empiric single-drug therapy.

Oseltamivir and zanamivir are drugs that block the surface protein neuraminidase and trap the virus within the infected respiratory epithelium preventing its dissemination. They should be administered, preferably within 48 hours of the onset of symptoms. They are active against both influenza A and B. In cases of severe pneumonia, medication should be provided even after 48 hours of symptom onset.

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