Viral pneumonia is an interstitial and parenchymal inflammation of the lungs caused by viruses invading the respiratory epithelium and alveolar epithelial cells. It can occur in both immunocompetent and immunosuppressed individuals. It is most common during the winter and spring seasons and can present as outbreaks or sporadic cases. Viruses are the second most common pathogens, after bacteria, causing community-acquired pneumonia in adults, and most cases resolve spontaneously. In recent years, the emergence of new mutant viruses (e.g., SARS coronavirus, H5N1, H1N1, H7N9) has led to epidemics with high mortality rates, making viral pneumonia a significant public health concern.
Etiology and Pathogenesis
Common causative viruses include influenza A and B viruses, adenoviruses, parainfluenza viruses, respiratory syncytial virus, and coronaviruses. Immunosuppressed hosts are particularly susceptible to herpesviruses and measles viruses. Bone marrow and organ transplant recipients are at higher risk for herpesvirus and cytomegalovirus pneumonia. Patients may be co-infected with more than one virus and often develop secondary bacterial infections, such as Staphylococcus aureus. Immunosuppressed individuals are also prone to secondary fungal infections. Viral pneumonia is primarily caused by inhalation of infectious droplets, leading to viral spread from the upper respiratory tract to the lower respiratory tract, often accompanied by tracheobronchitis. Occasionally, infection occurs through mucosal contact, and respiratory syncytial virus can be transmitted via airborne dust. In organ transplant cases, multiple blood transfusions or donor organs may lead to viremia and disseminated viral infections, typically without tracheobronchitis.
Pathology
Viruses invade the epithelium of the bronchioles, causing bronchiolitis. The infection may extend to the lung interstitium and alveoli, resulting in pneumonia. Extensive damage to airway epithelium occurs, with ulceration and fibrinous membrane formation on the mucosa. Pure viral pneumonia often manifests as interstitial pneumonia, characterized by significant mononuclear cell infiltration in the alveolar septa. Alveolar edema and the formation of protein- and fibrin-rich hyaline membranes increase the alveolar diffusion distance. Pneumonia can be focal or diffuse and may lead to consolidation. Viral inclusion bodies may be observed in some alveolar cells and macrophages. Inflammatory mediators act directly on bronchial smooth muscle, causing bronchospasm. After resolution of the infection, pulmonary fibrosis may remain as a sequela.
Clinical Manifestations
Viral pneumonia commonly occurs during viral epidemic seasons. Symptoms are usually mild and resemble those of mycoplasma pneumonia. However, the onset is more acute, with prominent systemic symptoms such as fever, headache, generalized muscle aches, and fatigue. Respiratory symptoms, including cough (with scant or white mucus sputum) and sore throat, often appear while acute influenza symptoms are still present. Severe pneumonia is more likely in children and older adults, manifesting as respiratory distress, cyanosis, lethargy, somnolence, and complications such as shock, heart failure, respiratory failure, or acute respiratory distress syndrome (ARDS). Chest signs are often absent, but severe cases may present with tachypnea, tachycardia, cyanosis, and dry or moist rales in the lungs.
Laboratory and Other Examinations
White blood cell counts are typically normal, slightly elevated, or low. Erythrocyte sedimentation rate (ESR) is usually within the normal range. Sputum smears show predominantly mononuclear cells, and sputum cultures often yield no pathogenic bacteria. Viral cultures are challenging and not routinely performed. In pneumonia patients, sputum smears showing scattered bacteria and numerous nucleated cells, or the absence of pathogenic bacteria, suggest the possibility of viral pneumonia. Detection of virus-specific IgM antibodies in serum can aid in early diagnosis. A fourfold or greater increase in antibody titers in serum between acute and convalescent phases is diagnostic. Polymerase chain reaction (PCR) testing for viral nucleic acids is valuable for identifying emerging or uncommon viruses.
Chest X-rays may show increased pulmonary markings, ground-glass opacities, small patchy infiltrates, or widespread infiltrates and consolidations. Severe cases may exhibit diffuse nodular infiltrates in both lungs, though lobar consolidation and pleural effusion are uncommon. Radiological features vary depending on the causative virus. Chest CT findings in viral pneumonia are diverse, including ground-glass opacities with lobular distribution, small nodular lesions, reticular or fibrotic changes, thickened bronchovascular bundles, segmental or lobar consolidation, mediastinal lymphadenopathy, and unilateral or bilateral small pleural effusions. Viral pneumonia resolves slowly and has a prolonged course.
Diagnosis
The diagnosis is based on clinical symptoms and imaging findings (X-ray or CT), with exclusion of pneumonia caused by other pathogens. Definitive diagnosis relies on etiological testing, including viral isolation, nucleic acid detection, and antibody testing. The presence of inclusion bodies in respiratory secretions suggests viral infection, though these may originate from sites other than the lungs. Lower respiratory tract secretions or lung biopsy specimens should be collected for viral culture and isolation. Serological tests commonly involve detecting specific IgG antibodies through complement fixation, hemagglutination inhibition, or neutralization tests, which are useful for retrospective diagnosis.
Treatment
Treatment is primarily symptomatic, with oxygen therapy as needed. Isolation and disinfection are crucial to prevent cross-infection.
Effective antiviral drugs include:
- Ribavirin: Broad-spectrum antiviral activity against respiratory syncytial virus, adenovirus, parainfluenza virus, and influenza virus. Dosage: 0.8–1.0 g/day in 3–4 divided doses orally; intravenous infusion or intramuscular injection at 10–15 mg/kg/day in 2 divided doses; or nebulized inhalation (10–30 mg per session with 30 mL distilled water, 2 sessions per day for 5–7 days).
- Acyclovir: Broad-spectrum, potent, and fast-acting antiviral effective against herpesviruses and varicella-zoster virus, especially in immunocompromised patients. Dosage: 5 mg/kg per dose via intravenous infusion, 3 times daily for 7 days.
- Ganciclovir: Inhibits DNA synthesis and is used for cytomegalovirus infections. Dosage: 7.5–15 mg/(kg·day) for 10–15 days.
- Oseltamivir: A neuraminidase inhibitor effective against influenza A and B viruses, with low resistance rates. Dosage: 150 mg/day in 2 divided doses for 5 days.
- Vidarabine: Broad-spectrum antiviral used for herpesvirus and varicella-zoster infections in immunocompromised patients. Dosage: 5–15 mg/(kg·day) via intravenous infusion for 10–14 days per course.
Antibiotics are generally not recommended for preventing secondary bacterial infections. However, if bacterial co-infection is confirmed, appropriate antibiotics should be promptly administered.