Viral pneumonia is interstitial and parenchymal inflammation caused by viral invasion of the respiratory epithelium and alveolar epithelial cells, and can occur in immunocompetent and immunosuppressed individuals, mostly in winter and spring, with outbreaks or sporadic cases. Viruses are the second most common pathogens of community acquired pneumonia in adults, and viral pneumonia can heal spontaneously. In recent years, new mutant viruses such as coronavirus, H5N1, H1N1, and H7N9 have emerged, causing pandemics and high mortality.
Etiology and pathogenesis
Common viruses include influenza A and B viruses, adenovirus, parainfluenza virus, respiratory syncytial virus, and coronavirus. Immunosuppressed hosts are susceptible to herpes virus and measles virus. Bone marrow transplant and organ transplant recipients are susceptible to herpes virus and cytomegalovirus pneumonia. Patients can be infected simultaneously with more than one virus, and often have secondary bacterial infections such as Staphylococcus aureus infection. Immunosuppressed hosts also often have secondary fungal infections. Viral pneumonia is mainly caused by inhaled viruses transmitted through human-to-human droplets. Upper respiratory tract viral infection extends downward, and is often accompanied by tracheobronchitis. Occasionally, mucosal contact infection is seen, and respiratory syncytial virus is transmitted through dust. In organ transplantation recipients, multiple blood transfusions and the transplanted organs can cause viral hematogenous dissemination of infection, usually without tracheobronchitis.
Pathology
Viruses invade the bronchiolar epithelium, causing bronchiolitis. The infection can spread to the pulmonary interstitium and alveoli, leading to pneumonia. The airway epithelium is extensively damaged, and ulcers occur on the mucosa, covered by a fibrin capsule. Simple viral pneumonia is mostly interstitial pneumonia, with massive mononuclear infiltration in the alveolar septa. The alveoli are edematous and covered by a hyaloid membrane containing protein and fibrin, increasing the alveolar diffusion distance. Pneumonia can be focal or diffuse, and can also be consolidation. Viral inclusion bodies can be seen in some alveolar cells and macrophages. Inflammatory mediators are released and act directly on bronchial smooth muscle, causing bronchospasm. Pulmonary fibrosis may remain after the lesion subsides.
Clinical manifestations
The disease often occurs in the epidemic season of viral diseases, and the symptoms are usually mild and resemble those of mycoplasmal pneumonia. However, the onset is rapid, and systemic symptoms such as fever, headache, generalized myalgia, and fatigue are more prominent. Respiratory symptoms such as cough, little or white mucus sputum, and pharyngitis often occur before the symptoms of acute influenza subside. Children and older adults are susceptible to severe pneumonia, manifested by dyspnea, cyanosis, lethargy, and listlessness, as well as complications such as shock, heart failure, respiratory failure, and ARDS. There are not significant chest signs. In severe patients, tachypnea, tachycardia, and cyanosis may occur, and dry and moist crackles in the lungs can be heard.
Laboratory and auxiliary examinations
The white blood cell count is normal, slightly elevated, or slightly declined, the erythrocyte sedimentation is usually within the normal range, the white blood cells seen in sputum smears are mostly monocytes, and sputum culture often does not grow pathogenic bacteria. Viral culture is difficult and cannot be conducted routinely. If sputum smears of pneumonia patients only show scattered bacteria and numerous nucleated cells, or no pathogens can be found, viral pneumonia should be suspected. Monitoring of the specific IgM antibodies in serum is helpful for early diagnosis. A fourfold or greater increase in the antibody titer between the acute phage and convalescent phase is of diagnostic significance. PCR detection of viral nucleic acid has diagnostic value for emerging mutant viruses or rare viruses.
Chest x-ray can show increased lung markings; ground-glass opacity; and small patchy infiltration, massive infiltration, and consolidation. In severe patients, chest x-ray shows diffuse nodular infiltration in both lungs, and occasionally lobar consolidation and pleural effusion. The different pathogens present different x-ray signs. The chest CT reveals lobular ground-glass opacity and small nodular lesions, as well as reticular and linear opacities, thickened bronchi and vascular bundles, and consolidation of the lobes and segments. Mediastinal lymphadenopathy and little unilateral or bilateral pleural effusion may be accompanied. Viral pneumonia resolves slowly and has a long course.
Diagnosis
The diagnosis is based on clinical symptoms, x-ray or CT imaging changes, and exclusion of pneumonia caused by other pathogens. The definite diagnosis depends on etiological examination, including viral isolation and detection of viral nucleic acid and viral antibodies. Inclusion bodies in the nucleus of the respiratory secretions can indicate viral infection, but the infections are not necessarily derived from the lungs. Further collection of lower respiratory tract secretions or lung biopsy specimens is required for culture and isolation of viruses. The common serological examinations, such as complement fixation test, hemagglutination inhibition test, and neutralization test, are to detect specific IgG antibodies for a retrospective diagnosis.
Treatment
Symptomatic treatment is the main regimen, and oxygen therapy is used when necessary. Attention should be paid to isolation and disinfection to prevent cross infection.
Ribavirin has broad-spectrum antiviral activity against respiratory syncytial virus, adenovirus, parainfluenza virus, and influenza virus. The treatment plan is oral ribavirin 0.8-1.0g/d in 3 - 4 divided doses; intravenous or intramuscular ribavirin 10 - 15mg/(kg.d) in 2 divided doses; or inhaled ribavirin 10 - 30mg diluted with distilled water 30ml twice a day; for 5 -7 days.
Acyclovir, with the characteristics of broad spectrum, strong effect, and rapid onset, is used to treat herpes virus and varicella virus infection. In immunocompromised or immunosuppressed patients, early administration is required. The treatment regimen is 5mg/kg intravenously 3 times a day for 7 days.
Ganciclovir can inhibit DNA synthesis and is used to treat cytomegalovirus infection. The treatment regimen is 7.5 - 15mg/(kg.d) for 10 - 15 days.
Oseltamivir is a neuraminidase inhibitor, has a good inhibitory effect on influenza A and B viruses, and has a low incidence of drug resistance. The treatment regimen is 150mg/d in 2 divided doses for 5 days.
Vidarabine has a wide range of antiviral effects and is mostly used to treat herpes virus and varicella virus infections in immunocompromised patients. The treatment regimen is 5 - 15mg/(kg.d) intravenously for 10 - 14 days.
In principle, antibiotics should not be used to prevent secondary bacterial infections. Once bacterial infections have been confirmed, sensitive antibiotics should be given.
The efficacy of glucocorticoids in viral pneumonia is still controversial, and glucocorticoids can be used if needed.