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Respiratory syncytial virus (RSV) is a large, enveloped RNA paramyxovirus. Two major strains (groups A and B) have been identified and often circulate concurrently.
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Almost all children are infected at least once by 2 years of age. Humans are the only source of infection. Initial infection occurs most commonly during the child's first year. Reinfection throughout life is common. In the United States, RSV usually occurs in annual epidemics during winter and early spring (predominantly November through March). Communities in the southern United States, particularly some communities in the state of Florida, tend to experience the earliest onset of RSV activity (as early as July). RSV is the most common cause of acute lower respiratory tract infection (ALRI) in children <1 year of age. RSV is associated with up to 120,000 pediatric hospitalizations (1–3% of children in the first 12 months of life) each year in the United States. Approximately 400 deaths are attributed to RSV annually. Globally, an estimated 3.4 million new episodes of severe RSV ALRI necessitating hospital admission occur in children <5 years, of whom up to 200,000 die as a complication of infection. Also, RSV is a common cause of nosocomial infection. It can persist on environmental surfaces for several hours and for a half-hour or more on hands. Infection among hospital personnel and others may occur by hand-to-eye or hand-to-nasal epithelium self-inoculation with contaminated secretions.
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The disease is generally limited to the respiratory tract. The inoculation of the virus occurs in the upper respiratory tract. The virus replicates in the nasopharynx and spreads to the small bronchiolar epithelium, sparing the basal cells. Subsequently, the virus extends to the type 1 and 2 alveolar pneumocytes in lung, presumably by cell-to-cell spread or via aspiration of secretions. In infants, the disease manifests itself as bronchiolitis or pneumonia. In very rare cases, RSV may be recovered from extrapulmonary tissues, such as liver, spinal, or pericardial fluid. Up to 20% of children with RSV bronchiolitis may be coinfected with another respiratory tract virus, such as human metapneumovirus or rhinovirus.
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Risk factors include infants <6 months of age, premature infants born <35 weeks' gestation, infants born with lung disease, infants <2 years of age with heart disease, infants with school-aged siblings, infants who attend day care, family history of asthma, regular exposure to secondhand smoke or air pollution, multiple birth babies, peak RSV season (fall to end of spring), being male, immunocompromised patients (eg, severe combined immunodeficiency, leukemia, or undergoing organ transplant), <1 month or no breast-feeding, and others sharing the bedroom with the infant. High altitude increases the risk of RSV hospitalization. Risk factors for more severe or fatal RSV disease include a premature infant, an infant with complex congenital heart disease (CHD), especially those that cause cyanosis or pulmonary hypertension; an infant with bronchopulmonary dysplasia (chronic lung disease [CLD]); and an infant with immunodeficiency with lymphopenia or receiving therapy that causes immune suppression.
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V. CLINICAL PRESENTATION
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RSV usually begins in the nasopharynx with coryza and congestion. During the first 2–5 days, it may progress to the lower respiratory tract with development of cough, dyspnea, and wheezing. RSV is the most common cause of bronchiolitis and pneumonia in infants <2 years old. Lethargy, irritability, and poor feeding are commonly present in young infants. Apnea may be the presenting symptom in ∼20% of infants hospitalized with RSV and may be the cause of sudden, unexpected death. Most previously healthy infants infected with RSV do not require hospitalization. RSV infection may predispose to reactive airway disease and recurrent wheezing during the first decade of life; the association between RSV bronchiolitis early in life and subsequent asthma remains poorly understood.
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Enzyme-linked immunosorbent assay (ELISA) and direct fluorescent antibody (DFA) tests utilize antigen capture technology that can be performed in <30 minutes on nasal wash or tracheal aspirate. Their sensitivity and specificity exceed 80–90% (in comparison with culture). False-positive test results are more likely to occur when the incidence of disease is low. Viral isolation from nasopharyngeal secretions in cell culture requires 1–5 days (shell vial techniques can produce results within 24–48 hours). Reverse transcriptase–polymerase chain reaction (RT-PCR) is an alternative to culture for confirming the result of rapid antigen detection assay (which is rarely needed). Culture and PCR may be needed to confirm rapid antigen detection initially to ...