Respiratory syncytial virus (RSV) is a large, enveloped, nonsegmented, negative-strand RNA virus of the genus Pneumovirus of the family Paramyxoviridae. The virus uses attachment (G) and fusion (F) surface glycoproteins for virus entry. Two major strains (groups A and B) have been identified and often circulate concurrently.
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 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). In the southern hemisphere, wintertime epidemics occur from May to September, with a peak in May, June, or 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. Globally, the annual rate of RSV hospitalization among children <5 years is approximately 4.4 per 1000; hospitalization rates are highest among children <6 months old (2%) and premature infants <1 year old (6.4%). In addition, RSV is a common cause of nosocomial infection in the neonatal intensive care unit (NICU). 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.
The disease is generally limited to the respiratory tract. RSV usually is transmitted by direct or close contact with contaminated secretions, which may occur from exposure to large-particle droplets at short distances (typically <6 feet) or from fomites. The inoculation of the virus occurs in nasopharyngeal or ocular mucous membranes after contact with virus-containing secretions or fomites. The virus replicates in the nasopharynx and spreads to the small bronchiolar epithelium, sparing the basal cells. Subsequently, the virus extends to type 1 and 2 alveolar pneumocytes in the 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 30% of children with RSV bronchiolitis may be coinfected with another respiratory tract virus, such as human metapneumovirus, rhinovirus, bocavirus, adenovirus, coronavirus, influenza virus, or parainfluenza virus.
Risk factors for RSV ALRI include infants <6 months of age, premature infants born <35 weeks’ gestation, infants with underlying lung disease such as chronic lung disease (CLD) of prematurity, infants <2 years of age with heart disease, infants with school-aged siblings, infants who attend daycare, 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 of or no breast feeding, and others sharing the bedroom with the infant. High altitude increases the risk of RSV hospitalization. Children with Down syndrome are at increased risk for severe RSV disease.
The incubation period ranges from 2 to 8 days. RSV usually begins in the nasopharynx with coryza and congestion. During the first 2 to 5 days, it may progress to the lower respiratory tract (20%–30%) 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 approximately 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. Most RSV hospitalizations occur in the first 3 months of life. 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.
Enzyme-linked immunosorbent assay and direct fluorescent antibody tests use antigen capture technology that can be performed in <30 minutes on nasal wash or tracheal aspirate. Their sensitivity is approximately 80%, and specificity is approximately 95% (in comparison with culture). False-positive test results are more likely to occur when the incidence of disease is low. Multiplex assays or viral respiratory panels (which test for multiple respiratory viruses with 1 test) may be preferred in many clinical settings because they are able to identify co-infection. Viral isolation from nasopharyngeal secretions in cell culture requires 1 to 5 days (shell vial techniques can produce results within 24–48 hours). Molecular diagnostic tests using reverse transcriptase–polymerase chain reaction (RT-PCR) are cleared by the US Food and Drug Administration and available widely; they increase RSV detection rates over viral isolation or antigen detection assays. RT-PCR is an alternative to culture for confirming the result of rapid antigen detection assay, which is rarely needed except to mark the start of the RSV season. Additionally, palivizumab exposure (see Section VII on management) may interfere with immunologic-based antigen detection assays (enzyme-linked immunosorbent assay and direct fluorescent antibody) as well cell culture, but it does not interfere with RT-PCR. Diagnostic serology is not helpful in infants because of the passive transplacental transfer of maternal antibody.
Chest radiograph usually reveals infiltrates or hyperinflation.
Blood gas analysis may show hypoxemia and occasionally hypercarbia. Development of hypercarbia is an ominous sign of impending respiratory failure.
Primary treatment of young infants hospitalized with ...