Causes and pathogenesis of respiratory syncytial infection

Respiratory syncytial infection is widespread and is registered all year round, but outbreaks occur more often in winter and spring. The source of infection is patients and, rarely, virus carriers. Patients excrete the virus for 10-14 days. The infection is transmitted exclusively by airborne droplets through direct contact. Transmission of infection through third parties and household items is unlikely. The susceptibility of different age groups to respiratory syncytial infection varies. Children under 4 months are relatively immune, since many of them have specific antibodies received from the mother. The only exception is premature babies, they do not have passive immunity and are therefore susceptible to RS infection from the first days of life. The greatest susceptibility to respiratory syncytial infection is noted at the age of 4-5 months to 3 years. At this age, all children have time to get sick with respiratory syncytial infection (especially in children's groups). In those who have recovered, specific IgA antibodies appear in the serum and discharge from the nasal mucosa. Secretory antibodies are an important factor of immunity in respiratory syncytial infection. Since acquired immunity is unstable, children may again become ill with respiratory syncytial infection upon repeated encounters with the respiratory syncytial virus. Such diseases proceed in a latent manner, but maintain the tension of specific immunity. Consequently, with the complete disappearance of specific antibodies against the respiratory syncytial virus, a manifest form of the disease occurs, and against the background of residual immunity - an latent, or inapparent, infection.

Causes of respiratory syncytial infection

The respiratory syncytial virus contains RNA, differs from other paramyxoviruses by its high polymorphism, the average particle diameter is 120-200 nm, and it is unstable in the external environment. There are 2 serovars of the virus that have a common complement-fixing antigen. The virus develops well in primary and transplantable cell lines (HeLa, Нер-2 cells, etc.), where syncytium and pseudogiant cells are formed. Unlike other paramyxoviruses, respiratory syncytial viruses have no hemagglutinin or neuraminidase.

Pathogenesis of respiratory syncytial infection

The virus enters the body by airborne droplets. Reproduction occurs in the epithelial cells of the mucous membrane of the respiratory tract. The pathological process quickly spreads to small bronchi and bronchioles, especially in young children. Persistence of the respiratory syncytial virus in epithelial cells causes their hyperplasia with the formation of symplasts, pseudogiant cells and hypersecretion, which leads to a narrowing of the lumen of small bronchi and bronchioles and complete blockage of their lumen with thick viscous mucus, deflated epithelium, leukocytes and lymphocytes. The drainage function of the bronchi is impaired, stasis, small atelectases develop, interalveolar septa thicken, which leads to a disruption of oxygen exchange and the development of oxygen starvation. The lungs are emphysematously dilated, dyspnea and tachycardia occur. The further course of respiratory syncytial infection is determined by the severity of respiratory failure and the superposition of bacterial infection.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ]