Enterovirus infections: causes and pathogenesis

Causes of enterovirus infections

The cause of enterovirus infections is intestinal viruses (multiplying in the gut and excreted from the body with faeces) of the genus Enterovirus of the family Picornaviridae (pico - small, RNA - RNA). The genus of enteroviruses combines polioviruses (3 serovars). Which are the causative agents of poliomyelitis, Coxsackie A viruses (24 serovars), Coxsackie B (6 serovars) and ECHO (34 serovars). And 5 human enteroviruses (unclassified viruses of 68-72 types). Enterovirus 70 causes acute hemorrhagic conjunctivitis, and enterovirus 72 - HAV. Enteroviruses are genetically heterogeneous.

The main features of these viruses are:

• small sizes of virions (15-35 nm);
• presence of RNA in the center of viral particles;
• protein molecules (capsomers) along the periphery of the virions.

Intestinal viruses are resistant to the environment, resistant to low temperatures, resistant to freezing and thawing (in faeces at low temperatures they remain viable for more than half a year). Resistant to 70% ethanol solution, 5% solution of lysol. In sewage, small reservoirs, depending on the temperature can persist up to 1.5-2 months. Intestinal viruses are sensitive to drying, at room temperature are kept up to 15 days. At a temperature of 33-35 ° C perish for 3 hours, at a temperature of 50-55 ° C - for several minutes, with boiling and autoclaving - instantly. Quickly die under the influence of formaldehyde, thiols, heterocyclic dyes (methylene blue, etc.), oxidizers (potassium permanganate and hydrogen peroxide), as well as ultraviolet irradiation, ultrasound, ionizing radiation. Free residual chlorine (0.3-0.5 mg / L) rapidly inactivates enteroviruses in aqueous suspensions, but the presence of chlorine-binding organic substances can reduce the effect of inactivation.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]

Pathogenesis of enterovirus infections

The pathogenesis of enterovirus infections has not been studied enough, since viruses can multiply in the intestinal wall without causing disease. The disease occurs when the resistance of the body decreases.

Enteroviruses penetrate the body through the mucous membrane of the upper respiratory tract and digestive tract, where their primary accumulation takes place. When the virus leaves the initial accumulation zone, it enters the regional lymph nodes and lymphatic formations of the intestine, where its replication continues. On the third day after the onset of the disease other organs are affected as a result of primary viremia. The variety of clinical forms of enterovirus infection is explained by the mutation of capsid antigens, the heterogeneity of the viral population, and the tropicity of the various genotypes of the pathogen to individual tissues (epithelial cells, nervous tissue and muscles).

In 1-2% of cases concurrently with the involvement of other organs or a little later, involvement in the CNS process is possible. Having penetrated into the central nervous system, the virus acts on the vascular plexuses of the brain, resulting in the production of an excessive amount of cerebrospinal fluid with the development of hypertensive-hydrocephalic syndrome, irritation of the nuclei of the vagus nerve and the vomiting center. Depending on the level of CNS lesion, serous meningitis, meningoencephalitis or poliomyelitis-like disease develop. To defeat the central nervous system enteroviruses, which have increased tropism to the nervous tissue.

In pregnant women as a result of viremia, intrauterine damage to the fetus is possible.

Enterovirus infection can be asymptomatic with the persistence of viruses in the intestines, muscles, parenchymal organs, and the central nervous system. There may be a chronic course of infection.

When pathomorphological examination of the organs of patients who died from Coxsackie virus infection (most often children of early age), myocarditis, infiltration of cardiac muscle by lymphocytes, histiocytes, plasma and reticular cells, eosinophils and polynucleated leukocytes are detected. In a number of cases, interstitial edema, thinning and necrosis of muscle fibers, scar changes and calcification foci are identified (in a number of cases, the development of transmural myocardial infarction was associated with myocarditis).

When meningoencephalitis occurs in the soft meninges of the brain and spinal cord, edema, hyperemia and perivascular lymphocytic-monocyte infiltration are noted. Diapedesis hemorrhages in the brain substance, perivascular infiltration and focal proliferation of glial cells, focal necrosis and polymorphonuclear infiltrates in the vascular plexuses of the ventricles of the brain are detected.

With epidemic myalgia, there are signs of acute or chronic myositis in the form of disappearance of transverse striation, swelling of individual fibers and in some cases - coagulation necrosis. Changes in the striated muscle are typical and pathognomonic for Coxsackie virus infection.

Epidemiology of enterovirus infections

The source of enteroviruses is a person (a patient or a virus carrier). In the spread of the disease an important role is played by convalescents, as well as by persons. Who were in contact with patients and convalescents.

The main mechanism of transmission of the pathogen is fecal-oral, the main transmission routes are water and alimentary. The most intensive virus is released in the first days of the disease, but in some cases, enterovirus can be released within a few months. Most often the transmission factors are water, vegetables, less often milk and other food products. Infection is possible during bathing in reservoirs contaminated with enteroviruses. The virus can be transmitted through dirty hands, toys. Given that in an acute period the virus is released from nasopharyngeal mucus, the air-drop route of transmission is not excluded. Transplacental transfer of enteroviruses from a sick mother to a fetus is possible.

The susceptibility is high. Frequent group diseases are observed in children's institutions, family outbreaks are possible. Asymptomatic virus carrying occurs in 17-46% of cases (more often in young children). After the transferred enterovirus infection, resistant type-specific immunity is produced. It is possible to develop cross immunity to certain types of enteroviruses.

Enterovirus infections are ubiquitous. Sporadic cases of the disease, outbreaks and epidemics of enterovirus infections are described in all countries of the world. In connection with a sharp decline in the incidence of poliomyelitis in recent years, the epidemiological significance of enterovirus infections is increasing. Mass migrations of people, the widespread use of tourism lead to the spread of new strains of enteroviruses in the collectives, to which people do not have immunity. On the other hand, there has been an increase in the virulence of some strains of the virus as a result of their natural circulation.

Enterovirus infections are diagnosed throughout the year, but for countries with a temperate climate, summer-autumn seasonality of morbidity is characteristic.

Enteroviral diseases have been registered in Ukraine since 1956.

[11], [12], [13], [14], [15]