Enterovirus infections - Causes and pathogenesis

Causes of enterovirus infections

Enterovirus infections are caused by intestinal viruses (reproducing in the intestine and excreted from the body with feces) of the genus Enterovirus of the family Picornaviridae (pico - small. RNA - RNA). The genus of enteroviruses includes polioviruses (3 serovars), which cause poliomyelitis, Coxsackie A viruses (24 serovars), Coxsackie B (6 serovars) and ECHO (34 serovars), as well as 5 human enteroviruses (unclassified viruses of types 68-72). Enterovirus 70 causes acute hemorrhagic conjunctivitis, and enterovirus 72 causes HAV. Enteroviruses are genetically heterogeneous.

The main signs of these viruses are:

• small size of virions (15-35 nm);
• the presence of RNA in the center of viral particles;
• protein molecules (capsomeres) on the periphery of virions.

Intestinal viruses are stable in the environment, resistant to low temperatures, resistant to freezing and thawing (in feces at low temperatures they remain viable for more than six months). Resistant to 70% ethanol solution, 5% lysol solution. Depending on the temperature, they can survive in wastewater and small reservoirs for up to 1.5-2 months. Intestinal viruses are sensitive to drying, and survive at room temperature for up to 15 days. At a temperature of 33-35 °C they die within 3 hours, at a temperature of 50-55 °C - within a few minutes, and instantly when boiled and autoclaved. They quickly die under the influence of formaldehyde, corrosive sublimate, heterocyclic dyes (methylene blue, etc.), oxidizers (potassium permanganate and hydrogen peroxide), as well as ultraviolet radiation, ultrasound, and ionizing radiation. Free residual chlorine (0.3-0.5 mg/l) rapidly inactivates enteroviruses in aqueous suspensions, but the presence of organic substances that bind chlorine can reduce the inactivation effect.

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Pathogenesis of enterovirus infections

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

Enteroviruses enter the body through the mucous membrane of the upper respiratory tract and digestive tract, where their primary accumulation occurs. When the virus goes beyond the initial accumulation zone, it enters the regional lymph nodes and intestinal lymphatic formations, where its replication continues. On the 3rd day from the onset of the disease, other organs are affected as a result of primary viremia. The diversity of clinical forms of enterovirus infection is explained by both the mutation of capsid antigens, the heterogeneity of the viral population, and the tropism of various genotypes of the pathogen to individual tissues (epithelial cells, nervous tissue, and muscles).

In 1-2% of cases, simultaneously with the damage of other organs or somewhat later, the central nervous system may be involved in the process. Having penetrated the central nervous system, the virus affects 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 damage to the central nervous system, serous meningitis, meningoencephalitis or poliomyelitis-like disease develop. CNS damage is caused by enteroviruses that have an increased tropism for nervous tissue.

In pregnant women, viremia may result in intrauterine damage to the fetus.

Enterovirus infection can be asymptomatic with persistence of viruses in the intestines, muscles, parenchymatous organs, and the central nervous system. Chronic infection is also possible.

Pathomorphological examination of organs of patients who died from Coxsackievirus infection (most often young children) reveals myocarditis, infiltration of the cardiac muscle by lymphocytes, histiocytes, plasma and reticular cells, eosinophils and polynuclear leukocytes. In some cases, interstitial edema, thinning and necrosis of muscle fibers, cicatricial changes and calcification foci are detected (in some cases, the development of transmural myocardial infarction was associated with previous myocarditis).

In meningoencephalitis, edema, hyperemia, and perivascular lymphocytic-monocytic infiltration are observed in the soft meninges of the brain and spinal cord. Diapedetic hemorrhages in the brain matter, perivascular infiltration and focal proliferation of glial cells, focal necrosis, and polymorphonuclear infiltrates in the vascular plexuses of the cerebral ventricles are detected.

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

Epidemiology of enterovirus infections

The source of enteroviruses is a person (patient or virus carrier). Convalescents, as well as persons who have been in contact with patients and convalescents, play a major role in the spread of the disease.

The main mechanism of transmission of the pathogen is the feco-oral route, the main routes of transmission are water and alimentary. The virus is most intensively released in the first days of the disease, but in some cases enteroviruses can be released for several months. Most often, water, vegetables, less often milk and other food products become transmission factors. Infection is possible when swimming in water bodies contaminated with enteroviruses. The virus can be transmitted through dirty hands, toys. Considering that in the acute period the virus is released from nasopharyngeal mucus, airborne transmission is also possible. Transplacental transmission of enteroviruses from a sick mother to the fetus is possible.

Susceptibility is high. Group diseases are often observed in children's institutions, family outbreaks are possible. Asymptomatic virus carriage occurs in 17-46% of cases (more often in young children). After an enterovirus infection, persistent type-specific immunity is developed. Cross-immunity to some types of enteroviruses may develop.

Enterovirus infections are widespread. Sporadic cases of the disease, outbreaks and epidemics of enterovirus infections have been described in all countries of the world. Due to the sharp decline in the incidence of poliomyelitis in recent years, the epidemiological significance of enterovirus infections is increasing. Mass migrations of people and widespread tourism lead to the spread of new strains of enteroviruses in groups, to which people have no immunity. On the other hand, an increase in the virulence of some strains of the virus has been noted as a result of their natural circulation.

Enterovirus infections are diagnosed throughout the year, but countries with a temperate climate are characterized by a summer-autumn seasonality of incidence.

Enterovirus diseases have been registered in Ukraine since 1956.

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