Norovirus infection

Mechanisms and transmission routes

The primary mechanism of infection transmission is fecal-oral. It occurs via several routes:

• Contact-household route: infection occurs via contaminated hands, toys, utensils, household items, and hardware.
• Waterborne route: via tap water, well water, boiled water, commercial ice, as well as open water bodies and swimming pools.
• Foodborne route: milk, various dairy products, and salads often serve as transmission factors.

An additional mechanism is aerogenic (airborne droplet). Viral RNA can be excreted in the patient's saliva from the 1st to the 10th day of illness.

Characteristics of the epidemic process

The disease spreads as sporadic cases, group outbreaks, and full-scale epidemics. Contagiousness among non-immune individuals is extremely high, ensuring rapid viral spread.

Following the infection, only a short-lived and type-specific immunity is formed, so the risk of reinfection is high. According to seroepidemiological studies, more than 90% of older children have antibodies to RTV (rotavirus, which has a similar clinical presentation). Viral agents are a major cause of nosocomial infections, accounting for 9% to 49% of hospital-acquired diarrheas, especially among premature infants and young children.

Pathogenesis and morphological changes

Detailed study of pathogenesis is hampered by the lack of an adequate experimental model. It is known that the virus actively penetrates mature enterocytes, where its replication and primary accumulation begin from the first days of illness.

As a result of viral activity, the following morphological changes in the gastrointestinal tract develop:

1. Atrophy and shortening of the small intestine villi.
2. Round-cell infiltration of the submucosal layer.
3. Round-cell infiltration of the lamina propria (lamina propria).

Differential diagnosis: Yersiniosis

Acute intestinal infections must be differentiated from the abdominal form of yersiniosis, which often simulates surgical pathology (appendicitis, mesenteritis, terminal ileitis).

The leading feature in yersiniosis is abdominal syndrome accompanied by fever (up to 38–39°C) and intoxication (myalgia, arthralgia, headache). Pain appears in the umbilical region and shifts to the right iliac region by the end of the 1st–2nd day. A forced patient position is characteristic — lying on the right side with bent legs. Positive Voskresensky, Sitkovsky, Rovsing, and Blumberg-Shchetkin signs are noted. A specific clinical sign is the so-called "raspberry tongue" (initially covered with a white coating, then clearing up).

Differential diagnosis: Botulism

If botulism is suspected (consumption of suspicious food products), a different algorithm of actions is required. Material for the sanitary and epidemiological station (15-20 ml of venous blood, 25-30 g of feces, vomitus) must be collected strictly BEFORE the administration of botulinum antitoxin and transported at a low temperature strictly without freezing.

To confirm the diagnosis, ELISA, inoculation into anaerobic media (Kitt-Tarozzi, Hottinger broth), and a biological assay on white mice (toxin neutralization reaction with type-specific antisera of types A, B, E) are used. Immunodiagnosis to detect antibodies in the patient is impossible, as the immunogenic dose of the toxin is lethal.

Class and exam questions

What else to study on this topic

• Specifics of conducting the mouse biological assay when botulism is suspected
• Variants of the abdominal form of yersiniosis
• Changes in the hemogram and ECG (ST segment) upon the development of toxic lesions
• Morphological picture of the lamina propria in acute intestinal infections
• The role of nosocomial infections in neonatology and pediatrics

Other topics in the "Acute Intestinal Infections" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.