Rotaviral Enteritis

Rotaviral gastroenteritis is an acute digestive tract infectious disease caused by rotavirus, also called autumn diarrhea. The pathogen is mainly transmitted via the digestive tract; main manifestations are acute fever, vomiting, and diarrhea, usually with a short course. It is one of the most common causes of diarrhea and can cause epidemics or pandemics. It mainly affects infants and young children, usually caused by group A rotavirus, with an autumn peak, hence called infantile autumn diarrhea. Worldwide, about 125 million cases of infant diarrhea occur annually due to rotavirus, mostly in developing countries. Group B rotavirus causes adult diarrhea.

Common Symptoms

Abdominal tenderness; borborygmus; diarrhea; abdominal pain; fatigue; low fever; nausea

Causes and Pathogenesis

Whether rotavirus causes disease depends on the infecting dose; a high viral load facilitates invasion. Rotavirus causes diarrhea through two routes: direct damage to small intestinal villous epithelial cells causing pathological changes, and metabolic products during replication acting on small intestinal endothelial cells, disrupting normal cellular function. Small amounts of virus are cleared by immunity without disease. Physiological host factors influence disease: when intestinal brush-border lactase (the rotavirus receptor) is abundant, as in infants, infection is more likely; lactase declines with age and susceptibility decreases. Reduced immunity from various conditions facilitates invasion. Pathogenesis: After reaching the small intestine, rotavirus enters epithelial cells via its outer capsid protein VP4 (attachment protein) binding to lactase on villous epithelial cells, multiplying in and destroying cells. Destruction of villous cells reduces disaccharidases such as lactase, blocking lactose conversion to monosaccharides; lactose accumulation creates high osmotic pressure in the small and large intestinal lumen, drawing water into the lumen and causing diarrhea and vomiting. Cuboidal epithelial cells from crypt bases then migrate upward to replace sloughed villous cells; since they are immature and in a high-secretion, low-absorption state, intestinal fluid retention prolongs diarrhea. The non-structural protein NSP4 synthesized during rotavirus replication acts as an enterotoxin, raising intracellular Ca2+ and small intestinal mucosal cAMP, also contributing to diarrhea. Severe diarrhea and vomiting can cause water, electrolyte, and acid-base disturbances. Pathology is reversible and mucosa usually remains intact; the small intestine is mainly affected, with biopsy showing shortened, blunted villi, lamina propria mononuclear infiltration, and irregular cuboidal epithelial cells with vacuolation or necrosis.

Treatment

Drug therapy, supportive therapy, symptomatic treatment, pediatric tuina therapy

Preventive Measures

Cutting transmission routes is the key to prevention. 1. Manage the source of infection: Early detection and isolation of patients; close observation of contacts and suspected cases. 2. Cut transmission routes: Strengthen food, water, and personal hygiene; disinfect patient feces; prevent contamination of drinking water and food. Hospitals must strictly disinfect infant and neonatal areas; incontinent children should be restricted from daycare or school. 3. Immunization: Rotavirus vaccines are clinically available; during epidemics, passive immunization of high-risk and susceptible groups has some preventive effect. Breast milk provides some protection; breastfeeding is recommended to reduce severity. Milk from cows immunized with bovine rotavirus contains IgA and IgG antibodies and also protects infants.

Department to Visit

It is recommended to visit the Gastroenterology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.