Rotavirus enteritis

　　First, etiology

　　1. The rotavirus belongs to the Reoviridae family, is a double-stranded RNA virus with a diameter of about 70nm, and is spherical. Under the electron microscope, the rotavirus has a unique morphology, such as wheel-shaped, hence the name. Its two outer shells enclose the central protein core, and the outer shell is wheel-shaped, surrounding the core gene-encoded protein. Vp1~Vp7 and five non-structural proteins (NSPI~4). Particles with a single shell are incomplete viruses and are not infectious.

　　2. According to the specificity of the capsid protein group antigen Vp6, it can be divided into seven serotypes (A~G). Most childhood infections are caused by type A. Types B and C mainly infect adults. Others are pathogens for animal infections. Non-A group rotavirus is also known as atypical rotavirus or pararotavirus, and infections can occur in humans, pigs, cattle, sheep, chickens, and other animals.

　　3. The rotavirus has strong resistance to the external environment, can survive for 7 months at room temperature, and can survive for several days or weeks in feces. It is acid-resistant and alkali-resistant. It can be inactivated by heating at 55°C for 30 minutes or formaldehyde.

　　Second, pathogenesis

　　1. Whether the rotavirus entering the body can cause disease depends on the number of infected viruses, the immune status of the body, and the physiological characteristics of the body. When the amount of invasive virus is large and the immune function is low, it is conducive to the invasion of the virus. When the content of lactase (the receptor of the rotavirus) on the brush border of the intestinal epithelium is high, such as in infancy, it is easy to be infected with rotavirus. With the increase of age, the amount of this enzyme decreases, and the susceptibility decreases.

　　2. After the rotavirus enters the body, it causes diarrhea through two pathways: one is that the rotavirus directly damages the small intestinal villous epithelial cells, causing pathological changes; the other is that the metabolic products of the rotavirus during the replication process act on the small intestinal endothelial cells, destroying the normal physiological function of the intestinal cells and causing diarrhea.

　　3. After the rotavirus invades the human body and reaches the small intestine, it enters the epithelial cells by binding its outer shell protein Vp4 (adsorption protein) to the lactase on the intestinal villus epithelial cells. It proliferates and destroys the epithelial cells, causing them to shed. Due to the destruction of the villous epithelial cells, the amount of disaccharidases such as lactase decreases, leading to the obstruction of the conversion of lactose to other monosaccharides. The accumulation of lactose in the intestinal lumen causes high osmotic pressure in the lumen of the small and large intestines, causing water to move into the intestinal lumen, resulting in diarrhea and vomiting. Subsequently, the cuboidal epithelial cells from the bottom of the crypts move upwards and replace the shed villous epithelial cells. Since their cell function is not mature, they are still in a high-secretion, low-absorption state, leading to intestinal fluid retention and prolonging the duration of diarrhea. The non-structural protein NSP4 synthesized during the replication of the rotavirus plays a role of an enterotoxin in the pathogenic process of the rotavirus, causing an increase in intracellular Ca2+ levels and promoting the rise of cAMP levels in the small intestinal mucosa, also participating in the formation of diarrhea. Severe diarrhea and vomiting can lead to water and electrolyte imbalance and acidosis.

　　The disease is reversible pathological changes, and the mucosa often remains intact. The main damaged part is the small intestine. Biopsy shows that the villi of the small intestine are shortened and blunt, the lamina propria is infiltrated with mononuclear cells, the epithelial cells are irregular, showing cuboidal shape, with vacuoles or necrosis.

　　Children with low immunity and a few patients with immune deficiency diseases may develop severe complications if not treated in time.

　　1. It can be complicated with intussusception, rectal hemorrhage, hemolytic uremic syndrome, encephalitis, and Reye syndrome, and so on.

　　2. Severe cases can die due to complications such as dehydration, pneumonia, toxic myocarditis, and so on. Toxic myocarditis refers to myocarditis caused by toxins or toxic substances. In addition to the myocardial damage caused by toxins and endotoxins in infectious diseases such as diphtheria, typhoid fever, and bacillary dysentery, certain biological toxins such as snake venom, poisonous mushrooms, fugu, aconite, and certain drugs or chemical substances such as emetine, antimony compounds, organophosphorus, organomercury, arsenic, carbon monoxide, lead, and aminophylline can all cause myocardial damage and produce toxic myocarditis. Toxic myocarditis is often an important manifestation of systemic poisoning.

　　1. The incubation period of infant patients is 24-72 hours, and the onset is often acute. Vomiting is often the first symptom, accompanied by diarrhea several times a day, mostly large amounts of watery stool, yellow-green, with a foul odor, and may have a small amount of mucus, without pus and blood. It can present as pseudo-cholera diarrhea. Patients have low fever, rarely exceeding 38°C. In the early stage of the disease, most patients have runny nose, sneezing, and slight cough. More than half of the children have varying degrees of dehydration and acidosis. Severe dehydration can lead to deterioration of the condition within a few hours and death. Generally, fever and vomiting subside within 48 hours, while diarrhea can last for more than a week. In severe cases, patients may not tolerate carbohydrates and may take several weeks to half a year to recover.

　　Newborns can also be affected, with mild diarrhea, abdominal distension, and blood-stained stools. X-ray examination may show abnormal intestinal shape, and even intestinal perforation may occur.

　　The incubation period of adult patients is shortest for a few hours and longest up to one week, averaging 2-3 days. The disease often starts abruptly, with abdominal pain and diarrhea as the main symptoms, accompanied by weakness, nausea, vomiting, and so on. The stool is mostly yellow watery stool, without mucus and blood, diarrhea usually occurs 5-9 times or more per day, and in severe cases, it can reach more than 20 times per day. The bowel sounds are enhanced, and abdominal tenderness is prominent around the umbilicus. Some patients have varying degrees of dehydration, and most patients have normal body temperature, while a few patients have low fever. The course of the disease is short, generally 3-5 days, mostly self-limiting, and a few can last for more than 9 days.

　　Early detection and isolation of patients with rotavirus enteritis are essential, and the excrement of patients should be disinfected; attention should be paid to water and food hygiene, and tableware should be disinfected; the baby room should have strict disinfection and isolation measures, and breastfeeding of infants should be promoted; for children aged 6-24 months, oral administration of attenuated vaccines containing various types of rotavirus can stimulate the local production of IgA antibodies, which is currently the most effective preventive measure.

　　1. Routine examination

　　The total white blood cell count is usually normal, with a slight increase in a few cases, and there may be an increase in lymphocytes in the cell classification. Fecal examination: The appearance is yellow watery diarrhea, without mucus, pus, or blood, and microscopic examination usually shows no abnormalities.

　　2. Virus antigen detection

　　Electron microscopy for detecting viruses in feces: Electron microscopy makes a specific diagnosis by observing the typical morphology, with a positive rate of up to 90%; this method is fast and accurate, but the equipment is expensive and the operation requirements are high, so it is often used in epidemiological investigations. Detection of virus-specific antigens: Many immunological methods can be used to detect rotavirus-specific antigens, such as enzyme immunoassay (EIA), complement fixation test (CF), immunofluorescence (IF) method, etc., among which EIA has the highest specificity and sensitivity and is easy to operate.

　　3. Detection of viral nucleic acids in feces

　　Polyacrylamide gel electrophoresis, nucleic acid hybridization, and polymerase chain reaction (PCR) methods can be used, among which nucleic acid hybridization has high specificity and PCR has high sensitivity, and is often used in molecular epidemiological research.

　　4. Serological detection of rotavirus

　　Detect specific antibodies in the patient's serum using immunological methods such as EIA, such as the antibody titer of the double serum samples from the acute and convalescent phases of the disease showing a 4-fold increase, which has diagnostic significance.

　　Children with rotavirus enteritis should stop eating milk and disaccharide foods and avoid unclean food. Breast milk contains specific rotavirus IgA, and breastfed infants are less likely or not likely to have rotavirus enteritis, so breastfeeding is recommended for infants and young children.

　　There is no specific treatment for rotavirus enteritis, and symptomatic treatment is mainly used. Stop milk and disaccharide foods; use antiemetics and sedatives when vomiting and diarrhea are severe; oral or intravenous fluid replacement to correct electrolyte imbalance.

　　Antibiotics may cause diarrhea or promote the growth of drug-resistant bacteria, so even if the pathogenic bacteria of gastroenteritis are clear, antibiotics are usually not recommended. However, antibiotics can be used for infections by other pathogenic bacteria (such as Campylobacter, Shigella, Vibrio cholerae, etc.) or in patients with traveler's diarrhea.