Bacterial dysentery in children

　　First, the cause of the disease

　　1. Pathogen

　　It is a Shigella, belonging to the genus Shigella of the family Enterobacteriaceae. It is a Gram-negative, aerobic, non-flagellated, non-motile, non-capsulated, and non-spore-forming bacillus. It is about 1 to 3 μm long; it can survive in water for 5 to 9 days, in food for 10 days, and is extremely sensitive to sunlight, dying after 30 minutes of exposure; it can be killed immediately at 60% humidity in 10 minutes and at 100℃; it can survive for several months in cold and humid places. It can survive for 1 to 2 weeks on vegetables, fruits, food, and contaminated items. Benzalkonium bromide (new disinfectant), bleaching powder, peracetic acid, lime milk, and Lysol can all kill it. It grows well on 37% culture media. Pure culture can be obtained using deoxycholate SS medium and methylene blue agar medium. The xylose lysine deoxycholate agar medium has a higher positive rate.

　　2. Classification

　　According to the structure of the O antigen of the bacterial body, it can be divided into 4 groups: A, B, C, and D, and within the group, it is divided into 47 serotypes (including subtypes):

　　(1) Group A: Shigella, this group does not ferment mannitol, has no ornithine decarboxylase, and has no serological relationship with other groups. This group has 1 to 12 serotypes. Serotype 1 is Shigella, serotype 2 is Schmitz, and the rest are Shigella flexneri.

　　(2) Group B: Flexneri Shigella, ferments mannitol, has no ornithine decarboxylase, and there is cross-agglutination among different types. There are already 13 serotypes (including subtypes and variants).

　　(3) Group C: Boydii Shigella, ferments mannitol, has ornithine decarboxylase, and there is no cross-agglutination among different types. There are 1 to 18 serotypes.

　　(4) Group D: Sonne Shigella, ferments mannitol, has ornithine decarboxylase, and slowly ferments lactose. There is only 1 serotype. However, in recent years, it can be divided into 2 strains according to its ability to ferment lactose, and 16 types according to its ability to produce colibactin.

　　3. Epidemic Strains

　　The Shigella genus has a large number of strains. Before the 1940s, group A was the main epidemic strain, almost disappeared in the early 1960s, but suddenly broke out in Central America in 1969-1970, and then in Bangladesh, South Asia from 1972 to 1978, followed by India, Sri Lanka, Nepal, Bhutan, Myanmar, Thailand, and other countries. Group B has been dominant in developing countries since the 1950s. Group D has been the leading strain in many developed countries since the 1960s, accounting for more than 95%. In 1984, among the 2274 Shigella strains collected in 14 provinces and cities in China, group B accounted for 65.8%, followed by group D with 25.1%, group A1 with 8.3%, and group C with 0.8%. Groups B and D were the main epidemic strains in the Beijing area from 1980 to 1992. More group D strains than group B were found in children. In 1986-1988, 113 Shigella strains were detected in children under 5 years old in 7 provinces and cities with exemplary maternal and child health demonstration counties, with group B, serotypes 1 and 2 of Flexneri being the most common, accounting for 72.6%, followed by group D (Shigella sonnei) with 11.5%, group A (Shigella) with 5.3%; at the same time, 66 Shigella strains were detected in children under 5 years old in Beijing, with group D (Shigella sonnei) being the most common, accounting for 66.6%, followed by group B (Flexneri) with 28.8%, group C (Bordetella) with 4.5%, and no group A (Shigella) was found.

　　4. Research on Resistance

　　Recent studies from China have shown that the resistance of Escherichia coli to various antibacterial drugs is increasing day by day. Due to the different antibacterial drugs used in different regions, the reported resistance rates also vary. In 1988, a resistance monitoring project led by the Capital Institute of Pediatrics involved 7 provinces and 1 city, showing that the resistance rate to tetracycline reached 71.1% to 83.6%, sulfonamide 54.4% to 74.8%, chloramphenicol 33.9% to 35.8%, furazolidone (痢特灵) 53.6% to 100%, and ampicillin (氨苄青霉素) 49.1% to 97.1%. The following antibiotics maintain a lower resistance rate, gentamicin 29.2% to 32.9%, polymyxin E 20%, amikacin (丁胺卡那霉素) 12.7% to 5.2%, kanamycin 21.2% to 33.6%, and neomycin, due to its reduced use in recent years, the resistance rate has decreased to 12.0% to 17.9%. Quinolone drugs have a good effect on intestinal pathogenic bacteria. According to the resistance test results of Beijing 302 Hospital, the resistance rate is very low, pipemidic acid 3.9% to 5.7%, norfloxacin 4.1%, enoxacin (氟啶酸) 0.7% to 0.9%, and ciprofloxacin is 0. In recent years, due to frequent use, the resistance of commonly used quinolones has increased, with norfloxacin resistance rate rising to 26.5% to 39.5%, and ciprofloxacin rising to 9.8% to 12%. Quinolones for dysentery are still the first choice of drugs. Berberine for dysentery remains stable with moderate sensitivity. When used in combination with other antibiotics, it has a synergistic effect and reduces resistance. Third-generation cephalosporins have good sensitivity.

　　II, Pathogenesis

　　1, Pathogenesis

　　All dysentery bacilli can produce endotoxins, and Shigella can also produce exotoxins. The above dysentery bacilli can all cause both typical and toxic dysentery in clinical practice. Identification of the bacterial serotype helps trace the source of infection, transmission routes, and predict the prognosis, as well as the selection of antibacterial drugs.

　　After the dysentery bacteria enter the gastrointestinal tract through the mouth, they must break through the defense of the gastrointestinal tract to cause disease. Dysentery bacteria have strong acid resistance, so they are easy to invade the intestines from the stomach and quickly reproduce in the alkaline environment of the intestinal fluid. Dysentery bacteria rely on their own invasive force to directly invade the intestinal mucosal epithelial cells and reproduce within them. Then they enter the lamina propria to continue reproducing and cause inflammatory reactions in the colon. Dysentery bacteria are engulfed by phagocytes in the lamina propria, and a small number of dysentery bacteria reach the mesenteric lymph nodes, which are also quickly eliminated by the mononuclear phagocyte system, thus septicemia caused by dysentery bacilli is extremely rare.

　　2, Pathophysiological changes

　　In addition to the inflammation of the colonic tissue, it can also cause microcirculatory disorders in the lamina propria, leading to变性 and necrosis of epithelial cells, forming superficial ulcers, thus causing abdominal pain, diarrhea, urgent need to defecate, mucous and purulent stools, and so on.

　　(1) Acute bacillary dysentery: The lesions of acute bacillary dysentery often involve the entire colon, with the sigmoid colon and rectum being most prominent. In severe cases, it can extend to the lower part of the ileum. It is mainly characterized by exudative inflammation and can be divided into:

　　①The congestion and edema stage: Initially, catarrhal inflammation is present, characterized by congestion and edema of the mucosa and submucosa, as well as infiltration of neutrophils and increased mucus secretion. Further development leads to a large amount of fibrinopurulent exudate covering the surface, followed by necrosis of the mucosal surface tissue and the exuded cells, which fuse to form a layer of grayish-white bran-like adherent material, i.e., pseudomembrane. Under the pseudomembrane, the remaining mucosa shows dilated and congested blood vessels, along with many neutrophil infiltrations. The submucosa is extremely congested and edematous.

　　② Ulcer formation stage: After the pseudomembrane of the mucosal epithelium falls off, ulcers form. These ulcers are generally small in area and superficial, with irregular edges. Although they penetrate into the submucosal layer, they rarely invade the muscular layer, so they do not cause perforation.

　　③ Ulcer healing stage: With the improvement of treatment and human resistance, inflammation subsides, and ulcers gradually heal. Small ulcers can heal through the regeneration of mucosal epithelium, while large ulcers heal through the proliferation of fibrous connective tissue to form scars. Sometimes the mucosa around the scar tissue proliferates, presenting as polyps. The intestinal lesions vary due to different pathogenic bacteria. The acute atypical dysentery is not staged, and the lesions are relatively mild, with some only having congestion and edema of the intestinal mucosa.

　　(2) Pathological changes of chronic bacillary dysentery: The lesions are most common in the rectum and sigmoid colon, followed by the ascending colon and the lower end of the ileum. The edema and thickening of the intestinal mucosa can also form ulcers, which often do not heal completely. Sometimes, although gradually healed, due to the large area of the ulcer, it can form concave scars, with polyps forming around. Sometimes the scar tissue contracts, causing intestinal stricture. Some ulcers heal incompletely, and mucosal adenomatous cysts can be seen on the mucosa. The cysts can continuously excrete Shigella, causing the disease to recur.

　　In children with acute bacillary dysentery, if vomiting and diarrhea are severe, complications such as water and electrolyte imbalance (dehydration, acidosis, hypokalemia, hyponatremia, hypocalcemia, etc.) may occur. Chronic bacillary dysentery has more complications, mainly due to malnutrition and low immune function. The most common are malnutrition and malnutrition edema, deficiency of various vitamins and trace elements, manifested as dry eye disease, malnutrition anemia, rickets. In severe cases, beriberi and scurvy may occur. The latter is rarely seen in China. Deep ulcers in the intestinal tract can lead to massive intestinal bleeding, frequent diarrhea can lead to rectal prolapse, long-term use of antibiotics can lead to intestinal flora disorder or fungal infection. In some severe cases of malnutrition, intestinal ulcers may not heal for a long time, leading to intestinal perforation.

　　I. Incubation period

　　From a few hours to 8 days, most of them are 1-3 days.

　　II. Clinical classification of bacterial dysentery

　　According to the course of the disease and the condition, it can be divided into acute bacillary dysentery, chronic bacillary dysentery, and toxic dysentery. Since the condition of toxic dysentery is special and will be described later, let's discuss acute bacillary dysentery and the general course of chronic bacillary dysentery first.

　　1. Acute bacterial dysentery

　　(1) Typical dysentery: The onset of typical cases is acute, with fever, body temperature ranging from low fever to high fever, diarrhea, stool 10-30 times a day, feces containing mucus and pus, nausea, vomiting, intermittent abdominal pain, mild tenderness in the abdomen, sometimes the sigmoid colon can be palpated as spasmodic in the lower left abdomen, hyperactive bowel sounds, a feeling of urgent defecation after defecation, general weakness, decreased appetite, in infants and young children, there may be high fever convulsions. Most children with acute dysentery can gradually improve and recover within a few days after reasonable treatment, with a good prognosis. Older children have stools that form quickly, while infants may have loose stools for several days, which is related to the slower recovery of the intestinal function in infants and young children.

　　(2) Atypical dysentery: without fever or only slight fever, without toxic symptoms, mild diarrhea, loose stools, the stool contains only mucus without pus and blood. Only a positive stool culture can be diagnosed. During an epidemic, the number of such cases may exceed that of typical cases, as they have similar symptoms to general enteritis and are easy to be ignored, often becoming carriers of dysentery.

　　2. Chronic bacterial dysentery

　　Dysentery that lasts more than 2 weeks is called persistent dysentery, and dysentery that lasts more than 2 months is called chronic dysentery. The main causes are mainly due to thin constitution, malnutrition, rickets, or anemia, or due to the fact that such children have not received reasonable treatment, causing the disease course to be long, gradually thinning, and the stool contains a large amount of mucus, which may not contain pus and blood, or there may be alternating mucus and purulent blood stools. The stool can still culture Shigella, but the positive rate is significantly lower than that of acute dysentery. Children with chronic dysentery who have severe malnutrition often easily develop some crises, and children may die unexpectedly due to electrolyte imbalance (low sodium, low potassium, low calcium) and severe myocardial damage. Such children are rarely seen in China but are often seen in other developing countries. Sometimes the symptoms of chronic dysentery may suddenly worsen, presenting as an acute attack.

　　To prevent dysentery, it is necessary to fully mobilize the masses, carry out extensive health education, and adopt comprehensive preventive measures: strengthen the health management of children, pay attention to personal hygiene, wash hands with soap before meals and after defecation; improve drinking water hygiene, prevent water sources from being contaminated, and do not drink unboiled water; strengthen stool management, the stool of patients should be soaked in 1% bleaching powder or poured with boiling water or sprinkled with quicklime before being poured into the drain or septic tank, the diapers and underpants of the sick children should be boiled or soaked in boiling water before washing; strengthen dietary hygiene, do not eat spoiled food, and wash fruits and vegetables before eating raw; strengthen environmental hygiene, eliminate flies and maggots, cover food storage to prevent insect contamination; for patients, early detection, early diagnosis, early isolation, and early treatment are the key to controlling the spread of dysentery. Atypical cases, asymptomatic carriers (rare in childhood), and chronic dysentery are important sources of infection, and they should be detected early, isolated, and treated. It is necessary to pay attention to the precipitating factors that lead to chronic dysentery, such as rickets, malnutrition, and other complications, and they should be dealt with promptly.

　　Collective kitchen staff and nursery workers should have regular stool examinations, and bacterial cultures should be done when necessary. If carriers are found, they should be dealt with promptly.

　　Firstly, blood routine examination

　　In acute cases, the total white blood cell count and neutrophils increase, while in chronic cases, there is often mild anemia.

　　Secondly, stool examination

　　1. Routine stool examination

　　The appearance shows mucous stool and purulent blood stool, under the microscope, there are more red blood cells, white blood cells, and phagocytes.

　　2. Stool culture

　　More than 70% can be cultured to produce pathogenic bacteria, and the pus and blood parts of the stool should be cultured before the application of antibiotics, the specimen should be fresh, and the positive ones should be drug sensitivity test.

　　3. Feces bacterial antigen detection

　　Fluorescent antibody staining method, immunofluorescence table bacterium method, latex agglutination test, synergistic agglutination test, PCR direct detection method, etc., are rapid, sensitive, and simple diagnostic methods.

　　Leeks, mutton, chili, fresh chili powder, strong tea, alcohol, various coffee drinks are all strong stimulants, causing vasoconstriction, making the mucosa congested, edematous, and damaged, so they should be avoided.

　　In addition, during the recovery period of patients with bacterial dysentery, due to weak digestion, it is still necessary to avoid raw and cold, hard, cool and slippery foods, such as cold dishes, beans, cold drinks, alcohol, melons and fruits, etc.

　　First, treatment

　　1. Acute bacterial dysentery

　　The focus is on controlling infection, doing a good job of fluid therapy and symptomatic treatment.

　　(1) Antimicrobial therapy: Since the widespread use of sulfonamide drugs and antibiotics, the resistance rate of Shigella has increased year by year. The bacteria are resistant to most of the sulfonamide drugs, chloramphenicol, tetracycline, streptomycin, furazolidone (Shidetong) and ampicillin (Ampicillin) (see pathogeny). According to the results of current drug sensitivity tests, the sensitive and effective drugs are as follows:

　　Quinolone drugs are relatively sensitive and are recommended as the first choice. As for the toxic reactions of quinolone drugs in children, in the 1970s, American scholars found joint cartilage damage in small animal experiments, while British scholars did not find skeletal damage in infants using the first generation quinolone drug naftidrofuryl acid, and considered there is a racial difference. In the following years, there have been no skeletal damage found in clinical applications in China, and many clinical data abroad show that the application of quinolone drugs in children is not consistent with experimental animals, showing a certain degree of safety. The Chinese Journal of Pediatrics (1996) organized a national expert discussion, believing that quinolone drugs should not be banned for children, but the indications should be strictly controlled, the dose should not exceed 10～15mg/kg per day, and the course should not exceed 7 days.

　　Norfloxacin (Norfloxacin, Furoxacin): 10～15mg/(kg·d), taken orally. The course is 5～7 days.

　　Ciprofloxacin (Ciprofloxacin, Ciprofloxacin): 10～15mg/(kg·d), taken orally in three doses. It can also be diluted with isotonic sodium chloride or glucose to 100～300ml for intravenous infusion, with infusion time not less than 30min.

　　Pipemidic Acid: 15～30mg/(kg·d), taken orally in three doses. As the second generation of quinolones, its efficacy is inferior to that of the above third generation quinolones, with relatively more side effects, and it is tend to be phased out.

　　Berberine (Coptis): 10～20mg/(kg·d), taken orally in three doses, for a course of 7 days.

　　Sulfamethoxazole/Trimethoprim (Combination Novomycin): 50mg/(kg·d), taken orally in two doses, for a course of 7 days.

　　⑥ Third-generation cephalosporins such as cefotaxime sodium (also known as cefotaxime sodium or Claforan), ceftriaxone sodium (also known as ceftriaxone sodium or Rocephin), etc., 100～150mg/(kg·d), administered intravenously twice a day, for severe patients who cannot take oral medications. Cefixime (cefixime, Siflox) can be taken orally at 3～6mg/(kg·d), taken twice a day.

　　⑦ Paromomycin (Paromycin): 40mg/(kg·d), taken 3～4 times orally.

　　⑧ Other antibiotics: Gentamicin, 10,000～20,000U/(kg·d), taken 3～4 times orally. Polymyxin E: 50,000～100,000U/(kg·d), taken 3～4 times orally. Oral drugs are not absorbed in the intestines and have no side effects. However, due to the lesions of dysentery invading the intestinal mucosa, their efficacy is not as good as systemic medications that can be absorbed.

　　(2) Fluid therapy: Correct the dehydration in a timely manner according to the degree of dehydration in the child (refer to the fluid therapy for pediatric diarrhea).

　　(3) Symptomatic treatment:

　　① Fever: >38.5℃ should be treated with aspirin or acetaminophen (paracetamol).

　　② Vomiting: Give domperidone (Motilium) orally, 0.3mg/(kg·time).

　　③ Abdominal pain: For mild cases, give scopalamine or atropine sulfate (654-2) orally. For severe cases, give atropine sulfate (654-2) intramuscularly, 1mg/(kg·time).

　　(4) Traditional Chinese medicine treatment: Traditional Chinese medicine refers to acute bacillary dysentery as damp-heat diarrhea, and uses Ge Gen, Huang Qin, Huang Lian, Ma Chi Xian, Fu Ling, and Che Qian Zi in the Ge Gen, Huang Qin, and Huang Lian decoction. For vomiting, add Ban Xia and Sheng Jiang. For abdominal pain, add Mu Xiang, Bai Shao, and Yuan Hu.

　　(5) General therapy and dietary management: The child should rest in bed, and gastrointestinal detoxification and isolation should be carried out according to local conditions. The child should continue to eat, and all the food they have eaten before can be eaten. For those with severe vomiting, short-term fasting can be given intravenous infusion.

　　2. Treatment of protracted and chronic dysentery

　　(1) Antimicrobial therapy: Similar to acute dysentery, it is best to culture the pathogenic bacteria and select antibiotics based on drug sensitivity tests. It is crucial to avoid blind and excessive use of antibiotics, as this can lead to intestinal flora disorder, microecological imbalance, and反而 promote the protraction of diarrhea.

　　(2) Fluid therapy: Protracted diarrhea in dysentery often accompanies malnutrition, with low sodium, low potassium, and usually presenting with hyponatremia and hypokalemia. Therefore, blood biochemical tests should be performed, and fluid replacement should be administered according to the nature of water and electrolyte disturbances.

　　(3) Nutritional therapy: Protracted and chronic dysentery often has nutritional disorders, so fasting is harmful. Improving the nutritional status of the child in a short period of time is the key to recovery from the disease, and it is necessary to provide enough calories. Protein supplementation helps in the disappearance of edema, the formation of antibodies, and the healing of lesions. Generally, it should not be less than 3g/(kg·d), and gradually increased to 4.5～5g/(kg·d). In addition, a variety of vitamins and trace elements should be provided. Intravenous nutrition, blood transfusion, or plasma transfusion should be given if necessary.

　　(4) Microecological Therapy: Many of these children have intestinal flora disorders and microecological imbalance. The addition of probiotics or lactic acid bacteria and other microecological preparations helps to restore intestinal microecological balance and rebuild the natural barrier of the intestines to promote recovery from the disease. However, attention should be paid to the quality of the preparation; preparations without sufficient amounts of viable bacteria are ineffective.

　　(5) Traditional Chinese Medicine Treatment: Traditional Chinese medicine believes that chronic diarrhea must be deficiency, and chronic dysentery belongs to spleen and stomach deficiency-cold diarrhea or spleen deficiency diarrhea according to traditional Chinese medicine syndrome differentiation. The specific differentiation and treatment with herbs are as follows:

　　①Spleen and stomach deficiency-cold diarrhea: Suitable for chronic dysentery after acute dysentery.

　　Symptoms: The course of the disease is more than 2 weeks, with varying degrees of severity, loose stools, pale and odorless, anorexia, yellowish complexion, pale tongue, thin and white coating, and fine and slippery pulse.

　　Treatment principle: Warming the middle-jiao and strengthening the spleen, astringing and stopping diarrhea. Prescription: Modified桃花汤.

　　Commonly used drugs: Myristica fragrans, Syzygium aromaticum, ferric pyrophosphate, Codonopsis pilosula, Atractylodes macrocephala, Atractylodes lancea, Poria, Dioscorea opposita, Punica granatum peel, Gastrodia elata tuber, and Prunus mume.

　　②Spleen deficiency diarrhea: Suitable for chronic dysentery with the following symptoms:

　　Symptoms: The course of the disease is protracted, with varying degrees of severity, onset and remission, loose stools, with milk residue or undigested food, pale and odorless, anorexia, fatigue, and emaciated or虚胖. The tongue is pale, the coating is thin and white, and the pulse is slow and weak.

　　Treatment principle: Strengthening the spleen and Qi, astringing and stopping diarrhea. Prescription: Modified Shen Ling Bai Zhu Powder.

　　Commonly used drugs: Codonopsis pilosula, Poria, Atractylodes macrocephala, Atractylodes lancea, Dioscorea opposita, Citrus reticulata Blanco, Cinnamomum cassia bark, or Gastrodia elata tuber, and ferric pyrophosphate.

　　Protrusion of the rectum: Add Astragalus and Cimicifuga.

　　II. Prognosis

　　Acute bacterial dysentery can recover quickly if treated promptly with sensitive antimicrobial drugs, and the prognosis is good. A study by Beijing 302 Hospital using a placebo showed that 70% of patients could recover spontaneously without antibiotic treatment. Severe malnutrition, low immune function in children infected with dysentery or with drug-resistant strains can lead to prolonged illness and severe consequences. In terms of various pathogenic bacteria, Shigella has the strongest virulence, followed by Flexneri, but sometimes infections caused by Flexneri can also be very severe. The infections caused by Shigella sonnei are generally mild, but if they cause toxic dysentery, they can also be severe.