| disease | Bacterial Dysentery |
| alias | Bacillary Dysentery |
Bacterial dysentery (bacillary dysentery) is a common acute intestinal infectious disease caused by dysentery bacilli, characterized by purulent inflammation of the colon as the main pathological change. It presents with clinical manifestations such as systemic toxic symptoms, abdominal pain, diarrhea, tenesmus, and the expulsion of pus and bloody stools.
bubble_chart Epidemiology
The disease occurs throughout the year but is more prevalent in summer and autumn, and is found worldwide.
- Source of infection: Patients and carriers, among which atypical cases and chronic sexually transmitted disease cases are particularly significant epidemiologically.
- Source of infection: Mainly transmitted orally through contaminated food, drinking water, hands, etc. During epidemic seasons, outbreaks can occur through food or water. The former is caused by consuming items contaminated by hands or flies, while the latter results from water sources polluted by feces leading to waterborne transmission. In non-epidemic seasons, infection can occur through contact with objects contaminated by patients or carriers.
- Population susceptibility: Regardless of age or gender, everyone is generally susceptible to the disease. After infection, only short-lived and unstable group and type immunity is produced, making reinfection or relapse likely.
Dysentery bacilli are Gram-negative facultative bacteria, non-motile, and grow well on ordinary culture media, with an optimal temperature of 37°C. They can survive for about 10 days in fruits, vegetables, and pickles; up to 24 days in milk; and for several weeks under dark, damp, or frozen conditions. Direct sunlight has a sterilizing effect, and heating at 60°C for 10 minutes kills them. Common disinfectants can also eliminate them.
All dysentery bacilli can produce internal toxins, cytotoxins, and enterotoxins (exotoxins). Shigella dysenteriae can also produce neurotoxins. Shigella species possess somatic O antigens and surface K antigens, which are specific to their groups and types. Based on generation and transformation reactions and antigen composition, dysentery bacilli can be divided into 4 groups:- Group A: Includes Shigella dysenteriae and its serotypes 1–15;
- Group B: Includes Flexneri and its serotypes: 1a–c, 2a–b, 3a–c, 4a–c, x, y, etc.;
- Group C: Includes Boydii and its serotypes 1–18;
- Group D: Includes Sonnei.
Dysentery bacilli have the ability to adhere to and invade the epithelial cells of the colon mucosa. Only strains that possess invasive capabilities toward the epithelial cells of the intestinal mucosa can cause typical lesions in the colon, whereas strains lacking such invasive abilities do not induce lesions. Gastric acid, short-chain fatty acids produced by intestinal flora, hydrogen peroxide, and large intestine bacteriocins, among others, can kill or antagonize dysentery bacilli. Secretory IgA and other specific antibodies produced by the human intestinal mucosa play a crucial role in repelling dysentery bacilli. Certain factors that significantly reduce the body's systemic and gastrointestinal local defense functions, such as chronic sexually transmitted diseases, excessive fatigue, overeating, and digestive tract disorders, facilitate the invasion of dysentery bacilli into the intestinal mucosa, leading to disease.
Toxic bacillary dysentery: The systemic toxic symptoms are inconsistent with the severity of intestinal lesions. Despite the presence of toxemia symptoms, the intestinal inflammatory response is extremely mild. In addition to the effects of dysentery bacilli internal toxins, it may be related to certain children having a specific constitution that elicits a strong reaction to bacterial toxins, leading to microvascular spasms, ischemia, and hypoxia. This can result in DIC, failure of vital organ functions, cerebral edema, and brain herniation.
bubble_chart Pathological Changes
Intestinal lesions are mainly distributed in the colon, most prominently in the rectum and sigmoid colon, but are also occasionally found in the ascending colon and the lower end of the ileum. The pathological changes in the acute phase consist of diffuse fibrinous exudative inflammation, with the intestinal mucosa showing diffuse congestion and edema, secreting large amounts of exudate, and occasionally forming microabscesses. Necrotic tissue sloughs off to form ulcers, which vary in depth but are confined to the submucosal layer, making intestinal perforation and hemorrhage rare. About one week after onset, the body produces antibodies, and the ulcers gradually heal. Toxins can also cause visceral lesions, manifesting as degeneration of the liver, renal tubules, myocardium, and brain cells. In toxic bacillary dysentery, colonic lesions are mild, but significant systemic changes include widespread small vessel spasms and increased exudation, with neural degeneration, infiltration, and punctate hemorrhage in the brainstem. The adrenal cortex may atrophy and hemorrhage. In chronic cases, the intestinal wall thickens, with polypoid hyperplasia at the edges of the ulcers. Healing leads to scar formation, resulting in intestinal stenosis.
The incubation period ranges from several hours to 7 days, with most cases occurring within 1 to 2 days. Shigella infections generally present with severe symptoms, while those caused by Shigella sonnei are milder, and infections by Shigella flexneri fall between the two but are more prone to becoming chronic. Clinically, it is often divided into acute and chronic intermediate stage [second stage].
(1) Acute Bacillary Dysentery
1. Typical Type: Sudden onset with fear of cold, shivering, and high fever, followed by abdominal pain, diarrhea, and tenesmus. Bowel movements occur 10–20 times a day, presenting as bloody or purulent stools with small volume. Tenderness in the left lower abdomen is accompanied by hyperactive borborygmus. Recovery usually occurs within 1–2 weeks, or the condition may transition to chronic.
2. Mild Type: Systemic toxic symptoms and intestinal manifestations are milder. Abdominal pain is not prominent, with diarrhea occurring fewer than 10 times daily. Stools are pasty or watery, containing small amounts of mucus, and tenesmus is not obvious. Vomiting may occur, and the course lasts 3–6 days, often mistaken for enteritis or colitis.
3. Toxic Type: More common in children aged 2–7 with a strong constitution. Sudden onset with high fever, lethargy, grayish complexion, cold extremities, weak and shallow breathing, recurrent convulsions, unconsciousness, and mottled skin. This may lead to respiratory and circulatory failure, but intestinal symptoms are mild or even absent (e.g., no abdominal pain or diarrhea). Rectal swabs or saline enemas are often required to collect stool samples, revealing mucopurulent stools with numerous pus cells and red blood cells under microscopy. Clinical manifestations can be categorized as: ① Shock Type: Primarily manifests as peripheral circulatory failure, mottled skin, cyanosis, significantly decreased or unmeasurable blood pressure, and varying degrees of impaired consciousness. ② Cerebral Type: Dominated by severe neurological symptoms, including cerebral edema and increased intracranial pressure, which may lead to brain herniation. Clinical features include convulsions, unconsciousness, and respiratory failure. Early signs include drowsiness, dysphoria, frequent vomiting, and rapid breathing. Late stage [third stage] presents with confusion, frequent convulsions, elevated blood pressure, dilated or unequal pupils, sluggish or absent light reflex, irregular breathing patterns (e.g., sighing respiration), eventually slowing or stopping. ③ Mixed Type: The most perilous prognosis, combining features of circulatory and respiratory failure.
(2) Chronic Bacillary Dysentery: A病程 exceeding 2 months is termed chronic bacillary dysentery. Factors predisposing to chronicity include: ① Inadequate treatment during the acute phase or infection with drug-resistant strains. ② Malnutrition. ③ Comorbid chronic conditions such as gastrointestinal disorders, cholecystitis, intestinal Chinese Taxillus Herb parasitosis, or immune dysfunction (e.g., SIgA deficiency). ④ Shigella flexneri infection.
1. Chronic Persistent Type: Following acute bacillary dysentery, symptoms persist long-term with varying degrees of abdominal discomfort, prolonged diarrhea, or alternating diarrhea and constipation. Stools frequently or intermittently contain mucus or blood, and intermittent bacterial shedding may occur over extended periods.
2. Chronic Latent Type: History of acute bacillary dysentery with prolonged absence of clinical symptoms, but positive stool cultures and abnormal findings on sigmoidoscopy. This type also serves as a significant pestilence source.
3. Acute Exacerbation Type: Chronic patients may experience acute exacerbations triggered by factors such as dietary indiscretion, cold exposure, or fatigue, with symptoms generally milder than during the acute phase.
bubble_chart Auxiliary Examination
(1) Blood Test: In acute sexually transmitted disease cases, there is a moderate increase in the total white blood cell count and neutrophils. Chronic sexually transmitted disease patients may exhibit grade I anemia.
(2) Stool Examination: Typical dysentery stools are devoid of fecal matter, scant in quantity, bright red and mucoid, and odorless. Microscopic examination reveals numerous pus cells and red blood cells, along with macrophages. Pathogenic bacteria can be detected through culture. However, improper sampling, prolonged storage of specimens, or prior antibiotic treatment in patients often yield unsatisfactory culture results. Commonly used differential culture media include SS agar and MacConkey agar.
(3) Other Examinations: Fluorescent antibody staining is one of the rapid diagnostic methods and is more sensitive than cell culture. In China, the immunofluorescent bacterial agglutination method is employed, which is simple, highly sensitive, and specific. Diagnosis can be made within 8 hours of sampling, and the bacteria can be further cultured for drug sensitivity testing. Sigmoidoscopy in the acute phase shows diffuse congestion, edema, significant exudation, and superficial ulcers in the intestinal mucosa, sometimes with pseudomembrane formation. In the chronic phase, the intestinal mucosa appears granular, with visible ulcers or polyps. Culturing secretions scraped from the lesions can improve detection rates. Additionally, X-ray barium studies in chronic patients may reveal intestinal spasms, motility changes, loss of haustration, luminal narrowing, thickening of the intestinal mucosa, or segmental changes. In recent years, the staphylococcal co-agglutination test has been used as a rapid diagnostic tool for bacillary dysentery, demonstrating good sensitivity and specificity.
During the epidemic season, the possibility of bacillary dysentery should be considered in individuals presenting with abdominal pain, diarrhea, and purulent bloody stools. Most patients in the acute phase exhibit fever, which often precedes gastrointestinal symptoms. A history of past episodes is crucial for chronic cases, and stool smear microscopy and bacterial culture aid in confirming the diagnosis. Sigmoidoscopy and X-ray barium examinations hold certain value in differentiating chronic bacillary dysentery from other intestinal disorders. In the epidemic season, children who suddenly develop fever and convulsions without other symptoms must be evaluated for toxic bacillary dysentery. Rectal swab specimens or saline enema samples should be collected as early as possible for smear microscopy and bacterial culture.
bubble_chart Treatment Measures
(1) Treatment of Acute Bacillary Dysentery
1. General and Symptomatic Treatment Patients should be isolated via the gastrointestinal route (until symptoms disappear and stool cultures are negative twice consecutively) and advised to rest in bed. The diet should generally consist of liquids or semi-liquids, avoiding foods that are high in residue, oily, or irritating. During the stage of convalescence, normal diet can be gradually resumed based on individual conditions. For those with signs of dehydration, oral rehydration salts can be administered. If oral intake is not possible due to vomiting, etc., intravenous infusion of normal saline or 5% glucose saline can be given, with the dosage adjusted according to the degree of dehydration to maintain water and electrolyte balance. For those with acidosis, alkaline fluids should be administered as appropriate. For spasmodic abdominal pain, atropine and abdominal hot compresses can be used, but drugs that significantly inhibit intestinal motility should be avoided to prevent prolonging the course of the disease and the duration of bacterial excretion. Although such drugs may relieve intestinal spasms and alleviate diarrhea, and to some extent reduce intestinal secretion, diarrhea is actually a manifestation of the body's defense mechanism and helps eliminate a certain number of pathogens and enterotoxins. Therefore, antispasmodics or drugs that inhibit intestinal motility should not be used long-term. Especially for patients with high fever, toxemia, or mucopurulent bloody stools, their use should be avoided to prevent worsening the condition. Such drugs should also not be used in infants and young children. Drugs that can act on and affect intestinal motility include atropine, belladonna mixture, pethidine, codeine, morphine, camphor tincture, diphenoxylate, and loperamide hydrochloride.
2. Etiological Treatment In recent years, drug-resistant strains of dysentery bacilli, especially multidrug-resistant strains, have been increasingly observed. When pathogenic bacteria are detected in stool cultures, drug sensitivity tests should be performed to guide rational drug use.
⑴ Sulfonamides: Sulfonamides Yaodui have antibacterial activity against dysentery bacilli, but synergistic effects can be achieved when combined with trimethoprim (TMP). For example, compound sulfamethoxazole (SMZ-TMP) tablets can be taken twice daily, two tablets each time (dosage reduced for children), with a treatment course of one week. Contraindications include severe liver or kidney disease, sulfonamide allergy, and leukopenia. In recent years, drug-resistant strains have increased; if efficacy is poor or absent, other antibacterial drugs should be used instead.
⑵ Quinolones: These drugs act on bacterial DNA gyrase, have bactericidal effects, and minimal side effects, making them the first-choice drugs for adult bacillary dysentery. However, as they may affect bone development in children, they are contraindicated for preschool children. Adult dosages are as follows: pipemidic acid 2g daily, divided into three oral doses, for 5–7 days; norfloxacin 600–800mg daily, divided into 2–3 oral doses, with the same treatment course; enoxacin, ofloxacin, and ciprofloxacin 600mg daily, divided into two oral doses, for 3–5 days.
⑶ Antibiotics: Oral administration is preferred whenever possible. Chloramphenicol and tetracyclines have poor activity against dysentery bacilli, and drug-resistant strains are increasingly common. Thus, in some large cities where antibiotics are widely used, chloramphenicol or tetracyclines should not be the first-choice drugs for acute bacillary dysentery, though they may still be used in rural areas. Furazolidone remains effective for this condition, but side effects such as vomiting are significant. For those who cannot tolerate oral administration, alternatives like gentamicin or ampicillin can be used.
The dose of gentamicin is 160–240mg/d, divided into two intramuscular injections; for children, 3–5mg/kg daily, divided into two intramuscular injections. The dose of kanamycin is 1–1.5g/d; for children, 20–30mg/kg daily, divided into two doses. The dose of ampicillin is 2–6g/d; for children, 50–100mg/kg daily, divided into four doses. The treatment course is 5–7 days for all. If necessary, TMP 0.1g twice daily can be added to enhance efficacy. In recent years, strains resistant to gentamicin and ampicillin have increased. Some have used amikacin at 15mg/kg daily for adults and 100mg/kg for children to treat bacillary dysentery with good results, but most authors believe this drug should not be a "first-line agent" to avoid increasing resistant strains.
(4) Chinese medicinals: Coptis Rhizome 0.3-0.4g, 4 times daily; Andrographis paniculata 4g, 4 times daily. The treatment course is 7 days for both.
(2) Treatment of Toxic Bacillary Dysentery This type progresses rapidly, and comprehensive measures should be taken promptly to rescue the patient based on the condition.
1. Antibacterial Treatment Use gentamicin or amikacin combined with ampicillin for intravenous injection. The dosage and administration are the same as in the acute phase. After the toxic symptoms improve, switch to general treatment for acute bacillary dysentery or change to oral compound sulfamethoxazole (SMZ-TMP) or norfloxacin. The total treatment course is 7–10 days. Fluoroquinolone intravenous injection and cefoperazone may also be used.
2. Treatment of High Fever and Convulsions High fever can easily lead to convulsions, worsening cerebral hypoxia and brain edema. Use metamizole and physical cooling. If ineffective or accompanied by restlessness, repeated convulsions, or twitching, administer sub-hibernation therapy with chlorpromazine and promethazine, 1–2 mg/kg each intramuscularly, or intravenously if necessary. After the condition stabilizes, extend the interval to one injection every 2–6 hours. Generally, 5–7 doses are sufficient before discontinuation, aiming to maintain body temperature around 37°C as quickly as possible. Chlorpromazine has a sedative effect on the central nervous system and reduces temperature, lowering tissue oxygen consumption and inhibiting the vasomotor center, which dilates small arteries and veins, thereby improving microcirculation and enhancing organ blood perfusion. Diazepam, chloral hydrate, or sodium barbital may also be administered.
3. Management of Circulatory Failure
(1) Volume Expansion: Due to reduced effective circulating blood volume, replenish blood volume by rapidly infusing low-molecular-weight dextran or glucose-sodium chloride solution intravenously. The initial dose is 10–20 ml/kg, with a total daily fluid volume of 50–100 ml/kg, adjusted based on the patient’s condition and urine output. If acidosis is present, administer 5% sodium bicarbonate (see the "Septic Shock" section for details).
(2) Use of Vasoactive Drugs: For microvascular spasms, use vasodilators such as tangut anisodamine. The adult dose is 10–20 mg per dose, and the pediatric dose is 0.3–0.5 mg/kg per dose. Alternatively, atropine may be used (adult dose: 1–2 mg per dose; pediatric dose: 0.03–0.05 mg/kg per dose). The interval and frequency of injections depend on the severity and urgency of symptoms. For mild cases, administer intramuscularly or intravenously every 30–60 minutes; for severe cases, administer intravenously every 10–20 minutes. Discontinue when the complexion turns rosy, circulation and breathing improve, limbs become warm, and blood pressure rises. Generally, 3–6 doses are effective. If peripheral circulation does not improve after the above treatments, consider combining dopamine with aramine.
(3) Cardiac Support: For left heart failure and pulmonary edema, administer cedilanid or similar treatments.
(4) Anticoagulation Therapy: For DIC, use heparin anticoagulation therapy, with dosage and course as for septic shock.
(5) Use of Adrenal Cortical Hormones: Administer hydrocortisone intravenously at 5–10 mg/kg daily to alleviate toxic symptoms, reduce peripheral vascular resistance, strengthen myocardial contraction, relieve brain edema, protect cells, and improve metabolism. The adult dose is 200–500 mg/day, generally for 3–5 days.
4. Treatment of Respiratory Failure Maintain airway patency, provide oxygen, and administer dehydration therapy (e.g., mannitol or sorbitol). Strictly control fluid intake. If necessary, administer lobeline or nikethamide intramuscularly or intravenously. Critically ill cases require respiratory monitoring, endotracheal intubation, or mechanical ventilation.
5. Correction of Edema and Electrolyte Imbalances Replenish lost fluids and potassium/sodium ions, but cautiously avoid excessive volume or rapid infusion to prevent pulmonary or brain edema.
(3) Treatment of Chronic Bacillary Dysentery Requires long-term, systematic treatment. Conduct stool cultures and bacterial sensitivity tests as frequently as possible. If necessary, perform sigmoidoscopy as a reference for drug selection and efficacy evaluation.
1. Application of Antibiotics First and foremost, it is essential to promptly isolate, identify, and conduct drug sensitivity testing for the pathogenic bacteria. Antibiotics to which the pathogenic bacteria are insensitive or those that have proven ineffective in the past should not be used. Most experts recommend the combined use of two different classes of antibacterial drugs, with adequate doses and a relatively long treatment course, which may need to be repeated for 1–3 cycles. The drugs available for selection are the same as those for acute bacillary dysentery.
2. Vaccine Therapy Autologous or mixed vaccines are administered subcutaneously every other day. The dose starts at 0.25 ml per day and gradually increases to 2.5 ml, with a treatment course lasting 20 days. The vaccine injection can induce systemic reactions, leading to local congestion, promoting regional blood flow, enhancing leukocyte phagocytosis, and facilitating the penetration of antibiotics into the affected area to exert their efficacy. Additionally, phage therapy may also be attempted.
3. Local Coloclysis Therapy This involves applying higher concentrations of medication directly to the affected area to enhance bactericidal effects and stimulate the regeneration of granulation tissue. It is generally performed as a retention enema. Commonly used medications include 100 ml of 5% garlic extract or 100–200 ml of 0.5–1% neomycin, administered once daily for a treatment course of 10–15 sessions. Some advocate adding 0.25% procaine or 25 mg of hydrocortisone to the enema solution to potentially improve efficacy.
4. Management of Intestinal Disorders Sedatives, antispasmodics, or astringents may be used as appropriate. For intestinal disorders following prolonged antibiotic therapy, lactasin, small doses of promethazine, compound diphenoxylate, or acupuncture at the Zusanli point may be administered. Alternatively, a retention enema with 100–200 ml of 0.25% procaine solution can be given nightly for a course of 10–14 days.
5. Management of Intestinal Dysbiosis Dairy and soy products should be restricted. For cases with reduced Escherichia coli counts, lactose and vitamin C may be given; for reduced enterococci, folic acid may be administered. Lactasin (containing anaerobic lactobacilli) at 4–6 g, Bacillus subtilis tablets (5 billion bacteria per tablet), or Bacillus subtilis solution (300 million viable bacteria per ml) at 100–200 ml may be used for enemas nightly for 2–3 weeks to promote anaerobic bacterial growth and restore intestinal flora balance. Bifico and Lizhu Changle can also regulate intestinal flora, with the former taken at 3–5 capsules per dose and the latter at 2 capsules per dose, both 2–3 times daily.
The treatment outcomes for chronic bacillary dysentery remain unsatisfactory. If significant symptoms persist and stool cultures are positive, isolation and treatment are necessary. Additionally, underlying factors contributing to chronicity, such as Chinese Taxillus Herb infestation or gastritis, should be investigated, and appropriate treatment for associated conditions should be provided. Given the prolonged course of chronic bacillary dysentery and its tendency for acute symptoms to resolve spontaneously, repeated stool cultures are essential to evaluate treatment efficacy.
Efforts should focus on three aspects: controlling the source of pestilence, cutting off transmission routes, and enhancing human resistance.
- Early detection of patients and carriers, timely isolation, and thorough treatment are crucial measures for controlling bacterial diseases. Personnel working in the catering industry, childcare, and water plants require longer-term follow-up and, if necessary, temporary suspension from their positions.
- To cut off transmission routes, implement the "three controls and one elimination" (i.e., managing water, feces, and food, as well as eliminating flies), and cultivate the habit of washing hands before meals and after using the toilet. Regular checks for carrier status should be conducted for staff in the catering industry and child institutions. Carriers should be treated immediately and temporarily reassigned.
- Protecting susceptible populations: Oral administration of live attenuated vaccines, such as the non-pathogenic but protective E.coli strain, can achieve an efficacy rate of 85–100%. Multivalent dysentery live vaccines are already being produced domestically.
During the stage of convalescence or the acute phase, multiple exudative large joint arthritis may occasionally occur, with joint redness and swelling, which subsides spontaneously within weeks. Severe cases in pregnant women may lead to late abortion or premature labor. Chronic bacillary dysentery with ulcerative colonic lesions may be complicated by malnutrition, anemia, vitamin deficiency, and neuroGuanneng symptoms. It can also cause hemolytic uremic syndrome, Reiter's syndrome, leukemoid reactions, etc. Pediatric patients may develop complications such as otitis media, angular cheilitis, and prolapse of the rectum. Septicemia is a rare complication, presenting with dual manifestations of bacillary dysentery and septicemia, but the condition is more severe with a high fatality rate, especially in infants under 1 year of age.
Acute bacillary dysentery should be differentiated from the following diseases.
- Amebic dysentery: The onset is generally slow, with few symptoms of toxemia, a milder sense of tenesmus, and fewer bowel movements. Abdominal pain is mostly on the right side. In typical cases, the stool appears like jam and has a foul odor. Microscopic examination reveals only a few white blood cells and red blood cells clumped together, often with Charcot-Leyden crystals, and amoebic trophozoites can be found. Sigmoidoscopy shows that the mucous membrane is mostly normal, with scattered ulcers. This disease is prone to complicating liver abscesses.
- Epidemic encephalitis B: The manifestations and epidemic season of this disease are similar to those of bacillary dysentery (severe or toxic type), but the latter has a more acute onset, progresses rapidly, and is prone to complicating shock. A warm saline enema can be performed for microscopic examination and bacterial culture.
- In addition, this disease should also be differentiated from Salmonella infection, Vibrio parahaemolyticus food poisoning, large intestinal bacillus diarrhea, Campylobacter jejuni enteritis, and viral enteritis. Chronic bacillary dysentery should be differentiated from chronic schistosomiasis, intestinal cancer, and nonspecific ulcerative colitis.
