Shigellosis

Introduction to Shigella It is a common intestinal infectious disease caused by Shigella. It used to be called bacterial dysentery (abbreviated as bacillary dysentery). Inflammation and ulceration of the colonic mucosa are the main pathological changes. Generally susceptible. There are two peaks in the age distribution. The first peak is preschool children, especially those under 3 years old. The second peak is young adults (20-40 years old), which may be related to increased opportunities for contact at work. Any factor that is sufficient to reduce resistance, such as malnutrition and overeating, is conducive to the occurrence of bacillary dysentery. Clinically, it can be seen that chills and high fever, abdominal pain, diarrhea, pus and bloody stools, and urgency and weight. It is distributed throughout the year and can be popular in summer and autumn. basic knowledge The proportion of illness: 0.1%-0.3% Susceptible people: no specific population Mode of infection: digestive tract spread Complications: bacteremia, hemolytic uremic syndrome, arthritis

Cause of Shigella

Antigen structure (20%):

According to the classification of the International Society for Microbiology in 1985, the pathogenic Shigella can be divided into four groups of 42 serotypes (10 in group A, 13 in group B, 18 in group C, and 1 in group D), Shigella Lipopolysaccharide is composed of lipid A, core polysaccharide and O-specific side chain. O antigen is the basis of its typing. The bacterium of Fusarium oxysporum O is encoded by chromosome, and the antigen of Song bacterium is encoded by the molecular weight of 120×106. In addition to the chromosomal coding, Shiga type I bacterium O antigen requires a small plasmid. Each group of Shigella has a complex antigenic configuration, and the serological specificity of each group has cross-reactivity, such as Fucobacterium. When the phage is integrated into the chromosome, the type conversion can occur, and after the plasmid of Shigella and Songella is lost, the colony changes from a smooth type to a rough type, that is, the pathogenicity is lost.

Resistance (25%):

Shigella is present in the feces of patients and carriers, and has strong viability in vitro. The resistance of the bacteria is greater than that of Fusarium, while the resistance of Shigella dysenteria is the lowest. Generally, the lower the temperature, the preservation of Shigella. The longer the time, such as 10 min death at 60 ° C; 30 min in direct sunlight; 20 days in water (37 ° C); 10 days on various objects (room temperature); 11 to 24 days on fruits and vegetables, Humans can cause disease by eating more than 10 bacteria. After eating contaminated food, it can cause food-type outbreaks. Shigella is sensitive to various disinfectants. For example, 0.1% of phenolic liquid can be killed within 30 minutes. Mercury (mercury), benzalkonium bromide (new hydrazine), peracetic acid, lime milk, etc. are also very sensitive.

Toxin (20%):

The pathogenicity of Shigella has an important relationship with its invasion process, including invasive epithelial cells that multiply in cells and spread to adjacent cells, causing cell death. There are multiple genes involved in invasion on the large plasmid of Shigella. It encodes a variety of proteins, for example, the invasiveness of Shigella is related to a variety of proteins encoded by a molecular weight of 140×106. In addition, the disseminated genes such as Fusarium also encode some proteins, which are also closely related to bacterial virulence. Relatedly, the above dysentery virulence gene is regulated by multiple genes on chromosomes and plasmids, including temperature-regulated genes (vir R), virulence expression at 37 ° C, and virulence at 30 ° C, Shigella Endotoxin can be produced after death, is an important factor causing systemic reactions such as fever, toxemia and shock, as well as the exotoxin of Shigella, which is injected into rabbits, causing paralysis in animals for 48 hours, so it is also known as Shiga neurotoxin, which is injected into the free intestinal segment of rabbits, can cause enterotoxin-like reactions, locally producing a large amount of liquid, and its electrolyte content is similar to that of intestinal fluid caused by cholera enterotoxin, but The former has a high protein content, and the exudation time is later, often after a partial injection of 105 min; except for a few reports, most of them believe that acyclic adenylase is not activated, and cholera enterotoxin is often found early in exudate (15-30 min) Mainly through the initiation of cyclic adenylase to cause hypersecretion, Shiga toxin lavage rabbit jejunum, does not cause mucosal changes, injection into the ileum segment, can cause intestinal villus shortening, epithelial cells from column to flat, lamina propria There is inflammatory cell infiltration, because Shigella toxin is unstable, it is difficult to purify successfully. Some people have found two different groups with partial purified products. One group can dissolve at pH 7.25, which can cause ileal sputum lesions and mouse death (neuropathy) Toxicity) can also cause Hela cytotoxicity; another group is only cytotoxic to Hela cells at pH 6.0. Recently, the purified Shiga toxin contains macromolecular subunits (molecular weight 30,000-35000) and five small molecules. Subunit (molecular weight 3000~11000), the pure product has both neurological, cellular and enterotoxin effects, and it is confirmed from the immune response that there is no enterotoxin in cholera or Escherichia coli. Recently, many reports have suggested that its cytotoxicity causes cell death by inhibiting intracellular protein synthesis. It is also believed that Shiga toxin is not a neurotoxin but an vascular toxin, which is caused by the action of toxin on the vascular endothelium. Often reversible, more importantly, it has recently been found that Shiga toxin is not only found in Shigella dysenteriae type 1, type 2 (Schmitz type), but also in Shigella flexneri 2a, Shiga toxin isolated from the above bacteria. There is cross-immunity, some people using Shila cells in the cytotoxicity of Hela cells may produce Shiga toxin, and it is also found that Shigella flexneri 2a, 3a, 4b can produce acid and heat stability. Enterotoxin, but its role in the pathogenesis is still unknown.

Pathogenesis

The development process of Shigella after entering the human body depends on the human condition and the interaction between the pathogenicity and quantity of the pathogen. It is currently believed that Shigella must have three conditions:

1 smooth lipopolysaccharide O antigen;

2 having a gene encoding that can invade and propagate in epithelial cells;

3 After the invasion, the toxin can be produced. The Shigella genus, including the first phase of the serovar and the type 2 of the Fusarium, must have a non-smooth O antigen, which is pathogenic, and the pathogenic O antigen has repeated aggregation. May, may be related to bacterial adhesion, but the more important factor of Shigella pathogenicity is invasiveness; invasive strains can cause suppurative cornea, conjunctivitis in guinea pigs, Hela cells can be infected in tissue culture, monkeys After oral administration, it can cause symptoms of dysentery. Although non-toxic strains can proliferate in the intestine, they do not cause lesions. Under electron microscope, pathogenic bacteria are surrounded by monolayer or bilayer membrane in colonic epithelial cells, but the micro-organs of cells can be Degeneration occurs, blisters appear on the surface of the cell membrane, mitochondrial sputum disappears, causing nuclear pyknosis or nuclear lysis. The endogenous cytotoxic process caused by Shigella may be related to bacterial metabolites, which may be a heat-labile substance; Bivalent ions such as calcium, magnesium, iron, etc. can enhance their cytotoxic effects. After swallowing Shigella, people with strong resistance can kill most of the bacteria, and normal intestinal flora has Shigella. Interference effect In immunocompetent patients, intestinal specific secretion of IgA can prevent the adhesion of Shigella to the intestinal mucosal epithelium, if the body's resistance declines, such as malnutrition, overeating, stomach acid deficiency, excessive fatigue, or infection a small amount Bacteria also cause disease. Watery diarrhea often occurs at the onset of symptoms, and then dysentery-like stools occur. However, some bacteria are given to the monkeys with 2a5×1010, and 31 of the 76 monkeys (41%) are affected. % only had symptoms of dysentery, 32% had only diarrhea, 39% had the above two symptoms. The mechanism of Shigella causing watery diarrhea is still unclear. Some people think that Shigella can proliferate in the small intestine and large intestine, but in Invasive lesions are not caused in the small intestine, and secretory diarrhea is caused by the enterotoxin produced. Since the number of enterotoxin receptors in intestinal epithelial cells of different humans or animals is not equal, some people or animals take the same amount of bacteria, and some appear. Water-like diarrhea symptoms, and some no, this has a certain relationship with the individual gene coding, Shigella can invade the colonic mucosa, and produce toxin-inhibiting protein synthesis to cause cell death, a wide range of colonic mucosal epithelial cells Attack and necrosis can cause pus and bloody stools, but it has also been found that most patients with diarrhea symptoms have no pathogenic bacteria in the jejunum, suggesting that bacteria that invade colonic epithelial cells produce toxins into the bloodstream, indirectly caused by toxins or by prostaglandins. Intestinal secretion increased, but some people directly injected the pathogen into the colon, did not cause watery diarrhea, thus negating the doctrine of toxin into the blood, Shigella invaded the colonic epithelial cells, through the basement membrane into the lamina propria, causing mucosal inflammation The reaction rarely enters the submucosal layer and rarely invades the blood circulation to cause sepsis. The Shigella sp. type I infection can cause hemolytic uremic syndrome, and Shigella flexneri is rare. It has been found that patients who cause this syndrome have internal Toxemia and circulating immune complexes, fibrotic thrombosis in the glomerulus, can cause necrosis of the renal cortex, suggesting endotoxemia caused by severe colitis of Shigella, leading to coagulopathy, renal microangiopathy and hemolysis Anemia, toxic bacillary dysentery is mainly seen in children, the pathogenesis is still unclear, may be related to specific physique, due to Shiga After endotoxin is absorbed into the blood from the intestinal wall, it can cause fever, toxemia and acute microcirculatory disorders. Endotoxin directly acts on the adrenal medulla and excites the sympathetic nervous system to release adrenaline, norepinephrine, etc., making the arterioles and Invasive contraction of the venule, due to the direct action of endotoxin or by stimulation of the mononuclear macrophage system, increased histidine decarboxylase activity, or release by lysosomal enzymes, resulting in the release of a large number of vasodilators, such as histamine, Bradykinin, globulin permeability factor, etc., make plasma extravasation, blood concentration; can also cause platelet aggregation, release platelet factor 3, promote intravascular coagulation, aggravate circulatory disorders, toxic bacteria, the above lesions are most prominent in brain tissue Brain tissue hypoxia can be complicated by cerebral edema. < Cerebral palsy can also cause respiratory failure. It is the main cause of death of toxic dysentery. Patients infected with Shigella, including Freund's and Song's bacteria for 1 week, can be serum. Antibodies against its lipopolysaccharide and invasive plasmid-encoding antigen (Ipa-s), including IgA, IgM and IgG antibodies, against Ipa-s in patients with high incidence of Shigella Increase is not very significant.

pathology:

The intestinal lesions of bacillary dysentery are mainly sigmoid colon and rectum, but in severe cases, the entire colon, ileocecal, and even the ileum can be involved. In a few cases, the ileum lesions can be more obvious than the colon, and even the rectal lesions are mild or near normal. The basic pathological changes of mucosa are diffuse fibrin exudative inflammation, partial damage of intestinal mucosa epithelium, formation of most irregular superficial ulcers, microscopic examination, partial exfoliation of mucosal epithelial cells; early villus top is most prominent, severe intestinal Mucosal necrosis can penetrate deep into the submucosa, but perforation is rare. In the submucosal tissue and lamina propria, neutrophils and phagocytic cells infiltrate. Mucosal epithelial cells are coated with a large amount of mucopurulent exudate. In severe cases, large intestinal mucosa falls off and necrosis Epithelial cells, fibrin, neutrophils and Shigella form a gray-white fiber pseudomembrane. In mild cases, only diffuse hyperemia and edema are found in the intestine, mucous bloody exudate is contained in the intestinal lumen, and intestinal infection can cause mesenteric infection. Lymph node enlargement, liver, kidney and other parenchymal organs have poisonous degeneration, chronic bacterial intestinal mucosal edema , thickening, often varying degrees of congestion, intestinal ulcers continue to form and continue to repair, mucosal epithelial cells in the ulcer repair, regeneration, formation of depressed scars and intestinal gland cysts and granulation tissue formation of intestinal polyps, a small number of cases due to intestinal Wall fiber scar tissue contraction and cause intestinal stenosis. In recent years, it has been found that the secretion of IgA in the intestinal tract of chronic bacillary dysentery is reduced. It is difficult to confirm the cause of chronic bacillary dysentery, inhibit the consequences of chronic intestinal lesions, and toxic bacillary dysentery. Intestinal lesions are mild, most of them only see congestion and edema. In some cases, there are superficial ulcers in the colon. The prominent pathological changes are brain and brain stem edema, neuronal degeneration, adrenal hyperemia in some cases, and adrenocortical atrophy.

Shigosis prevention

Prevention of bacillary dysentery should take comprehensive measures, with a focus on cutting off the route of transmission and at the same time managing the source of infection.

1. Manage the source of infection

Mainly for acute, chronic patients and carriers, relying on rural cooperative medical stations and urban medical units, organizing epidemic reports, early detection of patients, especially for mild atypical diseases, detailed registration for timely treatment, acute patients should be hospitalized or in Isolation, disinfection and thorough treatment in the home, the stool culture once every other day, can be released after two consecutive negatives. For the child care institutions, the food and beverage industry, the canteen staff and the water supply staff of the waterworks, regular stool training must be carried out. .

2. Cut off the route of transmission

Do: "Three tubes and one extinguish" (ie grasping drinking water, diet, management of feces, killing flies); "four to three don't" (to completely eliminate flies, wash hands before and after meals, eat raw fruits and vegetables to wash Hot, get the bacteria to report the treatment as soon as possible, do not drink raw water, do not eat rotten and unclean food, do not urinate with the ground), fly to prevent the formation of breeding grounds, according to the law of the growth and decline of flies, the annual anti-flying measures Special attention should be paid to the spread of bacillary dysentery in children's institutions and collective units. It is necessary to strictly implement various health systems, such as the hygiene system for food, food, living room, activity space and children's toys. Always check whether the water quality of centralized water supply is hygienic. It is required that the water quality of rural well water and river water should be paid special attention. Practice has proved that in addition to the four evils, hygiene, and purification of the environment are effective measures to cut off the transmission route.

3. Protect susceptible populations

In recent years, oral live vaccines have been mainly used, and three kinds of vaccines are generally used:

1 natural avirulent strain;

2 strains of toxic or non-toxic dysentery bacilli and E. coli;

3 variant strains, currently mainly used in the domestic strains, that is, the use of strain-based strains to prepare vaccines (variable non-toxic strains that can grow and reproduce on streptomycin-containing medium), China's trial production of monovalent or bivalent vaccines in 36 sites Observed tens of thousands of times, it proved that there is a good effect, the protection rate is 66.41% ~ 99.47%, live vaccines mainly through the stimulation of the intestinal secretion of secretory IgA and cellular immunity to obtain immunity, the immune period can be maintained 6 ~ 12 months, a small number of people may have diarrhea after taking it. Because Shigella is immunologically specific, sometimes it has a different type of fungus than the bacterin used, it has no protective effect. In some areas, it is suitable for local conditions. Prevention with Chinese herbal medicine, such as garlic, purslane, etc., also has a certain effect.

4. Wash hands thoroughly before handling food

Dirty clothes and sheets should be placed in a covered bucket and soaked in soapy water and then boiled for disinfection. Mosquito nets and barriers should be used in the house. Corresponding isolation measures (especially for the isolation of feces) should be taken for patients and carriers. An oral live vaccine is being developed, and field trials in endemic areas indicate promising prospects, but immunity is generally type-specific.

5. For personal hygiene , drink boiled water without drinking raw water. It is best to use pressurized water, wash fruits and vegetables with tableware and mouthwash with disinfected water; wash hands before and after meals, do not poop anywhere; eat cooked food without eating Cold salad, leftovers should be heated and eaten; make raw and cooked separately, prevent flies from crawling food; it is best not to participate in large-scale dinner activities, such as marriage, funeral, marriage, etc.;

Shigella complications Complications bacteremia hemolytic uremic syndrome arthritis

The main characteristics of typical Shigella disease are acute onset, fever, abdominal pain, pus and bloody stools, and moderate systemic poisoning symptoms. The diarrhea is more than 10 times a day or more. Severe patients are accompanied by convulsions, headaches, and whole body muscles. Soreness can also cause dehydration and electrolyte imbalance.

Parenteral complications of bacillary dysentery are rare.

1. Bacteremia: mainly seen in children, malnourished, sickle cell anemia and immunocompromised patients, more than 100 cases abroad, there are a few cases reported in China, the symptoms of bacteremia are more serious, the mortality rate is as high as 46 %, bacteremia is more common in 1 to 2 days after onset, antibiotic treatment is effective.

2. Hemolytic uremic syndrome: mainly seen in Shigella infection of dysentery, some cases have leukemia-like reactions at the beginning, followed by hemolytic anemia and DIC, acute renal failure in some cases, thrombosis and renal cortical necrosis in large and small arteries There are fibrin deposits in the glomeruli and arterial wall. In about half of the cases, the sputum test is positive. In most cases, the immune complex is positive in the serum. Endotoxemia may be related to the disease, but the endotoxemia caused by other bacteria has no similar performance. The prognosis of this disease is serious.

3. Arthritis: It occurs more than 2 weeks after the dysentery, which may be caused by allergic reaction, mainly involving large joints, which can cause knee and ankle joint swelling, exudation, antibodies to agglutinating Shigella in synovial fluid, serum The anti-"O" titer is normal, and hormone therapy can be quickly relieved.

Symptoms of Shigella disease Common symptoms Abdominal pain, abdominal distension, intestinal dysfunction, dehydration, diarrhea, chills, intestinal paralysis, light reaction, disappearance, nausea

Bacterial dysentery is characterized by fever, abdominal pain, diarrhea, sensation of urgency and mucus pus and blood. The basic pathological damage is hyperemia, edema, hemorrhage and other exudative inflammatory changes of the colonic mucosa. The incubation period is several hours to 7 days, most of which are 1 to 3 days, the length of incubation period and the severity of clinical symptoms depend on the age of the patient, the strength of the disease, the number of infected bacteria, the virulence and the type of bacteria, so any bacterial type can be light. Medium and heavy, but from a large number of case analyses, the symptoms caused by Shigella dysenteriae are heavier. According to recent epidemics in some parts of the country, fever, diarrhea, and pus and blood will last longer, but the prognosis is mostly good. The symptoms are mild, and there are many atypical cases, which are easy to be missed or misdiagnosed. There are more cases of children, and Fusarium dysentery is somewhere in between, but the time of sterilization is longer, and it is easy to turn to chronic. After 1 year of follow-up after treatment, 10% of patients with chronic disease, chronic diarrhea accounted for 10% to 20% of the total number of bacillary dysentery, according to the length of the disease and the severity of the disease can be divided into the following types:

Acute bacillary

According to the severity of toxemia and intestinal symptoms, it can be divided into four types.

(1) Ordinary type (typical): acute onset, chills, fever, mostly above 38 ~ 39 ° C, with dizziness, headache, nausea and other symptoms of systemic poisoning and abdominal pain, diarrhea, feces began to appear muddy or thin Water samples, the most, followed by mucus or mucus pus and blood, the amount is not much, daily defecation from ten to dozens of times, accompanied by urgency and heavy, left lower abdomen tenderness is obvious, can touch the intestinal cord, the course of about a week, A small number of patients may have severe vomiting, rehydration without timely dehydration, acidosis, electrolyte imbalance, secondary shock, typical acute bacterial dysentery is characterized by acute onset, fever, abdominal pain, pus and blood, and moderate body Symptoms of poisoning, diarrhea is more than 10 times a day or more, severe patients with convulsions, headache, body muscle aches, can also cause dehydration and electrolyte imbalance.

(2) Light (atypical): no obvious fever, acute diarrhea, stool 10 times / d, thin mucus, no pus, abdominal pain and lower left abdomen tenderness, light or lack of urgency, stool microscopic examination visible A small number of pus cells can be diagnosed by the growth of Shigella in stool culture.

(3) Heavy: more common in the elderly, frail, malnourished patients, acute fever, diarrhea 30 times / d or more, thin water pus bloody stool, occasionally discharged flaky pseudomembrane, even fecal incontinence, abdominal pain, after the emergency is heavy, late Severe abdominal distension and toxic intestinal paralysis may occur, often accompanied by vomiting. Severe water loss may cause peripheral circulatory failure. In some cases, toxic shock is prominent, body temperature does not rise, often acidosis and water, electrolyte imbalance, a few Patients may have heart, renal insufficiency, due to severe intestinal lesions, occasionally Shigella invade the blood circulation, causing sepsis.

(4) Toxic dysentery: more common in children 2 to 7 years old, most of the sick children are better in physical fitness, rare in adults, most of the onset is rapid, the fever is 39 ~ 41 ° C or higher, and irritability, paralysis, repeated convulsions, followed by Can appear pale, cold limbs, rapid toxic shock, long-term convulsions can lead to coma, and even respiratory failure, often after a few hours after the onset of dysentery-like stool, some cases of intestinal symptoms are not obvious, often Need to pass the enema or anal swab examination to find white blood cells in the stool, red blood cell side can be diagnosed, some cases began to be recessive bacillary dysentery, 1 to 2 days later turned into poisoning type, according to its main clinical manifestations, can be roughly divided into three types:

1 shock type (peripheral circulatory failure type): more common, with septic shock as the main performance, due to microcirculation vasospasm, leading to microcirculatory disorders, early grayish white, cold limbs, finger (toe) nails white, fast heart rate (150 ~ 160 times / min), pulse fineness increased, blood pressure decreased or not measured, lips, nail bed bun, aggravation of air, and can appear heart, kidney dysfunction symptoms.

2 brain type (respiratory failure type): is the most serious manifestation of toxic dysentery, due to cerebral vascular spasm caused by cerebral hypoxia, cerebral edema and even cerebral palsy, and central respiratory failure, due to frequent or persistent convulsions caused by coma At first, the respiratory rhythm is uneven, the depth is uneven, and then there is double inhalation, sigh-like breathing, jaw breathing and apnea; at the beginning, the pupil is suddenly big and small, and the pupils on both sides are not equal, and the reaction to light disappears. Sometimes, after 1 or 2 episodes of convulsions, the breathing stops suddenly.

3 mixed type: the most serious syndrome with circulatory failure, convulsions, respiratory failure and circulatory failure are three serious manifestations of toxic dysentery. Generally, convulsions first occur. If they are not rescued in time, they will rapidly develop into respiratory failure and circulation. Depletion.

2. Chronic bacteria

The pathogenesis of bacillary dysentery is repeated or delayed for more than 2 months, which is chronic bacillary dysentery. The causes of chronic bacillary dysentery can be roughly included in two aspects. On the one hand, the patient's resistance is low, such as acute phase failure, malnutrition, Gastrointestinal disorders, intestinal secretory IgA reduction, etc.; on the other hand, bacterial strains, such as Fusarium, are susceptible to chronic infection; some drug-resistant strains can also cause chronic diarrhea, which can be classified into three types according to clinical manifestations. .

(1) acute onset of chronic bacillary dysentery: a history of dysentery within six months, often induced by eating cold food or suffering from cold, fatigue and other factors, abdominal pain, diarrhea, pus and blood, fever is often not obvious.

(2) Chronic prolonged type: after the onset of acute bacillary dysentery, prolonged unhealed, often have abdominal pain, diarrhea, thin mucus or pus and blood, or constipation, alternating diarrhea, tenderness of the left lower abdomen, sputum and thickened sigmoid colon, long-term Diarrhea causes malnutrition, anemia, fatigue, etc., stool often intermittently sterilized, and the result of cultivating Shigella in stool is sometimes negative and sometimes positive.

(3) Chronic occult type: history of dysentery, no clinical symptoms, Shigella can be detected in stool culture, sigmoidoscopy can be found abnormally, chronic sputum is most common in chronic prolongation, chronic sputum acute attack Second, chronic occultity is a minority.

Shigosis examination

1. Blood: Acute dysentery often has leukocytosis, at (10 ~ 20) × 109 / L; neutrophils, nuclear left shift, mild cases of mild anemia.

2. Fecal examination: less stool, pus and mucus, microscopic examination of piles of pus cells, including red blood cells and macrophages, pus cells often in more than 10 / high power field, stool culture to isolate pathogenic bacteria Diagnosing and guiding treatment have important value. It is advisable to take specimens before the start of antibacterial therapy, take the pus and blood, and immediately send them for examination. If they are left for too long or mixed with urine, the positive rate can be affected. The disease period can be positive when taking specimens. As a result, the positive rate on the first day of onset was the highest, reaching 50%, down to 35% on the 6th day, and 14.8% on the 10th day. The multiple test can increase the positive rate. In order to facilitate the isolation of pathogenic bacteria, selective culture is often used. Base, in the past commonly used SS agar plate, in recent years, it has also been found to inhibit Shigella, using xylose-lysine deoxycholate agar plate, can increase the positive rate, the domestic also used HE agar (Hektoen enteric) culture The base and Mac Conkey agar plate have achieved good results, and the positive strains were isolated and the antibiotic sensitivity was measured in time, which has reference significance for guiding clinical drugs.

3. Rapid pathogen diagnosis: including immunofluorescence ball method, enrichment latex agglutination method, synergistic agglutination test, immunobright blue staining method, can quickly obtain positive results from feces, the positive rate can reach more than 90%, against bacillary dysentery Early diagnosis is helpful.

4. Monoclonal antibody point immuno-binding sandwich method (DIAB) and reverse indirect hemagglutination method: Recently, it has been used to detect the antigen of Fusarium dysenteriae in feces, which has good sensitivity and specificity and deserves further study.

5. DNA probe method: Some people used alkaline phosphatase-labeled probes and fecal specimens for hybridization. The early positive rate was up to 85%, which was significantly higher than the conventional culture positive rate of 56%, which increased the positive rate of early diagnosis.

6. Sigmoidoscopy: diffuse hyperemia and edema of acute colonic mucosa with superficial ulcers and exudates. Sigmoidoscopy is associated with increased patient suffering and is dangerous. It is generally not suitable for chronic bacillary dysentery. Visible colonic mucosa congestion, edema and superficial ulcers, mucosa can be granular and visible polyps and other proliferative changes, scraping mucus purulent secretions to culture can increase the positive rate.

7. X-ray examination : Chronic bacillary dysentery or barium enema, visible intestinal fistula, disappeared bag shape, thickened intestinal wall, narrowing of intestinal lumen and shortening of intestinal segment.

Diagnosis and identification of Shigella disease

The bacillary dysentery should be differentiated from various diarrheal diseases, and the toxic bacillary dysentery should be differentiated from the acute central nervous system infection in summer and autumn or septic shock caused by other causes.

1. Acute bacillary dysentery needs to be identified with the following diseases.

(1) Amoebic dysentery:

(2) Other bacterial intestinal infections:

1 Campylobacter jejuni enteritis: The incidence rate in developed countries exceeds that of bacillary dysentery and is close to Salmonella infection. The Shanghai area reports that it is the second most common intestinal tract in dysentery. The season and age are similar to those of dysentery, with fever and abdominal pain. , diarrhea or pus and blood mucus, a small number of people may have a history of contact with poultry or livestock, relying on clinical manifestations and fecal microscopy often difficult to identify, the use of special medium in the micro-aerobic environment to separate the bacteria,

2 E. coli infection: Some E. coli can invade the intestinal wall, can cause lesions caused by Shigella infection, have fever and mucus; some can produce heat-resistant or heat-labile enterotoxin, which can cause dilute watery stools, mainly Identification requires separation of stool culture and identification of pathogenic bacteria.

(3) Salmonella typhimurium, Proteus intestinal infection can cause diarrhea, especially the intestinal infection of Vibrio parahaemolyticus can cause bloody watery stools, the latter is more common in coastal areas, and more contaminated seafood History, can be a collective disease, abdominal pain is significant, a small number of urgency and heavy, feces cultured in 4% sodium chloride sputum or 4% sodium chloride agar plate, can get positive results.

(4) acute intussusception: more common in children, infants intussusception early without fever, due to abdominal pain and bursts of crying, bloody mucus can be discharged after a few hours of onset, microscopic examination of red blood cells, abdominal abdomen and mass .

(5) acute necrotizing hemorrhagic enteritis: more common in adolescents, fever, abdominal pain, diarrhea and bloody stools, severe toxemia, short-term shock, stool microscopic examination of red blood cells, often full abdominal tenderness and severe bloating , stool culture of Shigella-free bacteria.

(6) Toxic bacteria: the season of onset, age and high fever, convulsions, etc. are similar to epidemic encephalitis, but the toxic bacillary dysentery is fierce, early shock and/or respiratory failure, after enema with saline Examination of feces can be found in pus cells. The development of Japanese encephalitis is mild. It often enters coma or respiratory failure after a few days of fever. Shock is rare, and cerebrospinal fluid examination is positive. It is caused by Staphylococcus aureus sepsis or Gram-negative bacilli sepsis. Toxic shock, patients often have primary lesions such as sputum, or gallbladder, urinary tract infection, blood culture positive, late X-ray can be found that blood-borne Staphylococcus aureus pneumonia can be identified with toxic bacteria.

(7) Epidemic encephalitis B: The manifestations and epidemics of this disease are similar to those of bacillary dysentery (heavy and poisoned), the latter is more acute, rapid progress, and easy to have shock, can be heated by saline enema and microscopic examination and bacteria to cultivate.

The disease should be differentiated from viral enteritis.

2. Chronic bacillary dysentery should be differentiated from the following diseases:

(1) rectal cancer and colon cancer: colon cancer or rectal cancer is easy to be combined with intestinal infection. When there is secondary infection in cancer patients, diarrhea and pus and bloody stools may occur. Therefore, patients with chronic diarrhea, no matter what age, Routine anal examination and sigmoidoscopy should be performed. For suspected high-grade tumors, X-ray examination or fiberoptic colonoscopy should be performed.

(2) Schistosomiasis: There may be diarrhea and pus and bloody stools. There is a history of exposure to epidemic water in the epidemic area, often accompanied by hepatomegaly and eosinophilia in the blood. Fecal hatching and rectal mucosal biopsy can obtain positive results.

(3) Non-specific ulcerative colitis: an autoimmune disease with a long course of disease, with pus and blood or fever, sigmoid colonoscopy for intestinal mucosal congestion, edema and ulcer formation, mucosal fragility and easy bleeding, and intestines in the serum Lipopolysaccharide antibodies in mucosal epithelial cells are often associated with other autoimmune diseases, and antibacterial therapy is often ineffective.

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