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Shigella infection

  Bacterial dysentery (abbreviated as dysentery) also known as Shigella infection, is an intestinal infectious diarrhea caused by Shigella dysenteriae, one of the most common intestinal infectious diseases in summer and autumn. Shigella dysentery bacteria are divided into four groups: A group (Shigella dysenteriae), B group (Flexneri Shigella), C group (Bordetella Shigella), and D group (Sonnei Shigella). The main pathological changes are inflammation and ulcers of the colonic mucosa. Clinically, symptoms such as acute onset of chills and high fever, abdominal pain, diarrhea, purulent blood stools, and urgent need to defecate are common. It is scattered throughout the year and can cause outbreaks in summer and autumn.

Table of contents

1. What are the causes of shigellosis?
2. What complications can shigellosis lead to?
3. What are the typical symptoms of shigellosis?
4. How to prevent shigellosis?
5. What kind of laboratory tests should be done for shigellosis?
6. Diet taboo for shigellosis patients
7. Conventional methods of Western medicine for the treatment of shigellosis

1. What are the causes of shigellosis?

  The excrement of infected individuals and carriers in the convalescent period is the source of infection, the pathogenic bacteria are transmitted directly through the fecal-oral route, and people can become ill by eating food or objects contaminated with bacteria. Flies can act as mechanical vectors, and waterborne transmission is not common. Epidemics are most likely to occur in crowded populations with poor hygiene conditions, and shigellosis is particularly common in young children in epidemic areas, while adults have milder disease.

  First, the cause of disease

  Shigella is a short Gram-negative bacillus of the genus Shigella in the family Enterobacteriaceae, also known as dysentery bacillus. The bacteria are non-motile, short, and can be spherical-cylindrical in young culture. They have no capsule and no spores. Shigella is facultative anaerobic, but the most suitable for aerobic growth. After 24 hours of culture, it becomes an elevated, circular, transparent colony with a diameter of about 2mm and a neat edge. All Shigella can ferment glucose, produce acid, and do not produce gas except for Newcastle type and Manchester type Shigella. In addition to Shigella sonnei, they do not ferment lactose, and in addition to Shigella dysenteriae, they can ferment mannitol.

  1. Antigen structure:According to the classification of pathogenic Shigella by the International Microbiological Society in 1985, pathogenic Shigella can be divided into four groups of 42 serotypes (Group A: 10, Group B: 13, Group C: 18, Group D: 1), see Table 1. The lipopolysaccharide of Shigella is composed of lipid A, core polysaccharide, and O-specific side chain. The O antigen is the basis for typing. The O antigen of Shigella flexneri is encoded by the chromosome, the O antigen of Shigella sonnei is encoded by a plasmid with a molecular weight of 120×10^6, and the O antigen of Shigella type I, in addition to being encoded by the chromosome, also requires a small plasmid. Shigella strains in each group have complex antigenic structures, and there are cross-reactions in the serological specificity of each strain group. For example, if bacteriophages integrate into the chromosome of Shigella, a type conversion can occur. After the plasmid is lost in Shigella and Shigella sonnei, the colonies change from smooth to rough, that is, the pathogenicity is lost.

  2. Resistance:Shigella is present in the feces of patients and carriers, has strong viability in vitro, the resistance of Shigella sonnei is greater than that of Shigella flexneri, and the resistance of Shigella dysenteriae is the lowest. Generally, the lower the temperature, the longer the survival time of Shigella. For example, it dies within 10 minutes at 60℃; within 30 minutes under direct sunlight; survives for 20 days in water (37℃); survives for 10 days on various objects (room temperature); and survives for 11 to 24 days on vegetables and fruits. Eating 10 or more bacteria can cause illness in humans, and eating contaminated food can lead to large-scale foodborne outbreaks. Shigella is sensitive to various disinfectants, such as it can be killed within 30 minutes in a 0.1% phenol solution, and is also sensitive to mercuric chloride (mercuric chloride), benzalkonium bromide (new quickkill), peracetic acid, lime milk, etc.

  3. Toxin:The virulence of Shigella and its invasive process are closely related, including invasion of epithelial cells, proliferation within the cells, and spread to neighboring cells, causing cell death. Multiple genes related to invasion are present on the large plasmid of Shigella, encoding various proteins, such as the invasive power of Shigella, which is associated with proteins encoded by a plasmid with a molecular weight of 140×10^6. In addition, the dissemination genes of Shigella flexneri also encode some proteins that are closely related to bacterial virulence. The aforementioned virulence genes of Shigella are regulated by multiple genes on the chromosome and plasmids at multiple levels, including temperature-regulating genes (virR), with virulence expression at 37℃ and virulence disappearance at 30℃. All types of Shigella can produce endotoxins after death, which are important factors in systemic reactions such as fever, septicemia, and shock. There are also Shigella exotoxins, which, when injected into rabbits, can cause paralysis in the animals within 48 hours, hence they are also called Shigella neurotoxins. When injected into the free intestinal segment of rabbits, they can cause an enterotoxin-like reaction, producing a large amount of fluid locally, with its electrolyte content similar to that of cholera enterotoxin. However, the former has a higher protein content and a later onset of leakage, usually occurring after 105 minutes of local injection; except for a few reports, most believe that it does not activate cyclic adenosine monophosphate (cAMP) kinase. Cholera enterotoxin is often observed to produce leakage early (15~30 minutes), mainly by initiating cAMP kinase to cause excessive secretion. Washing the rabbit jejunum with Shigella toxin does not cause mucosal changes, but injecting it into the ileum segment can cause shortening of the intestinal villi, with the epithelial cells changing from columnar to flat, and inflammation cells infiltrating the lamina propria. Due to the instability of Shigella toxin, it is not easy to purify successfully. Some have found two different groups in a partially purified preparation, one group that can dissolve at pH 7.25, causing ileal loop lesions and death in mice (neurotoxicity), as well as HeLa cell toxicity; another group that only has cytotoxicity to HeLa cells at pH 6.0. Recently, it has been reported that purified Shigella toxin contains large molecular subunits (molecular weight 30,000~35,000) and five small molecular subunits (molecular weight 3,000~11,000), with the purified product having neurotoxic, cytotoxic, and enterotoxin effects, and confirmed by immune reactions to be unrelated to cholera or Escherichia coli enterotoxins. Recent reports suggest that its cytotoxic effect is due to inhibition of intracellular protein synthesis leading to cell death. Some also believe that Shigella toxin is not a neurotoxin but a vasoactive toxin, which causes secondary neurologic symptoms due to the action of the toxin on vascular endothelium, often reversible. More importantly, it has recently been found that Shigella toxin is not only present in Shigella dysenteriae type 1 and 2 (Schmitz type) but also in Shigella flexneri type 2a. The Shigella toxins isolated from the aforementioned bacteria have cross-immunogenicity. Some have found that all Shigella species have the potential to produce Shigella toxins. Some have also found that Shigella flexneri 2a, 3a, and 4b can produce acid- and heat-stable enterotoxins, but the role of these toxins in the pathogenesis is still unknown.

  二、发病机制

  志贺菌进入人体后的发展过程取决于人体情况和病菌的致病力与数量相互作用的结果。目前认为志贺菌致病必须具备三个条件:①具光滑型脂多糖O抗原;②具有能侵袭上皮细胞并在其中繁殖的基因编码;③侵袭后能产生毒素。志贺菌属,包括宋内菌第一相及福氏菌2a型,均必须具有不光滑型O抗原,才有致病性,致病性O抗原具有重复多聚物,可能和细菌黏附性有关。但是志贺菌致病的更重要的因素是侵袭力;有侵袭力的菌株在豚鼠可引起化脓性角膜、结膜炎,在组织培养上可以感染Hela细胞,猴子口服后可引起痢疾症状。无毒株虽可在肠内增殖,但不引起病变。在电镜下可见致病性细菌在结肠上皮细胞内被单层或双层膜包围,但细胞的微器官可以出现退行变,细胞膜表面出现小疱,线粒体嵴消失,引起核固缩或核溶解。志贺菌引起内源性细胞毒过程可能和细菌的代谢产物有关,可能为一种不耐热的物质;双价离子如钙、镁、铁等可以加强其细胞毒作用。人吞食志贺菌后,抵抗力较强的人其胃酸可将细菌大部杀死,正常肠道菌丛对志贺菌有干扰作用。具有免疫力的患者,肠道特异性分泌IgA,可以阻止志贺菌对肠黏膜上皮的黏附。如果人体抵抗力下降,如营养不良、暴饮暴食、胃酸缺乏、过度疲劳,即或感染小量细菌,亦引起发病。起病时常先有水样腹泻,然后出现痢疾样大便,但有人将福氏菌2a5×1010给猴子口服,76只猴子中31只(41%)发病,发病者中29%仅有痢疾症状,32%仅有腹泻,39%出现上述两种症状,志贺菌如何引起水样腹泻的机制尚不清楚。有人认为志贺菌在小肠及大肠中均可增殖,但在小肠内不引起侵袭性病变,由所产生的肠毒素引起分泌性腹泻。由于不同人或动物的肠上皮细胞的肠毒素受体数量不等,所以人或动物服等量细菌后,有的出现水样腹泻症状,有的则否,这和个体基因编码有一定关系。志贺菌可以侵袭结肠黏膜,并产生毒素抑制蛋白合成引起细胞死亡。结肠黏膜上皮细胞的广泛侵袭及坏死可以引起脓血便。但也有人发现出现水泻症状的患者空肠中多数并无致病菌,从而提出由侵入结肠上皮细胞的细菌产生毒素进入血流,由毒素或通过前列腺素间接引起小肠分泌增多。但有人直接将致病菌注入结肠,并未引起水样泻,因此否定了毒素入血的学说。志贺菌侵入结肠上皮细胞后,通过基底膜而进入固有层,引起黏膜炎症反应,很少进入黏膜下层,极少侵入血循环引起败血症。感染痢疾志贺菌I型可引起溶血性尿毒症综合征,福氏志贺菌则罕见。Someone has found that patients with this syndrome have endotoxemia and circulating immune complexes, with fibrous thrombus deposits in the glomeruli, which can cause renal cortical necrosis, indicating endotoxemia caused by severe Shigella colitis, leading to coagulopathy, renal microvascular lesions, and hemolytic anemia. Toxic Shigella dysentery is mainly seen in children, and the pathogenesis is not yet clear, possibly related to specific constitution. Since the endotoxin of Shigella can be absorbed into the blood from the intestinal wall, it can cause fever, toxemia, and acute microcirculatory disorders. Endotoxin acts directly on the adrenal medulla and excites the sympathetic nervous system to release adrenaline, norepinephrine, and other substances, causing spasm of small arteries and veins. Due to the direct action of endotoxin or through stimulation of the mononuclear phagocyte system, the activity of histidine decarboxylase increases, or through the release of lysosomal enzymes, leading to the release of a large amount of vasodilator substances, such as histamine, bradykinin, and globulin permeability factor, causing plasma extravasation and blood concentration; it can also cause platelet aggregation, release platelet factor 3, promote intravascular coagulation, and exacerbate circulatory disorders. The above lesions of toxic Shigella dysentery are most prominent in the brain tissue. Brain tissue hypoxia can lead to brain edema, and brain hernia can also cause respiratory failure, which is the main cause of death from toxic dysentery. After 1 week of infection with Shigella, including Shigella flexneri and Shigella sonnei, antibodies to its lipopolysaccharide and invasive plasmid-encoded antigen (Ipa-s) can appear in the serum, including IgA, IgM, and IgG antibodies. For patients in high-incidence areas of Shigella, the increase in antibodies to Ipa-s is not very significant.

  Pathology: The intestinal lesions of shigellosis mainly involve the sigmoid colon and rectum, but in severe patients, they can affect the entire colon, ileocecal region, and even the distal ileum. In a few cases, the damage to the ileum can be more pronounced than the colon, even with mild or near-normal rectal lesions. The basic pathological change of the intestinal mucosa is diffuse fibrin exudative inflammation. Partial damage to the intestinal mucosal epithelium forms multiple irregular superficial ulcers. Microscopic examination shows partial desquamation of mucosal epithelial cells; in the early stage, the tip of the villi is most prominent, and in severe cases, the necrosis of the intestinal mucosa can extend into the submucosa, but perforation is rare. Neutrophils and phagocytes infiltrate the submucosal tissue and lamina propria. The surface of the mucosal epithelial cells is covered with a large amount of mucopurulent exudate. In severe cases, large areas of the intestinal mucosa may slough off, forming a grayish white fibrous pseudomembrane composed of necrotic epithelial cells, fibrin, neutrophils, and Shigella. In mild cases, the intestines only show diffuse congestion and edema, with mucus-containing bloody exudate in the intestinal lumen. Severe intestinal infection can cause enlargement of mesenteric lymph nodes, toxic changes in the parenchymal organs such as the liver and kidneys. Chronic shigellosis shows edema and thickening of the intestinal mucosa, with varying degrees of congestion, continuous formation and repair of ulcers, and regeneration of mucosal epithelial cells at the site of ulcer repair, forming concave scars and visible intestinal adenoma mucosa cysts and granulation tissue forming intestinal polyps. In a few cases, intestinal stricture may be caused by contraction of the fibrous scar tissue of the intestinal wall. In recent years, it has been found that the secretion of IgA in the chronic shigellosis intestines is reduced, and it is currently difficult to determine whether it is the cause of the chronicization of shigellosis or the consequence of chronic intestinal lesions. The intestinal lesions of toxic shigellosis are mild, with most cases showing congestion and edema, and some cases have superficial ulcers in the colon. The prominent pathological change is edema of the brain and brainstem, and neuronal degeneration. In some cases, adrenal congestion and adrenal cortical atrophy may occur.

2. What complications can Shigella infection easily lead to

  The main characteristics of typical Shigella infection are acute onset, fever, abdominal pain, purulent and bloody stools, and moderate systemic toxic symptoms. Diarrhea can occur 10 or more times a day. Severe patients may have convulsions, headaches, and generalized muscle pain, and can also lead to dehydration and electrolyte disorders. Extraintestinal complications of shigellosis are not common.

  1. Bacteremia:Mainly seen in children with malnutrition, sickle cell anemia, and low immunity. There have been more than 100 cases abroad, and there are also a few cases reported in China. The symptoms are more severe in patients with bacteremia, with a mortality rate as high as 46%. Bacteremia is most common within 1~2 days after onset, and antibiotic treatment is effective.

  2. Hemolytic uremic syndrome:Mainly seen in Shigella dysenteriae infection. Some cases have a leukemoid reaction at the beginning, followed by hemolytic anemia and DIC. Some cases have acute renal failure, with thrombosis in the large and small arteries of the kidneys and necrosis of the renal cortex. The glomeruli and arterial walls have fibrin deposition. About half of the cases are positive in the limulus test, and most cases have positive immune complexes in the serum. Endotoxemia may be related to the onset, but endotoxemia caused by other bacteria does not have similar manifestations. The prognosis of the disease is severe.

  3. Arthritis:Mostly occurs within 2 weeks after dysentery, possibly due to an allergic reaction, mainly affecting large joints, and can cause redness, swelling, and effusion of the knee and ankle joints. The synovial fluid contains antibodies that agglutinate Shigella, and the serum anti-O titer is normal. Steroid therapy can quickly alleviate the symptoms.

3. What are the typical symptoms of Shigella disease?

  Bacterial dysentery is characterized clinically by fever, abdominal pain, diarrhea, tenesmus, and mucopurulent stools. Its basic pathological damage is the congestion, edema, and hemorrhage of the colonic mucosa, which shows exudative inflammatory changes. The incubation period ranges from a few hours to 7 days, most commonly 1~3 days. The length of the incubation period and the severity of clinical symptoms in dysentery Shigella patients depend on factors such as the patient's age, resistance strength, the number of infected bacteria, virulence, and strain. Therefore, any strain can have mild, moderate, or severe symptoms. However, from the analysis of a large number of cases, the symptoms caused by Shigella dysenteriae are more severe. According to the recent epidemic situation in some areas of China, fever, diarrhea, and purulent blood stools last longer, but the prognosis is generally good. Shigella sonnei dysentery has milder symptoms, more atypical cases, and is more likely to be missed or misdiagnosed, with more cases in children. Shigella flexneri dysentery is between the two, but the duration of excretion is longer, and it is more likely to become chronic. One-year follow-up after treatment shows that 10% become chronic, and chronic dysentery accounts for 10% to 20% or more of the total number of dysentery cases. It can be divided into the following types according to the duration and severity of the disease course:

  1. Acute bacillary dysentery

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

  1. Common type (typical):The onset is acute, with aversion to cold, fever, mostly above 38~39℃, accompanied by dizziness, headache, nausea, and systemic toxic symptoms, as well as abdominal pain, diarrhea, and the stool starts to be loose mud-like or watery. The most common form is mucus or mucopurulent stools with little quantity, ranging from ten to dozens of times a day for defecation, accompanied by tenesmus. There is marked tenderness in the lower left abdomen, and the spasmodic intestinal cords can be palpated. The course of the disease is about one week, and a few patients may develop secondary shock due to severe vomiting, inadequate fluid replacement leading to dehydration, acidosis, electrolyte disorder, and secondary shock. The main features of typical acute bacterial dysentery are acute onset, fever, abdominal pain, purulent blood stools, moderate systemic toxic symptoms, diarrhea presenting more than 10 times a day or more, and severe patients may have convulsions, headache, generalized muscle pain, and can also cause dehydration and electrolyte disorder.

  2. Mild type (atypical):No significant fever, acute diarrhea, stools less than 10 times per day, watery mucous stools, may be without pus and blood, with abdominal pain and left lower abdominal tenderness, mild or absent tenesmus, microscopic examination of stools may show a few pus cells, and culture of stools with the growth of Shigella can be diagnosed.

  3. Severe type:More common in elderly, weak, and malnourished patients, with acute onset of fever and diarrhea over 30 times per day, watery purulent stools, occasionally with the excretion of plate-like pseudomembranes, even incontinence of stools, marked abdominal pain and tenesmus, severe abdominal distension and toxic intestinal paralysis in the later stage, often accompanied by vomiting, severe dehydration can lead to peripheral circulatory failure. In some cases, toxic shock is the prominent manifestation, with body temperature not rising, frequent acidosis and water and electrolyte imbalance, and a few patients may have cardiac and renal insufficiency. Due to severe intestinal lesions, shigella may occasionally enter the blood circulation, causing sepsis.

  4. Toxic dysentery:More common in children aged 2 to 7, most of whom have good physical fitness, and it is rare in adults. Most cases have an acute onset, with a sudden high fever of 39-41℃ or higher, accompanied by restlessness, delirium, repeated convulsions, and then pale complexion, cold limbs, rapid onset of toxic shock, and in cases with prolonged convulsions, coma or respiratory failure may occur. Dysentery-like stools usually appear several hours after the onset, and in some cases, intestinal symptoms are not obvious, and stools may contain white blood cells and red blood cells, which can be diagnosed only after enema or anal swab examination. Some cases start as atypical bacillary dysentery and transform into toxic type 1 to 2 days later. According to its main clinical manifestations, it can be roughly divided into three types:

  (1) Shock type (peripheral circulatory failure type):More common, mainly manifested as infectious shock, due to microcirculatory vascular spasm, leading to microcirculatory disorders. In the early stage, the complexion may become pale and gray, the limbs may feel cold, the fingertips or toes may become pale, the heart rate may be fast (150-160 times/min), the pulse may become thin and rapid, the blood pressure may drop or cannot be measured, the lips and nail beds may become cyanotic, dyspnea may worsen, and symptoms of cardiac and renal insufficiency may appear.

  (2) Brain type (respiratory failure type):It is the most serious manifestation of toxic dysentery, caused by cerebral vascular spasm leading to cerebral hypoxia, cerebral edema, even cerebral hernia, and central respiratory failure. It may also lead to coma due to frequent or persistent convulsions, initially manifested as irregular breathing rhythm, uneven depth, and then appearing double inspiration, sighing breath, mandibular breathing, and respiratory arrest; at the beginning, the pupils may dilate and contract, and later, the pupils on both sides may not be equal in size, the light reflex may disappear, and sometimes sudden respiratory arrest may occur after 1 to 2 convulsions.

  (3) Mixed type:The most serious, with symptoms of circulatory failure, convulsions, respiratory failure, and circulatory failure are the three severe manifestations of toxic dysentery. Generally, convulsions appear first, and if not promptly rescued, they will rapidly develop into respiratory failure and circulatory failure.

  Second, chronic dysentery

  If the course of dysentery recurs or persists for more than 2 months, it is considered chronic dysentery. The reasons for the chronicity of dysentery can roughly be divided into two aspects: on the one hand, the patient's resistance is low, such as failure to treat during the acute stage, malnutrition, gastrointestinal diseases, and decreased intestinal secretory IgA; on the other hand, the bacterial strain, such as the Flexneri group bacteria, which is prone to chronic infection; some drug-resistant strain infections can also cause chronic dysentery. According to clinical manifestations, it can be divided into three types.

  1. Chronic dysentery acute attack type:Within half a year, there is a history of dysentery, often caused by eating cold food or catching a cold, fatigue, and other factors. Abdominal pain, diarrhea, purulent blood stool, and fever is usually not prominent.

  2. Chronic persistent type:After an acute dysentery attack, if not cured, there are often abdominal pain, diarrhea, loose mucus stool or purulent blood stool, or constipation alternating with diarrhea, left lower abdominal tenderness, palpable thickened sigmoid colon, long-term diarrhea leading to malnutrition, anemia, fatigue, and so on. Stool often intermittently excretes bacteria, and the results of Shigella stool culture are sometimes negative and sometimes positive.

  3. Chronic concealed type:Have a history of dysentery, no clinical symptoms, Shigella can be detected in stool culture, and abnormal findings can be found in sigmoidoscopy. Chronic dysentery is most common in chronic persistent type, followed by chronic relapsing type, and a few cases are of chronic concealed type.

4. How to prevent Shigellosis?

  The prevention of dysentery should adopt comprehensive measures, focusing on cutting off the route of transmission, while also managing the source of infection well.

  1. Manage the source of infection:Mainly for acute and chronic patients and carriers. Relying on rural cooperative medical stations and urban medical units, organize epidemic report, discover patients early, and especially for mild atypical diseases, make detailed records for timely treatment. Acute patients should be isolated and disinfected at home or in the hospital, and receive thorough treatment. A stool culture should be conducted every other day, and isolation can be lifted only after two consecutive negative cultures. For those working in child care institutions, the food and beverage industry, canteen cooks, and water supply staff at waterworks, regular stool cultures must be conducted.

  2. Cut off the route of transmission:Achieve the 'Three Controls and One Eradication' (that is, to manage drinking water, food, and feces well, and to eradicate flies); 'Four Shoulds and Three Should Nots' (to completely eradicate flies, wash hands before and after meals, wash and blanch vegetables and fruits when eaten raw, report and treat dysentery at an early stage, do not drink unboiled water, do not eat decayed and unclean food, and do not defecate or urinate at will). Prevent the formation of breeding grounds for flies, formulate annual fly eradication measures according to the law of the rise and fall of flies. Pay special attention to the spread of dysentery in children's institutions and collective units. It is necessary to strictly implement various hygiene systems, such as the hygiene system for tableware, food, living quarters, activity places, and children's toys. Regularly check whether the water quality of centralized water supply meets hygiene requirements. The water quality of wells and rivers in rural areas should be especially noted. Practice has proven that eradicating pests, maintaining hygiene, and purifying the environment are effective measures to cut off the routes of transmission.

  3. Protect susceptible populations:In recent years, mainly oral live vaccines have been used, generally using three types of vaccines: ① naturally non-toxic strains; ② strains of dysentery bacteria or non-toxic Shigella bacteria hybridized with Escherichia coli; ③ variant strains. Currently, China mainly uses variant strains, using the catabolic strain to prepare vaccines (which can grow and reproduce on culture media containing streptomycin). The monovalent or bivalent vaccines developed in China have been observed in 36 field trials involving tens of thousands of people, proving to have good effects with a protection rate of 66.41% to 99.47%. Live vaccines obtain immunity mainly by stimulating the intestinal tract to produce secretory IgA and cell-mediated immunity, with an immunity period that can last from 6 to 12 months. Some people may experience diarrhea after taking them. Due to the strain specificity of Shigella immunity, sometimes there may be an outbreak of a strain different from the vaccine used, which has no protective effect. In some areas, according to local conditions, traditional Chinese medicine is used for prevention during the epidemic process, such as taking garlic and Portulaca oleracea orally, which also has a certain effect.

  4. Wash hands thoroughly before handling food:Dirty clothes and bedding should be soaked in soapy water in a covered bucket and then boiled for disinfection. Houses should use mosquito nets and barriers. Appropriate isolation measures should be taken for patients and carriers, especially for fecal isolation. An oral live vaccine is under development, and field trials in epidemic areas have shown promising prospects, but the immunity is generally strain-specific.

  5. Personal hygiene:Do not drink unboiled water and drink boiled water instead. It is best to use water from a pressurized well. Wash fruits, vegetables, bowls, and chopsticks with disinfected water; wash hands before meals and after defecation; do not defecate on the ground; eat cooked food and not raw vegetables; heat leftovers before eating; separate raw and cooked foods to prevent flies from landing on food; it is best not to participate in large-scale catering activities such as weddings, funerals, and weddings; seek medical treatment in a timely manner after falling ill.

5. What laboratory tests are needed for Shigella infection?

  1. Blood count:Acute bacterial dysentery often has an increase in white blood cells, ranging from (10 to 20) × 10^9/L; an increase in neutrophils, with nuclear left shift, and mild anemia in chronic cases.

  2. Fecal examination:The fecal volume is small, and it is a purulent, bloody, and mucous stool. Microscopic examination shows clusters of pus cells, including red blood cells and macrophages, with pus cells often above 10 per high-power field. Isolation of pathogenic bacteria from fecal culture is of great value for diagnosis and guiding treatment. It is recommended to collect specimens before the start of antimicrobial therapy, take the purulent and bloody parts, and send them for examination immediately. Prolonged storage or mixing with urine may affect the positivity rate. The stage of illness at the time of specimen collection can affect the positive results, with the highest positivity rate on the first day of onset, reaching 50%, decreasing to 35% on the sixth day, and 14.8% on the tenth day. Multiple submissions can increase the positivity rate. To facilitate the isolation of pathogenic bacteria, selective media are often used. In the past, SS agar plates were commonly used, but recent findings have shown that they also have inhibitory effects on Shigella species. The use of xylose-lactose deoxycholate agar plates can increase the positivity rate. China also uses HE agar culture medium and MacConkey agar plates, which have achieved good results. Isolation of positive strains, timely determination of antibiotic sensitivity, is of reference significance for guiding clinical medication.

  3. Rapid pathogenic diagnosis:Including immunofluorescence bacterial agglutination method, enrichment latex agglutination method, synergistic agglutination test, immunofluorescence staining method, which can quickly obtain positive results from feces, with a positive rate of over 90%, which is helpful for the early diagnosis of Shigellosis.

  4. Monoclonal antibody sandwich immunoassay (DIAB) and reverse indirect hemagglutination method:Recently, some people have used it to detect antigens of Shigella flexneri in feces, with good sensitivity and specificity, worthy of further study.

  5. DNA probe method:Some people use alkaline phosphatase-labeled probes and fecal specimens for hybridization, with early positive rates reaching 85%, significantly higher than the 56% positive rate of conventional culture, thereby increasing the positive rate of early diagnosis.

  6. Sigmoidoscopy:Acute Shigellosis shows diffuse congestion and edema of the colonic mucosa, with superficial ulcers and exudates. Performing sigmoidoscopy only increases the patient's pain and carries certain risks, and is generally not recommended. Chronic Shigellosis shows colonic mucosal congestion, edema, and superficial ulcers, and the mucosa may appear granular and polyps and other proliferative changes can be seen. Scraping mucus and purulent secretions for culture can improve the positive rate.

  7. X-ray examination:Chronic Shigellosis can show changes such as intestinal spasm, disappearance of pouches, thickening of intestinal wall, narrowing of intestinal lumen, and shortening of intestinal segments when undergoing barium meal or barium enema.

6. Dietary taboos for Shigella infection patients

  1. Pay attention to drinking boiled water and eating cooked food. Wash fruits and vegetables before eating, and pay attention to the disinfection of bowls and chopsticks. Pay attention to personal hygiene and develop the good hygiene habit of washing hands before meals and after defecation.

  2. For diarrhea patients, the diet should be easy to digest and avoid cold, hard foods. Hot noodles, millet congee, and other foods can be consumed, with attention to small and frequent meals to reduce the burden on the gastrointestinal tract.

  3. For patients with dehydration, timely fluid replacement therapy is required. Pay attention to correcting electrolyte imbalance.

7. Conventional method of Western medicine for treating Shigella infection

  1. Treatment

  1. Acute Shigellosis

  (1) General treatment: Patients with obvious symptoms must rest in bed and follow the disinfection and isolation procedures for intestinal infectious diseases. Diet should consist mainly of liquid food. After the condition improves, switch to porridge, noodles, and other foods. Avoid cold, greasy, and刺激性 foods. If dehydration occurs, appropriate fluid replacement should be considered. For infants with dehydration within the range of 5% to 10% of body weight, the oral rehydration salt solution (ORS) recommended by the World Health Organization can be used, containing 20g of glucose, 3.5g of sodium chloride, 2.5g of sodium bicarbonate, and 1.5g of potassium chloride per liter of water. This solution has been tested in nearly 2000 cases across China, with an average efficacy rate of 96.9%. For patients with repeated vomiting or severe dehydration, consider initial intravenous fluid replacement, and as soon as possible switch to oral rehydration.

  (2) Antibacterial treatment: In recent years, the resistance of Shigella to various drugs and antibiotics has increased year by year. Currently, most Shigella strains are resistant to commonly used antibacterial drugs such as sulfonamides, streptomycin, chloramphenicol, and tetracycline, resulting in a corresponding decrease in clinical efficacy. Bacteria can show multiple drug resistance. Therefore, when choosing antibiotics for dysentery, it should be based on the local drug sensitivity test of the epidemic strain or the culture of the patient's stool samples to avoid indiscriminate and targeted misuse. In certain areas, attention should be paid to drug rotation. The evaluation of the efficacy of antibacterial drugs should be mainly based on the negative conversion rate of stool culture, and the negative conversion rate at the end of treatment should reach above 90%. Commonly used drugs include the following:

  ① Quinolone drugs: They have the advantages of a broad spectrum of antibacterial activity and easy oral absorption. In recent years, the number of resistant strains has gradually increased, and resistance can also be mediated by plasmids. For Shigella infection, ciprofloxacin 400-600mg per day is commonly used, taken in two or three doses orally, for a course of 3-5 days. Other new quinolone drugs are also effective against Shigella infection.

  ② Sulfamethoxazole/trimethoprim (sulfamethoxazole-trimethoprim combination): The dose is 2 tablets per time, twice a day, for a course of 7 days. According to our usage results, the cure rate can reach above 95%. In recent years, resistance has gradually increased, and there is a trend of decreasing efficacy. It is contraindicated for those with sulfonamide allergy, leukopenia, and liver or kidney dysfunction.

  ③ Antibiotics: Shigella has developed resistance to commonly used antibiotics such as chloramphenicol, streptomycin, and ampicillin. Some strains are still relatively sensitive to doxycycline. Most pathogenic bacteria are still sensitive to kanamycin and gentamicin in vitro, but they can only be administered by injection, with good immediate effects. Due to the low concentration of drugs in the intestinal wall tissue, they are not excreted into the intestinal lumen, making it difficult to clear bacteria, prone to recurrence, and therefore, it is advisable to be used in combination with oral methoxymethane. Studies outside of China have shown that cephalosporin antibiotics also have good efficacy against Shigella and can be chosen when necessary. When deciding to use antibiotics, the severity of the disease, the age of the patient (the treatment of acute infectious gastroenteritis in the section 265 of bacterial infections should be referred to for children), health status, the possibility of further spread, and the possibility of bacterial resistance to antibiotics should be considered. In addition, early use of appropriate absorbable antibacterial drugs can significantly alleviate symptoms and reduce the excretion of Shigella. For children, the preferred regimen is 4mg/kg of the TMP component in TMP-SMX every 12 hours; for adults, a double-strength tablet (TMP 320mg) every 12 hours. Adults can also use norfloxacin 400mg orally twice a day or ciprofloxacin 500mg orally twice a day. Many Shigella strains may be resistant to ampicillin and tetracycline.

  ④ Traditional Chinese medicine treatment: Berberine 0.3g/time, 4 times/day, for a course of 7 days. Alternatively, raw garlic can be taken orally, or the decoction of Aegopodium leavenworthii can be taken orally, or the decoction of Pulsatilla chinensis can be taken orally, all of which have certain effects.

  2. Early treatment of toxic dysentery should be pursued.

  (1) Antimicrobial treatment: Intravenous infusion administration should be adopted, and ciprofloxacin, levofloxacin (levorotatory ofloxacin), or cephalosporin antibiotics can be used. After the condition improves, oral administration can be changed, with the same dose and course as acute dysentery.

  (2) Anti-shock treatment:

  ① Expanding blood volume: Early rapid fluid infusion should be given, using dextran 40 immediately at a dose of 10-15ml/kg body weight and 5% sodium bicarbonate at a dose of 5mg/kg body weight, intravenous push within 30min-1h to rapidly expand blood volume. Subsequently, use 1/2 sodium-containing solution (half physiological saline and glucose injection), intravenous rapid infusion at a rate of 30-50ml/kg body weight, completed within 6-8h; if blood pressure does not rise, mannitol (20%) can be infused intravenously at a dose of 1g/(kg·time), which can absorb interstitial fluid and play a role in expansion, and can also prevent the occurrence of cerebral edema. After the shock improves, maintain fluid infusion mainly with glucose, with a ratio of 3:1 to 4:1 to sodium-containing fluids, with a maintenance volume of 50-80ml/kg body weight over 24 hours, infused slowly intravenously.

  ② Vasoactive drugs: Toxic dysentery is mainly characterized by high resistance and low output shock, and should be treated with anisodamine (which has the effect of antagonizing acetylcholine and dilating blood vessels) at a dose of 0.5-1mg/kg body weight, 20-40mg for adults, intravenous push, once every 5-15 minutes. Until the face turns red, the limbs become warm, breathing improves, and blood pressure recovers, it can be temporarily discontinued. If the effect after medication is not good, phenylephrine and norepinephrine can be used for intravenous infusion, or isoproterenol 0.1-0.2mg can be added to 200ml of 5% glucose injection for intravenous infusion, which can enhance myocardial contractility and has a certain effect on some high resistance and low output shocks.

  ③ Cerebral edema: When patients have frequent convulsions, deepening coma, irregular breathing, cyanosis of the lips, 20% mannitol or 25% sorbitol should be administered promptly, at a dose of 1.5-2g/(kg·time), 2-3 times/day, intravenous push. At the same time, dexamethasone should be administered intravenously, sodium intake should be restricted, and this has a certain effect on controlling cerebral edema.

  ④ Cooling and oxygen therapy: Fever patients should be given physical cooling, which can reduce oxygen consumption and alleviate cerebral edema. For patients with high fever and frequent convulsions, a short-term administration of chlorpromazine and promethazine in the form of a winter sleep mixture at 1-2mg/kg body weight, intramuscular injection, can enhance the effect of physical cooling.

  Other treatments such as hot water bags can help alleviate abdominal discomfort, but methylcellulose preparations that can be absorbed and reduce irritation have no effect on diarrhea and tenesmus. Anticholinergic drugs and camphorated opium tincture should be used as little as possible, as they can cause intestinal stasis, prolong the fever period, and cause persistent bacterial shedding in feces.

  3. Chronic bacillary dysentery:The main treatment is comprehensive, including the combination of overall and local, internal and external factors.

  (1) General treatment: Pay attention to the rhythm of life, eat easily digestible and nutritious food, avoid cold and greasy foods. And actively treat gastrointestinal diseases and intestinal parasitic diseases.

  (2) Antimicrobial treatment: If a positive result is obtained, appropriate antibiotics should be selected according to the drug sensitivity, or effective antimicrobial drugs that have never been used in the past should be used, combined with two courses of treatment. For patients with chronic intestinal mucosal lesions that do not heal for a long time, local enema therapy should be used at the same time, which can be 200ml of 5% to 10% garlic solution plus 20mg of prednisone and 10ml of 0.25% procaine, administered once a night, 10-14 days as a course of treatment.

  (3) Immunotherapy: Shigella vaccine therapy, it is best to use autogenous vaccine, injected subcutaneously once every other day, 10-14 days as a course of treatment.

  (4) Adjusting intestinal flora: Chronic bacillary dysentery often has flora imbalance due to long-term use of antimicrobial drugs. Normal intestinal flora is suppressed, and transient flora or invasive flora dominate. Fermentation-type patients should limit milk and soy products. Putrefaction-type should limit protein intake. When the number of Escherichia coli decreases, lactose and vitamin C can be given. When the number of Enterococcus faecalis decreases, folic acid can be given. In addition, oral administration of lactic acid bacteria or Bacillus subtilis and other probiotics can be used to support anaerobic bacteria in the intestines.

  (5) Traditional Chinese medicine treatment: According to the principle of diagnosis and treatment based on TCM, for chronic bacillary dysentery with yin deficiency, it is advisable to nourish yin and clear the intestines, and Zishu Zhayu can be used; for虚寒type, it is advisable to warm the spleen and kidney, and consolidate and firm, and真人养脏汤can be used.

  II. Prognosis

  Bacillary dysentery is often a self-limiting disease, which usually recovers within 1 to 2 weeks. The prognosis is related to the following factors: ①The elderly, infants and young children, and patients with weakened immune function have more complications and serious prognosis; ②The mortality rate of toxic dysentery is high, especially in respiratory failure; ③Shigella dysenteriae serogroup I causes more severe symptoms, while Shigella flexneri is more likely to cause chronic disease, and drug-resistant strains affect the efficacy; ④Appropriate antimicrobial drugs play an important role in clearing the infection. Improper use of medication, insufficient treatment duration, and untimely treatment all affect the efficacy.

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