Shigellosis (bacterial dysentery). Acute and Chronic Dysentery
Intestinal amoebiasis, Acute amoebic dysentery, Acute amoebiasis, Intestinal amoebiasis
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Acute amoebic dysentery (A06.0)
general information
Short description
Acute amoebic dysentery
- the main and most common form of amoebic invasion, characterized by a disorder of the stool with ulcerative lesions of the colon.
Flow period
The incubation period lasts from 1-2 weeks to 3 months or longer.
Classification
The disease can occur in severe, moderate and mild form.
Etiology and pathogenesis
When cysts enter the human small intestine, their membranes are destroyed and a four-nuclear maternal form of amoeba comes out of them, which, when divided, forms 8 single-nuclear amoeba. Under favorable conditions, they multiply, turning into vegetative forms that live in the proximal colon.
Amoeba's own enzymes have proteolytic activity, which ensures their penetration into the intestinal wall. In the intestine, cytolysis of the epithelium and tissue necrosis with the formation of ulcers occur. In intestinal amoebiasis, the pathological process is mainly localized in the blind and ascending colon. In some cases, there is a lesion of the rectum, less often - other parts of the intestine.
Epidemiology
Amoebiasis - intestinal anthroponosis. The transmission mechanism is fecal-oral. Various ways of transmission are possible: food, water, contact-household.
Sporadic morbidity is characteristic (the possibility of epidemic outbreaks is questioned). Diseases are recorded throughout the year, the peak incidence occurs during the hot months.
It occurs in all countries of the world, the highest incidence is typical for areas of tropical and subtropical climate, including in Central Asia and Transcaucasia. The ratio between incidence and carriage in endemic areas is 1:7, in the rest - from 1:21 to 1:23.
Factors and risk groups
Particularly susceptible to amoebiasis are women in the third trimester of pregnancy and the postpartum period (it is assumed that this is due to the peculiarities of the cellular immune response in pregnant women), as well as those who have received immunosuppressive therapy.
Clinical picture
Symptoms, course
The state of health remains satisfactory for a long time: intoxication is not expressed, the body temperature is normal or subfebrile. Only in a small number of cases, patients have general weakness, fatigue, headaches, loss of appetite, a feeling of heaviness in the epigastrium. Epigastrium - the region of the abdomen, bounded from above by the diaphragm, from below by a horizontal plane passing through a straight line connecting the lowest points of the tenth ribs.
, sometimes - short-term pain in the abdomen, flatulence.
The cardinal symptom of intestinal amoebiasis is a disorder of the stool. In the initial period, the stool is plentiful, fecal, with clear mucus, 4-6 times a day, with a pungent odor. Later, the frequency of bowel movements increases to 10-20 times a day, the stool loses its fecal character and is a vitreous mucus. In the future, blood is mixed with the stools and they take on the appearance of raspberry jelly.
In the acute form of the disease, constant or cramping pains in the abdomen of varying intensity are possible, which are aggravated by defecation. When the rectum is affected, painful tenesmus occurs Tenesmus - false painful urge to defecate, for example, with proctitis, dysentery
.
The abdomen is soft or slightly swollen, on palpation it is painful along the colon.
Acute symptoms of intestinal amoebiasis usually persist for no more than 4-6 weeks. Then, without specific treatment, as a rule, there is an improvement in well-being and relief of colitis syndrome. Duration of remission - from several weeks to several months. After remission, all or most of the symptoms of amoebiasis return.
Diagnostics
In the diagnosis of amoebiasis, a carefully collected epidemiological history, an anamnesis of the disease, and data from a clinical examination of patients matter.
Helps to recognize the disease sigmoidoscopy Sigmoidoscopy is a method for examining the rectum and sigmoid colon by examining the surface of their mucous membrane using a sigmoidoscope inserted into the intestinal lumen
and biopsy intestinal mucosa, X-ray examination.
Endoscopy colon reveals ulcers ranging in size from 2 to 10-20 mm in diameter, located most often on the tops of the folds. Ulcers have edematous, swollen, undermined edges; the bottom of the ulcer can reach the submucosa, covered with pus and necrotic masses. The ulcer is surrounded by a zone (belt) of hyperemia Hyperemia - increased blood supply to any part of the peripheral vascular system.
. The mucous membrane free from ulcers is changed a little, its small puffiness and a hyperemia can sometimes be observed.
Irrigoscopy Irrigoscopy - X-ray examination of the colon with retrograde filling with a contrast suspension
reveals uneven filling of the colon, the presence of spasm and rapid emptying of the intestine.
Laboratory diagnostics
The most important for the diagnosis of amoebic dysentery is the detection of a large vegetative form of amoeba in stool, a tissue form of amoeba in sputum, abscess contents and material from the bottom of ulcers. Detection of translucent forms and amoeba cysts in the feces is not enough for a final diagnosis.
Main Method amoeba detection - microscopy of native preparations of feces.
Differential Diagnosis
Amoebic dysentery is differentiated from other protozoal infections, dysentery, ulcerative colitis, and intestinal cancer.
Complications
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Acute and Chronic Dysentery
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Disease Code (ICD-10) A03.0
Dysentery (syn.: shigellosis) (dysenteria) - an infectious disease caused by shigella, occurring with symptoms of intoxication and a predominant lesion of the distal colon.
Distinguish between acute and chronic dysentery.
- Acute dysentery occurs in several variants (colitis, gastroenterocolitic and gastroenteric), each of which can be presented in mild, moderate and severe forms.
- Chronic dysentery has a recurrent or continuous course and can also occur in mild, moderate and severe form.
- There is also shigellosis (bacterioexcretion), which is considered as a subclinical form of the infectious process.
Acute dysentery
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Mild colitis disease is characterized by moderate or mild intoxication. It usually begins acutely with a short-term rise in temperature to 37-38 ° C. In the first hours of the disease, weakness, loss of appetite are observed, later moderate pains in the abdomen appear. Chair from 3-5 to 10 times a day. The stools are semi-liquid or liquid, often with mucus and sometimes streaked with blood. Patients remain able-bodied and often resort to self-treatment. On examination, the tongue is coated. The sigmoid colon is painful and spasmodic, rumbling is noted during its palpation. With sigmoidoscopy, catarrhal or catarrhal-hemorrhagic proctosigmoiditis and sphincteritis can be detected. Changes in the hemogram are insignificant. The disease lasts 3-5, less often 7-8 days and ends with recovery.
Colitis variant with moderate severity usually begins acutely, with chills, a feeling of "ache" and weakness throughout the body. The temperature rises to 38-39 ° C and stays at this level for 3-5 days, rarely longer. Anorexia, headache, nausea, sometimes vomiting, sharp cramping pains in the abdomen, tenesmus are often observed. Stool frequency 10-20 times a day. The stools quickly lose their fecal character and consist of mucus stained with blood. They can be sparse, in the form of a "rectal spit" or more abundant, mucous. The phenomena of hemocolitis are observed in 70-75% of patients. Acute phenomena on the 3rd–5th day of illness gradually subside. In the feces, the amount of mucus and blood decreases, the stool normalizes, but the coprogram remains pathological. Sigmoidoscopy reveals catarrhal-erosive proctosigmoiditis. Clinical recovery occurs by the end of the 2nd week of illness.
The heavy current of the political option dysentery is characterized by an acute onset with a rise in temperature to 39 ° C and above, a pronounced intoxication. There may be fainting, delirium, nausea, vomiting. Pain in the abdomen is pronounced and accompanied by painful tenesmus and frequent urge to urinate. Stools from 20-25 to 50 times a day, scanty, stool-free, muco-bloody. Sometimes the stools look like meat slops. Patients are lethargic, adynamic. The skin and mucous membranes are dry, blood pressure is reduced, there is a constant tachycardia. By the end of 1–2 days, a collaptoid state may develop. Tenesmus and spasms of the intestine can be replaced by its paresis, bloating, gaping anus and involuntary defecation. In the blood, leukocytosis or leukopenia is observed with a shift of the leukocyte formula to the left and toxic granularity in leukocytes. Palpation of the abdomen reveals spasm, soreness and rumbling of the large intestine (or only the sigmoid colon), flatulence. The severe condition of patients persists for 7-10 days. With sigmoidoscopy in case of Zone dysentery, catarrhal-hemorrhagic, catarrhal-erosive, less often ulcerative changes in the mucous membrane are determined. In severe cases of Flexner's dysentery, fibrinous-necrotic, fibrinous-ulcerative and phlegmonous-necrotic lesions of the colon mucosa are detected. The disease lasts 3-6 weeks or more.
In persons with immunodeficiency of various origins, there may be no pronounced fever, but the damage to the colon is of a total nature.
Gastroenterocolitic variant dysentery proceeds according to the type of food poisoning with a short incubation period, a rapid onset of the disease. The main syndrome at the onset of the disease is gastroenteritis, which is accompanied by severe symptoms of intoxication. In the future, the symptoms of enterocolitis begin to dominate. For the initial period, vomiting, profuse diarrhea, profuse watery stools without admixture of blood and mucus, diffuse pain in the abdomen are typical. Subsequently, the stool becomes less abundant, it contains impurities of mucus and blood. This variant can be mild, moderate or severe. When assessing the severity of the course of the disease, the degree of dehydration of the body is taken into account. In the case of a mild course of dysentery, there are no symptoms of dehydration. The moderate course of the disease is accompanied by dehydration of the 1st degree (fluid loss is 1-3% of body weight). In severe dysentery, dehydration of II-III degree develops (fluid loss is 4-9% of body weight).
The gastroenteric variant is close downstream to the initial period of the gastroenterocolitic variant. Its difference lies in the absence of symptoms of colitis in the later period of the disease (after 2–3 days of illness). Leading are the symptoms of gastroenteritis and signs of dehydration.
Erased flow dysentery occurs in all variants of the disease. It is characterized by mild abdominal pain and short-term (within 1-2 days) bowel dysfunction. The stools are semi-liquid, without blood and often without mucus. Body temperature is normal, but may be subfebrile. Often, palpation is determined by increased sensitivity of the sigmoid colon. In the coprogram, the number of leukocytes exceeds 20 in the field of view. Sigmoidoscopy reveals catarrhal proctosigmoiditis. The diagnosis is established after a thorough history of the disease, epidemiological history, as well as timely laboratory examination.
Protracted course of acute dysentery characterized by the persistence of clinical signs of the disease for 1.5–3 months. At the same time, in most patients, the phenomena of a sluggish inflammatory process in the intestine with the absence of its functional and morphological recovery in terms of up to 3 months are noted.
Complications: formidable, but relatively rare complications of the disease include toxic-infectious and mixed (toxic-infectious + dehydration) shocks. They develop during the height of the disease and have a serious prognosis. Complications of acute dysentery include its relapses, which are observed in 5-15% of cases. Some patients experience exacerbations of hemorrhoids, anal sphincter fissures. Debilitated patients may develop complications associated with the addition of secondary flora: pneumonia, ascending urogenital infection, and severe intestinal dysbacteriosis.
Rarer complications include perforation of intestinal ulcers with subsequent peritonitis, toxic dilatation of the intestine, thrombosis of mesenteric vessels, and rectal prolapse.
Acute dysentery relatively rarely becomes chronic (with Flexner's dysentery in 2-5%, with Sonne's dysentery - in 1% of cases).
Chronic dysentery
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There are two forms of chronic dysentery - recurrent and continuous.
Recurrent form occurs much more often than continuous and is characterized by alternating remissions and relapses of dysentery. The duration of each new return of the disease and light intervals may be different. The symptoms of damage to the distal colon predominate. However, a systematic examination of a patient with chronic dysentery can reveal signs of involvement in the pathological process of the stomach, small intestine, pancreas, and hepatobiliary system.
The clinical picture of relapse is similar to that of mild or moderate acute dysentery. Intestinal dysfunction is characterized by persistence and duration.
The central nervous system suffers to a greater or lesser extent. Patients are irritable, excitable, their performance is reduced, sleep is disturbed, headaches are frequent. Some of them have pronounced vegetative disorders (symptoms of vagotonia are more common).
Sigmoidoscopy reveals polymorphic changes in the mucous membrane of the rectum and sigmoid colon. During an exacerbation, the sigmoidoscopy picture resembles the changes characteristic of acute dysentery. However, their intensity in different areas is not the same. Alternation of bright hyperemia with paler areas of the mucous membrane is possible, on which an expanded vascular network is clearly visible. The mucous membrane in these places is thinned, dull, easily injured.
- A03.0. Dysentery caused by Shigella dysenteriae.
- A03.1. Dysentery due to Shigellaflexneri.
- A03.2. Dysentery caused by Shigella boydii.
- A03.3. Dysentery caused by Shigella sonnei.
- A03.8. Another dysentery.
- A03.9. Dysentery, unspecified.
ICD-10 code
A03 Shigelez
A03.0 Shigellosis due to Shigella dysenteriae
A03.1 Shigellosis due to Shigella flexneri
A03.2 Shigellosis due to Shigella boydii
A03.3 Shigellosis due to Shigella sonnei
A03.8 Other shigellosis
A03.9 Shigellosis, unspecified
What causes dysentery?
The Shigella species is ubiquitous and is a typical cause of inflammatory dysentery. Shigella is the cause of 5-10% of diarrheal diseases in many regions. Shigella are divided into 4 main subgroups: A, B, C and D, which in turn are divided into specific serotypes. Shigella flexneri and Shigella sonnei are found more frequently than Shigella boydii and especially the virulent Shigella dysenteriae. Shigella Sonnei is the most common isolate in the US.
The source of infection is the faeces of sick people and recovering carriers. Direct spread is via the fecal-oral route. Indirect spread occurs through contaminated food and objects. Fleas can serve as carriers of Shigella. Most often, epidemics occur in densely populated populations with inadequate sanitation measures. Dysentery is especially common in young children living in endemic regions. In adults, the resulting dysentery is usually not so acute.
Convalescent and subclinical carriers can be a serious source of infection, but long-term carriage of this microorganism is rare. Dysentery leaves little to no immunity.
The causative agent penetrates the mucosa of the lower intestine, which causes mucus secretion, hyperemia, leukocyte infiltration, edema, and often superficial ulceration of the mucosa. Shigella dysenteriae type 1 (not found in the US) produces Shiga toxin, which causes severe watery diarrhea and sometimes hemolytic uremic syndrome.
What are the symptoms of dysentery?
Dysentery has an incubation period of 1-4 days, after which the typical symptoms of dysentery appear. The most common manifestation is watery diarrhea, which is indistinguishable from diarrhea that occurs with other bacterial, viral, and protozoal infections, in which there is an increased secretory activity of intestinal epithelial cells.
In adults, dysentery may begin with episodes of cramping abdominal pain, urge to defecate, and defecation of shaped feces, followed by temporary relief of pain. These episodes are repeated with increasing severity and frequency. Diarrhea becomes pronounced, while the stool can be soft, liquid, contain an admixture of mucus, pus and often blood. Rectal prolapse and subsequent stool incontinence may be the cause of acute tenesmus. In adults, the infection may present without fever, with diarrhea without mucus or blood in the stool, and with little or no tenesmus. Dysentery usually ends in convalescence. In the case of a moderate infection, this occurs after 4-8 days, in the case of an acute infection, after 3-6 weeks. Severe dehydration with electrolyte loss and circulatory collapse and death usually occurs in debilitated adults and children under 2 years of age.
Rarely, dysentery begins suddenly with rice water diarrhea and serous (in some cases bloody) stools. The patient may vomit and quickly become dehydrated. Dysentery can manifest with delirium, convulsions, and coma. In this case, diarrhea is mild or absent. Death can occur within 12-24 hours.
In young children, dysentery begins suddenly. This causes fever, irritability or tearfulness, loss of appetite, nausea or vomiting, diarrhea, abdominal pain and bloating, and tenesmus. Within 3 days, blood, pus and mucus appear in the stool. The number of bowel movements can reach more than 20 per day, while weight loss and dehydration become acute. If left untreated, the child may die within the first 12 days of illness. In cases where the child survives, the symptoms of dysentery gradually decrease towards the end of the second week.
Secondary bacterial infections may occur, especially in debilitated and dehydrated patients. Acute mucosal ulceration can lead to acute blood loss.
Other complications are rare. These may include toxic neuritis, arthritis, myocarditis, and rarely intestinal perforation. Hemolytic uremic syndrome may complicate shigellosis in children. This infection cannot take a chronic course. Also, it is not an etiological factor in ulcerative colitis. Patients with the HLA-B27 genotype after shigellosis and other enteritis are more likely to develop reactive arthritis.
How is dysentery diagnosed?
Diagnosis is made easier by a high index of suspicion for shigellosis during outbreaks, the presence of the disease in endemic regions, and the detection of stool leukocytes on smears stained with methylene blue or Wright's stain. Stool culture is diagnostic and should therefore be performed. In patients with symptoms of dysentery (presence of mucus or blood in the feces), differential diagnosis of dysentery with invasive E. coli, salmonella, yersinia, campylobacteriosis, as well as amoebiasis and viral diarrhea is necessary.
The mucosal surface, when examined with a rectoscope, is diffusely erythematous with many small ulcers. Despite the fact that the number of leukocytes is reduced at the beginning of the disease, on average it is 13x109. Hemoconcentration is common, as is diarrhea-related metabolic acidosis.
