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l Acute infectious disease of intestine caused by dysentery bacilli l Place of lesion: sigmoid & rectum  Shigellosis is endemic throughout the world.

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Presentation on theme: "l Acute infectious disease of intestine caused by dysentery bacilli l Place of lesion: sigmoid & rectum  Shigellosis is endemic throughout the world."— Presentation transcript:

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2 l Acute infectious disease of intestine caused by dysentery bacilli l Place of lesion: sigmoid & rectum  Shigellosis is endemic throughout the world where it is held responsible for some 120 million cases of severe dysentery with blood and mucus in the stools

3  About 1.1 million people are estimated to die from Shigella infection each year, with 60% of the deaths occurring in children under 5 years of age.  about cases of shigellosis are reported each year among military personnel and travellers from industrialized countries  Since the late 1960s, pandemic waves of Shigella dysentery have hit sub-Saharan Africa, Central America and South and South-East Asia.

4 l Causative organism: dysentery bacilli, genus shigella, gram-stain negative, short rod,non-motile l Groups: 4 groups & 50 serotypes - S. Dysenteriae-the most severe - S. Flexnerii- endemic in developing countries. easily turn to chronic - S. Boydii - S. sonnei -the most mild

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6  Found only in the human intestinal tract.  Carriers of the pathogenic strain can excrete the organisms up to 2 wks after the infection &occasionally for longer periods.  Killed by drying

7  Transmitted by fecal-oral route  High incidence of shigellosis occur in areas of poor sanitation and where water supplies are polluted.  Lack of personal hygiene  Young children are more frequently affected than adults [> 6 months]  Horseflies are also thought to be important in transferring Shigella from faeces to food.  Epidemics can be caused by ingestion of contaminated milk and milk products.

8 Antigenic structure  Differentiation into groups (A, B, C, and D) is based on O antigen serotyping; K antigens may interfere with serotyping, but are heat labile.  Virulence factors  Shiga toxin – An A-B toxin produced by S. dysenteriae and in smaller amounts by S. flexneri and S. sonnei.  Enterotoxic, neurotoxic and cytotoxic effects  This Damages intestinal epithelium and glomerular endothelial cells (associated with HUS) plays a role in the ulceration of the intestinal mucosa.

9  These proteins are expressed at body temperature and upon contact with M cells in the intestinal mucosa they induce phagocytosis of the bacteria into vacuoles  Shigella destroy the vacuoles to escape into the cytoplasm  From there they spread laterally (Polymerization of actin filaments propels them through the cytoplasm.) to epithelial cells where they multiply but do not usually disseminate beyond the epithelium.

10  Adheres to small intestine receptors  Blocks absorption (uptake) of electrolytes, glucose, and amino acids from the intestinal lumen  Note: This contrasts with the effects of cholera toxin (Vibrio cholerae) and labile toxin (LT) of enterotoxigenic E. coli (ETEC) which act by blocking absorption of Na +, but also cause hypersecretion of water and ions of Cl -, K + (low potassium = hypokalemia), and HCO 3 - (loss of bicarbonate buffering capacity leads to metabolic acidosis) out of the intestine and into the lumen

11  B subunit of Shiga toxin binds host cell glycolipid  A domain is internalized via receptor-mediated endocytosis (coated pits)  Causes irreversible inactivation of the 60S ribosomal subunit, thereby causing:  Inhibition of protein synthesis  Cell death  Microvasculature damage to the intestine  Hemorrhage (blood & fecal leukocytes in stool)  Neurotoxic Effect: Fever, abdominal cramping are considered signs of neurotoxicity

12  Shigellosis is primarily a pediatric disease, and is restricted to the GI tract.  Mean infective dose:  Mouth colon invade M cells and subsequently spread to mucosal epithelial cells cause microabscess in the wall of colon and terminal ileum necrosis of the mucous membrane, superficial ulceration, bleeding, and formation of pseudomembrane.

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16 Two-stage disease:  Early stage:  Watery diarrhea attributed to the enterotoxic activity of Shiga toxin following ingestion and noninvasive colonization, multiplication, and production of enterotoxin in the small intestine  Fever attributed to neurotoxic activity of toxin  Second stage:  Adherence to and tissue invasion of large intestine with typical symptoms of dysentery  Cytotoxic activity of Shiga toxin increases severity

17  Common Type Incubation period: 1-3 days  Sudden onset of abdominal pain, fever and watery diarrhea, number of stools increase, less liquid, often contain mucus and blood, rectal spasms with resulting lower abdominal pain (tenesmus)  symptoms subside spontaneously in 2-5 days in adult cases, but loss of water and electrolytes frequently occur in children and the elderly. a small number of patients remain chronic carriers.

18  Some cases are accompanied by hemolytic uremic syndrome (HUS), characterized by acute hemolysis, renal failure, uremia, and disseminated intravascular coagulation.  Death can occur from circulatory collapse or kidney failure.  Total WCC is raised with neutrophilia  Infection with S. dysenteriae can lead to leukemoid reaction developing 5-10 days after infection caused by an endotoxin.  S. sonnei is not very pathogenic, therefore infections are rarely serious.

19 Acute dysentery mild type: caused by S. sonnei low fever or no fever Abdominal pain is mild stool mixed with mucus, without blood & pus diagnosis by isolation bacteria

20 Abrupt onset, high fever, Temperature rise to 40 o C Listlessness, lethargy, convulsion, coma. circulatory & respiratory collapse diarrhea mild or absent at beginning shock form: septic shock brain form: respiratory failure mixed form

21 l Chronic dysentery: > 2 months Chronic delayed type: diarrhea long-time and repeated Chronic obscure type: acute history in 1 year, no symptoms, stool culture Pos. or sigmoidscopy Acute attack type: same as common acute dysentery

22  Blood picture: total WBC count increase, neutrophils increase  Stool examination: direct microscopic exam.: WBC, RBC, pus cells bacteria culture:  Sigmoidoscope: shallow ulcer, scar, polyps

23  oral rehydration therapy, intravenous fluid replacement  Antibiotic treatment: chloramphenicol, ceftriaxone, ciprofloxacine, tetracycline, and trimethoprim- sulfamethoxazole. Drug resistance is common.  Restoration of electrolytes  Opiates and anti-diarrhoea medications should be avoided.

24  Humans are the only reservoir for shigellae.  Transmission of shigellae: water, food, fingers, feces, and flies.  Most cases occur in children under 10 years of age.  Prevention and control of dysentery:  1. Sanitary control of water, food and milk; sewage disposal; and fly control.  2. Isolation of patients and disinfection of excreta.  3. Detection of subclinical cases and carriers.


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