shigellosis ( bacillary dysentery )
DESCRIPTION
SHIGELLOSIS ( Bacillary Dysentery ). Acute infectious disease of intestine caused by dysentery bacilli 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. - PowerPoint PPT PresentationTRANSCRIPT
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SHIGELLOSIS
(Bacillary Dysentery)
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INTRODUCTION Acute infectious disease of intestine caused by
dysentery bacilli 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
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EPIDEMIOLOGY 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 500 000 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.
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AETIOLOGY
Causative organism: dysentery bacilli, genus shigella, gram-stain negative, short rod,non-motile
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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NORMAL HABITAT
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
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TRANSMISSION
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.
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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.
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OUTER MEMBRANE AND SECRETED PROTEINS
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.
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SHIGA TOXIN ENTEROTOXIC EFFECT:
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 HCO3
- (loss of bicarbonate buffering capacity leads to metabolic acidosis) out of the intestine and into the lumen
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CYTOTOXIC EFFECT: 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
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PATHOGENESIS AND IMMUNITY
Shigellosis is primarily a pediatric disease, and is restricted to the GI tract.
Mean infective dose: 103. 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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INVASION OF INTESTINAL WALL BY SHIGELLA
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SHIGELLOSIS
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
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CLINICAL DISEASE: ACUTE DYSENTERY
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.
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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.
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Acute dysenterymild type: caused by S. sonneilow fever or no feverAbdominal pain is mildstool mixed with mucus, without blood & pusdiagnosis by isolation bacteria
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TOXIC TYPE:
Abrupt onset, high fever, Temperature rise to 40oCListlessness, lethargy, convulsion, coma.circulatory & respiratory collapsediarrhea mild or absent at beginning
shock form: septic shock brain form: respiratory failure mixed form
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CHRONIC DYSENTERY
Chronic dysentery: > 2 monthsChronic delayed type: diarrhea long-time and
repeatedChronic obscure type: acute history in 1 year, no
symptoms, stool culture Pos. or sigmoidscopyAcute attack type: same as common acute
dysentery
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LABORATORY DIAGNOSIS Blood picture: total WBC count increase, neutrophils increase Stool examination:direct microscopic exam.: WBC, RBC, pus cellsbacteria culture:
Sigmoidoscope: shallow ulcer, scar, polyps
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TREATMENT
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.
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PREVENTION AND CONTROL
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.