Shigella, Shigellosis
Shigella, Shigellosis
Shigella, Shigellosis
Dr.T.V.Rao MD
Dr.T.V.Rao MD
Shigella is one of the most infectious of bacteria and ingestion of as few as 100200 organisms will cause disease. Most individuals are infected with shigellae when they ingest food or water contaminated with human fecal material. Shigella can survive up to 30 days in milk, eggs, cheese or shrimps.
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Definition
An enterobacteriaceae Gram negative bacilli. Readily growth O2 + An O2. Metabolically active, fermenting a variety of substrates. Mostly non-motile, non sporing, non acid fast, 2-4um x 0.4 -0.6um rounded ends.
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CLASSIFICATION
4 SPECIES/SUBGROUPS BASED ON BIOCHEMICAL AND SEROLOGICAL CHARACTERS SHIGELLA DYSENTERIAE : 12 Serotypes SHIGELLA FLEXNERI : 6 serotypes SHIGELLA BOYDII : 18 SHIGELLA SONNEI : 17 Colicins types
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Taxonomy
Family Enterobacteriaceae
1. Shigella dysenteriae: most serious form of bacillary dysentery 2. Shigella flexneri: shigellosis in underdeveloped countries 3. Shigella sonnei: shigellosis in developed countries 4. Shigella boydii
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1. Non-mannitol-fermenters Shigella dysenteria 2. Mannitol-fermenters Shigella flexneri Shigella boydii Shigella sonnei
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Mannitol negative
Mannitol positive
Shigella dysenteria
Lactose fermenter
Indole negative
Indole positive
Shigella sonnei
Shigella boydii
CULTURAL CHARACTERISTICS All members of Shigella are aerobic and facultative anaerobes. Grow readily in culture media at pH 6.4 to 7.8 at 10 oC - 40 oC, with optimum of 37 oC. After 24 hours incubation, Shigella colonies reaches a diameter of about 2 mm. The colonies are circular, convex, colorless, but moderately translucent with smooth surface, and entire edges.
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PATHOGENESIS
SOURCE : MAN: CASE OR CARRIER MODE OF SPREAD: CONTAMINATED FINGERS, FOOD, FLIES, FOMITES PERSON TO PERSON TRANSMISSION INFECTIVE DOSE: 10-100 VIABLE BACILLI HIGHEST CONCENTRATION IN STOOL DURING EARLY/ACUTE INFECTION 103 TO 109 VIABLE BACILLI PER GRAM OF STOOL POST CONVALESCENT SHEDDING : LOW COUNTS 102 TO 103
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Transmission
Faecal-oral transmission is the main path of Shigella infection. Other modes of transmission include ingestion of contaminated food or water, contact with infected objects, or sexual contact. Outbreaks of Shigella infection are common in places where sanitation is poor.
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Penetrate through mucosal surface of colon (colonic mucosa) and invade and multiply in the colonic epithelium but do not typically invade beyond the epithelium into the lamina propria
(thin layer of fibrous connective tissue immediately beneath the surface epithelium of mucous membranes)
Preferentially attach to and invade into M cells in Peyers patches (lymphoid tissue, i.e., lymphatic system) of small intestine
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PATHOGENIC DETERMINANTS
O antigen: The ability to survive the passage through the host defenses may be due to O antigen. Invasiveness: Virulent Shigella penetrate the mucosa and epithelial cells of the colon in an uneven manner. Intracellular multiplication leads to invasion of adjacent cells, inflammation and cell death. Cell death is probably due to cytotoxic properties of shiga toxin that interfere with protein synthesis. The cellular death and resulting phagocytosis response by the host accounts for the bloody discharge of mucus and pus and shallow ulcers characteristic of the disease. Other toxins: It has a protein toxin which may be neurotoxic, cytotoxic, and enterotoxic. The enterotoxic property is responsible for watery diarrhea.
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PATHOGENICITY
Shigella dysenterys form a powerful exotoxin, it is associated with epidemics of bacillary dysentery. In man, shigellosis begins with symptoms of acute gastro-enteritis which is accompanied by abdominal pain and diarrhea.
As it progresses, diarrhea becomes more frequent and is usually accompanied Dr.T.V.Rao MD 18 colicky pain.
PATHOGENICITY
Later diarrhea losses its fecal characteristic and is followed by mucus with pus and blood. The disease is usually accompanied by fever and marked prostration. It is also known that children are more frequently attacked than adult persons and the symptoms are more severe.
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Penetrate through mucosal surface of colon (colonic mucosa) and invade and multiply in the colonic epithelium but do not typically invade beyond the epithelium into the lamina propria
(thin layer of fibrous connective tissue immediately beneath the surface epithelium of mucous membranes)
Preferentially attach to and invade into M cells in Peyers patches (lymphoid tissue, i.e., lymphatic system) of small intestine
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Note: This contrasts with Salmonella which multiplies in the phagocytic vacuole
Actin filaments propel the bacteria through the cytoplasm and into adjacent epithelial cells with cell-to-cell passage, thereby effectively avoiding antibody-mediated humoral immunity (similar to Listeria monocytogenes)
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and invade into M cells in Peyer's patches of small intestine M cells typically transport foreign antigens from the intestine to underlying macrophages, Shigella can lyse the phagocytic vacuole (phagosome) and replicate in the cytoplasm
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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 Dr.T.V.Rao MD 25
Pathogenesis and Virulence Factors (cont.) Shiga Toxin Effects in Shigellosis (cont.) 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)
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Clinical Syndromes
Process involves: 1. Ingestion 2. Non-invasive colonization and cell multiplication 3. Production of the enterotoxin by the pathogenic bacteria in the small intestine; Second stage: Adherence to and tissue invasion of large intestine Typical symptoms of dysentery Cytotoxic activity of Shiga toxin increases severity
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Clinical Features
FEVER BLOODY DIARRHOEA ABDOMINAL CRAMPS TENESMUS MUCUS , PUS CONVULSIONS MILD INFECTION :WATERY STOOL BACTEREMIA - RARE REITER,S SYNDROME HEMOLYTIC UREMIC SYNDROME
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Epidemiology Shigellosis is a major cause of diarrheal disease (developing nations) Major cause of bacillary dysentery (severe second stage form of shigellosis) Leading cause of infant diarrhea and mortality (death) in developing countries
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Epidemiology
Shigella occurs naturally in higher primates Spread from human to human via the fecal-oral route Less frequently, transmission by ingestion of contaminated food or water Outbreaks usually occur in close
communities; Secondary transmission occurs frequently
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Epidemiology
Low infectious dose (102-104 CFU) with 1-3 day incubation period Carriage of the organism persists for approximately one month following convalescence
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Epidemiology
HUMAN FECAL ORAL ROUTE ( water ,, food ,, feces ,, flies ) PERSON PERSON CONTACT CHIILDHOOD IID :: 10 - 100 ORGANIISMS HIIGH IINFECTIIVIITY IIP - 1 4 DAYS SOURCE - CASES ,, CARRIIERS DAYCARE CENTERS,, MENTAL IINST.. TRAVEL ,, HOMOSEXEUAL Dr.T.V.Rao MD
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LABORATORY DIAGNOSIS The only satisfactory method of laboratory diagnosis is to cultivate the bacilli from the patient. In the early stages of acute shigellosis, isolation of the causative organism from the feces is usually accomplished without difficulties by using the same special media and methods employed for salmonella
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LAB DIAGNOSIS
COLONIES ON MA/DCA : NLF PALE AND TRANSLUCENT COLONIES PICKED UP FOR THE FOLLOWING TESTS: HANGING DROP : NON MOTILE GRAMS :GNB BIOCHEMICAL TESTS : IMVIC ++-ANEROGENIC FERMENTERS SLIDE AGGLUTINATION WITH SPECIFIC HTS Dr.T.V.Rao MD
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Laboratory Identification:
Closely related to Escherichia Species (serogrouping and biochemical analysis Stool specimens and rectal swabs should be cultured soon after collection or placed in appropriate transport medium (Cary-Blair medium)
Readily isolated on selective/differential agar media (XLD, SS, and brilliant green agar)
Lactose nonfermenter
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Prevention
SUPPLY OF PURE WATER PERSONAL HYGIIENE ( HANDS) SEWAGE DIISPOSAL FOOD HYGIIENE IINSECT CONTROL (FLIIES) VACCIINE (ORAL) - 6 MONTHS
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Developed countries too Suffer Shigella Infections In developed countries, singlesource, food or water-borne outbreaks occur sporadically, and pockets of endemic shigellosis can be found in institutions and in remote areas with substandard sanitary facilities.
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Programme Created by Dr.T.V.Rao MD for Medical and Paramedical Students in the Developing World Email [email protected]
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