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  1. 1. Shigella Dr Sabrina Moyo Department of Microbiology and Immunology
  2. 2. Definition <ul><li>An enterobacteriaceae </li></ul><ul><li>Gram negative bacilli. </li></ul><ul><li>Readily growth O2 + An O2. </li></ul><ul><li>Metabolically active, fermenting a variety of substrates. </li></ul><ul><li>Mostly non-motile, non sporing, non acid fast, 2-4um x 0.4 -0.6um rounded ends. </li></ul>
  3. 3. Morphology & Physiology <ul><li>   Small Gram-negative, facultatively anaerobic, coliform bacillus </li></ul><ul><li>   Non-motile (no H antigen) </li></ul><ul><li>   Possess capsule (K antigen) and O antigen </li></ul><ul><li>   K antigen not useful in serologic typing, but can interfere with O antigen determination </li></ul><ul><li>   O antigens : A, B, C, D correspond respectively to the four species </li></ul><ul><li>   Non-lactose fermenting </li></ul><ul><li>   Bile salts resistant: trait useful for selective media </li></ul><ul><li>ferment glucose </li></ul><ul><li>reduce nitrates (NO 3 to NO 2 or N 2 ) </li></ul><ul><li>are oxidase negative </li></ul>
  4. 4. Taxonomy <ul><li>Family Enterobacteriaceae </li></ul><ul><li>Shigella dysenteriae : most serious form of bacillary dysentery </li></ul><ul><li>Shigella flexneri : shigellosis in underdeveloped countries </li></ul><ul><li>Shigella sonnei : shigellosis in developed countries </li></ul><ul><li>Shigella boydii </li></ul>
  5. 5. Taxonomy <ul><li>Classification: 4 groups or species on the based on difference in O antigen and some biochemical reactions </li></ul><ul><li>Group A - S. dysenteriae 1-10 </li></ul><ul><li>group B - S. flexneri 1-6 </li></ul><ul><li>group C - S. boydii 1-15 </li></ul><ul><li>group D - S. sonnei 1 </li></ul>
  6. 6. Clinical Syndromes (Shigellosis) <ul><li>   Ranges from asymptomatic infection to severe bacillary dysentery </li></ul><ul><li>   Two-stage disease: watery diarrhea changing to dysentery with frequent small stools with blood and mucus, tenesmus , cramps, fever </li></ul><ul><li>Early stage : </li></ul><ul><li>   Watery diarrhea attributed to the enterotoxic activity of Shiga toxin </li></ul><ul><li>   Fever attributed to neurotoxic activity of toxin   </li></ul>
  7. 7. Clinical Syndromes <ul><li>Process involves: </li></ul><ul><li>1. Ingestion </li></ul><ul><li>2. Non-invasive colonization and cell multiplication </li></ul><ul><li>3. Production of the enterotoxin by the pathogenic bacteria in the small intestine; </li></ul><ul><li>  Second stage : </li></ul><ul><li>   Adherence to and tissue invasion of large intestine </li></ul><ul><li>   Typical symptoms of dysentery </li></ul><ul><li>   Cytotoxic activity of Shiga toxin increases severity </li></ul>
  8. 8. Epidemiology <ul><li>   Shigellosis is a major cause of diarrheal disease (developing nations) </li></ul><ul><li>   Major cause of bacillary dysentery (severe second stage form of shigellosis) </li></ul><ul><li>    Leading cause of infant diarrhea and mortality (death) in developing countries </li></ul>
  9. 9. Epidemiology <ul><li>Shigella occurs naturally in higher primates </li></ul><ul><li>Spread from human to human via the fecal-oral route </li></ul><ul><li>  Less frequently, transmission by ingestion of contaminated food or water </li></ul><ul><li>   Outbreaks usually occur in close communities; </li></ul><ul><li>   Secondary transmission occurs frequently </li></ul>
  10. 10. Epidemiology <ul><li>  Low infectious dose (10 2 -10 4 CFU) with 1-3 day incubation period </li></ul><ul><li>Carriage of the organism persists for approximately one month following convalescence </li></ul>
  11. 11. Pathogenesis & Immunity <ul><li>Invasiveness involves attachment (adherence) and internalization </li></ul><ul><li>Controlled by a multi-gene virulence plasmid </li></ul><ul><li>Organisms penetrate through colonic mucosa </li></ul><ul><li>invade and multiply in the colonic epithelium </li></ul><ul><li>Not beyond the epithelium into the lamina propria </li></ul>
  12. 12. Pathogenesis & Immunity <ul><li>  Bacterial cells preferentially attach to and invade into M cells in Peyer's patches of small intestine </li></ul><ul><li>M cells typically transport foreign antigens from the intestine to underlying macrophages, </li></ul><ul><li>Shigella can lyse the phagocytic vacuole (phagosome) and replicate in the cytoplasm </li></ul>
  13. 13. Pathogenesis & Immunity <ul><li>Exotoxin (Shiga toxin) is neurotoxic , cytotoxic , and enterotoxic , encoded by chromosomal genes, </li></ul><ul><li>Enterotoxic effect : Shiga toxin adheres to small intestine receptors </li></ul><ul><li>Blocks absorption (uptake) of electrolytes, glucose, and amino acids from the intestinal lumen </li></ul>
  14. 14. Pathogenesis & Immunity <ul><li>Cytotoxic effect: B subunit of Shiga toxin binds host cell glycolipid in large intestine , </li></ul><ul><li>Inactivate the 60S ribosomal subunit, </li></ul><ul><li>Inhibit protein synthesis, causing cell death, microvasculature damage to the intestine, and hemorrhage (blood and fecal leukocytes in stool) </li></ul><ul><li>   Neurotoxic effect: Fever, abdominal cramping are considered signs of neurotoxicity </li></ul>
  15. 15. Laboratory Identification : <ul><li>Closely related to Escherichia </li></ul><ul><li>Species (serogrouping and biochemical analysis </li></ul><ul><li>Stool specimens and rectal swabs should be cultured soon after collection or placed in appropriate transport medium ( Cary-Blair medium) </li></ul><ul><li>Readily isolated on selective/differential agar media ( XLD , SS , and brilliant green agar </li></ul><ul><li>Lactose nonfermenter </li></ul>
  16. 16. Treatment, Prevention & Control : <ul><li>Dehydration is problem to attend </li></ul><ul><li>Treat carriers, major source of organisms; Cirpflxacin , Erythromycin </li></ul><ul><li>Antibiotic resistance is a major problem </li></ul><ul><li>Proper sewage disposal and water chlorination </li></ul><ul><li>Oral vaccines of Shigella : E. coli hybrids or Shigella mutants offers immunity for six months to one year </li></ul>
  17. 17. <ul><li>THANK YOU! </li></ul>