BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000

Shigella Summary

Morphology & Physiology:

  Small Gram-negative, facultatively anaerobic, coliform bacillus

  Non-motile (no H antigen)

  Possess capsule (K antigen) and O antigen

  K antigen not useful in serologic typing, but can interfere with O antigen determination

  O antigens: A, B, C, D correspond respectively to the four species

  Non-lactose fermenting

  Bile salts resistant: trait useful for selective media

Taxonomy:

  Family Enterobacteriaceae

  All Enterobacteriaciae:

1. ferment glucose
   

2. reduce nitrates (NO₃ to NO₂ or all the way to N₂)
   
3. are oxidase negative

   Four species:

1. Shigella dysenteriae: causes most serious form of bacillary dysentery
2. Shigella flexneri: most common cause of shigellosis in underdeveloped countries
3. Shigella sonnei: most common cause of shigellosis in developed countries
4. Shigella boydii

Clinical Syndromes (shigellosis):

  Ranges from asymptomatic infection to severe bacillary dysentery

  Two-stage disease: watery diarrhea changing to dysentery with frequent small stools with blood and mucus, tenesmus, cramps, fever

  Early stage:

  Watery diarrhea attributed to the enterotoxic activity of Shiga toxin

  Fever attributed to neurotoxic activity of toxin

  Process involves:

1. Ingestion
2. Noninvasive 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

Epidemiology:

  Shigellosis is a major cause of diarrheal disease throughout the developing nations of the world

  Major cause of bacillary dysentery (severe second stage form of shigellosis) in pediatric age group (1-10 years old) via fecal-oral transmission

  Estimated 15%-20% of pediatric diarrhea in United States

  Leading cause of infant diarrhea and mortality (death) in developing countries

  Shigella occurs naturally in higher primates, so shigellosis is spread from human to human via the fecal-oral route primarily by contaminated hands (ingestion is portal of entry)

  Less frequently, transmission by ingestion of contaminated food or water

  Outbreaks usually occur in close communities; Daycare facilities account for a large proportion of cases that occur in the U.S.

  Secondary transmission occurs frequently

  Low infectious dose (10²-10⁴ CFU) with 1-3 day incubation period

  Carriage of the organism persists for approximately one month following convalescence

Pathogenesis & Immunity:

 

  Organisms penetrate through colonic mucosa (mucosal surface of colon) and invade and multiply in the colonic epithelium but do not typically invade beyond the epithelium into the lamina propria

  Bacterial cells preferentially attach to and invade into M cells in Peyer's patches of small intestine (lymphoid tissue, i.e., lymphatic system)

  M cells typically transport foreign antigens from the intestine to underlying macrophages, but Shigella can lyse the phagocytic vacuole (phagosome) and replicate in the cytoplasm ( 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)

  Exotoxin (Shiga toxin) is neurotoxic, cytotoxic, and enterotoxic, encoded by chromosomal genes, with two domain (A-5B) structure similar to the Shiga-like toxin of enterohemorrhagic E. coli (EHEC) (except that Shiga-like toxin is encoded by lysogenic bacteriophage)

  Enterotoxic effect: Shiga toxin adheres to small intestine receptors and 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 LT (labile toxin produced by enterotoxigenic E. coli, i.e., ETEC) which block absorption of Na⁺, but 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)

  Cytotoxic effect: B subunit of Shiga toxin binds host cell glycolipid in large intestine, A1 domain internalized via receptor-mediated endocytosis (coated pits) and causes irreversible inactivation of the 60S ribosomal subunit, thereby inhibiting protein synthesis, causing cell death, microvasculature damage to the intestine, and hemorrhage (blood and fecal leukocytes in stool)

  Neurotoxic effect: Fever, abdominal cramping are considered signs of neurotoxicity

Laboratory Identification:

  Closely related to Escherichia

  Four distinct species differentiated on basis of serogrouping and biochemical analysis

  Stool specimens and rectal swabs should be cultured soon after collection or placed in appropriate transport medium (e.g., Cary-Blair medium)

  Readily isolated on selective/differential agar media (e.g., XLD, SS, and brilliant green agar

  Lactose nonfermenter

Treatment, Prevention & Control:

  Dehydration is problem to attend

  Treat carriers, major source of organisms; Ampicillin and trimethoprim-sulfamethoxazole are effective antibiotics that reduce duration of carriage

  Antibiotic resistance is a major problem

  Proper sewage disposal and water chlorination

  Oral vaccines of Shigella: E. coli hybrids or Shigella mutants offers immunity for six months to one year

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