SHIGELLA SPP.

Features of SHIGELLA SPP.

• 4 serogroup based on O antigen

  1. Shigella dysenteriae (serogroup A)

• Produce Shiga toxin

• Severe disease

• Cannot ferment mannitol

• Complication : hemolytic uremic syndrome

  
  

  2. Shigella flexneri (serogroup B)

• In sexual transmitted infection

• Associated with Reiter’s syndrome

3. Shigella sonnei

• late lactose fermenter

• B-D-galactosidase and ornithine decarboxylase +ve

4. Shigella boydii

Characteristics of Shigella spp. compared to Salmonella spp.

1. Highly selective agars

• to isolate and identify Gram -ve enteric pathogen Salmonella and Shigella spp.

2. Xylose-Lysine Deoxycholate agar

• Shigella spp.

→ red/ pink colonies

→ not ferment xylose

→ No H2S produce

3. Salmonella-Shigella agar

• Non lactose fermenter

• Colorless colonies

• No black center

• No H2S produced

  
  

Virulence factor of Shigella spp.

1. Shiga toxin

• produced by S.dysenteriae type 1

• Produce dysentery diarrhea

2. Lipopolysaccharide

• act as endotoxin

• Activated once cell is destroyed

• Damages adjacent epithelium

3. Type III secretion system

• plasmid encoded

• Invasion and entry

• Modulate actin tail formation for invasion

Pathogenesis

INTRACELLULAR MOVEMENT

• transcytosis via M-cells of epithelium — cross intestinal barrier

• Enter intestinal epithelium— M cell engulf Shigella spp in vacuole

• Shigella able to escape and travel to laminate propria

• Macrophages will phagocytose Shigella

• Shigella able to evade degradation by induce apoptosis of macrophages and produce pro inflammatory cell death

INTERCELLULAR MOVEMENT

• invade adjacent colonic epithelium cell from basolateral side

• T3SS deliver effectors to modulate actin

• Develops actin tail and able to moves freely across cells

• Shigella reproduce rapidly

• Invasion causing acute inflammatory cascade

• Massive release of cytokines (IL 1 beta, IL8)

• Neutrophil infiltration

• Microabscesses and necrotic lesion in mucosa

• Acute inflammatory colitis

• Dysentery, fever and abdominal pain

SHIGA TOXIN OF S.DYSENTERIAE 1

• B subunit of Shiga toxin bind to Gb3 of surface host cell

• A subunit internalized the toxin via endocytosis

• Transport to Golgi apparatus and endoplasmic reticulum

• Cleaves to A1 and A2 subunit

• A1 subunit will bind to 28s rRNA and cleaves it

• Lead to cessation of protein synthesis

• Cell death and necrosis

• Tissue destruction and hemorrhagic colitis

Laboratory diagnosis

1. Sample

• stool sample — immediate transport and workup

2. Stool microscopy

• presence of RBC and pus cell

3. Direct plating on special or selective agar

• Mac Conley agar → non lactose fermenter

• Salmonella-Shigella agar → good growth, non lactose fermenter, no H2S

• Xylose-Lysine Deoxycholate→ non xylose fermentation, no H2S

4. Biochemical test

• TSI agar : A/K, gas-, H2S-

• Late lactose fermenter : S.sonnei

• Mannitol fermentation : non fermenter for S.dysenteriae

• B-D-galactosidase and ornithine decarboxylase → +ve for S.sonnei

Mode of transmission

• Fecal oral transmission

• Person to person spread