SHIGELLA

The genus Shigella contains fewer species than the genus Salmonella and is antigenically less complex. It belongs to the Enterobactericeae family. Clinical dysentery may be caused by Shigella, Salmonella, Entamoeba histolytica.

Gram

ve rods

Non

motile

Facultative

anaerobes but grows best aerobically.

Non

lactose fermenters.

Resistant

to bile salts.

Mannitol fermentation

positive

negative

Shigella sonnei

Shigella flexneri

Shigella boydii

Shigella dysenteria

Yellow color indicates mannitol fermentation

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 reach a diameter of about 2 mm. The colonies are circular, convex, colorless, but moderately translucent with smooth surface

Specimens for culture includes fresh stool, mucus flecks, and rectal swabs.

Shigella release toxic lipopolysaccharide. Endotoxin contributes to

the irritation of the

bowel wall.

(shiga bacillus) produces a heat labile exotoxin known as Shiga toxin. Shiga toxins inhibits protein synthesis within target cells. Effects the gut and the CNS. It has 3 types of effects 1. Enterotoxin 2. Cytotoxin 3. Neurotoxin

S dysenteriae type 1

Carriers of pathogenic strains can excrete the organism up to two weeks after infection and occasionally for longer periods. Shigella are killed by drying. Shigella are transmitted by the fecal-oral rout. The highest incidence of Shigellosis occur in areas of poor sanitation and where water supplies are polluted.

The ability to survive from the host defenses may be due to O antigen. O antigens of shigella are lipopolysaccaride in nature. Other toxins: It has a protein toxin which may be neurotoxic, cytotoxic, and enterotoxic. The enterotoxic property is responsible for watery diarrhea.

 Penetrate the

mucosa and epithelial cells of the colon in an uneven manner.  Intracellular multiplication leads to inflammation and cell death

Early stage: y Watery diarrhea attributed to the enterotoxic activity of Shiga toxin following ingestion and invasive colonization, multiplication, and production of enterotoxin in the small intestine y Fever attributed to neurotoxic activity of toxin

Adherence and tissue

invasion of large intestine with typical symptoms of dysentery

Cytotoxic activity of Shiga toxin increases severity

The Shigella first cross the mucous membrane

Shigella are taken up by M-cells in large intestine by endocytosis.

The M cell passes the Shigella on to a macrophage

Macrophages then take up the shigella

Macrophages that take up the shigella are killed and release organism.

The bacteria multiply and enter the epithelial cells.

Actins filament quickly form a tail and push the bacteria into next cell.

Infected cells die  Acute inflammatory response occurs with bleeding & abscess formation


 Water

and electrolytes replacement. Antibiotic therapy is required to eliminate the organism. Due to the emergence of resistant strains of shigella, antibiotic sensitivity, must be performed on any shigella to determine suitable antibiotics

Sulfonamides Tetracycline Chloramphenicol Ampicillin Streptomycin

are known to be effective against

shigella.

Short lived; Preparation of oral live attenuated vaccine is the way to stimulate mucosal IgA Prevention Sanitary precautions. Good personal hygiene (hand washing).