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home - Colon - Colonic Infection - Shigella Written by Dr Sebastian Zeki
Knowledge

Recognises the range of important inflammatory conditions of the
intestine other than inflammatory bowel disease
Knows the range of potential aetiologies including infection and
ischaemia
Understands how diverticular disease can give rise to complications mini-CEX, SCE 1
Knows how diseases can affect the peritoneum and how such
conditions can present both in the acute and chronic situation
Knows the range of both acute and chronic intestinal infections and
their various presentations
Knows the means of investigations of infectious diseases and
understands the principles and use of antimicrobial therapy

Skills
Makes a full clinical assessment of patients presenting with infective
and inflammatory conditions
Recognises the potential urgency of the clinical situation. Selects
appropriate investigations and treatments

Behaviours
Manages patients with inflammatory and infective conditions carefully,
competently and sympathetically.

Shigella

Step 1: Bacterium released into cell cytoplasmStep 2: Host actin organises to form a tail behind the bacterium Step 3: Tail motors protrusions into other cellsStep 4: Protrusions are then endocytosedStep 5: Bacterium enter the cell. M-cell Inflammatory Response Shigella effector proteins variably block induction of NFkB signaling, alter signaling via the MAPK kinase pathway , and alter transcription of immunomodu-latory proteins thus altering the immune system to its advantage Shigella infection is generally limited to the intestinal mucosaShigella bacteremia v. rare 100 organisms cause diseaseShigella are relatively resistant to killing by stomach acid Shigella species 1.S. dysenteriae 2. S. Flexneri3. S. sonnei, 4. S. Boydii -Direct person-to-person spread -Contaminated food and water Clinical ManifestationsFever — in 35 % .Abdominal pain —in 85 % .Mucoid diarrhea —in 77 %.Bloody diarrhea —in 40% .Watery diarrhea — in 35 %.Vomiting — in 35 %. 1-7 day incubation Lasts up to 7 days if left untreated Colonic perforation — Rare/ Usually in children or severely malnourished.Assoc. with S. dysenteriae 1 or S. flexneri.Toxic megacolon — Assoc with S. dysenteriae 1 / The incidence is 3 %.Associated with level of inflammationIntestinal obstruction — Assoc with S. dysenteriae 1/Incidence of 2.5 %.Severe colonic disease may result in intestinal obstruction.Proctitis or rectal prolapse — In children TreatmentIt is usually self limiting.Give antibiotics ( ciproflox-cin or azithromycin) if stool culture +ve for public health reasons and reduces fever by 2 days. Can be shed for up to 6 weeks after symptoms have resolved DIagnosisHot stool is needed for diagnosis. Systemic complications Metabolic disturbances — Volume depletion rare as low stool vol.Hyponatremia due to SiADHA protein-losing enteropathy. Bacteremia —Incidence 5%/ More commoon in kidsAssoc with deathNot increased in HIV Hemolytic-uremic syndrome Shigella. can cause HUS by cytotoxic damage to vascular endothelium by Shiga-toxin from S. dysenteriaeNo role for antibiotics. Reactive arthritis —Reiter’s 2weeks after S. flexneri infection regardless of antibiotics70% HLA-B27 positive- mechanism is probably molecular mimicry to this Neurologic disease —Seizures are due to feverLeast common with S. dysenteriae No sequelae/ no assoc with shiga toxinEncephalopathy with lethargy, confusion, and headache has been noted in up to 40 % kidsEkiri syndrome associated with S. sonnei-characterized by seizures and coma with high fever and few dysenteric symptoms. Leukemoid reaction — Usually in kids.Predicts worse prognosis Dec NaDec Protein Gut complications EnterotoxinsAll species produce the virulence plasmid-encoded ShET2 .S.dysenteriae 1 produce Shiga toxin (Stx) similar to the Stx1 and 2toxins of E.coli 0157:H7- this mediates hemolytic-uremic syndrome.Each enterotoxin induces intestinal secretion of solutes and water. 1 2 3 4 5 Shigella Pathogenesis Written by Dr Sebastian Zeki

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