Shigella : Clinical Findings, Pathogenesis, Lab Diagnosis and Treatment
Introduction:
SOURCE:
- MAN: CASE OR CARRIER
MODE OF SPREAD:
- CONTAMINATED FINGERS, FOOD, FLIES, FOMITES
- PERSON TO PERSON TRANSMISSION
- Gut pathology is due to toxin
INFECTIVE DOSE:
- 10-100 VIABLE BACILLI
- HIGHEST CONCENTRATION IN STOOL DURING EARLY/ACUTE INFECTION:
- 103 TO 109 VIABLE BACILLI PER GRAM OF STOOL
PATHOGENESIS
Invasiveness (main):
- Bacteria invade basolateral surface of colon epithelium
- Intracellular replication
- Cell to cell spread with the help of microbial protein
- ICS A (ATP-ase)
- Host protein cadherin L – CAM.
- Responsible for late dysentery.
- Nontoxic mutants can cause dysentery but non-inttasive can’t produce dysentery.
Toxins:
- Endotoxin
- LPS
- Cause irritation of bowel.
Shigella Dysenteriae-
- Produces heat labile exotoxin (Shigabacillus exotoxin)
Affect gut and CNS:
- Show neurotoxicity on blood vessel of CNS
- Can lead to miningsmus and coma.
- Cytotoxicity = Verotoxin I or Shiga like toxin
- Toxin has two peptide subunit.Toxins produce early, non bloody voluminous diarrhea.
- A unit (N-glycosidase) of cytotoxin hydrolyzes adenine from specific sites of 60s RNA
- Inhibits protein synthesis.
- Contributes to fatal nature.
CLINICAL SYMPTOMS:
- Shigella Associated with hemolytic uremic Syndrome
- 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 diarrhoea attributed to the enterotoxic activity of Shiga toxin
- Fever attributed to neurotoxic activity of toxin
- Majority of lesion are in distal colon.
COMPLICATIONS
- Toxic dilatation
- Colonic perforation
- Thrombotic thrombocytopenic purpura
- Reactive arthritis
- Reiter’s syndrome.
- HUS
- Schistocytes are suggestive of hemolytic-uremic syndrome (HUS)
DIAGNOSIS
- Sampling: fresh stool, mucus flakes and rectal swabs
- Selenite F broth(0.4%) is used as enrichment and transport media (for 9-12hours)
- Total blood count reveals anemia and thrombocytopenia, and schistocytes
- Increase blood urea nitrogen(BUN)
- Invasive test for shigella is Rabbit ileal loop
TREATMENT:
- Oral rehydration therapy (No antibiotics) for mild to moderate dehydration.
- Ciprofloxacin, Fluoroquinol, Azithromycin, Pivmecillinam, Ceftriaxone
- Preventing infected individuals from handling food
- DOC for multiresistant Nalidixic acid.
Exam Important
Introduction:
- PERSON TO PERSON TRANSMISSION
- Gut pathology is due to toxin
INFECTIVE DOSE:
- 10-100 VIABLE BACILLI
Toxins:
- Endotoxin
- LPS
- Cause irritation of bowel.
Shigella Dysenteriae-
- Produces heat labile exotoxin (Shiga bacillus exotoxin)
Affect gut and CNS:
- Show neurotoxicity on blood vessel of CNS
- Cytotoxicity = Verotoxin I or Shiga like toxin
- Toxins produce early, non bloody voluminous diarrhea.
CLINICAL SYMPTOMS:
- Shigella Associated with hemolytic uremic Syndrome
- 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 diarrhoea attributed to the enterotoxic activity of Shiga toxin
- Fever attributed to neurotoxic activity of toxin
- Majority of lesion are in distal colon.
COMPLICATIONS
- HUS
- Schistocytes are suggestive of hemolytic-uremic syndrome (HUS)
DIAGNOSIS
- Sampling: fresh stool, mucus flakes and rectal swabs
- Selenite F broth(0.4%) is used as enrichment and transport media (for 9-12hours)
- Total blood count reveals anemia and thrombocytopenia, and schistocytes
- Increase blood urea nitrogen(BUN)
- Invasive test for shigella is Rabbit ileal loop
TREATMENT:
- Oral rehydration therapy (No antibiotics) for mild to moderate dehydration.
- Ciprofloxacin, Fluoroquinol, Azithromycin, Pivmecillinam, Ceftriaxone
- DOC for multiresistant Nalidixic acid.
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