SHIGELLOSIS COLITIS

 

SHIGELLOSIS COLITIS

 

DEFINITION:

A bacterial infection of the colon caused by Shigella resulting in a dysenteric diarrhea.

EPIDEMIOLOGY:

  • incidence: ?
  • risk factors:
    • age: peaks between 2.3 years, rare in infants < 6 months
    • season: warm months, rainy season (in Tropics)
    • route: direct: fecal-oral
    • indirect: water, food (salads)
    • environ: endemic - daycare, families, institutions, gays epidemic - especially S. dysenteriae
  • incubation period: 3-4 days

PATHOGENESIS:

1. Background

  • Shigella is a gram negative rod
    • four species responsible for dysentery:
    • 1. Serogroup A - S. dysenteriae
    • 2. Serogroup B - S. flexneri
    • 3. Serogroup C - S. boydii
    • 4. Serogroup D - S. sonnei
  • S. sonnei and flexneri are the most common species causing dysentery in both developing and developed countries.
  • the virulence property of Shigella is invasiveness due to a group of genes encoded on a large (120-140 megadalton) plasmid which are involved in cell invasion and killing (EIEC harbours this virulence plasmid and thus behaves like shigella).
  • chromosomal genes are important for full virulence, i.e. shigatoxin. Shigatoxin is a protein-inhibiting exotoxin produced only by S. dysenteriae serotype 1 and EHEC.
  • Shigella are tranferred mainly by a fecal-oral route and are highly infectious with only 10-100 organisms needed to cause dysentery. These organisms can survive the acidity of the stomach for as long as 4 hours.
  • Once inside the epithelial cells, shigella multiply in the lamina propria & submucosa. Multiplication is an essential step as dysentery will not occur without it. Thus, invasion and multiplication of the Shigella are essential to the virulence.
  • With multiplication comes local inflammation, edema, hyperemia, and epithelial cell dysfunction. Microabscesses form behind obstructed crypts and superficial ulcers may lead to bleeding.
  • A fibrous exudate containing PMN covers the mucosal lining of the colon. Because of the superficial nature of the Shigella infection, intestinal perforation does not occur and bacteremia is unusual. Pathologically, major damage occurs in the distal colon and rectum although a pancolitis may occur with extension to the terminal ileum

CLINICAL FEATURES:

1. Prodrome

  • several days of abdominal cramps of variable severity, urgency, painful defecation, vomiting, anorexia, high fever, generalized toxicity; signs may include abdominal distension & tenderness, hyperactive bowel sounds, and tender rectum

2. Diarrhea

  • initially large volume watery diarrhea -> frequent small volume dysenteric stools (bloody diarrhea)
  • may have up to 20 stools per day
  • stools with blood, pus, mucous, viscous, odourous, WBC, RBC's
  • can be mild and self-limiting lasting 1-2 weeks, (10% > 10 days) or severe with a fever > 40 C with chills, severe tenesmus, and guarding

3. Gastrointestinal Manifestations

  • rapid dehydration with electrolyte & metabolic disturbances -> acute renal failure (ATN)
  • persistent chronic diarrhea (in malnourished children)
  • significant blood loss -> hypotension
  • intussusception
  • peritonitis

4. Central Nervous System Manifestations

  • most common extraintestinal manifestation occurring in up to 40% of patients
  • not due to the presence of a neurotoxin
  • seizures:
    • 12-45% risk of both afebrile and febrile seizures
    • increased risk if temperature > 40 C, less than 3 years of age, family history of seizures
  • meningismus (not meningitis) - associated with delirium, headache, nuchal rigidity, fainting, lethargy before or after the onset of the diarrhea

5. Others

1. Associated with S. Dysenteriae - serotype 1

  • thought to be secondary to the shigatoxin
  • hemolytic uremic syndrome (HUS)
  • hemolytic anemia
  • sepsis
  • gastrointestinal manifestations:
    • rectal prolapse
    • toxic megacolon
    • pseudomembranous colitis

2. Associated with S. Flexneri

  • conjunctivitis, iritis, corneal ulcers
  • pneumonia
  • cholestatic hepatitis
  • sterile joint effusions or arthritis (2-5 weeks after enteritis)
  • Reiter Syndrome
  • cystitis
  • vaginitis (with blood-tinged discharge)

3. Ekiri Syndrome

  • extreme toxicity
  • seizures
  • hyperpyrexia
  • rapid demise without sepsis or dehydration

4. Rare Complications

  • nephritis with hematuria
  • SIADH
  • DIC
  • death - 25-50% when associated with risk factors: sepsis, malnutrition, age <6 months

INVESTIGATIONS:

1. Stool

1. Culture

  • gold standard but still problems
  • from direct swab of a rectal ulcer or from stool
  • with MacConkey's agar or selective medium - XLD or SS agar
  • WBC's, RBC's

2. Biopsy

1. Pathology

  • ulcerations, pseudomembranes, epithelial cell death with PMN and mononuclear infiltration extending from the mucosa -> muscularis mucosae
  • submucosal edema

3. Colonoscopy

  • localized or diffuse mucosal edema, ulcerations, friable mucosa with blood and exudate

4. Serum

  • hyponatremic dehydration
  • hypocalcemic and hyponatremic (risks for seizures)
  • usually leukocytosis (5-15) with left shift (bandemia)
  • blood cultures + in 5% of cases
  • secretory IgA and IgG develop days -> weeks after infection and may be serotype specific or offer cross-protection

5. Cerebral Spinal Fluid

  • meningitis rare
  • pleocytosis with minimally elevated protein levels

MANAGEMENT:

1. Supportive

  • oral rehydration fluid (ORF) or intravenous rehydration, etc

2. Medications

  • 1. TMP-SMX - empiric drug of choice, oral or IV x 5 days
  • 2. Ampicillin - many strains now resistent (S. sonnei)
  • 3. Nalidixic Acid
  • 3. Prevention

    1. Prolonged breastfeeding

    • breastmilk contains antibodies to Shigella

    2. Handwashing Techniques

    • after defecation, during food preparation & consumption

     

     

     

    Pediatric Database - SHIGELLOSIS COLITIS

    Pediatric Organization - Pedbase [at] Gmail.com