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:
- Shigella is a gram negative rod
- four species responsible for dysentery:
- 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:
- 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
- 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:
- 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
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