2. Definition
“Bacillary dysentery” – an anthroponosis
infectious disease with faecal-oral mechanism
of transmission, caused by Shigella,
characterized by clinical syndrome of fever,
acute colitis involving mainly the distal colon
and the rectum (intestinal cramps, and
frequent passage of small, bloody,
mucopurulent stools).
3. Historical data
Hippocrates suggested the name
“Dysentery” – abdominal pains with bloody
diarrhoea
Avicenna – first described the disease
The discovery of Shigella is attributed to the
Japanese microbiologist Kiyoshi Shiga who
isolated the Shiga bacillus (now known as
Shigella dysenteriae type 1).
5. Aetiology
Gram-negative rod
Non-spore-forming
Nonmotile
Produces entero-, cyto-, neurotoxin
Grows on MacConkey medium
Perishes at 60°С within 30 min, at 100°С – 1 min
Resistant to drying & low temperature
Sensitive to disinfectants
8. Aetiology
Pathogenecity of Shigella:
- endotoxin: intoxication
- enterotoxin: increases secretion of water and
electrolytes
- cytotoxin: affection of epithelial cells of bowel
- neurotoxin: (Shigella dysenteriae type 1)
10. Epidemiology
Anthroponosis, enteric infection
Mechanism of transmission – faecal-oral
Source of infection:
- patients with acute shigellosis (excretion
of Shigella is greatest)
- patients with chronic shigellosis
- shigella carriers
Season – summer-autumn
Immunity – serotype specific, not more than 1
year
11. Routs of transmission
Food Drinking Person
water to person
cEndogenous Contaminated Faecal
pathogens with faeces contamination
Not cooked Contact,
thoroughly fingers put in
mouth
12. Distribution
The prevalence of the species associated with dominant
route of transmission in that very area
Sh. Dysenteriae type 1 is more prevalent in
developing countries (Africa, South-East Asia, Latin
America) where personal and general hygiene is below
standard
Sh. flexneri – in the least developed countries (watery
route of transmission)
Sh. sonnei – in economically emerging countries
and in the industrialized world (contaminated dairy
products)
Sh. boydii – in Indian subcontinent
13.
14. Pathogenesis
Enter via gastro-intestinal tract (through oral
contamination)
Resistance to low-pH conditions allows shigella
to survive passage through the gastric barrier
Destructed by HCl, lysozyme and releasing
endotoxin intoxication
In small bowel multiply and release enterotoxin
binds to a receptors diarrhoea
Invasion of shigella in large bowel occurs later,
but more extensive
15. Pathogenesis
Attach and invade the М-cell (microfold cell)
located in Peyer patches
Delivery of Shigella to macrophages (МF)
Shigellae survive phagocytosis by inducing
programmed cell death (apoptosis)
Death of MF (apoptosis) leads to release of IL-1,
IL-6, TNF- (proinflammatory cytokines)
Chemotaxis activation attraction of PMNs into
the infected tissues colonocytes inflammation
destabilizes the integrity of the intestinal wall
rearrangement of actin filaments in the host
cells cell-to-cell passage occurs
16. Pathogenesis of colitic syndrome
1. Disorder of intestine innervation,
inflammation of mucous membrane: sharp
spastic abdominal pain
2. Irregular contractions of different parts of
bowel: small volume stool with
inflammatory exudate (mucus, blood)
3. Rectal and sigmoid colon muscles cramps:
false urges to defecate and tenesmus
21. Classification
By duration According to
clinical variant
According to
the severity
• Acute
• Chronic
• Colitic
• Gastroentero-
colitic
• Gastroeneritic
(Sonnei)
• Mild
• Moderate
• Severe
22. Clinical features
Incubation period – 2-5 days
The presentation and severity of shigellosis depends
to some extent on the infecting serotype but even
more on the age, immunologic and nutritional status
of the host.
Severe shigellosis caused by Sh. dysenteriae type 1
and Sh. Flexneri
Shigellosis caused by Sh. boydii similar to Sh. sonnei
23. Colitic variant
The most frequent variant (90%) with
intoxication & distal hemorrhagic colitis
Intoxication syndrome:
- acute onset
- fever 1-3 days
- weakness, headache, dizziness
- anorexia
24. Colitic variant
Distal haemorrhagic colitis:
1. abdominal cramps in left lower abdominal part
2. tenesmus and false urges to defecate
3. very frequent, small volume stool with blood
and mucus - “rectal sputum“
4. palpation of the sigmoid colon is painful
5. incompletely closed anus (anal dysenteric
syndromes rarely)
* Unlike most diarrheal syndromes, dysenteric
syndromes rarely present with dehydration as a
major feature.
25.
26.
27. Gastroenteritic variant
Intoxication
Nausea, vomiting,
Diffuse abdominal pain, cramps,
Large volume watery stool
Dehydration (I-II degree)
Gastroenterocolitic variant
The same symptoms +
after 2-3 days - small volume stool with
mucus & blood
28. Shigellosis caused by Sh. dysenteriae type 1
Severe course (mortality 15 times higher, than in
cholera)
Chills, fever up to 40°C
Large volume watery stool “meat water“ small
volume stool with mucus & blood
Tenesmus, abdominal cramps
Rectal prolapse, toxic megacolon
Vomiting, dehydration of II-IV degree
Convulsions, collapse, impairment of consciousness
(till coma)
Infectious-toxic chock, sepsis
Haemolytic-uremic syndrome (in the second week)
35. Complications
Acute life-threatening complications most often
- in children <5 years of age (particularly those who
are malnourished)
- in elderly patients.
Risk factors for death in a clinically severe case
include:
- nonbloody diarrhea,
- moderate to severe dehydration,
- bacteremia,
- absence of fever,
- abdominal tenderness,
- rectal prolapse.
36. Complications
Major complications are predominantly
intestinal:
- toxic megacolon,
- intestinal perforations,
- rectal prolapse
- metabolic (e.g., hypoglycemia, hyponatremia,
dehydration).
* Bacteremia is rare and is reported most
frequently in severely malnourished and HIV-
infected patients.
37. Toxic megacolon
is a consequence of severe inflammation extending to
the colonic smooth-muscle layer and causing paralysis
and dilatation.
abdominal distention and tenderness, with or without
signs of localized or generalized peritonitis.
on abdominal x-ray - marked dilatation of the
transverse colon (with the greatest distention in the
ascending and descending segments);
thumbprinting caused by mucosal inflammatory
edema;
loss of the normal haustral pattern associated with
pseudopolyps,
If perforation occurs, radiographic signs of
pneumoperitoneum may be apparent.
38. Thumbprinting sign
The normal haustra become thickened at regular intervals appearing
like thumbprints projecting into the aerated lumen.
39. Megacolon
Predisposing factors should be
investigated:
- hypokalemia
- use of opioids, anticholinergics, loperamide,
psyllium seeds, and antidepressants
40. HUS
is a nonimmune (Coombs test–negative) hemolytic anemia
defined by a diagnostic triad:
- microangiopathic hemolytic anemia (hemoglobin level
typically <80 g/L [<8 g/dL]),
- thrombocytopenia (mild to moderate in severity;
typically <60,000 platelets/μL),
- acute renal failure due to thrombosis of the
glomerular capillaries (with markedly elevated
creatinine levels).
Anemia
is severe, with fragmented red blood cells (schizocytes) in
the peripheral smear,
high serum concentrations of lactate dehydrogenase
free circulating hemoglobin,
elevated reticulocyte counts.
50. Pathogenetic therapy
Spasmolytics or antimotility agents (no-
spa, mebeverine, papaverine) are
suspected of increasing the risk of toxic
megacolon and HUS (in children infected
by EHEC strains).
For safety reason, it is better to avoid
antimotility agents in bloody diarrhoea.
51. Conclusion
Shigellosis is the most common cause of
acute bloody diarrhoea
Characterized by development of
proctosigmoiditis
Can lead to chronic dysentery
Every case should be treated by
antibacterial drugs
