Shigellosis is a bacterial infection caused by Shigella bacteria that is transmitted through the fecal-oral route. It causes acute bloody diarrhea and abdominal cramps. There are four species of Shigella that can cause disease with varying levels of severity. Complications can include toxic megacolitis, intestinal perforation, and hemolytic uremic syndrome. Diagnosis is made through stool culture. Treatment involves rehydration and antibiotic therapy with fluoroquinolones or sulfonamides depending on severity. Preventing transmission through proper hygiene is important for controlling outbreaks of this infectious disease.

1. SHIGELLOSIS
UTM
Department of Infectious Diseases
2023

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).

4. Aetiology
Family – Enterobacteriaceae
Genus – Shigella
4 species:
 Shigella dysenteriae (10 serotypes)
 Shigella flexneri (6 serotypes)
 Shigella sonnei
 Shigella boydii (15 serotypes)

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

6. Shigella

7. Shigella

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)

9. Aetiology
Sh.dysenteriae Sh.flexneri Sh.sonnei Sh.boydii
Serotypes 10 6 - 15
Lactose
fermentation
- - + -
Mannit
fermentation
- + + +
Pathogenicity > > > >
M.I.D.
High level of
infectivity
101 102 107 -
Stability < < < <
Route of
transmission
person-to-person watery food -

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

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

17. M-cell

18. Acute inflammation
Shigella
1.
2.
IL-1
IL-6
TNF-
3.
4.
IL-8
5.
M-cell

19. Pathology
The colon mucosa damage stages:
 Acute catarrhal inflammation
 Fibrinous-necrotic
 Formation of ulcers
 Recovery of ulcers

20. The mucosa inflammation & ulceration

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.

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)

29. Laboratory diagnosis
 Stool culture (in 22-80%) –”gold standard”
 Stool microscopy (high PMNs and
erythrocytes counts)
 Serologic tests:
- ELISA
- indirect hemagglutination
- immunofluorescence

30. Growth of Shigella on
selective culture medium

31. Instrumental method
Rectoromanoscopy - procrosigmoiditis:
 catarrhal
 catarrhal-haemorrhagic
 ulcerative

32. Rectoromanoscopy

33. Rectoromanoscopy

34. Complication
Intestinal Extraintestinal
 Rectal prolapse
 Intestinal perforation
 Toxic megacolon
 Bacteremia
 Mesenteric vessels
thrombosis
 Hemolytic-uremic
syndrome (HUS)
 Secondary infection,
(Pneumonia)
Postinfectious
arthropathy (after
infection with S.flexneri)

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.

41. Rectal prolaps

42. Toxic megacolon

43. Treatment
 Diet
 Etiotropic therapy (3-5 days – for
immunocompetent patients, 7-10 days –
for immunocompromised)
 Pathogenetic therapy

44. Differential diagnosis
 Infectious diarrhea caused by other invasive
pathogens:
- Salmonella,
- Campylobacter jejuni,
- Clostridium difficile,
- Yersinia enterocolitica,
- Entamoeba histolytica
 IBD:
- Crohn’s disease,
- Ulcerative colitis, etc.

45. Etiotropic therapy
Mild form
 Nitrophurans
- Furazolidone
- Ercefuryl
 4-oxiquinolones
- Intetrix

46. Etiotrop therapy
Moderate form
 Sulfonamides
- Sulfamethoxazole-trimethoprim
 Fluoroquinolones
- Ciprofloxacin
- Ofloxacin
- Norfloxacin

47. Etiotropic therapy
Severe form
 Fluoroquinolones IV +
- aminoglycosides (Gentamicin)
- cephalosporins (Ceftriaxone, Cefazolin)

48. Pathogenetic therapy
 Rehydration
- Oral (Rehydron, Oralit, Citroglucoso-
lane)
- Parenteral (Ringer, Ringer-Lactate,
Quartasol etc.)

49. Pathogenetic therapy
Enterosorbents
- Smecta
- Enterosorb
Digestive enzymes
- Creon
- Festal
- Mezym-forte

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

52. Thank you for your kind attention!