Bacillary Dysentery.pdf in adults humans

Urinary tract infections in adults male

1. Bacillary Dysentery
Dr. Mohamed Sakr, M.D.
Medical Microbiology and Immunology

2. Bacillary Dysentery (Shigellosis)
Shigellosis is a strictly human disease with no animal
reservoirs. It is one of the most common causes of
infectious diarrhea, caused by the bacteria of the genus
shigella.
The genus is divided into four species, which are defined
by biochemical reactions and specific O antigens
organized into serogroups.
• Group A= Shigella dysenteries (most common cause)
• Group B= Shigella flexneri
• Group C= Shigella boydii
• Group D= Shigella sonnei

3. Shigellosis
Shigella sonnei is the most common in developed
countries and generally causes a watery diarrhea.
Shigella flexneri, the most common species in
developing countries, but it is more likely to cause
bloody diarrhea.
Shigella dysenteriae causes dysentery characterized
by tenesmus and the production of scant, bloody
stools.

4. Bacillary Dysentery (Shigellosis)
Shigella is Gram-negative, facultative aerobic, non-spore-
forming, rod-shaped bacteria. All of them are nonlactose
fermenter except Shigella sonnei is late lactase fermenter
All Shigella species are nonmotile (they lack
flagella and thus H antigens).

5. Virulence of Shigella
A number of plasmid and chromosomal encoded
proteins. These proteins:
•Invasion plasmid antigens (Ipa),
•Surface presentation antigens (Spa),
•Membrane excretion proteins (Mxi),
•Virulence proteins (Vir).
- Endotoxin: all shigellae release their toxic
lipopolysaccharide Upon autolysis. This endotoxin
probably contributes to the irritation of the bowel wall.

6. Virulence of Shigella
- Shigella Dysenteriae Exotoxin
S dysenteriae type 1 (Shiga bacillus) produces a heat-
labile exotoxin that affects both the gut and the central
nervous system. The exotoxin is a protein Acting as an
enterotoxin, it produces diarrhea. Acting as a
“neurotoxin,” contribute to the extreme severity and
fatal nature of S dysenteriae infections and to the
central nervous system reactions observed in them (ie,
meningismus, coma) .
Hemolytic uremic syndrome has been linked to
shigella

7. Shiga toxin
Shiga toxins act to
inhibit protein
synthesis within target
cells the protein (A
subunit) inactivates
60S subunit of the
ribosome, thereby
stopping protein
synthesis. As they
mainly act on the
vascular endothelium,
a breakdown of the
lining and hemorrhage
eventually occurs

8. Mode of transmission
•Mainly by direct or indirect fecal-oral transmission
from a patient or carrier.
•Transmission through water and milk may occur as a
result of direct fecal contamination
•Flies can transfer organisms from latrines to a non-
refrigerated food
Period of communicability: During acute infection and
until the infectious agent is no longer present in feces,
usually within four weeks after illness.

9. Pathogenesis
•Shigellae are highly communicable. Shigella is acid-
resistant and survives passage through the stomach to reach
the intestine.
•Invasion of the mucosal epithelial cells (M cells) by induced
phagocytosis, escape from the phagocytic vacuole,
multiplication and spread within the epithelial cell
cytoplasm, and passage to adjacent cells.
•The Shigella transcytose through M cells into the
underlying collection of macrophages. Inside macrophages,
the organisms escape from the phagosome to the cytoplasm
and activate apoptosis in the macrophage. Bacteria released
from the dead macrophage contact the basolateral side of
enterocytes.

10. Pathogenesis
•Micro abscesses in the wall of the large intestine and
terminal ileum lead to necrosis of the mucous membrane,
superficial ulceration, bleeding, and formation of a
“pseudomembrane” on the ulcerated area. This consists of
fibrin, leukocytes, cell debris, a necrotic mucous membrane,
and bacteria.
•Shigella infections are almost always limited to the
gastrointestinal tract; bloodstream invasion is quite rare.

11. Pathogenesis
•Micro abscesses in the wall of the large intestine and
terminal ileum lead to necrosis of the mucous membrane,
superficial ulceration, bleeding, and formation of a
“pseudomembrane” on the ulcerated area. This consists of
fibrin, leukocytes, cell debris, a necrotic mucous membrane,
and bacteria.
•Shigella infections are almost always limited to the
gastrointestinal tract; bloodstream invasion is quite rare.

12. Pathogenesis

13. Clinical Manifestations
Incubation period: usually 1-3 days.
•Watery diarrhea is followed by fever, rapid pulse and
vomiting.
•A clinical triad consisting of cramps, painful straining to
pass stools (tenesmus), and a frequent, small-volume,
bloody, mucoid fecal discharge.
•Generalized abdominal tenderness.
•Most infections are self-limiting however, in children and
elderly adults, loss of water and electrolytes may lead to
dehydration, acidosis, and even death. The illness caused by
S dysenteriae may be particularly severe.

14. Diagnosis
Specimens: include fresh stool, mucus flecks, and
rectal swabs for culture.
Microscopy: Large numbers of pus cells, some red
blood cells and mucus often are seen.
Culture: The materials are streaked on differential
media (eg, MacConkey) and on selective media
Xylose Lysine Deoxycholate agar (XLD agar), which
suppress other Enterobacteriaceae and gram-positive
organisms.

15. Diagnosis
•Isolates are identified with further biochemical tests.
• Lactose non fermenting colonies are inoculated into
Triple sugar iron agar (TSI) agar.
•Slide agglutination tests using O group-specific
antisera (A, B, C, D) confirm both the species and
the Shigella genus.
•The colicin typing: method for differentiating
epidemic strains of Shigella sonnei for tracing the
source of infection.

16. Mention the
method and
interpretation of
colicin typing
?


Increase your
knowledge

17. Treatment
Fluid and electrolyte replacement
Co-trimoxazole or ciprofloxacin in severe cases or Nalidixic
acid in the case of resistance.
Prevention and control
•Detection of carriers and treatment of cases will interrupt an
epidemic.
•Hand washing after toilet and before handling or eating Food .
•Proper excreta disposal especially from patients, convalescent
and carriers.
• Adequate and safe water supply.
•Control of flies.
•Cleanliness in food handling and preparation.