Bacillary

Dysentery

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 DEFINITION

• Bacillary dysentery can be caused by

many kinds of bacteria such as:
• genus shigellae
• enteroinvasive E.coli (EIEC)
• campylobacter fetus subspecies jejuni:
(helicobacter) etc.

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 Bacillary Dysentery

• Shigellosis is an acute bacterial

infection caused by the genus shigellae,
resulting in colitis, and affecting
predominantly the rectosigmoid colon.

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 Bacillary Dysentery

• Shigellosis is characterized by fever,

abdominal pain, diarrhea, tenesmus &
dysentery. And in severe cases, infectious
shock and /or toxic encephalopathy can be
seen.

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 ETIOLOGY

• 1.Shigellae are gram-negative bacilli

belonging to the family Enterobacteriaceae.
• 2. On the basis of antigenic &
biochemical properties, shigellae are
divided into four species:
Group A S. dysenteriae
Group B S. flexneri
Group C S. boydii
Group D S. sonnei 5
 ETIOLOGY

• 3. S.dysenteriae 1 causes epidemics with

more severe clinical manifestations and
higher mortality than other serotypes.
• 4. Each type of shigella can release
endotoxin which is responsible for the main
toxic symptoms. S.dysenteriae can produce
exotoxin (shiga toxin) that always exacerbate
the clinical manifestations such as diarrhea.
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 EPIDEMIOLOGY

• 1. Source of infection: patients &

the carriers.
• The atypical & chronic patients &
the carriers are always out of attention
because of their light symptoms,
thereupon they are more important in
epidemiology.
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 EPIDEMIOLOGY

• 2. Route of transmission:
• Shigellosis is transmitted by the
fecal-oral route through contaminated
hands, foods, water etc.
• Transmission always occurs
through close person-to-person contact.

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 EPIDEMIOLOGY
• 3. Susceptible group:
• All the people are susceptible to shigella
but crowded living condition, poor water
supply and other low standards of hygiene
all contribute to an increased risk of
infection.
• Children have the greatest risk of
developing shigellosis because of bad
health habits.
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 EPIDEMIOLOGY

• 4. Epidemic feature:
• Relapse & reinfection is common
• Summer & autumn

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 PATHOGENISIS
& PATHOLOGY

• 1.Since the microorganisms are

relatively resistant to acid, shigllae pass
the gastric barrier more readily than other
enteric pathogens. About 200 bacilli can
produce shgellosis, which is much fewer
than typhoid & cholera.

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 PATHOGENISIS
& PATHOLOGY

• 2. During the incubation period(usually

12 to 72h), the organisms tranverse the
small bowel, penetrate colonic epithelial
cells, and multiply intracellularly & then
lead to an acute inflammatory response.
After the epithelial cells containing bacteria
are lysed, there come the superficial
ulcerations .
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 PATHOGENISIS
& PATHOLOGY

• 3.Inflammation is confined to the

rectum and rectosigmoid colon & in
severe cases, there may be pancolitis.
• 4. Diarrhea results from:

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 PATHOGENISIS
& PATHOLOGY

• 5.Bacteremia is infrequency. One reason

is the ulceration is superficial(virulence),
another is that shigella is susceptible to
serum complement-mediated bacteriolysis.
• 6.Toxic shigellosis always occur in those
whose immunity is strong enough to kill
great deal of shigellae or those who get in
much endotoxin directly.
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 CLINICAL MANIFESTATIONS

• 1. The severity of shigellosis is

mainly related to the different strain
of infecting organism , and so as
mortality rate. (S.dysenteriae.1)

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 CLINICAL MANIFESTATIONS

• 2. Most patients with shigellosis

begin their illness with a nonspecific
prodrome. Fever, crampy abdominal
pain, watery diarrhea are the most
common early symptoms & coincide
with infection of the small intestine.

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 CLINICAL MANIFESTATIONS

• The height of fever: varies from 38 to

40 degrees celsius.
• Abdominal tenderness: often marked in
the left lower quadrant over the sigmoid
colon but may also be generalized, always
with the sensation of bowel movement &
the feeling will not disappear after
defacation.
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 CLINICAL MANIFESTATIONS

• Frequency and volume of diarrhea

varies too, mainly basing on the
destruction of local mucosa by shiga
toxin. This phase of illness lasts for
several days in most patients.

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 CLINICAL MANIFESTATIONS

• With the infection of colon,

tenesmus, fecal urgency & the passage
of bloody mucoid stools occur.
• The amount of blood on the stools is
usually small.

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 CLINICAL MANIFESTATIONS

• 3. Patients with mild disease develop only

prodrome or experience only watery diarrhea
without dysentery.
• 4. In severe cases, dehydration, electrolyte
disturbance, acidosis, circulatory failure,
unconsciousness etc. can be present, which
are often the causes of death, especially in
children.
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 CLINICAL MANIFESTATIONS

• Shigellosis can be acute or

chronic.
• Shigellosis lasts more than 2
months is chronic and usually
caused by group B.
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 LABORATORY TESTS

• Bloody and purulent are grossly apparent in

severe bacillary dysentery.
• Even in milder cases, microscopic examination
of the stool often reveals numerous leukocytes and
erythrocytes.

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 LABORATORY TESTS

• The presence of a bundant

polymorphonuclear leukocytes helps in
distinguishing shigellosis from diarrhea
syndromes caused by viruses &
enterotoxigenic bacteria.
• The fecal leukocyte examination is not
helpful in distinguishing shigellosis from
diarrhea illness caused by other invasive
enteric pathogens (such as salmonella,
campylobacter & Yersinia etc.).
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 LABORATORY TESTS

• The peripheral white cell count is of

little diagnostic value, since it may range
from less than 3000 to more than 30,000.
• Sigmoidoscopic examination reveals
diffuse erythema, with a mucopurulent layer
and mucosa with shallow ulcers 3 to 7 mm
in diameter.

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 DIAGNOSIS

• Shigellosis should be considered in any

patient with acute onset of fever and diarrhea:
• Epidemiology
• History
• Examination of the stool is essential
• Definitive diagnosis depends upon shigellae
isolation. (usually for three successive days)
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 TREATMENT

• The correction of fluid, electrolyte

& acid-base disturbances are the
mainstay of therapy & particularly
important in elderly & very young
patients.

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 TREATMENT

• Antibiotics: Fluoroquinolones such as

norfloxacin & ciproxacin are the most
effective drugs.(not approved for pediatric
use because of the side-effect on epiphysis
growth).
• No quinolone resistance was encountered
• Contraindications: children, pregnant
women etc.
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 TREATMENT

• Trimethoprim-sulfamethoxazole(80
mg & 400 mg respectively each tablet):
• 5 days both for adults & children
• 2 tablets bid p.o. for adults
• 10 mg/kg/day & 50 mg/kg/day
respectively for children

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 TREATMENT

• Amipicillin:
• 0.5 q.i.d p.o.
• For 5 days
• Effective for sensitive organisms

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 TREATMENT

• Antiperistaltic agents should be

avoided.

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 PREVENTION

• The most important control measure is to

institute proper sanitary & hygienic measures.
• Hand washing is extremely important in
decreasing direct transmission.
• Asymptomatic and convalescent carriers
should be excluded from food preparation and
handling.
• A live attenuated oral vaccine is under
development.
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