Transcript Bacillary Dysentery (shigellosis)

INTRODUCTION
 Acute infectious disease of intestine caused by
dysentery bacilli
 Place of lesion: sigmoid & rectum

Shigellosis is endemic throughout the world
where it is held responsible for some 120
million cases of severe dysentery with blood
and mucus in the stools
EPIDEMIOLOGY

About 1.1 million people are estimated to die from
Shigella infection each year, with 60% of the
deaths occurring in children under 5 years of age.

about 500 000 cases of shigellosis are reported
each year among military personnel and
travellers from industrialized countries

Since the late 1960s, pandemic waves of Shigella
dysentery have hit sub-Saharan Africa, Central
America and South and South-East Asia.
AETIOLOGY
 Causative organism: dysentery bacilli, genus shigella,
gram-stain negative, short rod,non-motile
 Groups: 4 groups & 50 serotypes
- S. Dysenteriae-the most severe
- S. Flexnerii- endemic in developing
countries. easily turn to chronic
- S. Boydii
- S. sonnei -the most mild
NORMAL HABITAT

Found only in the human intestinal tract.

Carriers of the pathogenic strain can excrete
the organisms up to 2 wks after the infection
&occasionally for longer periods.

Killed by drying
TRANSMISSION

Transmitted by fecal-oral route

High incidence of shigellosis occur in areas of poor
sanitation and where water supplies are polluted.

Lack of personal hygiene

Young children are more frequently affected than
adults [> 6 months]

Horseflies are also thought to be important in
transferring Shigella from faeces to food.

Epidemics can be caused by ingestion of
contaminated milk and milk products.
Antigenic structure
 Differentiation
into groups (A, B, C, and D) is based
on O antigen serotyping; K antigens may interfere
with serotyping, but are heat labile.
 Virulence
factors
toxin – An A-B toxin produced by S.
dysenteriae and in smaller amounts by S. flexneri and
S. sonnei.
 Enterotoxic, neurotoxic and cytotoxic effects
 Shiga

This Damages intestinal epithelium and glomerular
endothelial cells (associated with HUS) plays a role in the
ulceration of the intestinal mucosa.
OUTER MEMBRANE AND SECRETED PROTEINS

These proteins are expressed at body temperature and
upon contact with M cells in the intestinal mucosa they
induce phagocytosis of the bacteria into vacuoles

Shigella destroy the vacuoles to escape into the
cytoplasm
From there they spread laterally (Polymerization of
actin filaments propels them through the cytoplasm.) to
epithelial cells where they multiply but do not usually
disseminate beyond the epithelium.

SHIGA TOXIN ENTEROTOXIC EFFECT:

Adheres to small intestine receptors

Blocks absorption (uptake) of electrolytes, glucose,
and amino acids from the intestinal lumen
 Note: This contrasts with the effects of cholera
toxin (Vibrio cholerae) and labile toxin (LT) of
enterotoxigenic E. coli (ETEC) which act by
blocking absorption of Na+, but also cause
hypersecretion of water and ions of Cl-, K+ (low
potassium = hypokalemia), and HCO3- (loss of
bicarbonate buffering capacity leads to metabolic
acidosis) out of the intestine and into the lumen
CYTOTOXIC EFFECT:




B subunit of Shiga toxin binds host cell glycolipid
A domain is internalized via receptor-mediated
endocytosis (coated pits)
Causes irreversible inactivation of the 60S ribosomal
subunit, thereby causing:
 Inhibition of protein synthesis
 Cell death
 Microvasculature damage to the intestine
 Hemorrhage (blood & fecal leukocytes in stool)
Neurotoxic Effect: Fever, abdominal cramping are
considered signs of neurotoxicity
PATHOGENESIS AND IMMUNITY

Shigellosis is primarily a pediatric disease, and is
restricted to the GI tract.

Mean infective dose: 103.

Mouth
colon
invade M cells and
subsequently spread to mucosal epithelial cells
cause microabscess in the wall of colon and
terminal ileum
necrosis of the mucous
membrane, superficial ulceration, bleeding, and
formation of pseudomembrane.
INVASION OF INTESTINAL WALL BY SHIGELLA
SHIGELLOSIS
Two-stage disease:
 Early stage:



Watery diarrhea attributed to the enterotoxic
activity of Shiga toxin following ingestion and
noninvasive colonization, multiplication, and
production of enterotoxin in the small intestine
Fever attributed to neurotoxic activity of toxin
Second stage:


Adherence to and tissue invasion of large intestine
with typical symptoms of dysentery
Cytotoxic activity of Shiga toxin increases severity
CLINICAL DISEASE: ACUTE DYSENTERY

Common Type Incubation period: 1-3 days

Sudden onset of abdominal pain, fever and
watery diarrhea, number of stools increase, less
liquid, often contain mucus and blood, rectal
spasms with resulting lower abdominal pain
(tenesmus)

symptoms subside spontaneously in 2-5 days in
adult cases, but loss of water and electrolytes
frequently occur in children and the elderly. a
small number of patients remain chronic carriers.

Some cases are accompanied by hemolytic uremic
syndrome (HUS), characterized by acute hemolysis,
renal failure, uremia, and disseminated intravascular
coagulation.
Death can occur from circulatory collapse or
kidney failure.
 Total WCC is raised with neutrophilia
 Infection with S. dysenteriae can lead to
leukemoid reaction developing 5-10 days after
infection caused by an endotoxin.
 S. sonnei is not very pathogenic, therefore
infections are rarely serious.

Acute dysentery
mild type:
caused by S. sonnei
low fever or no fever
Abdominal pain is mild
stool mixed with mucus, without blood & pus
diagnosis by isolation bacteria
TOXIC TYPE:
Abrupt onset, high fever, Temperature rise to
40oC
Listlessness, lethargy, convulsion, coma.
circulatory & respiratory collapse
diarrhea mild or absent at beginning
shock form: septic shock
brain form: respiratory failure
mixed form
CHRONIC DYSENTERY
 Chronic dysentery: > 2 months
Chronic delayed type: diarrhea long-time and
repeated
Chronic obscure type: acute history in 1 year, no
symptoms, stool culture Pos. or sigmoidscopy
Acute attack type: same as common acute
dysentery
LABORATORY DIAGNOSIS
 Blood picture: total WBC count increase,
neutrophils increase
 Stool examination:
direct microscopic exam.: WBC, RBC, pus cells
bacteria culture:
 Sigmoidoscope: shallow ulcer, scar, polyps
TREATMENT

oral rehydration therapy, intravenous fluid
replacement

Antibiotic treatment: chloramphenicol, ceftriaxone,
ciprofloxacine, tetracycline, and trimethoprimsulfamethoxazole. Drug resistance is common.

Restoration of electrolytes

Opiates and anti-diarrhoea medications should be
avoided.
PREVENTION AND CONTROL

Humans are the only reservoir for shigellae.

Transmission of shigellae: water, food, fingers, feces,
and flies.

Most cases occur in children under 10 years of age.

Prevention and control of dysentery:

1. Sanitary control of water, food and milk; sewage
disposal; and fly control.

2. Isolation of patients and disinfection of excreta.

3. Detection of subclinical cases and carriers.