Shigellosis
bacillary dysentery
细菌性痢疾
Center of Infectious Disease
Guangzhou eighth people’s Hospital
He Xi
83710422, gz8hhexi@126.com
DEFINITION.
• Shigellosis is an acute bacterial infection
caused by the genus Shigella resulting in
colitis affecting predominantly the
rectosigmoid colon.
• "Bacillary dysentery" is synonymous with
shigellosis.
• The disease is characterized by abdominal
pain, diarrhea, bloody fecal, tenesmus, fever,
and toxemia.
ETIOLOGY.
Shigellae
nonmotile
gram-negative bacilli
belonging to the tribe
escherichia, family
Enterobacteriaceae.
Four species of shigellae
(on the basis of antigenic
and biochemical properties)
ETIOLOGY.
• S. dysenteriae (group A)
• S. flexneri (group B)
• S. boydii (group C)
• S. sonnei (group D).
• Shiga toxin is produced by S. dysenteriae
serotype 1 and in lesser amounts by other
serotypes.
• sensitive to desiccation, but may survive
several months in food or water
EPIDEMIOLOGY.
1.Infectious source :
Humans and higher primates
(during clinical illness and for
up to 6 weeks after recovery)
2.Transmission route:
fecal-oral route
3. susceptible people :
all people are susceptible ,
Children between 2 and 3
years old have the greatest
risk.
PATHOGENESIS
• shigellae ingested pass the gastric barrier( more readily
than other enteric pathogens) traverse the small bowel
penetrate colonic epithelial cells multiply intracellularly
an acute inflammatory response ensues in the colonic mucosa
( prodromal symptoms) epithelial cells containing
bacteria are lysed resulting in superficial ulcerations and
shedding of shigella organisms into stools
Diarrhea results because of impaired absorption of water and
electrolytes by the inflamed colon.
PATHOGENESIS
PATHOLOGY.
The mucosa is friable and covered with a layer
of polymorphonuclear leukocytes.
Formation of crypt abscesses.
Pseudomembranous type of colitis may
develop.
EVOLUTION OF CLINICAL SYNDROMES
Stages
•Prodrome
•Nonspecific diarrhea
•Dysentery
•Complications
•Postdysenteric Syndromes
Factors
•Infecting species
•Age of the host
•Presence of the risk factors
•Specific immunity of the host
PRODROME
• Time: earliest
• Symptoms and signs:
Fever, chills, myalgias
anorexia, nausea, vomiting
NONSPECIFIC DIARRHAE
• Time: 0~3 days
• Symptoms and signs:
Abdominal cramps, loose stools, watery
diarrhea
DYSENTERY
• Time: 1-8 days
• Symptoms and signs:
Frequent passage of blood and mucus
tenesmus
rectal prolapse
abdominal tenderness
COMPLICATIONS
• Time: 3-10 days
• Symptoms and signs:
Dehydration, seizures, septicemia, leuke-
moid reaction,
hemolytic uremic syndrome,
ileus, peritonitis
POSTDYSENTERIC SYNDROMES
• Time: 1-3 weeks
• Symptoms and signs:
Arthritis, Reiter's syndrome
BLOODY MUCOPURULENT STOOLS
LAB. EXAMINATIONS
1. Stool routine
blood and pus are grossly apparent (or under
microscope, erythrocyte and leukocyte,
macrophge more diagnostic value)
2. Blood routine
elevated leukocyte count
3. Stool culture
to isolate shigellae
plus drug sensitive test
BARIUM ENEMA EXAMINATION
DIAGNOSIS.
(1)epidemiological data
Shigellosis should be considered in any patient with acute
onset of fever and diarrhea,especially in summer season.
(2)clinical manifestations
(3)lab.examination
DIFFERENTIAL DIAGNOSIS
• E. coli enteritis
• Salmonella enteritis
• Viral diarrhea
• Amoebic dysentery
• Acute hemorrhagic enteritis
• Bacterial food poisoning
• Toxic dysentery
• Chronic dysentery: rectal cancer, ulcerative
colitis
TREATMENT.
(1)antimicrobials
In adults, fluoroquinolones, for example ciprofloxacin given orally in a
dose of 500 mg twice daily for 5 days or 1 gram as a single dose is the
treatment of choice when the susceptibility of a strain is unknown.
In children, treatment should be trimethoprim-sulfamethoxazole,
ampicillin, or cephalosporin
(2) the patient should be treated with appropriate intravenous or oral
electrolyte repletion fluids in quantities adequate to correct clinical
signs of saline depletion.
(3)The treatment of patients with the toxic type should be considered
comprehensively.
PREVENTION.
*Individuals excreting shigellae should be excluded from
all phases of food handling until negative cultures have
been obtained from three successive stool specimens
collected after completion of antimicrobial therapy.
*In institutional outbreaks, strict and early isolation of
infected individuals is mandatory.
*The most important control measure is rigorous
handwashing.
*Reporting of shigellosis cases to health authorities
should be mandatory.
*no vaccine is now commercially available,but some
under test (live attenuated FS streptomycin dependent
strain)
霍乱 Cholera
DEFINITION.
*an acute watery diarrheal disease
*caused by Vibrio cholerae
*occurs both sporadically and large outbreaks
*extreme fluid loss of solute-rich body fluids
*depleting circulating plasma volume, producing
vascular collapse and death in hours.
ETIOLOGY.
•V cholerae
*short, slightly curved
*rapidly motile
*uniflagellate
*gram-negative
*grow aerobically on
relatively simple
media.
ETIOLOGY
*belonging to Enterobacteriaceae
*V cholerae is a fragile organism and cannot withstand
drying, mild oxidation, or acid conditions. Thus a variety
of disinfectants are effective
*many O serogroups of V cholerae, but only serogroups 1
and 139 Bengal cause epidemic human disease.(WHO: 3
groups, 1.O1: two main biotypes, “classical” and ”el Tor“;
2.non O1:>200 serotypes, but only O139 cause cholera;
3.untypical O1)
*produces a potent exotoxin (choleragen), producing
secretion and malabsorption of sodium ion and water
*O139 Bengal is currently responsible for major epidemics.
Epidemiology
• 1.Infectious source: cases and carriers
Contamination of household food and water sources is the
rule.
Most often raw or undercooked shellfish or fresh vegetables
washed with contaminated water are responsible.
2. Mode of Spread.
Fecal-oral route
cholera is mainly waterborne.
occasionally, contaminated foods spread disease.
3. Susceptibility
in areas where cholera occurs each year, children younger
than 5 are the main victims. Older children and adults in such
endemic areas have acquired a lasting and strongly protective
local intestinal immunity.
PATHOGENESIS.
• V cholerae is ingested reach the duodenum and
jejunum (where alkaline pH, nutrients, and bile salts
favor rapid multiplication) penetrate mucous layers
and attach to the brush border of the intestinal
epithelium secrete a potent exotoxin(a protein
consisting of five B subunits that bind irreversibly to the
receptor(GMI-ganglioside) on the cell surfaces) A
subunit is linked to the B aggregate and gains entry
once binding has occurred A subunit producing
increased adenylate cyclase activity raised cyclic
AMP levels in the enterocytes stimulation of crypt
cells to secrete chloride, drawing with them cations and
water from the blood stream into the gut Iumen
Pathology
*severe dehydration
*"rice water stool“ in the colon
*heart ,liver and spleen,etc. shrunken.
There is no cellular damage and no inflammation
or loss of plasma proteins or formed elements of
the blood.
CLINICAL MANIFESTATIONS.
• Incubation period 1-3 days
1.diarrhea and vomiting stage(a few hours to
2 days):
diarrhea without abdominal pain, The fluid
lost in cholera is a slightly fishy-smelling
nonfecal whitish mucous-flecked liquid
("rice water stool"). Projectile vomiting
usually after diarrhea.
CLINICAL MANIFESTATIONS.
• 2.dehydration stage: (a few hours to 3 days)
Without fluid replacement, cholera patients demonstrate
signs of severe volume depletion:
sunken eyes, poor skin turgor （ elasticity), hoarse voice,
extreme thirst, faint heart sounds, weak or absent
peripheral pulses, and severe muscle cramps.
Patients are oriented but appear apathetic except for thirst.
If patients survive and have not received adequate
hydration, fever secondary to sepsis and pneumonia are
common, and pulmonary edema can ensue with even
modest fluid replacement.
3. Convalescence stage
Laboratory examination
1.phase or dark-field microscopy examination and
immobilizing test
darting motility of vibrios can be recognized in fresh wet
preparations. To be certain that these motile bacteria are V
cholerae, serogroup I antisera can be applied to wet
preparations, immobilizing the organisms in a rapid and
specific diagnostic test.
Laboratory examination
• 2.bacterium culture
* a stool sample or rectal swab can be incubated in an
enrichment medium for vibrios, such as alkaline peptone
water, for 12 to 18 hours.
*Stool culture is best done on a selective medium, since
colonies of V cholerae may be overgrown or are easily missed
on standard enteric media. A simple method uses TCBS agar,
which is very stable and selective for vibrios. *Opaque flat
yellow colonies form on TCBS agar in 18 hours at 37'C.
*Confirmation of serogroup and serotype can be done by
direct slide agglutination with specific antisera
*Biotyping requires more elaborate procedures, but
resistance to polymyxin B is a quick way to recognize the eltor
biotype.
DIAGNOSIS.
1.epidemiological data
Travel to or residence in a cholera-
endemic area
should raise the index of suspicion.
2.clinical manifestation
3.lab.examination
Differential diagnosis
Diseases which should be differentiated
include bacterial food poisoning, bacillary
dysentery, etc.
TREATMENT.
1.isolate patients and carriers
2.Symptomatic and supportive therapy
**replacement of the lost volume:
A. oral rehydration
*Advanced oral hydration solutions based on rice or
other starchy foods hydrate efficiently and reduce
diarrhea and vomiting substantially as compared
with intravenous treatment or glucose-based oral
rehydration solutions.
(In all except the most severe cases, oral
rehydration therapy is sufficient to treat cholera,
especially if started as soon as diarrhea begins)
B. Intravenous rehydration
*Intravenous replacement for patients who are
depleted and in shock should be given rapidly through a
large-bore needle to ensure infusion rates of 50 to 100
ml per minute until a strong radial pulse has been
achieved. Remaining fluid deficits may then be replaced
less rapidly over 2 hours.
1 (As soon as patients are strong enough to drink, oral
rehydration therapy should begin, preferably with a
rice- or other cereal-based solution of the proper solute
composition. If this is done adequately, no further
intravenous fluids are needed)
*Thirst and urination are adequate guides to volume
replacement therapy
3.antibiotics
Adjunctive antibiotic therapy may be
indicated. Tetracycline and doxycycline
have been effective when resistance is
not present.
As with other Enterobacteriaceae,
resistance arises quickly and must be
monitored
PREVENTION.
*Safe water supplies and appropriate disposal of human
waste prevent spread of cholera but may not be
achievable.
*A variety of disinfectants are effective for soiled articles.
Bleaching powder is frequently used.
*Handwashing with soap before food handling is
important.
*Patients suspected to have cholera should be reported to
state health authorities.
*There are effective killed bacterial and toxoid oral
vaccines as well as very promising genetically altered live
vaccines.
