Bacillary Dysentery

(shigellosis)
Dept. Of Infectious Disease
Wang Jingyan

Definition
Acute infectious disease of intestine caused by
dysentery bacilli
Place of lesion: sigmoid & rectum
Pathological feature: diffuse fibrious exudative
inflammation
Clinical manifestation: fever, abdominal pain,
diarrhea, tenesmus , stool mixed with blood,
mucus & pus. Even companied with marked
toxicity and shock,toxic-encepholopthy.
Etiology
Causative organism: dysentery bacilli, genus
shigella, gram-stain negative, short rod,non-motile
Groups: 4 groups & 50 serotypes
- S. Dysenteriae-the most sever
- S. Flexnerii-the epidemic group and
easily turn to chronic
- S. Boydii-tropical and subon
- S. sonnei-the most mild
Etiology
Pathogenicity:
- virulence
(endotoxin) - interotoxin (exotoxin)
- invasiveness
(attach-penetrate-multiply)

Resistance: Strong.1-2week in fruits,vegetable and
dirty soil. heat for 60 30 min


Epidemiology
Source of infection:
- patients
- carriers
Route of transmission: fecal-oral route
Suceptibility of population:immunity after
infection is short and unstead,no cross-immune

Epidemic features:
- season: summer & fall
- Flexneri, Soneii, dysentery
- age: younger children

Pathogenesis
Number of bacteria
toxicity
immunity
invasiveness
- attachment
- penetration
- multiplication
Pathogenesis-common
Bacteria
intestine
Normal bacteria flora
sIg A
Prevent attaching
Penetrate mucus
Multiply in epithelia
cell & proper lamina
endotoxin
Endogenous pyrogen
fever
Inflammation
vessel contraction
Superficial mucosal in,nec and
ulcer
Diarrhea mixed with blood & pus,
abdominalache
Pathogenesis-toxic
Strong - allergy to endotoxin
Demethyl-adrenaline
Micro-circulatory failure
Shock, DIC, cerebral edema
cerebral hernia
Pathology
Site of lesion: entire large bowel-colone,
sigmoid & rectum
Feature:
acute: diffuse fibrinous exudative
inflammation, hyperemia, edema,
leukocyte infiltration, superficial necrosis
chronic: edema, polypoid hyperplasis
toxic: endothelial cell of micro-capillary
necrosis
Clinical manifestation
Incubation period: 1-2 day, (Hrs. To 7 days)
Acute dysentery
common type:
onset in sudden, shiver, high fever
abdominal pain
diarrhea:stool mixed with blood, mucus & pus
tenesmus, continence
Clinical manifestation
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
Clinical manifestation
Acute dysentery:
Toxic type:
Age: 2 to 7 yrs.
Abrupt onset, high fever, Trise to 40
o
C
Listlessness,lethargy,convulsion,coma.
circulatory & respiratory collapse
diarrhea mild or absent at beginning
shock form: septic shock
brain form: respiratory failure
mixed form
Clinical manifestation
Chronic dysentery: > 2 months
Chronic delayed type:diahhrea 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 Findings
Blood picture: total WBC count increase,
neutrophils increase
Stool examination:
direct microscopic exam.: WBC, RBC, pus cells
bacteria culture:
Sigmoidoscope: shallow ulcer,scar, polyps
Differential diagnosis
Acute dysentery
Amebic dysentery
Entameba histolytica
stool: reddish brow, like jam
flask-shaped ulcer,Amebic trophozoite
Enteritis caused by E. Coli,
salmonella,viral diarrhea
Intussusception: jelly-like stools, abdominal
mass and absence of fever
Differential diagnosis
Chronic dysentery
Rectal & colonic carcinoma: no cure for long-
term,drop of weiht of body
non-specific ulcer colitis: no cure for long-term,culture
of stool is negetive, sigmoidoscope:hemorrhage,
ulcer,lead pipe.
Chronic schistosomiasis Japonica
a. co ntact with the disease-water
b. hepatomegaly and splenomegaly
c .founding the ova of schistosomiasis Japonica
Toxic dysentery
Encephalitis B
brain form:Japaness B encephalitis
a.stool
b.CFS-IgM
c.slowly
d.shock rarely

Treatment
Common dysentery
Toxic dysentery
general treatment
Pathogenic treatment :ofloxine or Amp. Given
by IV
Synptomatic treatment:Control high fever,
convulsion: sub-winter sleep
Treatment of shock:same as ECM
Treatment of cerebral edema: same as EBC
Treatment
Chronic dysentery
General therapy:live,nurishing,diet,avoid
overwork,excise.
Etiologic therapy: sensitive antibiotics used
in turn or combined use;according to results of
culture;enema;expectant treatment.
Prevention
Control the source of infection: until
culture negative
Interruptted the route of transmission:
method of mainly
Protct the susceptability:F2a-secratory
IgA protect 80%-6-12mon
return