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Bacillary Dysentery
(shigellosis)
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 40oC
 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

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Dysentery

  • 2. 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.
  • 3. 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
  • 4. 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
  • 5. 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
  • 6. Pathogenesis  Number of bacteria  toxicity  immunity  invasiveness - attachment - penetration - multiplication
  • 7. 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
  • 8. Pathogenesis-toxic Strong - allergy to endotoxin Demethyl-adrenaline Micro-circulatory failure Shock, DIC, cerebral edema cerebral hernia
  • 9. 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
  • 10. 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
  • 11. 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
  • 12. Clinical manifestation  Acute dysentery: Toxic type:  Age: 2 to 7 yrs.  Abrupt onset, high fever, Trise 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
  • 13. 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
  • 14. 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
  • 15. 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
  • 16. 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
  • 17.  Toxic dysentery  Encephalitis B brain form:Japaness B encephalitis a.stool b.CFS-IgM c.slowly d.shock rarely
  • 18. 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
  • 19. 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.
  • 20. 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