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 Penetrate mucus Normal bacteria flora sIg A Multiply in epithelia cell & proper lamina Prevent attaching endotoxin Inflammation vessel contraction Endogenous pyrogen fever 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