Download Bacillary Dysentery (shigellosis)

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Plasmodium falciparum wikipedia , lookup

Trichinosis wikipedia , lookup

Sarcocystis wikipedia , lookup

Chagas disease wikipedia , lookup

Diarrhea wikipedia , lookup

Typhoid fever wikipedia , lookup

Clostridium difficile infection wikipedia , lookup

Hepatitis B wikipedia , lookup

Hepatitis C wikipedia , lookup

Leptospirosis wikipedia , lookup

Rocky Mountain spotted fever wikipedia , lookup

Yellow fever in Buenos Aires wikipedia , lookup

Coccidioidomycosis wikipedia , lookup

Oesophagostomum wikipedia , lookup

Gastroenteritis wikipedia , lookup

Schistosomiasis wikipedia , lookup

Traveler's diarrhea wikipedia , lookup

Transcript
Bacillary Dysentery
(shigellosis)
Dept. Of Infectious Disease
Huang
Fen
Definition
Acute infectious disease of intestine
caused by dysentery bacilli
Place of lesion: sigmoid & rectum
Pathological feature:
diffuse fibrious exudative
inflammation
Definition
Clinical manifestation:
fever, abdominal pain, diarrhea,
tenesmus , stool mixed with
mucus blood, & pus.
even companied with shock and
toxic encepholopthy.
Etiology
Causative organism:
dysentery bacilli, genus shigellae,
gram-stain negative,
short rod, non-motile
Groups: 4 serogroups 47 serotypes
S. Dysenteriae
the most severe
Etiology
S. Flexneri
the epidemic group and
easily turn to chronic
S. Boydii
tropical areas
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 and carriers
Route of transmission:
fecal-oral route
Suceptibility of population:
immunity after infection is short
and unsteady, no cross-immune
Epidemiology
Epidemic features:
season: summer & fall
Flexneri, Soneii,
age: younger children
Pathogenesis
number of bacteria
pathogenicity
toxicity
invasiveness
attachment
penetration
multiplication
immunity
common
Bacteria
intestine
penetrate mucus
multiply in epithelia
cell & proper lamina
inflammation
vessel contraction
normal intestinal flora
sIg A
prevent attaching
endotoxin
endogenous pyrogen
superficial mucosal necrosis
and ulcer
fever
diarrhea mixed with blood & pus,
abdominal pain
interotoxin
Pathogenesis-toxic
strong - allergy to endotoxin
demethyl-adrenaline
micro-circulatory failure
shock, DIC,
cerebral edema
cerebral hernia
Pathology
site of lesion:
entire colon -sigmoid & rectum
feature:
acute:
diffuse fibrinous exudative inflammation,
hyperemia, edema, leukocyte
infiltration, necrosis,
superficial ulceration.
Pathology
chronic: edema, ulceration,
polypoid hyperplasia,
toxic: hyperemia, edema,
Clinical manifestation
Incubation period:
1-2 day, (hours to 7 days)
Acute dysentery
common type
mild type
toxic type
Clinical manifestation
common
type:
acute onset ,
shiver, high fever
abdominal pain
diarrhea: stool mixed with
mucus, blood & pus
tenesmus,
Clinical manifestation
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
toxic type:
age: 2 to 7 yrs.
abrupt onset, high fever, T> 40oC
convulsion repeatedly, altered
consciousness
circulatory & /or respiratory collapse
diarrhea mild or absent at beginning
Clinical manifestation
shock form: septic shock
brain form:
listlessness,lethargy,convulsion,
coma.
respiratory failure
mixed form
Clinical manifestation
chronic dysentery: > 2 months
chronic delayed type
chronic obscure type
acute attack type
Clinical manifestation
chronic
delayed type:
long-time diarrhea and repeated
chronic
obscure type:
acute history in 1 year, no symptoms,
stool culture positive or sigmoidscopy
acute
attack type:
same as common acute dysentery
Laboratory Findings
Blood picture:
WBC count increase,
neutrophils increase
Stool examination:
direct microscopic examination:
WBC, RBC, pus cells
Laboratory Findings
bacteria culture:
PCR :DNA
Serologic examination:
Sigmoidoscopy: chronic patients
shallow ulcer
scar
polyp
Diagnosis
Epidemiologic data:
contact history
Clinical manifestation:
Laboratory findings:
Differential diagnosis
acute dysentery
amebic dysentery
Entamoeba histolytica
stool: reddish brown, like jam
flask-shaped ulcer,
amebic trophozoite
Differential diagnosis
enteritis caused by E. Coli,
salmonella, virus.
intussusception:
jam-like stools,
abdominal mass
absence of fever
Differential diagnosis
chronic dysentery
rectal & colonic carcinoma:
no cure for long-term,
drop of weight of body
non-specific ulcer colitis:
no cure for long-term,
culture of stool is negative,
Differential diagnosis
sigmoidoscopy: hemorrhage,
ulcer,
X-ray : lead pipe.
chronic schistosomiasis Japonica
contact with the contaminated water
hepatomegaly and splenomegaly
founding the ovum of schistosomiasis
Differential diagnosis
toxic dysentery
encephalitis B:
high fever,convulsion,coma.
• <24h
• circulatory failure
• stool examination
• CSF
• meningeal irritation
• specific IgM
Treatment
Common dysentery
general treatment:
isolation
diet
fluid and electrolyte
pathogenic treatment:
norfloxacin 0.2~0.4 q6h po 5~7d
Ampicillin given by po or iv
Getamycin
Treatment
symptomatic treatment:
Toxic dysentery
general treatment
pathogenic treatment:
L-ofloxacin: 0.2 bid ivdrop
cefotaxime:
Ampicillin :
Treatment
symptomatic treatment:
• control of high fever,convulsion:
subhibernation
• treatment of shock:
654-2: 1- 2mg/kg
• treatment of cerebral edema:
20% mannitol
respiratory failure
Treatment
chronic dysentery
general therapy:
live, avoid overwork
exercise
diet
Treatment
etiologic therapy:
sensitive antibiotics, according to
results of culture
used in turn or combined use
enema.
Prevention
Control the source of infection:
until culture negative
Interrupting the route of transmission:
Protecting the susceptible population:
F2a: secretary IgA
protect rate: 80%
6-12mon