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8/10/2019 Disentriadaada
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DISENTRI
Departemen Ilmu Penyakit DalamFakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara
Dr. dr. Shahrul Rahman, Sp.PD, FINASIM
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Definisi : adalah suatu penyakit saluran pencernaan
yang ditandai dengan muntah dan diare.
Etiologi : Bakteri, amuba, virus, jamur, toksin,
parasit, makanan.Yang paling sering pada orang dewasa di negara
berkembang :
Vibrio Kolera Kolera
Amuba Disentri amuba
Shigella Disentri basiler
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Disentri Amuba •Def. Adalah infeksi pada kolon disebabkan oleh
Entamuba histolitika.•Entamuba histolitika.
–Motil, pseudopodia, oval, fagositosis.
–Lingk. Hidup : anaerob atau kadar O2 5%.
–Bentuk : tropoziod dan kista. –Tropozoid : bentuk minuta & magna.
•Minuta : non patogenik, memakan bakteri&cairan usus
•Magna :
–Patogenik, memakan eritrosit/hematofagous –Bisa menginfasi sampai submukosa, membentuk
koloni >> tjd ulkus pada dinding usus.
•
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Kista:
- bulat/agak oval
- inti 1 - 4 buah.
- infektif.
Patogenesa :◦ Kista tertelan ->>pecah/menetas di usus halus --
>>amuba berinti 4 keluar dari kista ->>tjd pembelahansitoplasmik ->>terbentuk 8 tropoz.
◦ Tropoziod menginvasi kolon ->>tjd fokus lesi
->>beberapa fokus bergabung mjd ulkus (berbentuk spt.
botol) ->> ulkus makin dalam
->> mencapai p. darah ->>vaskulitis ->>trombus
->> nekrosis ->> perdarahan.
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Tanda & Gejala Klinis :
•Asimtomatis : E.histolitika hidup scr komensal.
•Ringan : –Abd. discomfort, freq. BAB bertambah, lemah, diare dan
obstipasi silih berganti, kalau kronis BB menurun, gejala
menghilang ->>bbrp bulan muncul lagi.
•Berat : –Diare lendir dan darah, tenesmus, kolik, muntah,
kram otot perut, BB menurun, demam, lemah, nyeri tekan
perut kanan bawah/seluruh abdomen, hiperperistaltik.
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•Laboratorium:
- Tinja mikroskopis:- Dgn eosin 1% + brilliant crystal blue 0,2%
- Diperiksa < 30 menit stlh pengambilan.
- Jangan kena air ok merusak tropozoit.
- Terdapat tropozoit.Tanda: bergerak, tdp pseudopodi jernih,
plasma mengandung eritrosit.
- Kultur tinja : Medium : Diamond’s, Lock Egg Serum
- Serologis : ELISA, Complement fixation.
- PCR.
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•Diagnosa Banding :
- Tuberkulosis intestinalis.
- Ca kolon.- Inflammatory bowel disease.
- Disentri basiler.
- Demam tifoid.
- Brusellosis. Pengobatan:
•Asimtomatik : Diloksanid furoat 3 x 500 mg : 10
hari Paromomycin 3 x 500 mg : 10 hr
•Simtomatik : Metronidazole 3 x 750 mg : 10 haribersama dengan diloksanid furoat
atau
• paromomycin.
•Obat alternatif : emetin, dihidroemetin.
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•Komplikasi :Intestinal :
1. Perdarahan massif.2. Perforasi usus.3. Apendisitis amuba.4. Ameboma (penebalan ddg usus, mirip Ca)
5. Striktur kolon.Ekstraintestinal:
1. Amebiasis hati ( Abses hati amuba)2. Amebiasis pleuropulmonal
(empiema, abses, fistula hepatopleural)3. Amebiasis perikardial.4. Amebiasis serebral.5. Amebiasis kulit.
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DISENTRI BASILER Nama lain Sigellosis.
Etiologi : Shigella sonnei (paling sering)
Shigella flexneri
Shigella dysentriae (jarang, berat).
Gejala klinik :◦ Diare mula-mula cair, kemudian bercampur darah dan
lendir.
◦ Tenesmus.
◦
Demam, menggigil, sakit kepala, anoreksia, lemah.◦ Dehidrasi
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Definition
Acute infectious disease ofintestine caused by dysenterybacilli
Place of lesion: sigmoid &rectum
Pathological feature:
diffuse fibrious exudativeinflammation
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Definition
Clinical manifestation:fever, abdominal pain,
diarrhea, tenesmus , stool
mixed with mucus blood &pus.
even companied with shock
and toxic encephalopathy.
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DEFINITIONS
Enterotoxin = an exotoxin with enteric activity, i.e.,
affects the intestinal tract
Dysentery = inflammation of intestines (especially
the colon (colitis) of the large intestine) with
accompanying severe abdominal cramps,
tenesmus (straining to defecate), and frequent, low-
volume stools containing blood, mucus, and
fecal leukocytes (PMN’s) Bacillary dysentery = dysentery caused by
bacterial infection with invasion of host cells/tissues
and/or production of exotoxins
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Etiology
Causative organism: dysentery bacilli, genus
shigellae,gram-stain negative,
short rod, non-motileGroups: 4 serogroups 47
serotypesS. Dysenteriae
the most severe
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Etiology
S. Flexneri
the epidemic group and
easily turn to chronic
S. Boydii
tropical areas
S. sonnei
the most mild
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Etiology
Pathogenicity:- virulence
endotoxin - interotoxin (exotoxin)- invasiveness
(attach-penetrate-multiply) Resistance:Strong, 1-2 week in fruits,vegetableand dirty soil, heat for 60 30 min
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Coliform bacilli (enteric rods)
Nonmotile gram-negative facultative anaerobes
Four species Shigel la sonnei (most common in industrial world)
Shigella flexneri (most common in developing countries) Shigel la boyd i i
Shigel la dysenter iae
Non-lactose fermenting
Resistant to bile salts
General Character ist ics o f Sh igel la
E id i l d Cli i l S d
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Shigellosis = Generic term for disease
Low infectious dose (102-104 CFU) Humans are only reservoir
Transmission by fecal-oral route
Incubation period = 1-3 days
Watery diarrhea with fever; changing to dysentery Major cause of bacillary dysentery (severe 2nd stage)
in pediatric age group (1-10 yrs) via fecal-oral route
Outbreaks in daycare centers, nurseries, institutions
Estimated 15% of pediatric diarrhea in U.S. Leading cause of infant diarrhea and mortality
(death) in developing countries
Epidem iology and Clin ical Syndromes
o f Sh igel la
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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
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Epidemiology
o f Sh igel la
Infect ion
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Pathogenesis
number of bacteriapathogenicity
toxicity
invasiveness
attachment
penetration
multiplication
immunity
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common Bacteria
intestine
normal intestinal flora
sIg A
prevent attaching
penetrate mucus
multiply in epitheliacell & proper lamina
endotoxin interotoxin
endogenous pyrogen
fever
inflammation
vessel contraction
superficial mucosal necrosis
and ulcerdiarrhea mixed with blood & pus,
abdominal pain
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Pathogenesis-toxic
strong - allergy to endotoxin
demethyl-adrenaline
micro-circulatory failure
shock, DIC, cerebral edema
cerebral hernia
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Shigellosis
Two-stage disease: Early stage: Watery diarrhea attributed to the enterotoxic
activity of Shiga toxin following ingestion and
noninvasive colonization, multiplication, andproduction of enterotoxin in the small intestine
Fever attributed to neurotoxic activity of toxin
Second stage: Adherence to and tissue invasion of large
intestine with typical symptoms of dysentery
Cytotoxic activity of Shiga toxin increases
severity
Pathogenesis o f Shigella
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Pathogenesis and Virulence Facto rs (cont.)
Virulence attributable to:
Invasiveness
Attachment (adherence) and internalization
with complex genetic control
Large multi-gene virulence plasmid regulated bymultiple chromosomal genes
Exotoxin (Shiga toxin)
Intracellular survival & multiplication
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Penetrate through mucosal surface of colon
(colonic mucosa) and invade and multiply in the
colonic epithelium but do not typically invade
beyond the epithelium into the lamina propria (thinlayer of fibrous connective tissue immediately beneath the
surface epithelium of mucous membranes)
Preferentially attach to and invade into M cells in
Peyer’s patches (lymphoid tissue, i.e., lymphatic system)of small intestine
Invasiveness in Shigel la -Associated Dysentery
Pathogenesis and Virulence Facto rs (cont.)
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M cells typically transport foreign antigens from
the intestine to underlying macrophages, but
Shigel la can lyse the phagocytic vacuole
(phagosome) and replicate in the cytoplasm Note: This contrasts with Salmonella which
multiplies in the phagocytic vacuole
Actin filaments propel the bacteria through the
cytoplasm and into adjacent epithelial cells withcell-to-cell passage, thereby effectively avoiding
antibody-mediated humoral immunity (similar
to Listeria monocytogenes)
Pathogenesis and Virulence Facto rs (cont.)
Invasiveness in Shigel la -Associated Dysentery(cont.)
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C
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Methods That Circum vent
Phagocy t ic K il ling
, Shigel la spp.
Shigel la spp .
,
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Enterotoxic, neurotoxic and cytotoxic
Encoded by chromosomal genes
Two domain (A-5B) structure Similar to the Shiga-like toxin of
enterohemorrhagic E. co li (EHEC)
NOTE: except that Shiga-like toxin is encoded by
lysogenic bacteriophage
Pathogenesis and Virulence Facto rs (cont.)
Characteristics of Shiga Toxin
P h i d Vi l F
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Shiga Toxin Effects in Shigellosis
Enterotoxic Effect: Adheres to small intestine receptors
Blocks absorption (uptake) of electrolytes,
glucose, and amino acids from the intestinal
lumen Note: This contrasts with the effects of cholera toxin
(Vibrio cholerae) and labile toxin (LT) of
enterotoxigenic E. coli (ETEC) which act by blocking
absorption of Na+, but also cause hypersecretionof water and ions of Cl-, K+ (low potassium =
hypokalemia), and HCO3- (loss of bicarbonate
buffering capacity leads to metabolic acidosis) out of
the intestine and into the lumen
Pathogenesis and Virulence Facto rs (cont.)
P th i d Vi l F t ( t )
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Cytotoxic Effect: B subunit of Shiga toxin binds host cell glycolipid
A domain is internalized via receptor-mediated
endocytosis (coated pits)
Causes irreversible inactivation of the 60Sribosomal subunit, thereby causing:
Inhibition of protein synthesis
Cell death
Microvasculature damage to the intestine
Hemorrhage (blood & fecal leukocytes in stool)
Neurotoxic Effect: Fever, abdominal cramping are
considered signs of neurotoxicity
Shiga Toxin Effects in Shigellosis (cont.)
Pathogenesis and Virulence Facto rs (cont.)
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Pathology
site of lesion:entire colon -sigmoid &
rectum
feature:acute: diffuse fibrinous exudative
inflammation,hyperemia, edema, leukocyte
infiltration, necrosis,superficial ulceration.
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Pathology
chronic: edema, ulceration,
polypoidhyperplasia,
toxic: hyperemia, edema,
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Clinical manifestation
Incubation period:1-2 day, (hours to 7 days)
Acute dysenterycommon type
mild type
toxic type
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Clinical manifestation
common type: acute onsetshiver, high fever
abdominal paindiarrhea: stool mixed withmucus, blood & pus
tenesmus
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Clinical manifestation
toxic type:
age: 2 to 7 yrs.abrupt onset, high fever, T> 40oC
convulsion repeatedly, alteredconsciousnesscirculatory & /or respiratorycollapsediarrhea mild or absent at beginning
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Clinical manifestation
shock form: septic shock
brain form: listlessness,lethargy, convulsion, coma.respiratory failure
mixed form
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Clinical manifestation
chronic dysentery: > 2
months
chronic delayed type
chronic obscure type
acute attack type
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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
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Laboratory Findings
Blood picture: WBC count increase,
neutrophils increaseStool examination:direct microscopic
examination: WBC, RBC, pus cells
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Laboratory Findings
bacteria culture
PCR :DNASerologic examination
Sigmoidoscopy: chronicpatients
shallow ulcerscarpolyp
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Diagnosis
Epidemiologic data:
contact history
Clinical manifestation
Laboratory findings
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Differential diagnosis
acute dysenteryamebic dysentery Entamoeba histolytica
stool: reddish brown, like jam
flask-shaped ulcer,
amebic trophozoite
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Differential diagnosis
enteritis caused by E. Coli ,salmonella, virus.
intussusception: jam-like stools,
abdominal mass,
absence of fever
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Differential diagnosis
chronic dysenteryrectal & colonic carcinoma:
no cure for long-term,drop of weight of bodynon-specific ulcer colitis:
no cure for long-term,
culture of stool is negative,
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Differential diagnosis
sigmoidoscopy: hemorrhage, ulcer,X-ray : lead pipe.
chronic schistosomiasis
Japonicawith the contaminated waterhepatomegaly and splenomegalyf ounding the ovum of schistosomiasis
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Differential diagnosis
toxic dysentery
encephalitis B:high fever, convulsion,coma.
<24h•circulatory failure•stool examination•CSF•meningeal irritation•specific IgM
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TreatmentCommon dysenterygeneral treatment:
isolation
dietfluid and electrolyte
pathogenic treatment:
norfloxacin 0.2~0.4 q6h po5~7d
Ampicillin given by po or iv
Gentamycin
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Treatment
symptomatic treatment:
Toxic dysentery
general treatmentpathogenic treatment:
L-ofloxacin: 0.2 bid ivdrop
cefotaxime
Ampicillin
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Treatment
chronic dysenterygeneral therapy:
live, avoid overworkexercise
diet
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Treatment
etiologic therapy: sensitive antibiotics, according to
results of culture
used in turn or combineduse enema.
Rehidrasi.
Antibiotika :
◦ Kotrimoksazol tidak lagi mjd antimikroba empirik◦ Siprofloksasin 2 x 500-750 mg
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Prevention
Control the source of infection:until culture negative
Interrupting the route oftransmissionProtecting the susceptible
population:F2a: secretary IgA
protect rate: 80%6-12mon