DISENTRI

dr Shahrul Rahman, Sp.PD

Departemen Ilmu Penyakit Dalam
Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara

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

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.

Kista:
- bulat/agak oval
- inti 1 - 4 buah.
- infektif.
Patogenesa

Kista tertelan ->>pecah/menetas di usus halus

-->>amuba berinti 4 keluar dari kista ->>tjd pembelahan
sitoplasmik ->>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.

Tanda & Gejala Klinis :

Asimtomatis
Ringan :

: E.histolitika hidup scr komensal.

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.

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 : Diamonds, Lock Egg Serum
- Serologis : ELISA, Complement fixation.
- PCR.

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

atau

: Metronidazole 3 x 750 mg : 10 hari

bersama dengan diloksanid furoat

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.

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

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 encephalopathy.

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, lowvolume stools containing blood, mucus, and
fecal leukocytes (PMNs)
Bacillary dysentery = dysentery caused by
bacterial infection with invasion of host cells/tissues
and/or production of exotoxins

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

General Characteristics of Shigella

Coliform bacilli (enteric rods)
Nonmotile gram-negative facultative anaerobes
Four species

Shigella sonnei (most common in industrial world)

Shigella flexneri (most common in developing
countries)
Shigella boydii
Shigella dysenteriae

Non-lactose fermenting
Resistant to bile salts

Epidemiology and Clinical Syndromes

of Shigella

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

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

Epidemiology
of Shigella
Infection

Pathogenesis
number of bacteria
pathogenicity
toxicity
invasiveness
attachment
penetration
multiplication
immunity

common
Bacteria
intestine
penetrate mucus
multiply in epithelia
cell & proper lamina

normal intestinal flora

sIg A
prevent attaching

endotoxin
interotoxin
inflammation
vessel contraction
endogenous pyrogen
superficial mucosal necrosis
and ulcer
fever
diarrhea mixed with blood & pus,
abdominal pain

Pathogenesis-toxic
strong - allergy to endotoxin
demethyl-adrenaline
micro-circulatory failure
shock, DIC,

cerebral edema
cerebral hernia

Pathogenesis of Shigella
Shigellosis

Two-stage disease:
Early stage:

Watery diarrhea attributed to the enterotoxic

activity of Shiga toxin following ingestion and
noninvasive colonization, multiplication, and
production 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 and Virulence Factors (cont.)

Virulence attributable to:

Invasiveness
Attachment (adherence) and internalization
with complex genetic control
Large multi-gene virulence plasmid regulated by
multiple chromosomal genes
Exotoxin (Shiga toxin)
Intracellular survival & multiplication

Pathogenesis and Virulence Factors (cont.)

Invasiveness in Shigella-Associated Dysentery

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 (thin
layer of fibrous connective tissue immediately beneath the
surface epithelium of mucous membranes)

Preferentially attach to and invade into M cells in

Peyers patches (lymphoid tissue, i.e., lymphatic system)
of small intestine

Pathogenesis and Virulence Factors (cont.)

Invasiveness in Shigella-Associated Dysentery(cont.)

M cells typically transport foreign antigens from
the intestine to underlying macrophages, but
Shigella 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 with
cell-to-cell passage, thereby effectively avoiding
antibody-mediated humoral immunity (similar
to Listeria monocytogenes)

Methods That Circumvent

Phagocytic Killing

, Shigella spp.

,
Shigella spp.

Pathogenesis and Virulence Factors (cont.)

Characteristics of Shiga Toxin

Enterotoxic, neurotoxic and cytotoxic
Encoded by chromosomal genes
Two domain (A-5B) structure
Similar to the Shiga-like toxin of
enterohemorrhagic E. coli (EHEC)
NOTE: except that Shiga-like toxin is encoded by
lysogenic bacteriophage

Pathogenesis and Virulence Factors (cont.)

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 hypersecretion
of 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 Factors (cont.)

Shiga Toxin Effects in Shigellosis (cont.)

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 60S
ribosomal 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

Heparin-binding epidermal growth

factor on heart & nerve surfaces

Pathology
site of lesion:
entire colon -sigmoid &
rectum
feature:
acute:

diffuse fibrinous exudative

inflammation,
hyperemia, edema, leukocyte
infiltration, necrosis,
superficial ulceration.

chronic: edema, ulceration,

polypoid
hyperplasia,
toxic: hyperemia, edema,

Pathology

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

shock form: septic shock

brain form: listlessness,
lethargy, convulsion, coma.
respiratory failure
mixed form

Clinical manifestation

Clinical manifestation
chronic dysentery: > 2

months
chronic delayed type
chronic obscure type
acute attack type

chronic

delayed type:

chronic

obscure type:

long-time diarrhea and repeated

acute history in 1 year, no symptoms,
stool culture positive or sigmoidscopy
acute

attack type:

same as common acute dysentery

Clinical manifestation

Laboratory Findings
Blood picture:
WBC count increase,
neutrophils increase

Stool examination:
direct microscopic
examination:
WBC, RBC, pus cells

bacteria culture
PCR :DNA
Serologic examination
Sigmoidoscopy: chronic
patients
shallow ulcer
scar
polyp

Laboratory Findings

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

enteritis caused by E. Coli,

salmonella, virus.
intussusception:
jam-like stools,
abdominal mass,
absence of fever

Differential diagnosis

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,

sigmoidoscopy: hemorrhage,
ulcer,
X-ray : lead pipe.
chronic schistosomiasis Japonica

with the contaminated water

hepatomegaly and splenomegaly
founding the ovum of schistosomiasis

Differential diagnosis

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
Gentamycin

symptomatic treatment:
Toxic dysentery
general treatment
pathogenic treatment:
L-ofloxacin: 0.2 bid ivdrop
cefotaxime
Ampicillin

Treatment

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.
Rehidrasi.
Antibiotika :
Kotrimoksazol tidak lagi mjd antimikroba empirik
Siprofloksasin 2 x 500-750 mg

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

Prevention

Sekian