DISENTRI

Dr. dr. Shahrul Rahman, Sp.PD, FINASIM

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 : 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.
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 : Metronidazole 3 x 750 mg : 10 hari
bersama dengan diloksanid furoat
atau
paromomycin.
Obat alternatif : emetin, dihidroemetin.
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, low-
volume 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 normal intestinal flora

sIg A
multiply in epithelia prevent attaching
cell & proper lamina

inflammation endotoxin interotoxin

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
considered signs of neurotoxicity
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:
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

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