Disentriadaada

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



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 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.



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 : Diamond’s, 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 haribersama 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 ofintestine caused by dysenterybacilli

Place of lesion: sigmoid &rectum

Pathological feature:

diffuse fibrious exudativeinflammation



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 (PMN’s) 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-motileGroups: 4 serogroups 47

serotypesS. 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,vegetableand dirty soil, heat for 60 30 min



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



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



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

o f Sh igel la

Infect ion



Pathogenesis

number of bacteriapathogenicity

toxicity

invasiveness

attachment

penetration

multiplication

immunity



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



Pathogenesis-toxic

strong - allergy to endotoxin

demethyl-adrenaline

micro-circulatory failure

shock, DIC, cerebral edema

cerebral hernia



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



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



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




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)


Invasiveness in Shigel la -Associated Dysentery(cont.)



C



Methods That Circum vent

Phagocy t ic K il ling

, Shigel la spp.

Shigel la spp .

,



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


Characteristics of Shiga Toxin

P h i d Vi l F



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


P th i d Vi l F t ( t )



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.)




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,

polypoidhyperplasia,

toxic: hyperemia, edema,



Clinical manifestation

Incubation period:1-2 day, (hours to 7 days)

Acute dysenterycommon type

mild type

toxic type




common type: acute onsetshiver, high fever

abdominal paindiarrhea: stool mixed withmucus, blood & pus

tenesmus




toxic type:

age: 2 to 7 yrs.abrupt onset, high fever, T> 40oC

convulsion repeatedly, alteredconsciousnesscirculatory & /or respiratorycollapsediarrhea mild or absent at beginning




shock form: septic shock

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

mixed form




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



Laboratory Findings

Blood picture: WBC count increase,

neutrophils increaseStool examination:direct microscopic

examination: WBC, RBC, pus cells



Laboratory Findings

bacteria culture

PCR :DNASerologic examination

Sigmoidoscopy: chronicpatients

shallow ulcerscarpolyp



Diagnosis

Epidemiologic data:

contact history


Laboratory findings



Differential diagnosis

acute dysenteryamebic 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




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,




sigmoidoscopy: hemorrhage, ulcer,X-ray : lead pipe.

chronic schistosomiasis

Japonicawith the contaminated waterhepatomegaly and splenomegalyf ounding the ovum of schistosomiasis




toxic dysentery

encephalitis B:high fever, convulsion,coma.

<24h•circulatory failure•stool examination•CSF•meningeal irritation•specific IgM



TreatmentCommon dysenterygeneral treatment:

isolation

dietfluid and electrolyte

pathogenic treatment:

norfloxacin 0.2~0.4 q6h po5~7d

Ampicillin given by po or iv

Gentamycin



Treatment

symptomatic treatment:

Toxic dysentery

general treatmentpathogenic treatment:

L-ofloxacin: 0.2 bid ivdrop

cefotaxime

Ampicillin



Treatment

chronic dysenterygeneral therapy:

live, avoid overworkexercise

diet



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



Prevention

Control the source of infection:until culture negative

Interrupting the route oftransmissionProtecting the susceptible

population:F2a: secretary IgA

protect rate: 80%6-12mon

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