DISENTRIdr Shahrul Rahman, Sp.PDDepartemen Ilmu Penyakit DalamFakultas KedokteranUniversitas Muhammadiyah Sumatera Utara

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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 AmubaDef. 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 ususMagna : 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 BASILERNama 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

DefinitionAcute 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

EtiologyS. Flexneri the epidemic group and easily turn to chronicS. Boydii tropical areasS. sonnei the most mild

EtiologyPathogenicity: - virulence endotoxin - interotoxin (exotoxin) - invasiveness (attach-penetrate-multiply) Resistance: Strong, 1-2 week in fruits,vegetable and dirty soil, heat for 60 30 min

Coliform bacilli (enteric rods)

Nonmotile gram-negative facultative anaerobes

Four speciesShigella sonnei (most common in industrial world)Shigella flexneri (most common in developing countries)Shigella boydiiShigella dysenteriae

Non-lactose fermenting

Resistant to bile salts

General Characteristics of Shigella

Shigellosis = Generic term for disease

Low infectious dose (102-104 CFU)Humans are only reservoirTransmission by fecal-oral routeIncubation period = 1-3 daysWatery diarrhea with fever; changing to dysenteryMajor cause of bacillary dysentery (severe 2nd stage) in pediatric age group (1-10 yrs) via fecal-oral routeOutbreaks in daycare centers, nurseries, institutionsEstimated 15% of pediatric diarrhea in U.S.Leading cause of infant diarrhea and mortality (death) in developing countries

Epidemiology and Clinical Syndromes of Shigella

Epidemiology

Source of infection: patients and carriersRoute of transmission: fecal-oral routeSuceptibility of population: immunity after infection is short and unsteady, no cross-immune

Epidemiology Epidemic features:season: summer & fallFlexneri, Soneii, age: younger children

Epidemiology of Shigella Infection

Pathogenesisnumber of bacteria pathogenicitytoxicityinvasivenessattachmentpenetrationmultiplication immunity

commonBacteriaintestinenormal intestinal florasIg A prevent attachingpenetrate mucusmultiply in epithelia cell & proper laminaendotoxin interotoxinendogenous pyrogenfeverinflammationvessel contractionsuperficial mucosal necrosis and ulcerdiarrhea mixed with blood & pus, abdominal pain

Pathogenesis-toxicstrong - allergy to endotoxindemethyl-adrenalinemicro-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, and production of enterotoxin in the small intestineFever attributed to neurotoxic activity of toxin

Second stage: Adherence to and tissue invasion of large intestine with typical symptoms of dysenteryCytotoxic activity of Shiga toxin increases severity

Pathogenesis of Shigella

Pathogenesis and Virulence Factors (cont.) Virulence attributable to:

InvasivenessAttachment (adherence) and internalization with complex genetic controlLarge multi-gene virulence plasmid regulated by multiple 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 (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

Invasiveness in Shigella-Associated DysenteryPathogenesis and Virulence Factors (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 cytoplasmNote: 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)

Pathogenesis and Virulence Factors (cont.)Invasiveness in Shigella-Associated Dysentery(cont.)

Methods That Circumvent Phagocytic Killing, Shigella spp.Shigella spp.,

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.)Characteristics of Shiga Toxin

Shiga Toxin Effects in ShigellosisEnterotoxic Effect: Adheres to small intestine receptorsBlocks absorption (uptake) of electrolytes, glucose, and amino acids from the intestinal lumenNote: 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.)

Cytotoxic Effect: B subunit of Shiga toxin binds host cell glycolipidA 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 neurotoxicityShiga Toxin Effects in Shigellosis (cont.)Pathogenesis and Virulence Factors (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, polypoid hyperplasia,toxic: hyperemia, edema,

Clinical manifestationIncubation period: 1-2 day, (hours to 7 days)Acute dysenterycommon type mild typetoxic type

Clinical manifestationcommon type: acute onset shiver, high feverabdominal paindiarrhea: stool mixed with mucus, blood & pustenesmus

Clinical manifestationmild type: caused by S. sonneilow fever or no feverabdominal pain is mildstool mixed with mucus, without blood & pusdiagnosis by isolation bacteria

Clinical manifestationtoxic type: age: 2 to 7 yrs.abrupt onset, high fever, T> 40oCconvulsion repeatedly, altered consciousnesscirculatory & /or respiratory collapsediarrhea 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 monthschronic delayed typechronic obscure typeacute attack type

Clinical manifestationchronic delayed type: long-time diarrhea and repeatedchronic obscure type: acute history in 1 year, no symptoms, stool culture positive or sigmoidscopyacute 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 :DNASerologic examinationSigmoidoscopy: chronic patients shallow ulcer scar polyp

DiagnosisEpidemiologic data: contact historyClinical manifestationLaboratory findings

Differential diagnosis acute dysenteryamebic dysentery Entamoeba histolytica stool: reddish brown, like jam flask-shaped ulcer, amebic trophozoite

Differential diagnosisenteritis caused by E. Coli, salmonella, virus.intussusception: jam-like stools, abdominal mass, absence of fever

Differential diagnosis chronic dysenteryrectal & 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 with the contaminated water hepatomegaly and splenomegaly founding the ovum of schistosomiasis

Differential diagnosis

toxic dysentery encephalitis B: high fever, convulsion,coma.

TreatmentCommon dysenterygeneral treatment: isolation diet fluid and electrolytepathogenic treatment: norfloxacin 0.2~0.4 q6h po 5~7d Ampicillin given by po or iv Gentamycin

Treatmentsymptomatic treatment:Toxic dysentery general treatmentpathogenic treatment: L-ofloxacin: 0.2 bid ivdrop cefotaxime Ampicillin

Treatment chronic dysenterygeneral therapy: live, avoid overwork exercise diet

Treatmentetiologic therapy: sensitive antibiotics, according to results of culture used in turn or combined use enema. Rehidrasi.Antibiotika :Kotrimoksazol tidak lagi mjd antimikroba empirikSiprofloksasin 2 x 500-750 mg

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

Sekian

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