UnPar-Final Modul Gastro 2013

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    Dr. Agnes Kurniawan,

    PhD, SpParK

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    GI Module Feb 2013-AK-UniB/UnPar 2

    1. To acquire knowledge on protozoa and

    worms which often leads to gastrointestinal

    disorders

    2. To understand the life cycle, epidemiology,clinical symptoms, diagnosis, treatment and

    prevention of the protozoa and worms

    causing GI disorders

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    Trichuris trichiura

    Taenia saginata

    E. histolytica

    Cyclospora cayetanensis

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    WORM

    PROTOZOA

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    = Whipworm, a roundworm/nematode, STH

    Commonly infect children

    Epidemiology : warm, humid climates, crowded

    Mode of infection : ingested of mature eggs

    Risk factor : poor hygiene, sanitation, raw vegetables

    Mature egg ingested hatch in the small intestine

    larvaeadult worm in caecum/ascending colon

    egg adult female = 60-70 days

    egg infective stage:36 wks, soil

    eggs produced: 3000-10.000/day

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    Adult:

    - female 5 cm, male 4 cm

    - anterior portion whip like- live in colon ascendens and caecum

    - no lung cycle: egg ingested hatch in thesmall intestine larvae adult worm in

    caecum/ascending colon

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    < 10 worms asymptomatic

    Heavy infection

    diarrhea, dysentery,anemia, rectal prolapse,growth retarded

    Note : dysentry : frequent, painfulpassage of stool that contains amixture of mucus, water, and

    blood.

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    The anterior part of the worm dip into the

    intestinal mucosa irritation trauma and

    inflammation of the intestinal mucosa and

    bleeding -- sucked by the worms

    anemia

    Parasitology Lab Diagnosis

    Microscopy :Wet smear : T. trichiura eggs in the stool

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    Treatment

    - Mebendazol 2x100 mg for 3 days (>2 yo)

    2x200 mg for 3 days (adult)

    - Albendazol 400 mg, single dose

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    1. BREAK THE WORM LIFE CYCLE- environmental sanitation : use of toilet

    for defecation, not using stool forfertilizer

    - good personal hygine : handwashingwith soap & water, wash well the fruitsand vegetables

    - mass treatment when prevalence > 30%

    2. HEALTH EDUCATION

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    Definitive host: man

    Adult worm: in the middle third small intestine

    Intermediate host : cattle

    larva (cyst) in muscles Mode of infection:

    - 1. in cattle: grazing on moist pasture contaminatedwith eggs ofT. saginata from human stool

    - 2. in man: consuming uncooked/rare cooked beefwith larvae (cysticercus bovis)

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    LIFE CYCLE

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    LIFE CYCLE & PREVENTION

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    Proglotid: crawling out of anus

    GI complaints: nausea, diarrhea, abdominal

    pain

    Systemic symptoms: fatigue, hunger,

    dizziness, moderate loss of weight

    Rare symptoms: vomiting of segments,

    obstruction of bile ducts, pancreatic ducts orappendix

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    eggs in stool

    proglotid crawling out

    of anusTreatment

    praziquantel 10mg/kg, single dose

    albendazole

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    EVALUATION OF TREATMENT- Relieve of symptoms- Parasitology lab examination :

    1. 24 hours collected stool after th/:

    scolex + proglottids

    2. stool, 3 months after th/:

    negative for eggs and

    or segments

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    E. histolytica: histo=tissue ; Lysis = dissolve,

    destroyed

    Aetiology of intestinal and extra intestinal

    amebiasisHost : human

    Habitat : colon

    Distribution : cosmopolitan, in tropical and

    subtropical countries

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    2 stages: trophozoite and cyst

    TROPHOZOITE :

    - 2 forms : histolytica (pathogen) and minuta

    (apathogen). Size : 10-60 um, entameba nucleus

    Endoplasm: fine granules, contains bacteriaor food metabolites

    If contains red blood cells erythrophago-cytosis typical for E. histolytica infection

    Live 2 hours outside the host

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    Size: 10-20 um

    round/oval shape

    Structure: cyst wall, endoplasm with 1,2 or 4

    nuclei

    Endoplasm : chromatoid body (cigar form) &

    glycogen vacuol (food storage)

    apathogenic Infective stage : mature cyst (cyst

    with 4 nuclei)

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    Ingestion of mature cyst

    Excystation in the stomach with the help of

    gastric juice trophozoite release colon

    multiplication by binary fission

    invadethe mucose ( cause symptoms ) or transform

    into cyst stage (encystation )

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    Trophozoites express gal/gal nac lectins

    antigen on its surface stick to colonic

    epithelial cells present amoebapores and

    excrete cysteine proteinases (amebapain dan

    hystolisine) lyse extracellular protein matrix

    epithelial cell lysis tissue necrosis,

    further invasion to submucose flask shape

    ulcer

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    Form : bottle shape, small opener at the top, wide

    at the bottom, irregular rim, slightly elevated

    Inflammation, with blood and secondary infectionwith bacteria

    Progression to submucose area along the lateral

    axis of colon

    Excretion of trophozoite into the lumen invadeother healthy area of colon or excreted with stool

    dysentric stool (mucous and blood )

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    1. Carrier state:

    - intestinal amebiasis

    - parasite multiplies in the body

    - stools : cysts ++

    - clinical signs /symptoms : none

    - cause : low virulent strain, low number of

    infection, adequate immune status

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    2. Intestinal amebiasis

    - dysentery, colitis, appendicitis, toxic

    megacolon, amebomas

    - Abdominal pain- Diarhoea with mucous and bloody stool ,

    frequency up to 10 x/day

    - Fever, loss of appetite, decrease body weight

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    The most common extraintestinal complication

    of amebiasis (8.5% of cases).

    Hepatic infection occurs because colonic

    trophozoites ascend via the portal vein

    invade the parenchyma

    Cause : toxin release & hepatocyte damage

    Usually develop within days - months after dysentri

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    Symptoms : fever (>90% acute cases), dullpleuritic right upper quadrant pain radiating to

    the right shoulder, hepatomegali and pleural

    effusions.

    Acute form: often very high fever, continuous orintermittent + chills

    Chronic forms : fever is low, develops gradually,

    without chills or sweating

    Right / left lobe

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    Occasionally spread into the overlying

    abdominal wall or form portal venous amebic

    thrombi.

    Hematogenous dissemination to the brain israre

    Diarrhea (2%), with 4 - 5 x/ day,watery stool,

    with mucus and blood, tenesmus, abdominal

    cramping and distension due to potassium loss

    Jaundice is an unusual feature(5%)

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    the abscess extends upward the diaphragm,

    pleura empyema .

    Invasion of the lung parenchyma by E.

    histolytica development of interstitialpneumonitis, liquefaction & formation lung

    abscess

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    1. Microscopic Faeces : trophozoite (invasive stage) and /

    cysts (non invasive stage)

    The 2 stages represent two separatespecies : E. histolytica & E. dispar which

    are morphologically indistinguishable

    unless E. histolytica is observed with

    ingested red blood cellsCysts: found in formed stool

    Trophozoites: found in diarrheal stool

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    Body fluid: trophozoite

    Stool examination is best performed 3X in a

    week to exclude false negative

    2. Serology test ( Antibody detection)

    IHA, ELISA

    To diagnose extraintestinal amebiasis

    Performed together with the microscopic

    examination of the abscess fluid and radio

    diagnostic

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    3. Antigen Detection

    ELISA

    Specimens: stool, serum, abscess fluid, saliva

    Specific for E. histolytica ( cannot for E.dispar)

    4. Polymerase chain reaction (PCR)

    to differentiate E. Histolytica from E. dispar

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    TREATMENTDrugs:

    - metronidazole (trophozoite & cyst form)

    - chloroquine (trophozoite form)

    - paromomycin (trophozoite form)

    Intestinal Amebiasis: paromomycin 25-35

    mg/kgbb/hari, 3x/day, 7 days

    Extraintestinal Amebiasis : metronidazol 3x750mg/hari 7-10 days + abscess drain

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    Improving sanitation and hygine individuals

    Health education on mode of transmission

    Water treatment : chlorination and filtration

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    Coccidia

    Host: man

    Epidemiology : developing countries

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    Oocyst: 8-10 um

    Immature (unsporulated) oocyst excreted instools sporulation 1 several weeks inwarm and humid climate

    Mature Oocyst : 2 sporocysts @ foursporozoites

    Infection : ingestion of mature oocysts

    Source of infection : contaminated food /

    vegetables, water such as raspberry

    Parasite lives intracytoplasmic develop inthe jejunal enterocytes

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    Diareanorexia, flatulance, epigastric pain,

    nausea, vomitus, low grade fever Immune competent : acute, light diarrheaAIDS : chronic diarrhea, severe

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    1. Microscopic :

    - oocyst in the stool, duodenal aspirates,duodenal/jejunal biopsy

    - 3 stools every 2-3 days- safranin / acid fast stainings

    2. UV fluorecense microscope

    3. PCR

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    Treatment : trimetoprim + sulfametoksazol,

    metronidazol, siprofloksasin

    Prevention : Improving sanitation and hygine

    individuals, health education, watertreatment, proper washing of raw vegetables

    and fruits

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    THANK YOU