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    Growth and development failure (failure

    to thrive) due to parasitic infections

    Lisawati Susanto & Taniawati Supali

    Department of Parasitology, Faculty of Medicine,

    University of Indonesia

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    Definition

    is a description applied to children whose

    current weight or rate of weight gain is

    significantly below that of other children of

    similar age and sex.

    height or weight less than the third to fifth

    percentiles for age on more than one

    occasion.

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    Failure to thrive

    In general, the rate of change in weight

    and height may be more important than

    the actual measurements.

    It is important to determine whether failure

    to thrive results from medical problems or

    factors in the environment, such as abuse

    or neglect.

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    Etiology of failure to

    thrive

    Chromosome abnormalities, such as Downsyndrome and Turner syndrome

    Abnormalities in the gastrointestinal system, whichmay result in malabsorption or absence of digestiveenzyme, resulting inadequate nutrition.

    Abnormalities of the endocrine system, such asgrowth hormone deficiency

    Damage to the brain or central nervous system,which may cause feeding difficulties

    Anemia

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    Giardia lamblia

    Ascaris lumbricoides

    Hookworms

    Some parasites within their life cycle pass through

    gastrointestinal system

    http://en.wikipedia.org/wiki/Image:Digestive_system_diagram.svghttp://en.wikipedia.org/wiki/Image:Digestive_system_diagram.svghttp://en.wikipedia.org/wiki/Image:Digestive_system_diagram.svghttp://en.wikipedia.org/wiki/Image:Digestive_system_diagram.svg
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    Parasitic infection and failure to thrive

    Chronic parasitic infections may cause

    disturbances on food absorption in the GI

    tract system effecting the host nutrition.

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    Parasitic infection and failure to thrive

    In general parasitic infections could be

    divided into two classifications: helminthes

    (metazoa) and protozoa

    Helminthes:Ascaris lumbricoides, hook

    worm

    Protozoa: Giardia lamblia

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    Class Species Infective stage

    Nematoda Ascaris lumbricoidesHookworms

    Mature egg

    Filariform larva

    Protozoa Giardia lambia Cyst

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    Risk factors

    Defecation habits

    Geophagia (eating soil)

    Cultural differences relating to personal

    and food hygiene

    Inadequate sanitation

    Poor socio-economic conditions

    Occupation such as farmer, mining labour

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    Ascaris lumbricoides

    Ascariasis is a disease caused by Ascarislumbricoides (round worm), which is the mostprevalent intestinal worm infection in the world.

    The adult worm lives in the lumen of smallintestine

    Eggs are found in the soil, infection occurs whena person accidentally ingests (swallow) infectiveeggs.

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    Ascariasis

    Route of infection:

    Children/Human become infected after

    touching their mouth with their hands

    contaminated with eggs from soil or othercontaminated surfaces

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    Life cycle ofA. lumbricoides

    Human ingested embryonatedegg. In the stomach, larvaehatch from the eggs. and arecarried via the hepatic portalvein, then systemic circulationto the lungs, mature in the

    lungs (10 -14 days), penetratethe alveolar walls, ascend thebronchial tree to the throat,and are swallowed.

    Once swallowed, they reach the

    intestines and develop intoadults worms. Adult female

    worms lay eggs that are then

    passed in feces; this cycle will

    take between 2 3 months

    Eggs are passed in the stool.

    Unfertilized eggsmay be ingested butnot infective.

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    Pathogenesis

    Heavy infection children with malnutrition

    Acute inflammatory response

    Proinflammatory Monokines (IL-1, IL-6, TNF-)

    Appetite

    Loss of protein raise resting energy expenditure

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    Pathogenesis

    Adult worms in the small intestine

    Direct competition with the host for nutrients

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    Adult worms

    Protease inhibitors & anti-trypsine

    Ascaris lumbricoides

    secreting

    Interfering host digestion Enable to ingest the meal

    before host absorption

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    Adult worms

    Abnormalities of small intestine

    Changes in the absorption of fat and xylose

    Ascaris lumbricoides

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    Symptoms of ascariasis

    Commonly infected persons: No symptoms

    Immature worms enter the small intestine and

    mature into adult worms.

    - abdominal symptoms: abdominaldiscomfort-fullness, malabsorption.

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    Ascariasis

    Complications:

    Adult worms move to bile duct and

    interfere the lipid digestion.

    Heavy infection in children:

    loss of appetite and insufficient absorption of

    digested foods can occur as a large number

    of parasites take nourishment from the hosts

    body Nutritional deficiencies

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    Treatment

    Drug of choice:

    Albendazole - 400 mg (single dose)

    Mebendazole - 500 mg (single dose)Pyrantel pamoat - 10 mg/kg BW (single

    dose)

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    Prevention

    Sanitary disposal of feces through the

    implementation of latrines

    Health education: personal hygiene and food

    hygiene

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    Hookworm

    There are two species of hookworm which infect human

    Ancylostoma duodenaleAncylostoma duodenale Necator americanusNecator americanus

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    Hookworm

    Disease:

    Ancylostomiasis

    Necatoriasis

    Route of infection:

    Ancylostoma duodenale : oral, percutaneous

    Necator americanus : percutaneous

    Filariform larva (infective stage)

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    Hookworm

    Hookworm eggs require warm, moist,

    shaded soil to hatch into larvae.These barely visible larvaepenetrate the skin(often throughbare feet), are carried to the lungs,go through the respiratory tract tothe mouth, are swallowed, and

    eventually reach the small intestine.This journey takes about a week. Inthe small intestine, the larvaedevelop into half-inch-long worms,attach themselves to the intestinalwall, and suck blood. The adult

    worms produce thousands of eggs.These eggs are passed in the feces(stool). If the eggs contaminate soiland conditions are right, they willhatch, molt, and develop intoinfective larvae again after 5 to 10

    days.

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    Hookworm

    Worms live in the small intestine by attaching to

    the mucose via the buccal capsule.

    Worms feed on host mucosa and blood.

    Worms change position of attachment site every

    4 6 hours in response to tissue depletion andor the onset of local inflammation.

    (The blood is still coming out from the old attachment site for

    several day)

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    Pathogenesis

    The adult worms move several times a day to different

    attachment sites in the intestinal mucosa.

    The worms eat villous tissue and also suck blood

    directly from their site of attachment to the intestinal

    mucosa and submucosa.

    The worms secrete an anticoagulant that blocks the

    action of host factor Xa and VII a/tissue factors. Blood

    loss continues after the worms move to a new location.

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    Pathogenesis

    The combination of constant blood loss due tohookworm infection and poor iron intake in thediet results in iron deficiency anaemia.

    The severity of iron-deficiency anemia

    depends upon the species of hookworms inthe intestine (A. duodenale ingests 4-5 timesmore blood each day than N. americanus)

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    Adult worms

    Suck host blood Secrete anti-coagulant

    from the capillaries of blocking factorsIntestinal mucosa Xa dan VII a

    Loss of blood plasma & Blood lost

    Its constituents

    Hypoproteinemia Anaemia

    Pathogenesis

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    Hookworm

    Heavy infection with hookworm can create

    serious health problems for newborns,

    children, pregnant women, and persons

    who are malnourished.

    Head ofA. duodenale Head of N. americanus

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    Symptoms

    Heavy infection can cause anemia, abdominalpain, diarrhea, loss of appetite, and weight loss.

    When children are continuously infected by manyworms, the loss of iron and protein can retardgrowth and mental development, sometimesirreversibly.

    Anaemia in Children can impair their educationalperformance.

    a

    Hookworms on the bowel mucosa

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    Diagnosis

    The examination of stool sample for the

    presence of eggs is the most reliable

    means of diagnosis.

    The recommended procedure is the Kato-

    Katz technique which is able to count the

    number of eggs to determine intensity

    of infection

    Egg counts express as EPG (eggs per gram

    of faeces)

    Rhabditiform larva

    Egg

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    Treatment

    Drug of choice:Albendazole 400 mg (single dose)

    Mebendazole -100 mg (twice a day for 3consecutive days)

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    Prevention

    Sanitary disposal of feces through the

    implementation of latrines

    Health education: personal hygiene and food

    hygiene Encouraging use of shoes or other footwear

    (hookworms).

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    Giardia lamblia(Giardiasis)

    Zoonosis

    Host: animal and human

    Trophozoite Cyst

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    Life cycle ofG.lamblia

    Giardia lamblia exists in two forms, an

    active form called a trophozoite, andan inactive form called a cyst. Theactive trophozoite attaches to thelining of the small intestine with asucker and is responsible forcausing the signs and symptoms ofgiardiasis. The trophozoite cannot live

    long outside of the body, therefore itcannot spread the infection to others.The inactive cyst, on the other hand,can exist for prolonged periodsoutside the body. When it is ingested,stomach acid activates the cyst, andthe cyst develops into the disease-causing trophozoite. It takes ingestionof only ten cysts to cause infection.Trophozoites are important not onlybecause they cause disease, theyalso produce cysts that exit the bodyin faeces and spread infection toothers.

    http://www.medicinenet.com/script/main/art.asp?articlekey=3400http://www.medicinenet.com/script/main/art.asp?articlekey=3400
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    Pathogenesis

    The mucosal factors :

    The intestinal mucosa isdamaged by the attachment oftrophozoites on the epithelialbrush border.

    Absorptive activities areblocked due to thetrophozoites "blanketing" theintestinal mucosa and causingfunctional mucosal obstruction

    and interference in absorptionof fats and fat-soluble vitamins.

    The mucosal and luminal factors involved in the pathogenesis.

    The luminal factors : The increased number of anaerobic

    & aerobic bacteria in the smallintestine leads to the deconjugationof bile salts. The bile salts are then

    taken up by the trophozoitesstimulating parasite growth.

    The consumption of host bile salts inchronic infection deplete the bile saltpool and thus contribute to fatmalabsorption.

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    Clinical presentation

    The clinical presentation of the disease is

    influenced by the host's immune response to

    the parasite and the parasite load in the

    small intestine.

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    Symptoms

    10-25 cysts are capable of causing clinical

    disease.

    Symptoms of giardiasis normally begin 1

    to 2 weeks (average 7 days) after

    becoming infected.

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    Symptoms

    Commonly no symptoms at all.

    Diarrhea: Stools become malodorous, mushy, and greasy.

    Watery diarrhea may alternate with soft stools or evenconstipation.

    Flatulence

    Steatorrhea

    Stomach cramps

    Nausea. These symptoms may lead to weight loss and

    dehydration.

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    Symptoms

    These symptoms may lead to weight loss.

    Weight loss occurs in more than 50% of

    patients and averages 10 pounds per person. Chronic illness may occur with adults

    presenting with long-standing malabsorptionsyndrome and children with failure to thrive.

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    Symptoms

    The disease is more prevalent in children.

    The symptoms of giardiasis causedehydration due to diarrhea, therefore

    drink plenty of fluids .

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    Laboratory examination

    Stool examination

    Trophozoites may be found in fresh, watery

    stools.

    Cysts are passed in soft and formed stools.

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    Laboratory examinations

    Stool antigen detection ELISA to detect giardia specific antigen 65

    kDa (GSA-65)

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    ELISA Results

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    Other tests

    Detection of trophozoites in duodenalfluid can be done by String test /Entero test.

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    Treatment

    Metronidazole 3 x 250 750 mg for 7 10

    days

    Tinidazole: 2 g- single dose

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    Prevention

    Washing hand after defecation.

    Chlorination, sedimentation, and filtrationmethods to purify public water supplies.

    Drinking water can be purified by usingfiltration (pore size,

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