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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
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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.
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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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