Reading on ascariasis is too important to mange those who are at risk

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PEDIATRIC
ASCARIASIS/HOOK
WORM
ESRAEL DIGA

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PRESENTATION OUTLINE
 Introduction
 Pathophysiology
 Epidemiology
 Clinical presentation
 DDX
 Work up
 Rx and management
 Medication
 prevention

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INTRODUCTION
 A. lumbricoides which causes ascariaisis is
the largest worms (nematodes)
 Female measures 50 by 0.5 cm
 It present in the GI tract
 The parasite is acquired through ingestion of
embryonated egg
 It is usually asymptomatic

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CONTINUED
 AL has been present in humans for many
thousand years
 Science only began to elucidate its biology in
17th
century
 Effective chemotherapy was only developed
in the 20th
C
 1758 Linnaeus proposed the name AL
 In 1862, Ransome reported that finding eggs
in fecal samples was a reliable means of dx

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CONTINUED
 In 1862, Davaine concluded that ingestion of
embryonated eggs produced ascariasis

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CONTINUED
 The genus Ascaris is composed of 17 species
 AL has high host specificity for humans and
rarely for pigs
 A. suum has high host specificity for pigs

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LIFE CYCLE
 Life cycle data come from investigation of A
suum in pigs and AL in mice
 Little is known about the interaction of AL
larvae and humans
 Human ingest al eggs which contains stage 2
larvae
 The egg hatch in the jejenum release the
stage 2 larvae

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CONTINUED
 They then penetrate the small intestine wall , inter
portal venous circulation
 Migrates to the liver
 The larvae then migrates via the venous circulation
to the pulmonary circulation and to the lungs
 They then break into alveolar spaces and molt into
stage three and four larvae
 Then ascend the trachea, are swallowed, return to
small intestine, molt for the final time and develop
into mature adult , all over 14-20 days
 Total elapsed time from ingestion of eggs to mature
adult 18-42 days

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CONTINUED
 The size range of the mature female is 20-40cm
times 0.5- 0.6 cm
 The mature male 12-24 by 0.3-0.4 cm -
 Female produces approximately 200,000 eggs per
day
 In the presence of male eggs are fertilized by
copulation
 Female only infection produces non-fertilized
non-infective eggs
 male only infections produces no eggs
 The pre patent period from ingestion of egg to
detection of eggs in feces is 76-76 days

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CONTINUED
 The Life span of AL is 1-2 days
 Eggs fertilized and unfertilized released into
environment
 Unfertilized eggs do not become infective
 Fertilized eggs can not infect untile they
embryonate outside human body

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CONTINUED
 To become infective, eggs must complete
embryonization while in the soil
 The zygote develops into a stage 1 larva and
molts to a stage 2 larva within the egg shell
 This occurs over 10-14 days at 28-32°C (82.4-
89.6°F) and over 45-55 days at 16-18°C
(60.8-64.4°)
 Several factors favor survival of the egg

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THIS INCLUDES
Amount of moisture in the soil (ie, clay soil vs sandy soil)
Protection from direct sunlight (quickly kills eggs)
Temperatures of 5-34°C (41-93.2°F): A temperatures of
40°C (104°F) is lethal. A temperature of 38°C (68.4°F) is
lethal after 8 days.
 Soil humidity of more than 4%: The length of survival is
4.5 hours or less with soil humidity of less than 4%,
varies at 4-50% soil humidity, and is best at more than
50% soil humidity

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CONTINUED
 Freezing at –15°C to –12°C (0.4-5°F) for 90
days kills all eggs except those at the single
blastomere stage
 Depth in the soil is another major influence
 Experimentally, under similar climatic
conditions, eggs survive 21–29 days on the
surface
 1.5 years or less at a depth of 10-20 cm, and
2.5 years or less at a depth of 40-60 cm

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CONTINUED
 Under experimental conditions, eggs have
sHowever, in general, eggs are expected to
survive 28-84 daysurvived for 6-14 years in
the soil
 However, in general, eggs are expected to
survive 28-84 days
 In areas of endemicity, particularly where
night soil (human feces) or untreated
wastewater is used as fertilizer, the egg
concentration is 100 eggs per gram of soil

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PATHOPHYSIOLOGICAL
MECHANISM
 Adult worms move throughout the GI tract
 and move in and out of orifices (eg, biliary
tract, pancreas, appendix, diverticula,
Meckel diverticulum
 become incarcerated, leading to obstructive
pathology
 The worms may die, leading to inflammation,
necrosis, infection, and abscess formation

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CONTINUED
 Larvae during migration may be deposited in
the brain, spinal cord, kidney, or other
organs, leading to granuloma formation,
 They may become entwined in a bolus and
obstruct the small bowel; this is most
common in the terminal ileum
 This condition may be precipitated by the
administration of an antihelminthic drug
 Only a small percentage of Ascaris infections
produce serious, acute pathology

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EPIDEMIOLOGY
 In the United States, more than 4 million
individuals are believed to be infected with
Ascaris species
 Most infected persons are immigrants from
developing countries

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INTERNATIONAL STATISTICS
 Worldwide, more than 1.4 billion people are
infected with ascariasis
 The distribution of cases is as follows:
 South America, Central America, and the
Caribbean - 8.3%
 Africa and the Middle East - 16.7%
 Asia and the Oceania region - 75%

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COMPLICATIONS
 Intestinal obstruction - 63%
 Bile duct obstruction - 23%
 Perforation, peritonitis, or both - 3.2%
 Volvulus - 2.7%
 Hepatitic abscess - 2.1%
 Appendicitis - 2.1%
 Pancreatitis - 1%
 Intussusception - 0.5%
 Cebral encephalitis - 1%

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CONTINUED
 Sepsis, sepsis syndrome, septic shock
 Ascaris pneumonia
 Löeffler syndrome
 Asthma exacerbation
 Other ectopic migration

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HISTORY
 Most individuals are asymptomatic, even in
communities where the prevalence is high
 The most common manifestation is
asymptomatic passage of an adult worm via
the rectum
 Less frequently, a worm migrates to the
oropharynx and is coughed out
 Ascaris eggs are often found in the stools of
asymptomatic individuals in endemic areas

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CONTINUED
 Some individuals with known significant
worm burdens report anorexia, abdominal
discomfort, and diarrhea
 however, these symptoms cannot be directly
attributed to ascariasis

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PULMONARY ASCARIASIS
 Symptoms develop 1-2 weeks after infection
 they vary from none to life-threatening
(rare), depending on sensitization or
considerable migrating worm burden
 Symptoms include
 chest pain (burning, aggravated by cough),
 cough (dry),
 dyspnea, fever, sputum (may be blood-
tinged), and wheezing

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CONTINUED
 A massive infestation can lead to Löeffler
syndrome
 transient eosinophilia, transient lung
infiltrates
 ascariasis remains the most common cause of
this syndrome worldwide
 In areas of continuous transmission,
pulmonary symptoms tend to be less evident

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INTESTINAL OBSTRUCTION
 Partial or complete obstruction secondary to
an entangled worm bolus can occur at any age
 however, 85% of cases occur in children aged
1-5 years and most occur at terminal ileum
 The worm bolus may also cause
intussusception or volvulus
 Severe, sharp, colicky abdominal pain with
associated vomiting predominates
 The vomit may contain worms
 Complete obstruction may begin subsequent
to the administration of an antihelminthic

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CONTINUED
 particularly in the setting of acute abdominal
pain or partial bowel obstruction
 Specific concern surrounds the
administration of pyrantel pamoate, which
causes a spastic paralysis of the worms
 Complete obstruction has also been reported
with piperazine (flaccid paralysis of worms)
and mebendazole (single large dose)

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HEPATOBILIARY AND PANCREATIC
ASCARIASIS AND OTHER GI DISEASES
 Migrating adult worms (most common), worm
fragments, or eggs can cause
 acalculous cholecystitis
 ascending cholangitis
 appendicitis
 biliary colic
 gastric hemorrhage
 granulomatous peritonitis
 liver abscess
 Meckel diverticulum inflammation
 obstructive jaundice
 Pancreatitis
 peritonitis
 peritoneal granulomatosis (ie, ductal and/or intestinal
perforation or migration through perforation

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EXTRA-GI CONDITIONS
 Worms may migrate to the upper respiratory
tract (ie, throat, nose, lacrimal ducts, and
inner ear
 Experimental studies report that the
migrating larvae can enter many tissues,
including the brain, kidney, and lymph nodes,
but cannot survive
 Several case reports have suggested
encephalopathy secondary to Ascaris larvae

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DIFFERENTIAL DIAGNOSES
Appendicitis Imaging
Asthma
Hypersensitivity Pneumonitis
Pediatric Cholecystitis
Pediatric Gallstones (Cholelithiasis)
Pediatric Malabsorption Syndromes
 Pediatric Pancreatitis and Pancreatic Pseudocyst

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LABORATORY STUDIES
 A microscopic examination finding of eggs in
the feces confirms the diagnosis
 This is performed using a direct method
(stool mixed with saline) or after
concentrating the stool
 Fertilized eggs are easier to identify than
unfertilized eggs and decorticate eggs
 Male-only ascaris infections produce no eggs
 Microscopic examination of gastric contents
may reveal larvae and eggs

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CHEST RADIOGRAPHY
 According to Löeffler, "The x-ray shadows are
 variable, unilateral or bilateral,
 fleecy or dense and small and round
 big and irregular; they may be very
extensive
 CT
 MRI

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TREATMENT AND MGT
Pulmonary cases
 Most cases are asymptomatic
 Most symptomatic cases are mild and self-
limited (days) and do not require therapy
 Bronchospasm can be managed with
conventional therapy
 Severe cases can be managed with systemic
steroids and oxygen supplementation

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PARTIAL SMALL BOWEL
OBSTRUCTION
 In the absence of signs of toxicity
 , fever, tachycardia
 , protracted vomiting, peritoneal signs
 persisting abdominal pain, or a palpable
mass
 in the same site for more than 24 hours,
several conservative management strategies,
including supportive care, have proven
efficacious

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HEPATOBILIARY AND
PANCREATIC ASCARIASIS
 This typically manifests as biliary colic,
 acalculous cholecystitis, ascending
cholangitis, pancreatitis, or hepatic abscess.
 Ascariasis is a common cause of these
conditions in endemic countries

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SURGICAL CARE
Intestinal obstruction
Appendicitis
Volvulus
Intussusception
 Ischemic bowel

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MEDICATIONS
 Several drugs are efficacious for the treatment of
ascariasis, including the asymptomatic intestinal
phase;
 this involves the periodic deworming of children
(symptomatic and asymptomatic), a reduction of the
public health burden
 The efficacy for albendazole, mebendazole, and
pyrantel is 88%, 95%, and 88%, respectively.
 For hookworm, a common infecting STH, the efficacies
for the same medications are 72%, 15%, and 31%,
respectively;
 therefore, using albendazole is more efficacious, when
a coinfection of ascaris and hookworm is suspected

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CONTINUED
 In general, antihelminthic drugs are not
recommended in patients from endemic
areas
 who have acute abdominal pain, with or
without partial bowel obstruction,
 Albendazole has the advantages of pediatric
dosing for individuals younger than 2 years,
 good tolerability, and efficacy in the
treatment of ascariasis, hookworm infection,
pinworm infection, strongyloidiasis, and
trichuriasis.struction

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MEBENDAZOLE
 Causes worm death by selectively and
irreversibly blocking uptake of glucose
 other nutrients in susceptible adult intestine
where helminths dwell
 Causes slow immobilization and death of
organisms
 Administration over 3 d reduces risk of worm
bolus formation
 Available as a 100-mg chewable tablet that
can be swallowed whole, chewed, or crushed
and mixed with food

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ALBENDAZOLE
 Broad-spectrum anthelmintic agent
 effective against Ascaris species, hookworm,
tapeworm, liver fluke, and pinworms.
 Decreases ATP production in worm,
 causing energy depletion, immobilization,
and finally death.

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PIPERAZINE
 Causes flaccid paralysis of the helminth by
blocking response of Ascaris species worm to
acetylcholine;
 thus, expels the worm by normal intestinal
peristalsis

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IVERMECTINE
 Binds selectively with glutamate-gated
chloride ion channels in invertebrate nerve
and muscle cells, causing cell death.
 Half-life is 16 h; metabolized in liver

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PREVENTION
 Prevention consists of improved sanitation
and education about the disease
 In endemic areas, school screening has
demonstrated effectiveness in detection and
early treatment of asymptomatic carriers
 Benefits in health and educational
performance have been reported with
 large-scale treatment of school-aged
children every 6 months in countries where
ascariasis is a public health problem

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CONTINUED
 Three strategies have been identified to
control STH infections
 chemotherapy, health education, and
sanitation

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SANITATION
 Sanitation in developed countries is currently
too expensive
 to be provided to the more than 2 billion
people who lack safe disposal of their feces

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HOOK WORM
 Hookworm infections are common in the tropics and
subtropics
 The prevalence of hookworm infection is highest in sub-
Saharan Africa, followed by Asia, Latin America, and the
Caribbean
 Infection is rare in regions with less than 40 inches of
rainfall annually
 There are two species of hookworm that cause human
infection
 Ancylostoma duodenale (in Mediterranean countries,
Iran, India, Pakistan
 Necator americanus (in North and South America,
Central Africa, Indonesia, islands of the South Pacific,
and parts of India)

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THREE FAVORABLE CONDITIONS
FOR TRAANSIMISSION
 Three conditions are important for
transmission of hookworm infection:
 human fecal contamination of soil
 favorable soil conditions for larval survival (moisture,
warmth, shade)
 contact of human skin with contaminated soil
 Individuals who walk barefoot or with open
footwear in fecally contaminated soil are at
risk for infection

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LIFE CYCLE
 begins with passage of eggs from an adult
host into the stool
 Hookworm eggs hatch in the soil to release
rhabditiform larvae that mature into
infective filariform larvae
 Infection is transmitted by larval penetration
into human skin
 as few as three larvae are sufficient to
produce infection

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CONNTINUED
 From the skin, larvae migrate into the blood
vessels and are carried to the lungs
 Approximately 8 to 21 days following
infection, larvae penetrate into the
pulmonary alveoli
 ascend the bronchial tree to the pharynx,
and are swallowed
 In addition to percutaneous larval
penetration (the principal mode of
transmission), A. duodenale infection may
also be transmitted by the oral route

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CONTINUED
 In the small intestine, the larvae mature into adult
worms
 attach to the intestinal wall with resultant blood loss
 A. duodenale larvae may persist within tissues before
returning to the intestine with delay in egg laying
 Following fertilization by adult male worms, gravid
female adults lay eggs within the bowel
 Eggs become detectable in feces about six to eight
weeks following infection with N. americanus
 Most adult worms are eliminated in one to two years
though infection can persist for many years

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CLINICAL MANIFESTATION
 The potential manifestations reflect the four
phases of hookworm infection
 Dermal penetration by infecting larvae
 Transpulmonary passage
 Acute gastrointestinal symptoms
 Chronic nutritional impairment

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CUTANEOUS MANIFESTATIONS
 Dermal penetration of the skin frequently
produces a focal pruritic maculopapular
eruption at the site of larval penetration
(termed "ground itch")

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TRANSPULMONARY PASSAGE
 Transpulmonary passage is usually
asymptomatic
 A mild cough and pharyngeal irritation may
occur during larval migration in the airways,
though eosinophilic pulmonary infiltrates
 Pulmonary symptoms attributable to
hookworm have not been observed
experimentally infected volunteers

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ACUTE GASTROINTESTINAL
SYMPTOMS
 Patients may experience gastrointestinal
symptoms at the time of larval migration to
the small intestine
 Nausea, diarrhea, vomiting, midepigastric
pain (usually with postprandial accentuation)
 increased flatulence

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CHRONIC NUTRITIONAL
IMPAIRMENT
 The major impact of hookworm infection is
on nutritional status
 his is particularly important in endemic areas
where children and pregnant women may
have limited access to adequate nourishment
 In addition, maternal hookworm infection is
associated with low birth weight

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CONTINUED
 Hookworms cause blood loss during
attachment to the intestinal mucosa by
lacerating capillaries
 ingesting extravasated blood
 this process is facilitated by the production of
anticoagulant peptides that inhibit activated
factor X and factor VIIa/tissue factor complex
 inhibit platelet activation
 lead to anemia and contribute to impaired
nutrition, especially in patients with heavy
infection

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DIAGNOSIS
 Clues to the presence of hookworm infection
include clinical manifestations as described
above
 The diagnosis is established by stool
examination; there are no reliable serologic
tests available

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STOOL EXAMINATION
 Stool examination for the eggs of N. americanus
or A. duodenale is useful for detection of
clinically significant hookworm infection
 Fecal egg excretion becomes detectable about
eight weeks after dermal penetration of N.
americanus infection
 up to 38 weeks after dermal penetration of A.
duodenale
 Stool examination for detection of hookworm
infection is insensitive
 Serial examinations may be required to make
the diagnosis.

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CONTINUED
 The eggs of N. americanus and A. duodenale
are morphologically indistinguishable
 Speciation is not necessary for clinical
purposes and is only possible if adult worms
are detected in stool or at endoscopy

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EOSINOPHILIA
 Otherwise unexplained eosinophilia may be a
major clue to the presence of a parasitic
infection
 Eosinophilia has been attributed to persistent
attachment of adult worms to the intestinal
mucosa
 The degree of eosinophilia with hookworm
infection is usually mild and varies during the
course of the disease

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TREATMENT
 Iron replacement alone can lead to
restoration of a normal hemoglobin level in
individuals with hookworm infection
 but anemia recurs unless anthelminthic
therapy is given

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CHEMOTHERAPY

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HEALTH EDUCATION
 In terms of education, better-educated
households have better health
 The challenge is to educate communities
without clashing with local customs and
cultures

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CHEMOTHERAPHY
 The goal is to reduce the intensity of STH
infections in the community
 Three chemotherapy strategies have been
field tested for reducing the intensity of STH
infections in the community:
 1/universal/mass treatment (all ages, both
sexes, no exceptions)
 2/targeted treatment (defined age, sex, or
other identifier)
 3/selected treatment (current diagnosis of
STH infection)

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CONTINUED
 Only universal and targeted treatments are
effective
 Selected treatment does have a role, although
it does not reduce community STH infection
intensity
 Treatment delivered to children through the
schools at intervals of a year, 6 months, 4
months, or 3 months has been shown to be
effective
 When given every 3 months to children in one
study, a significant decrease in adult intensity
was noted, as wellective

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CHALLENGES IN OUR SPECIFIC
COMMUNITY
 Not familiar with ways of trnsmission
 Considering worms as parts of organ system
 The association between ascariasis and BUDA
 low socio economic status
 Poor hand washing practices/sanitation and
hygiene
 Educational status
 Open defecation in rural areas/ no
appropriate toilets
 Accesseblity for cean drinking water

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WAY FORWARD