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Pediatric Ascariasis: Background, Pathophysiology, Epidemiology http://emedicine.medscape.


Pediatric Ascariasis
Updated: Jan 05, 2015
Author: William H Shoff, MD, DTM&H; Chief Editor: Russell W Steele, MD more...


Ascaris lumbricoides, which causes ascariasis, is the largest of the round worms (nematodes),
with females measuring 30 cm x 0.5 cm. It is present in the GI tract (small intestine) of 1.21.5
billion individuals in tropical and subtropical areas, making it the most common nematode infection
in the world. The number of cases in the United States is estimated to be 4 million, with
transmission occurring in the Gulf States and southern New Mexico and southern Arizona. See the
image below.

The roundworm Ascaris lumbricoides causes ascariasis. Worms can reach 10-30 cm in length. Clinical disease
results from effects of pulmonary larval migration, intestinal obstruction, or migration through the biliary tree.

The parasite is acquired through ingestion of embryonated eggs. Ascariasis is usually

asymptomatic but can be complicated by several conditions, including appendicitis, bowel
perforation, cholecystitis, intestinal obstruction (large numbers), malabsorption (eg, lactose,
nitrogen, vitamin A), and pancreatitis. The mortality rate is 5% if complications occur. When the
parasite migrates through the lung early in its parasitic cycle, it can also cause pneumonitis. The
mainstays of chemotherapy include albendazole, mebendazole, and pyrantel pantoate (for
alternatives, see Medication).

A lumbricoides is one of the soil-transmitted helminths (STH), a group that includes 16 worms.
Many individuals are infected with 2-3 of the 3 major parasites (ie, A lumbricoides, Trichuris
trichiura, and hookworm).

Table 1. Major Soil-Transmitted Helminths [1, 2] (Open Table in a new window)

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Parasite* Disease Prevalence

Common roundworm 800 million to

A lumbricoides
infection, ascariasis 1.4 billion

Whipworm infection, 600 million to 1

T trichiura
trichuriasis billion

Necator americanus and

580 million to
Hookworm infection
Ancylostoma duodenale 1.2 billion

Threadworm infection,
Strongyloides stercoralis 30-300 million

4-28% of
Enterobius vermicularis Pinworm infection

Toxocara canis and

Visceral larva migrans and 2-80% of

Toxocara cati ocular larva migrans children

*All major parasites are found in tropical,

subtropical, and temperate climates.

Table 2. Minor Soil-Transmitted Helminths [1, 2] (Open Table in a new window)

Minor Parasite Disease Distribution

Ancylostoma braziliense Cutaneous larva migrans Costal regions worldwide

Uncinaria stenocephala Cutaneous larva migrans Costal regions worldwide

Ancyclostoma canium Eosinophilic enteritis Australia

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Ancylostoma ceylanicum Hookworm infection Asia

Oesophagostomum bifurcum Nodular worm infection North America

Strongyloides fuelleborni Swollen belly syndrome West Africa

Ternidens diminutus False hookworm infection Southern Africa

By chronically infecting school-aged children, usually in developing countries, these parasites

significantly contribute to cognitive deficits, growth stunting, mental retardation, and malnutrition.
The 3 most important infections are ascariasis (A lumbricoides) , trichuriasis (T trichiura), and
hookworm (N americanus and A duodenale); often, all 3 parasites can be found in a single
individual. The combined disease burden of the STHs is estimated to be equivalent to malaria or

Although A lumbricoides has been present in humans for many thousands of years, science only
began to elucidate its biology in the 17th century, and effective chemotherapy was only developed
in the late 20th century. The earliest recovered eggs are from the 30,000-year-old Upper-
Paleolithic site of Arcy-sur-Cure in Yonne, France. Infertile eggs have been reported in coprolites
dating to 2277 BCE from an archeological site at Los Gavilanes, Peru. Desiccated human feces
from Big Bone Cave, Tennessee dating to approximately 2177 BCE contained A lumbricoides. In
the Nubian aspect of the Nile River, eggs have been recovered inside a mummy dating to
2050-1750 BCE.

In 1683, Tyson discussed " Lumbricus teres observations on the Round Worm bred in human
bodies.that common Round Worm which children u[s]ually are troubled with." In 1758, Linnaeus
proposed the name Ascaris lumbricoides. In 1856, Ransom reported that finding eggs in fecal
samples was a reliable means of diagnosis. In 1862, Davaine concluded that ingested
embryonated eggs produced ascariasis and that the infected host would produce eggs in feces
that could pass the infection to another host. In the 1980s, several reviews noted the public health
impact of STH infection and suggested control strategies using antihelminthic drugs, some of
which were introduced in the 1960s (eg, pyrantel pantoate) and 1970s (eg, mebendazole).

The genus Ascaris is composed of 17 species. A lumbricoides has a high host specificity for
humans and, rarely, for pigs. It has been reported in other hosts, including cats, chimpanzees,
domestic dogs, gibbons, gorillas, guinea-pigs, lambs, macaques, monkeys, rabbits, rats, and
squirrels; however, it has not been demonstrated to achieve sexual maturity or to produce fertile
eggs in these hosts.

Ascaris suum has a high host specificity for domestic pigs and, rarely, humans. It has been
reported in other hosts, including domestic cattle, gorillas, goats, lambs, monkeys, mice, rabbits,
and rats. As with A lumbricoides, A suum has not been demonstrated to achieve sexual maturity or
to produce fertile eggs in these hosts. The other 15 species of Ascaris are not reported in humans.
Therefore, A lumbricoides does not have an animal reservoir.

Species in the genus Ascaris are transmitted via the fecal-oral route, primarily from ingestion of

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agricultural products or food contaminated with parasite eggs.

Life cycle

Life cycle data come from investigations of A suum in pigs and A lumbricoides in mice. Little is
known about the interaction of A lumbricoides larvae and humans.

Humans ingest A lumbricoides eggs, which contain stage 2 larvae and measure 50-70 m x 40-50
m. The eggs hatch in the jejunum and release the stage 2 larvae. They then penetrate the small
intestinal wall (some evidence suggests the large intestine), enter the portal venous circulation,
and migrates to the liver over 2-8 days. According to data from mice, they measure 258 m x 14
m at this stage.

The larvae then migrate via the venous circulation to the pulmonary circulation and to the lungs.
Here, the larvae measure 564 m x 28 m. They then break into the alveolar spaces, molt to the
stage 3 larvae, grow to 1,7002,000 m, and molt to stage 4 larva, all over 4-14 days. They then
ascend the trachea, are swallowed, return to the small intestine (usually intestine), molt for the
final time, and develop into mature adults, all over 14-20 days. The total elapsed time in humans
from the time of ingestion to development of mature adults is 18-42 days.

The size range of the mature female is 20-40 cm x 0.50.6 cm; the mature male is somewhat
smaller at 12-25 cm x 0.3-0.4 cm. The Ascaris genus contains the largest of the nematode
parasites; the migration through the tissues appears to confer this size advantage. In general,
alimentary tract nematodes (700 species) that migrate through tissues grow faster.

Females produce approximately 200,000 eggs per day (134,462-358,750), although this number
fluctuates. In the presence of a male, the eggs are fertilized by copulation. Female-only infections
produce nonfertilized eggs that cannot become infective. Male-only infections produce no eggs.
The prepatent period (time from ingestion of the egg to detection of the eggs in feces) is 67-76
days (67 d in children < 4 y). A suum infections in humans have a similar life cycle, with a
prepatent period of 24-29 days.

The life span of A lumbricoides is 1-2 years. Eggs, fertilized and unfertilized, are released to the
environment via feces. Unfertilized eggs do not become infective. Fertilized eggs cannot infect
until they embryonate outside the human body under proper conditions. Fertile eggs have 4
layers. The outer layer, which is not always present, consists of an extruded, sticky
mucopolysaccharide from the parent female worm. This provides adhesiveness thought to be
advantageous, allowing the eggs to stick to many types of surfaces. The other 3 layers are
secreted by the embryo and include an outer thin proteinaceous membrane, a middle protein and
chitin layer that provides structural strength, and the inner ascaricide layer, which consists of
protein (25%) and unsaponifiable lipid (75%). This inner ascaroside layer is selectively permeable
and is important for the survival of the egg in various conditions.

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 28-32C (82.4-89.6F) and over 45-55 days at 16-18C (60.8-64.4F). Several factors favor
survival of the egg, including the following:

Amount of moisture in the soil (ie, clay soil vs sandy soil)

Protection from direct sunlight (quickly kills eggs)
Temperatures of 5-34C (41-93.2F): A temperatures of 40C (104F) is lethal. A temperature

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of 38C (68.4F) 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
Formation of stage 2 larvae in the egg

Freezing at 15C to 12C (0.4-5F) 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 2129 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. Eggs and infective larva can survive over winter
to infect in warmer weather. Under experimental conditions, eggs have survived 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. Eggs can be spread through the soil by earthworms,
insects (eg, termites), and other burrowing animals. Egg-contaminated dust can be spread by
wind and can lead to human infection via inhalation and swallowing.

In endemic areas eggs contaminate numerous domestic and public sites, including the following:

Chopping boards
Door handles
Fingernail dirt
Nasal discharge
Paper money
Public baths and restrooms
Public transportation (eg, buses)
Public squares (eg, sand, lawns)
School rooms
Wash basins

The average number of female offspring that attain reproductive capacity (reproductive number)
produced by one adult female A lumbricoides worm is 1-6.

A lumbricoides and A suum

Evidence suggests that these parasites are separate species, although they are closely related. A
lumbricoides infects humans almost exclusively and rarely infects pigs. A suum infects pigs almost
exclusively and rarely infects humans. A lumbricoides has occasionally been reported in other
animals, such as bears and primates, and A suum has occasionally been reported in cattle or

Morphologically, they are essentially indistinguishable; however, several reports cite differences in

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the denticles as a distinguishing characteristic. The morphology of the sex chromosomes exhibits
differences, suggesting that the species are different. Species differences in the internal
transcribed sequences of the ribosomal DNA have been reported, allowing differentiation. Protein
profiles using 2-dimensional electrophoresis reveal reproducible differences. The current
consensus is that these are, in fact, different species; however, they are closely related enough
biologically that data on the life cycle and pathology of A suum have been extrapolated to

Pathophysiological mechanism

Adult worms move throughout the GI tract and move in and out of orifices (eg, biliary tract,
pancreas, appendix, diverticula, Meckel diverticulum) and may become incarcerated, leading to
obstructive pathology. The worms may die, leading to inflammation, necrosis, infection, and
abscess formation. If they migrate through an existing perforation in the bowel wall secondary to
tuberculosis or typhoid, they can cause a granulomatous peritonitis. Larvae during migration may
be deposited in the brain, spinal cord, kidney, or other organs, leading to granuloma formation,
inflammation, or infection. They may become entwined in a bolus and obstruct the small bowel;
this is most common in the terminal ileum, although other, more proximal, sites have been rarely

This condition may be precipitated by the administration of an antihelminthic drug (see

Medication). Eggs may be deposited in the liver or biliary tract. If they gain entry to the blood, they
are deposited in extraneous sites, leading to local reactions.

Only a small percentage of Ascaris infections produce serious, acute pathology; however,
because about one quarter of the human population is infected, the number of cases is significant.


Humans make antibodies in response to Ascaris antigens and infection; immunoglobulin (Ig) E is
predominant. [3] The response is heterogeneous and is believed to confer some immunity.
Evidence also suggests that whatever immunoprotection is conferred is not immunoglobulin-

Whether the presence of Ascaris infection increases risk or causes allergic disease or may have a
protective effect remains controversial. Several studies demonstrate an association between
Ascaris infection, seropositivity, or sensitization and allergic symptoms, sensitization, or asthma
risk. [4, 5, 6, 7] Some studies demonstrate a negative association. [8, 9]

An association has been reported between egg excretion in children and increased prevalence of
allergic disorders (eg, asthma) compared with children who do not excrete eggs. Because
ascariasis and other helminthic infections are long-lived without producing consistently serious
symptoms, a significant immunomodulatory relationship must occur between the infection and the
human host, the details of which have not been fully clarified. Future research may lead to the
development of vaccines and other interventions that will permit better control and treatment of
this pervasive parasitic disease.


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United States

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, although the species
are endemic in the southeastern United States in rural, low-income families.

During April 2010March 2013, the Maine Department of Health and Human Services investigated
multiple cases of ascariasis that had been reported by health-care providers, veterinarians, and
patients. All of the cases were in persons who had lived or worked on Maine farms and had
frequent exposure to pigs. After investigation, 14 persons on seven farms in Maine were identified
with Ascaris infection. [10]


Worldwide, more than 1.4 billion people are infected with ascariasis. The distribution of cases is as

South America, Central America, and the Caribbean - 8.3%

Africa and the Middle East - 16.7%
Asia and the Oceania region - 75%

Ascariasis is present in at least 150 of the 218 countries in the world. Prevalence estimates widely
vary among countries and within communities inside these countries.


Annual mortality estimates range from 10,000-200,000. Currently, the rate is believed to be 10,000
deaths per year based on more detailed calculations.

Morbidity is proportional to the worm burden. A large majority of cases are asymptomatic.
Intestinal obstruction, the most common complication of ascariasis, has been reported with as few
as 4 worms. The average worm burden in numerous nonfatal case reports was 59 worms (range,
4-990); in fatal cases, the average worm burden was 659 (range, 23-1978).

Based on numerous reports in the literature, a rough estimate of the occurrence (percent of total
complications) of complications is as follows: [2]

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%
Cerebral encephalitis - 1%
Intussusception - 0.5%

Other sites of pathology (< 0.5%) include Meckel diverticulum, the gallbladder, ears, eyes, nose,
lungs, kidneys, vagina, urethra, heart, placenta, spleen, thoracic cavity, umbilicus, pericecal mass,
jejunostomy tube, and erythema nodosum. In endemic regions, ascariasis is a significant part of
the differential diagnosis for intestinal obstruction, appendicitis, biliary tract disease, pancreatitis,
intussusception, and volvulus.

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Public health issues

A lumbricoides and other STHs have been shown to play a significant role in childhood
malnutrition, which leads to growth retardation, cognitive impairment, and poor academic
performance, resulting in a poorer quality of life and less ability to contribute to society. For the 3
major STHs, the disability-adjusted life years lost is 39 million years. Ascariasis accounts for 10.5
million years, hookworm infection accounts for 22.1 million years, and trichuriasis accounts for 6.4
million years. In comparison, malaria accounts for 35.7 million years.

Deworming with medications is one of many public health strategies to reduce infection rates and
worm burden. Many studies demonstrate that after deworming, reinfection at the pretreatment
level returns within 2-6 months, particularly, among the poor and socially disadvantaged. Several
factors play a role in reinfection, including swimming in polluted rivers, absence of parent (at work)
to supervise children, absence of toilet in house, running barefoot, eating without washing hands,
geophagy (eating soil), eating unwashed fruits and vegetables, and chores that require contact
with floors and ground. [11, 12, 13]


No racial predilection is recognized.


Hepatobiliary and pancreatic ascariasis (HPA) occurs with a greater frequency in women than men
(76% in one series). [14] In the same series, biliary surgery was more frequent in women (77%) and
was an important risk factor for HPA. No other sex association is reported.


Intestinal obstruction predominates in young children (85% of cases occur in children aged 1-5 y)
but can occur at any age.

HPA is more common in adults than in children. In one large series of 500 patients, the age range
was 4-70 years (median, 35 y). [15]

Clinical Presentation

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