Pediatric Ascariasis

Updated: Oct 06, 2023
  • Author: William H Shoff, MD, DTM&H; Chief Editor: Russell W Steele, MD  more...
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Practice Essentials

Ascaris lumbricoides, which causes ascariasis, is the largest of the round worms (nematodes), with females measuring 30 cm × 0.5 cm. It is present in the GI tract (small intestine) of 1.2-1.5 billion individuals in tropical and subtropical areas, making it the most common nematode infection in the world. [1] 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 ascarias 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 [2, 3] (Open Table in a new window)




A lumbricoides

Common roundworm infection, ascariasis

800 million to 1.4 billion

T trichiura

Whipworm infection, trichuriasis

600 million to 1 billion

Necator americanus and

Ancylostoma duodenale

Hookworm infection

580 million to 1.2 billion

Strongyloides stercoralis

Threadworm infection, strongyloidiasis

30-300 million

Enterobius vermicularis

Pinworm infection

4-28% of children

Toxocara canis and

Toxocara cati

Visceral larva migrans and ocular larva migrans

2-80% of children

*All major parasites are found in tropical, subtropical, and temperate climates.

Table 2. Minor Soil-Transmitted Helminths [2, 3] (Open Table in a new window)

Minor Parasite



Ancylostoma braziliense

Cutaneous larva migrans

Costal regions worldwide

Uncinaria stenocephala

Cutaneous larva migrans

Costal regions worldwide

Ancyclostoma canium

Eosinophilic enteritis


Ancylostoma ceylanicum

Hookworm infection


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 tuberculosis.



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.

Whether A suum and A lumbricoides are separate species remains controversial; however, evidence suggests that they may be distinct entities.



Species in the genus Ascaris are transmitted via the fecal-oral route, primarily from ingestion of 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 µm x 40-50 µm. 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 µm x 14 µm at this stage.

The larvae then migrate via the venous circulation to the pulmonary circulation and to the lungs. Here, the larvae measure 564 µm x 28 µm. They then break into the alveolar spaces, molt to the stage 3 larvae, grow to 1,700–2,000 µm, 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 0.5–0.6 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 28-32°C (82.4-89.6°F) and over 45-55 days at 16-18°C (60.8-64.4°F). 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 5-34°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

  • Formation of stage 2 larvae in the egg

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. 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: [3]

  • Chopping boards

  • Coins

  • Door handles

  • Dust

  • Fingers

  • Fingernail dirt

  • Fruit

  • Furniture

  • Insects

  • Nasal discharge

  • Paper money

  • Pickles

  • Public baths and restrooms

  • Public transportation (eg, buses)

  • Public squares (eg, sand, lawns)

  • School rooms

  • Underclothes

  • Vegetables

  • 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 sheep.

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

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 reported.

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. [4] The response is heterogeneous and is believed to confer some immunity. Evidence also suggests that whatever immunoprotection is conferred is not immunoglobulin-based.

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. [5, 6, 7, 8] Some studies demonstrate a negative association. [9, 10]

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.



United States statistics

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 2010–March 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. [11]

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%

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.

A meta-analysis by Holland et al found that the greatest prevalence of high-intensity Ascaris infection is in Latin America and the Caribbean region (8.4% of infected persons). [12]

Race-, sex-, and age-related demographics


No racial predilection is recognized.


Hepatobiliary and pancreatic ascariasis (HPA) occurs with a greater frequency in women than men (76% in one series). [13] 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. [14]

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]



Prognosis is excellent for the treatment of asymptomatic ascariasis. In some instances, a second treatment may be necessary to completely clear the worms. This has been demonstrated to significantly reduce the number of complications. The concern in endemic countries is that reinfection will occur.

In children in endemic countries, treatment results in demonstrated improvement in cognitive development, school performance, and weight gain.

The prognosis is good for patients with partial bowel obstruction who do not have toxicity and who are nonseptic, provided the patient is treated early with conservative management (see Medical Care).

The prognosis in patients with bowel obstruction who do not have toxicity or sepsis is good if the patient is treated early with appropriate surgical intervention (see Surgical Care).


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: [3]

  • 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 a meta-analysis by Mewara et al, ocular complications were reported exclusively among children and adolescents. [16] In endemic regions, ascariasis is a significant part of the differential diagnosis for intestinal obstruction, appendicitis, biliary tract disease, pancreatitis, intussusception, and volvulus.

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. [17, 18, 19]  A study by Clarke et al reported that for hookworm and Ascaris lumbricoides, mass deworming led to a significant reduction in prevalence in children when compared to targeted deworming. [20]


Complications include the following:

  • Intestinal obstruction: In some instances, treatment that involves an antihelminthic in an asymptomatic individual who is passing Ascaris eggs or who is involved in a mass treatment program precipitates partial or complete bowel obstruction. This situation cannot be predicted. If the patient has abdominal (nonsurgical) pain that may be related to ascariasis, conservatively treating the patient without administering an antihelminthic until the symptoms abate and then treating with antihelminthics under close observation is judicious (see Medical Care). Untreated intestinal obstruction may lead to bowel necrosis, peritonitis, sepsis, and death.

  • Volvulus

  • Intussusception

  • Hepatobiliary disease

  • Pancreatitis

  • Appendicitis

  • Bowel perforation

  • Peritonitis

  • Sepsis, sepsis syndrome, septic shock

  • Ascaris pneumonia

  • Löeffler syndrome

  • Asthma exacerbation

  • Encephalitis

  • Other ectopic migration