Updated: Oct 01, 2021
  • Author: Amber Mahmood Bokhari, MBBS; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Ascariasis is the most common helminthic infection, with an estimated worldwide prevalence of 804 million cases in 2013. [1, 2, 3]  It is caused by Ascaris lumbricoides, which is the largest parasite from the class of nematodes commonly known as roundworms. Usually A lumbricoides or A suum infection is asymptomatic. Ascariasis is most prevalent in children of tropical and developing countries, [4] where they are perpetuated by contamination of soil by human feces or use of untreated feces as fertilizer and the water or food contaminated by the eggs is ingested. [5] For more information on ascariasis in children, see the Medscape article Pediatric Ascariasis. Symptomatic ascariasis occurs during the adult worm's intestinal or larval migration phase and may manifest as growth retardation, pneumonitis, intestinal obstruction, or hepatobiliary and pancreatic injury. Ascariasis may exist as a zoonotic infection associated with pigs and use of hog manure and is caused by Ascaris suum [6, 7] which is very similar to Ascaris lumbricoides  [8, 9] but, in most endemic areas, it is most likely transmitted from person to person. [10]

The image below depicts a roundworm that infects humans through soil contaminated by human feces.

Adult Ascaris lumbricoides.
Adult Ascaris lumbricoides.

See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.



Ascaris lumbricoides is the largest of the common nematodes (roundworms) that infect humans. Adult A lumbricoides are white or yellow and 15-35 cm long (Fig 9-12-1). They live 10 to 24 months in the jejunum and middle ileum of the intestine. Each day, female A lumbricoides produce 240,000 eggs (Fig 9-12-12), which are fertilized by nearby male worms. The eggs are oval, 45-70 x 35-50 microns in size with a thick outer shell. A Chinese study showed that 45% of infected persons shed only fertilized eggs, 40% shed fertilized and unfertilized eggs, and 20% shed only unfertilized eggs. Unfertilized eggs accounted for only 6-9% of eggs shed. Fertilized eggs released into favorable soil may become infectious within 5-10 days. [11] Eggs may remain viable in soil for up to 10 years. Infection occurs through oral ingestion of food or water contaminated by soil that contains embryonated eggs from human or pig feces that hatch in the small intestine within 4 days or direct ingestion of infected uncooked pig or chicken liver containing larvae. Although the eggs can persist in water treated by chemicals, they can be eradicated by boiling or filtering water sources. (Fig 9-12-12). [12, 13]

Adult Ascaris lumbricoides.
Adult Ascaris lumbricoides.
Ascaris lumbricoides egg. Ascaris lumbricoides egg.
Life cycle of Ascaris lumbricoides. Courtesy of th Life cycle of Ascaris lumbricoides. Courtesy of the Centers for Disease Control and Prevention (CDC) [].

Adult worms (females 20 to 35 cm; males 15 to 30 cm) (1)  live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces (2) . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3) , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4) , the larvae hatch out of eggs (5) , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs (6) . The larvae mature further in the lungs (10-14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7) . Upon reaching the small intestine, they develop into adult worms (1) . Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years. [14]

Larva of A lumbricoides hatching from an egg. Cour Larva of A lumbricoides hatching from an egg. Courtesy of the Centers for Disease Control and Prevention (CDC) [].

[14]  Reproduced from: Centers for Disease Control and Prevention. DPDx: Ascariasis. Available at:

Larvae are released from the Ascaris eggs in the small intestine within 4 days of ingestion. These larvae migrate through cecum and proximal colon and penetrate the intestinal mucosa and reach the liver via the portal circulation. They enter the heart through the hepatic veins, infiltrate the lymphatics and end up in the lungs where they mature in about 2 weeks. The mature larvae cause symptoms of pneumonitis and ascend the trachea by the cough reflex. They are swallowed by the host to mature into adult worms in the intestinal tract where each female worm lays over 200,000 eggs daily within 1 to 11 weeks of infection. [15]  Eggs are infective only if both male and female worms are present. Although the majority of worms are found in the lumen of the jejunum, they may be seen in any part of the intestine as well as ectopic sites such as the kidneys or brain. Adult worms can live up to 2 years and are passed in the stool. The worm burden increases with reinfections in endemic areas and can be as high as 200 worms per individual. [16]

A significant exposure may produce subsequent pneumonia and eosinophilia. Symptoms of pneumonitis include wheezing, dyspnea, nonproductive cough, hemoptysis, and fever. Larvae are expectorated and swallowed, eventually reaching the jejunum, where they mature into adults in approximately 65 days. Adult worms feed on digestion products of the host. Children with a marginal diet may be susceptible to protein, caloric, or vitamin A deficiency, resulting in retarded growth and increased susceptibility to infectious diseases such as malaria. [17] Large and tangled worms may cause intestinal (usually ileal), common duct, pancreatic, or appendiceal obstruction. Mean worm burden varies from more than 16 to 4 and appears related to host factors, particularly age, geophagy, [18] and immunity. Worms do not multiply in the host. For infection to persist beyond the 2-year maximum lifespan of the worms, re-exposure must occur. Some children appear to become very heavily infested, probably from multiple cumulative exposures over time and/or relative immunodeficiency. [19]

Ascaris lumbricoides suum, a swine nematode, is thought responsible for zoonotic infection. Distinguishing this worm from A lumbricoides is difficult, as it differs by only 6 (1.3%) nucleotides in the first internal transcribed spacer (ITS-1) and by 3%-4% in the mitochondrial genome sequence. [19] A suum appears to responsible for most ascariasis cases in well-developed countries with excellent sanitation (eg, Denmark, [20] United States, [9] UK [21] ). In this setting, infected persons have a low worm burden and may present with only cough, acute eosinophilia, or eosinophilic liver lesions visible on CT scans. However, a molecular genetic study from China casts doubt that infections in pigs are the cause of most human infection. [10]

Ascariasis is transmitted mainly by ingestion of food or water that has been contaminated by the fertilized infected eggs of A. lumbricoides or A. suum. Poor hand hygiene, polluted water and unsanitary food preparation play major role in reinfections in endemic areas and lingers in families and group homes with shedding of eggs by asymptomatic individuals. No immunity develops with past infections or treatment and other parasitic infections may coexist. A. suum infection is common in pig farmers and eating uncooked meat or vegetables grown in soil fertilized by pig manure. [22, 23]




United States

In 1974, an estimated 4 million people, mainly in the southeast United States, had ascariasis. Recent estimates of ascariasis prevalence are much lower. Immigrants from countries with a high prevalence of ascariasis comprise most recent cases. In the past, it was most prevalent in the southeast United States, but after introduction of modern waste management systems and sanitation, the numbers have sharply declined. [24]


The prevalence of ascariasis is highest in children aged 2 to 10 years, with the highest intensity of infection occurring in children aged 5 to 15 years who have simultaneous infections with other soil-transmitted helminths, such as Trichuris trichiura and hookworm. The warm, wet climate of tropical countries with suboptimal sanitation is a very favorable environment for the transmission of helminth infections. The prevalence decreases after the age of 15 years. A Vietnamese study found that adult women living in rural areas, especially those exposed to human night soil and living in households without a latrine, were at surprisingly high risk for ascariasis. [25] In regions with soil-transmitted diseases, ascariasis tends to be more geographically dispersed than Trichuris or hookworm. [26]

The Centers for Disease Control and Prevention (CDC) estimated that that there are more than one billion cases of A. lumbricoides infection worldwide. [27, 28] Ascariasis rates in 2005 were as follows: 86 million cases in China, 204 million elsewhere in East Asia and the Pacific, 173 million in sub-Saharan Africa, 140 million in India, 97 million elsewhere in South Asia, 84 million in Latin America and the Caribbean, and 23 million in the Middle East and North Africa. Between 1990 and 2013, the disease burden of ascariasis was estimated to have decreased by 75%. [2] Survey data, however, are corrupted by lack of standardized diagnostic methods. [29]

Because the lifespan of adult worms in the intestine is only 1 to 2 years, persistent infection requires frequent re-exposure and reinfection. The frequency and intensity of infection remain high throughout life in endemic areas and pose a risk to both elderly and young persons. In a recent study in rural southwest Nigeria, the intensity of excreted eggs per gram of feces among infected persons was 2371 for Ascaris species, 1070 for hookworm, and 500 for Trichuris species, with only slightly lower rates among persons in urban areas. [30]

Estimates of disability-adjusted years of life due to ascariasis have fallen because of development and management programs during the 1990s, especially in Asia, but still constitute a significant burden in some countries. Current ascariasis-associated disability-adjusted life years (DALYs) are approximately 1 million, [2] with nonsurgical morbidity mostly associated with wasting syndrome in children. [2]

A suum infections have been seen in countries where pigs are raised and pig manure is used as a fertilizer. [12, 31]  These have been reported in China, [32]  Japan, [31] Thailand, Lao People's Democratic Republic, Myanmar, [33] the United States, [34]  and Europe. [8, 20]


Most A lumbricoides or A suum infections are asymptomatic especially in adults. Severe, symptomatic ascariasis is most common in children. Intestinal obstruction caused by heavy worm burden (≥60) is the most common presenting manifestation of disease. An estimated 2 per 1000 infected children develop intestinal obstruction per year. [35] Among children aged 1 to 12 years who presented to a Cape Town hospital with abdominal emergencies between 1958-1962, symptomatic A lumbricoides infection was responsible for 12.8% of cases, with 68% of those due to intestinal obstruction, usually at the terminal ileum. The peak incidence was at age 2 years in a series from Colombia and age 4.8 years in a series from Turkey.

The prevalence of infection in Vietnam is estimated at 44.4%, more commonly in the northern peri-urban and rural areas of the country. [36] In Vietnam, vegetable cultivation using night soil fertilizer places adult women at especially high risk. Children with chronic ascariasis may experience decreased growth and development due to decreased food intake.

The disease is commonly symptomatic during the early phase larval migration stage with pulmonary symptoms and in late-phase adult worm intestinal stage and manifests as intestinal, hepatobiliary, or pancreatic symptoms. Within weeks of new infection, pulmonary manifestations may be seen but are uncommon in patients from endemic areas or reinfections. This was demonstrated by a study of 13,00 patients in and endemic region of Columbia with only 4 cases of Loeffler syndrome. [37, 38, 39]

Adults with ascariasis are more likely to develop biliary complications due to migration of adult worms, possibly provoked by other illnesses such as malarial fever. In Damascus, of 300 adults referred for complications of ascariasis between 1988 and 1993, 98% had abdominal pain, 4.3% had acute pancreatitis, 1.3% had obstructive jaundice, and 25% had worm emesis. Twenty-one to 80% of patients had undergone previous cholecystectomy or endoscopic sphincterotomy.

Adult Ascaris lumbricoides in biliary system. Adult Ascaris lumbricoides in biliary system.

Because of improved access to care and availability of ultrasonography, biliary ascariasis has been increasingly recognized and reported from endemic areas. [40] In Kashmir, it may account for up to 36% of patients presenting with biliary or pancreatic disorders and is reported to cause 20% of biliary disease in the Philippines. [40]  A review of biliary ascariasis suggests that this association may be causative as a result of dilatation of the common bile duct and elevation of cholecystokinin levels with resultant relaxation of the sphincter of Oddi. [41]

A report from India indicated that, of consecutive patients diagnosed with biliary ascariasis, 80% presented with recurrent abdominal pain, 30% with acute cholecystitis, 25% with obstructive jaundice, 25% with cholangitis, only 5% with pancreatitis, 5% with perforated viscus, and 5% with hepatolithiasis. Only 25% of the Indian patients required surgery, and conservative medical therapy with oral anthelminthics has recently been recommended. [40]

A postcholecystectomy syndrome of pain and jaundice is frequently due to ascariasis in endemic areas, presumably owing to enhanced patency of the biliary system after surgical or endoscopic sphincterotomy. [42]

Intestinal obstruction, usually of the terminal ileum in children, is the most commonly attributed fatal complication, resulting in 60,000 deaths per year. [3] Besides direct obstruction of the bowel lumen, toxins released by live or degenerating worms may result in bowel inflammation, ischemia, and fibrosis.


See International and Mortality/Morbidity.



Universal treatment is effective in endemic areas regardless of asymptomatic infections. However in non-endemic areas, screening or empiric treatment is based on the high pretest probability, especially in patients with history of travel to endemic areas or exposure to infected populations. Immediate cure rates after single-dose albendazole in South Africa were 95%, with egg reduction rates of more than 99%. [43]

Most treated patients become reinfected within months unless they are relocated to an area of significantly improved sanitation.


Patient Education

Because of the limited (2-year) lifespan of the disease, education on hand hygiene, fecal waste disposal, and general public health could be instrumental in breaking the cycle of infection in households and communities. [3]