Ascaris Lumbricoides

Updated: Jan 10, 2023
Author: Aaron Dora-Laskey, MD, MS; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD 



Intestinal nematode infections affect one fourth to one third of the world's population. Of these, the intestinal roundworm Ascaris lumbricoides is the most common. While the vast majority of these cases are asymptomatic, infected persons may present with pulmonary or potentially severe gastrointestinal complaints. Ascariasis predominates in areas of poor sanitation and is associated with malnutrition, iron-deficiency anemia, and impairments of growth and cognition.

Ascaris lumbricoides is shown in the image below.

Adult Ascaris lumbricoides. Adult Ascaris lumbricoides.


A lumbricoides is the largest of the intestinal nematodes affecting humans, measuring 15-35 cm in length in adulthood. Infection begins with the ingestion of embryonated (infective) eggs in feces-contaminated soil or foodstuffs.[1] Once ingested, eggs hatch, usually in the small intestine, releasing small larvae that penetrate the intestinal wall. Larvae migrate to the pulmonary vascular beds and then to the alveoli via the portal veins usually 1-2 weeks after infection, during which time they may cause pulmonary symptoms (eg, cough, wheezing). During the time frame of pulmonary symptoms, eggs are not being shed, and thus diagnosis via stool ovas and parasites is not possible. Eggs are not shed in stool until roughly 40 days after the development of pulmonary symptoms.

After migrating up the respiratory tract and being swallowed, they mature, copulate, and lay eggs in the intestines. Adult worms may live in the gut for 6-24 months, where they can cause partial or complete bowel obstruction in large numbers, or they can migrate into the appendix, hepatobiliary system, or pancreatic ducts and rarely other organs such as kidneys or brain. From egg ingestion to new egg passage takes approximately 9 weeks, with an additional 3 weeks needed for egg molting before they are capable of infecting a new host.

Life cycle of Ascaris lumbricoides. Life cycle of Ascaris lumbricoides.



United States

In the United States, approximately 4 million people are believed to be infected.[2] High-risk groups include international travelers, recent immigrants (especially from Latin America and Asia), refugees, and international adoptees. Ascariasis is indigenous to the rural southeast, where cross-infection by pigs with the nematode Ascaris suum is thought to occur. (Children aged 2-10 years are thought to be more heavily infected in this and all other regions.)


Worldwide, 1.4 billion people are infected with A lumbricoides, with prevalence among developing countries as low as 4% in Mafia Island, Zanzibar,[3] to as high as 90% in some areas of Indonesia. Local practices (eg, termite mound–eating in Kenya[4] ) may predispose to ascariasis in some populations. Further risk factors include other forms of geophagia and cat/dog ownership. In some regions, Ascaris infection is thought to contribute significantly to the burden of abdominal surgical emergencies.


The rate of complications secondary to ascariasis ranges from 11-67%, with intestinal and biliary tract obstruction representing the most common serious sequelae. Although infection with A lumbricoides is often asymptomatic, it is responsible for an estimated 730,000 cases of bowel obstruction annually, 11,000 of which are fatal.[5] In one series of pregnant patients in Bangladesh, biliary ascariasis was responsible for a plurality (28%) of nonobstetric etiologies of acute abdomen.[6]

Owing to similarities in the means of infection, many individuals infected with Ascaris are also co-infected with other intestinal parasites.  


No racial predilection is known. A genetic predisposition has been described in a study of families from Nepal.[7]


Male children are thought to be infected more frequently, owing to a greater propensity to eat soil.


Children, because of their habits (eg, directly or indirectly consuming soil), are more commonly and more heavily infected than adults. Neonates may be infected by transplacental infection. Frequently, families may be infected and reinfected in group fashion due to shared food and water sources as well as hygiene practices.


The prognosis for ascariasis is excellent. However, in higher worm burden infections, serious complications such as obstruction are more common.

Patient Education

Recommend good personal hygiene and food handling techniques: discriminate defecation, hand-washing, cleaning fruits and vegetables, and avoiding soil consumption. Educational programs should also address the use of human feces as fertilizer, a practice that persists in many communities internationally.




Most patients are asymptomatic. When symptoms occur, they are divided into 2 categories: early (larval migration) and late (mechanical effects).

In the early phase (4-16 d after egg ingestion), respiratory symptoms result from the migration of larvae through the lungs. Classically, these symptoms occur in the setting of eosinophilic pneumonia (Löffler syndrome).

  • Fever

  • Nonproductive cough

  • Dyspnea

  • Wheezing

In the late phase (6-8 wk after egg ingestion), gastrointestinal symptoms may occur and are more typically related to the mechanical effects of high parasite loads.

  • Passage of worms (from mouth, nares, anus)

  • Diffuse or epigastric abdominal pain

  • Nausea, vomiting

  • Pharyngeal globus, "tingling throat"

  • Frequent throat clearing, dry cough

  • Complications - Mechanical small bowel obstruction, volvulus, intussusception, biliary obstruction, appendicitis, pancreatitis


General symptoms include the following:

  • Fever

  • Jaundice (in biliary obstruction)

  • Cachexia (due to malnutrition)

  • Pallor (anemia)

  • Urticaria (early infection)

Pulmonary symptoms include the following:

  • Wheezing

  • Rales

  • Diminished breath sounds

Abdominal symptoms include the following:

  • Abdominal tenderness, which may be diffuse (in obstructive infections), epigastric (pancreatitis), or localized to the right lower (appendicitis) or right upper quadrant (hepatobiliary infections)

  • Peritoneal signs in cases of bowel perforation

  • Obstructive symptoms (nausea/vomiting/constipation/distention)

Migrating larvae may transmit other organisms, causing bacterial pneumonia or cholangitis. Rare cases of airway obstruction and laryngeal spasm[8] have also been reported. Other much less common presentations include lacrimal drainage obstruction,[9] small bowel intussusception,[10] acute interstitial nephritis,[11] urinary tract obstruction,[12] and encephalopathy.[13]


Symptoms are typically associated with early larval migration, heavy intestinal burdens of adult worms, or aberrant worm migration. Worm migration may be stimulated by anesthetic agents, fever, or subtherapeutic anthelmintic treatment, or by use of certain anthelmintics (eg, pyrantel pamoate).


Complications may be attributed to larval migration typically involving the lungs, and intestinal tract producing vague symptoms but may as well involve the kidneys, brain, and heart.

Severe complications later in disease are usually attributable to mechanical obstruction of intestines or biliary tree secondary to high worm burden.

Complications may arise early in disease due to allergic reaction to Ascaris infection (urticaria).

Malnutrition, anemia, growth, and developmental retardation (subject to some debate)



Differential Diagnoses



Laboratory Studies

Early infection (larval migration)

Complete blood count (CBC) may show eosinophilia.

Sputum analysis may reveal larvae or Charcot-Leyden crystals (collections of crystalloid composed of eosinophilic proteins).

Stool examination findings are typically normal in absence of previous infection (during the first 40 d).

Ascaris -specific antibodies may be found (not useful in acute infection and not protective).

Increases in IgE and later IgG may be found.

Established infection (adult phase)

Stool examination findings include characteristic eggs. Adult females lay about 200,000 eggs per day, aiding microscopic identification of characteristic eggs.

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

Ascaris lumbricoides egg in feces (formalin-ethyl Ascaris lumbricoides egg in feces (formalin-ethyl acetate sedimentation method).

Other diagnostic tests (eg, polymerase chain reaction [PCR]) have been described for identifying infection with soil-transmitted helminths; however, these are typically used for population-based treatment programs in endemic areas.[14]

Imaging Studies

Early infection (larval migration)

Chest radiography may reveal patchy infiltrates of eosinophilic pneumonia.

Established infection (adult phase)

Abdominal radiography may reveal signs of bowel obstruction (eg, air-fluid levels) or the "cigar bundle" appearance of a worm bolus. On computed tomography (CT) scanning, Ascaris worms may be visualized as linear or cylindrical filling defects in the presence of contrast or may be identifiable in groups or masses (sometimes having a whirled appearance).[15]

Some authors have recommended ultrasonography as the initial imaging study of choice, especially when pretest suspicion of pancreatobiliary involvement is high. Diagnosis of Ascaris infection has been described using point-of-care emergency department ultrasonography (POCUS).[16] Sensitivity may be increased by left lateral decubitus positioning, oral fluids, and gentle transducer pressure to induce worm movement. While hepatobiliary ascariasis has been described in several case reports and is sometimes evidenced by the movement of live worms, experienced operators may also be able to diagnose intestinal complications using POCUS, including small bowel obstruction and (rarely) intussusception.[17]

Magnetic resonance cholangiopancreatography (MRCP) may detect adult worms in bile or pancreatic ducts, though its availability may be limited.[18]

Alternatively, endoscopic retrograde cholangiopancreatography (ERCP) has the advantage of being both diagnostic and therapeutic when pancreato-biliary complications are suspected.[19] Diagnosis of ascariasis using capsule endoscopy has also been described.[20]



Emergency Department Care

Early infection (larval migration)

Inhaled beta-agonists may be indicated.

Steroids for pulmonary symptoms are controversial.

Whether anthelmintic therapy is effective against larval stages is unclear. (Stool ova microscopy will likely be negative at this phase). Because infection in the early phase is rarely serious, generally treatment is delayed until definitive diagnosis can be made.

Established infection (adult phase)

Benzimidazoles are the mainstay of treatment of symptomatic and asymptomatic infections. They are poorly systemically absorbed and thus have low human toxicity and exert their action directly on worms. The most common members of this family are albendazole and mebendazole.

Treatment of bowel obstruction includes intravenous hydration, nasogastric suctioning, electrolyte monitoring, and laparotomy if conservative measures fail. Colonoscopy and esophagogastroduodenoscopy (EGD) may be useful in removing obstructing masses of worms.

Piperazine citrate, a helminth paralytic, has been suggested in cases of obstruction; however, it is no longer commercially available in the United States.

Hepatobiliary ascariasis typically responds to similarly conservative therapy, but it may require invasive intervention (eg, ERCP) should this fail, or if there are coexisting stones or strictures. It may also be indicated in cases of pyogenic cholangitis and acute pancreatitis.


Bowel or hepatobiliary obstruction may require surgical or gastroenterologic consultation.


Screening programs for the carrier state may assist in eradication in endemic areas.

Given the association with poverty and malnutrition, long-term control will require sustained economic growth in developing countries and the creation of sanitation and education systems including those to reduce the use of human feces for fertilizer.

Many nations have such high rates of Ascaris infection that they empirically treat some age groups without testing. Medication choices and the frequency of testing vary from country to country, but data are favorable for reducing the load of parasites in the community and as well for reducing individual morbidity and mortality associated with infection.

Further Outpatient Care

Primary care follow up is suggested to confirm cure.

Presumptive administration of albendazole to all immigrants at risk for parasitosis has been suggested and shown to save lives and money. However, current recommendations do not include its implementation.

Follow-up stool ova and parasite microscopic testing is warranted post treatment to ensure clearance of parasite infection and as well to monitor for re-infection, which can be common.

Further Inpatient Care

Further inpatient care is warranted for patients with complications due to worm migration.



Medication Summary

Benzimidazoles are effective for the treatment of intestinal ascariasis, although some authors recommend against their use in the first year of life and during pregnancy due to their teratogenic effects in animal studies. The most commonly recommended agents are albendazole and mebendazole.[21] Ivermectin and pyrantel pamoate are alternatives, the latter having been suggested for pregnant patients in whom benzimidazoles are contraindicated. An anthelmintic agent from China, tribendimidine (at a dose of 300 mg), has been shown to be as efficacious as albendazole.[22, 23]


Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Albendazole (Albenza)

Decreases ATP production in worm, causing energy depletion, immobilization, and finally death.

Mebendazole (Vermox)

Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.

Pyrantel pamoate (Antiminth)

Depolarizing neuromuscular blocking agent; inhibits cholinesterases, resulting in spastic paralysis of worm.

Ivermectin (Stromectol)

Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death.