How to Cite This Chapter: Mach T, Nowak S, Zaborowski P. Ascariasis. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed December 11, 2023.
Last Updated: January 28, 2022
Last Reviewed: January 28, 2022
Chapter Information

Etiology and pathogenesisTop

1. Etiologic agent: Ascaris lumbricoides, a 15 to 35 cm-long nematode (roundworm) and parasite of the small intestine in humans. Infection occurs through swallowing invasive eggs (ie, eggs that have matured to the invasive stage). In moist soil with an optimum temperature of 25 degrees Celsius, the maturation takes ~3 weeks. The larvae hatched in the small intestine (rhabditiform larvae) penetrate the gastrointestinal (GI) walls and migrate through the portal circulation to the liver (where the maturation begins), then to the right atrium and ventricle and, eventually, to the lungs (from alveolar capillaries, the larvae break into the alveolar lumen, where the first and second molting occurs). Then they ascend the bronchial tree to the larynx and throat, where they are swallowed. Swallowed larvae return to the small intestine to undergo final maturation. Mature forms may survive for 1 to 2 years. After 2 to 3 months from infection, the female starts producing large numbers of eggs, which are excreted with stool.

2. Reservoir and transmission: The reservoir is humans. Transmission is via the oral route (consumption of vegetables and fruit from farms in which human feces are used as fertilizers) or dirty hands contaminated with soil containing the eggs.

3. Risk factors: Consumption of unwashed raw fruit and vegetables (eg, strawberries grown in fields where human feces are used as fertilizers), geophagy.

4. Incubation and contagious period: The period from infection to the development of pulmonary manifestations is 4 to 16 days; parasites reach full maturity and eggs appear in stool after 2 to 3 months. The patient is not contagious for contacts. In moist soil the eggs remain invasive for 7 to 10 years (they are resistant to freezing); they may be destroyed by prolonged exposure to direct sunlight and temperatures >40 degrees Celsius.


Ascariasis occurs worldwide, with ~25% of the global population being affected (in some regions, eg, in Africa and some countries in Asia, it is >50%). It is typically more common in rural areas. In Europe the prevalence of ascariasis is significantly smaller.

Clinical features and natural historyTop

The clinical course depends on the intensity of invasion. If the invasion is minor, the disease is usually asymptomatic. Nonspecific GI symptoms may occur, such as abdominal discomfort and altered bowel movement pattern. In more severe invasion typical pulmonary symptoms appear. Occasionally, when the number of adult worms is very large, GI complications requiring surgical intervention may develop.

Types of ascariasis:

1. Pulmonary ascariasis: Migration of the larvae to the lungs may manifest as cough with expectoration, and sometimes as fever. Auscultation is usually unremarkable. Plain chest radiography may reveal migrating opacities (corresponding to inflammatory infiltrates). Other findings include peripheral blood eosinophilia (formerly termed Löffler syndrome). In some patients urticaria may be observed. Charcot-Leyden crystals are found in bronchoalveolar lavage fluids.

2. Intestinal ascariasis: Abdominal discomfort or pain (sometimes colicky), less frequently nausea. Massive invasion (>60 worms) may also cause weight loss and malnutrition, mechanical intestinal obstruction, appendicitis, and diverticulitis. Rarely, if parasites penetrate the intestinal wall, peritonitis may develop. The presence of intestinal ulcerations, for instance, caused by typhoid fever or tuberculosis, may facilitate intestinal perforation.

3. Hepatobiliary ascariasis: Worms may migrate into the bile ducts or pancreatic ducts and cause an inflammatory reaction with bile retention (cholangitis) or pancreatic juice retention (acute pancreatitis). There are reports of liver abscesses in cases where a dead worm was found in the biliary tract.


Microscopic detection of A lumbricoides eggs in stool (direct fecal smear or formalin-fixed smear). The analysis should be performed ≥3 times every 2 to 3 days. Stool analysis does not detect immature worms or single male parasites (absence of eggs). In 3% of cases ascariasis is diagnosed on the basis of the presence of adult worms in a stool or vomit.

Differential Diagnosis

Other nematode infections such as enterobiasis (this is differentiated on the basis of microscopic examination of eggs), as well as other causes of dyspepsia, abdominal pain, or biliary tract diseases (results of the microscopic stool examination are decisive).


Elimination of the Etiologic Agent

1. Treat all patients with parasitic infection (including asymptomatic individuals). In the case of mixed infections, start from the treatment of ascariasis and subsequently treat other nematode infections. Since stool examination does not detect immature forms of A lumbricoides, empiric treatment is justified in patients with suspected ascariasis.

2. Antiparasitic treatment:

1) First-line treatment: Oral mebendazole 100 mg bid for 3 days or 500 mg in a single dose; or a single dose of oral albendazole 400 mg on an empty stomach (irrespective of the patient’s age).

2) Second-line treatment: A single dose of oral pyrantel 10 mg/kg (maximum 1 g/d). This treatment is recommended in pregnant or breastfeeding patients.

If no adult parasite has been recovered from stool during the treatment of laboratory-confirmed ascariasis, the therapy should be repeated.

3. Surgical treatment (laparotomy and worm removal) is indicated in patients with complications (see above).

Symptomatic Treatment

Pulmonary ascariasis: Administer an inhaled beta2-agonist or oral glucocorticoid. Do not use antiparasitic agents in this phase, as their efficacy against larvae in the lungs is not confirmed and the clinical course of invasion at this early stage is rarely severe. A follow-up stool examination should be performed after several months and appropriate therapy should be introduced if intestinal ascariasis is confirmed.


The criterion for the complete cure is absence of A lumbricoides eggs in 3 consecutive stool samples obtained 2 weeks after treatment completion.


Specific Prevention


Nonspecific Prevention

1. Washing hands before meals and after contact with soil.

2. Preventing geophagy in children.

3. Thorough washing of fruits and vegetables, avoiding consumption of food from unknown sources.

4. Banning the use of human feces to fertilize fruit or vegetable plantations (this may cause epidemics). Ascaris eggs are resistant to freezing and can remain invasive in soil for years. They are killed during the cooking process.

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