Ascariasis

 

Ascariasis

Introduction

Ascariasis is an infection of the small intestine caused by the nematode Ascaris lumbricoides. Ascaris lumbricoides is the largest intestinal nematode to infect humans. It is also known as the common roundworm. Historically, it was sometimes confused with the earthworm due to its resemblance. The specific name lumbricoides is derived from Lumbricus, the Latin word for earthworm.

Ascaris species are very large nematodes. Adult females measure 20 to 35 cm in length, and adult males measure 15 to 30 cm. In some sources, female length is noted as 20-40 cm and male length as 15-30 cm or 15-31 cm. While A. lumbricoides is the primary species involved in human infections globally, Ascaris derived from pigs (often referred to as A. suum) may also infect humans. These two are closely related, and hybrids have been identified, making their status as distinct species contentious.

Geographical Distribution

Ascariasis occurs worldwide. It is most common in tropical and subtropical areas where sanitation and hygiene are poor. The burden is highest in these regions. Main epidemic regions with a prevalence rate of approximately 10-90% include countries in South East Asia, Africa, and Latin America. The infection is generally rare to absent in developed countries. However, sporadic cases may occur in rural, impoverished regions of developed countries.

Habitat

The adult worm lives in the lumen of the small intestine. Specifically, 85% are found in the jejunum and 15% in the ileum. Humans are the only natural host and reservoir of infection. Natural infections with A. lumbricoides sometimes occur in monkeys and apes.

 Morphology

Adult Worm: Resembles an earthworm. It is elongated and cylindrical, tapering at both ends, with the anterior end being more pointed or slender than the posterior. The freshly excreted worms are yellowish-pink in color, gradually changing to white.The worm is sexually dimorphic.

Male Worm: Smaller than the female. Measures 15-30 cm or 15-31 cm in length and 2-4 mm or 3-4 mm in diameter or thickness. The posterior end is curved ventrally to form a hook and carries 2 copulatory spicules. The male tail has numerous genital papillae ventrally.

Female Worm: Larger than the male. Measures 20-35 cm or 20-40 cm in length and 2-6 mm or 4-6 mm in diameter or thickness. The posterior extremity is straight and conical.

Egg: Two types are liberated: fertilized and unfertilized.

• Fertilized Egg:
• Shape: Round to oval.
• Size: 50-75 µm x 40-50 µm or 60 x 40 µm.
• Covering: Surrounded by a thick smooth translucent shell consisting of three layers: the outer coarsely mamillated albuminoid coat (often stained brown by bile) (giving a rough surface), a thick transparent middle layer, and an inner lipoidal vitelline membrane. Some eggs found in feces may lack the outer mamillated coat and are called decorticated eggs.
• Bile Staining: Bile-stained, golden brown in saline mount.
• Floatation: Floats in saturated salt solution.
• Unfertilized Egg:
• Shape: Elongated and larger than fertile eggs (up to 90 µm in length). May be round to oval.
• Covering: Albuminous coat is thinner, distorted, and scanty. Bile Staining: Bile-stained, golden brown in saline mount.
• Floatation: Doesn’t float in saturated salt solution.

Life Cycle

• The life cycle of Ascaris completes in a single host, the human. There is no intermediate host.
• Stage I: Eggs in feces: Sexually mature females produce approximately 200,000 eggs per day which are passed with the feces in an unembryonated and non-infective form.
• Stage II: Development in soil: Embryonation occurs in soil given optimum conditions of warm temperature (20-25°C or 20°C to 30°C), sufficient moisture, and oxygen. The infective larva (L3) develops within the fertile egg in 18 days to several weeks or about 3-6 weeks or 10-40 days, during which the embryo moults twice.
• Stage III: Human infection and liberation of larvae: Humans get infected by ingesting embryonated eggs through contaminated food and water, especially fresh vegetables grown in fields manured with human feces ('night soil') or by direct transmission to the mouth through dirty fingers (fecal-oral route, geophagia) where soil contamination is heavy due to indiscriminate defecation. The inhaled eggs (via windswept dust) may also be swallowed.
• Stage IV: Migration of larvae through lungs: After infective eggs are swallowed, the larvae hatch in the duodenum, penetrate the intestinal mucosa, and are carried via the portal, then systemic circulation to the liver within 4-7 days of infection. They then travel via blood to the heart and to the lungs by pulmonary circulation. The larvae mature further in the lungs (10 to 14 days), where they moult twice and grow much bigger (from 0.2 mm to 2.0 mm). They break through the capillary wall and reach the lung alveoli.
• Stage V: Re-entry to stomach and small intestine: From the alveoli, the larvae ascend the bronchial tree to the throat and are swallowed, reaching the small intestine again.
• Development into adult worms: Upon reaching the small intestine, they develop into adult worms. They undergo two more moults, and sexual maturation occurs within 6-10 weeks.
• The female starts discharging eggs in the intestinal lumen, which are excreted along with feces, continuing the life cycle.

Pathogenesis

• There are two phases in ascariasis contributing to pathogenesis:
• Phase I: Migrating larvae:
• The migrating larvae cause pathological lesions.
• The severity depends on the sensitivity and nutritional status of the host and the number of migrating larvae.
• During migration and moulting through the lungs, larvae may cause pneumonia characterized by low-grade fever, cough, and other allergic symptoms, such as transient eosinophilic pneumonitis (Loeffler’s disease), elevated IgE, bronchospasm, dyspnea and wheezing, fever, and non-productive cough and chest pain.
• The sputum may be blood-tinged, and larvae may occasionally be found in it or more often in gastric washings.
• Phase II: Adult worm:
• Few worms in the intestine may produce no major symptoms or sometimes cause abdominal pain, especially in children. Most infections are asymptomatic.
• High worm burdens may cause abdominal pain and intestinal obstruction and potentially perforation in very high-intensity infections. Heavy worm burden in children can lead to intussusception and total obstruction.
• Large numbers of adult worms affect the nutritional status of the host, causing malnutrition, weight loss, diarrhea, and growth retardation in children. They can cause malabsorption of nutrition and protein-energy malnutrition and vitamin A deficiency.
• The metabolites of living or dead worms are toxic and immunogenic, producing allergic toxins that manifest as fever, conjunctivitis, and irritation. Hypersensitivity to worm antigens can also lead to urticaria, angioneurotic edema, and wheezing.
• Adult worms can produce trauma in host tissue.
• They may wander and block the appendical lumen or common bile duct and even the small intestine. They can enter the liver parenchyma, causing liver abscesses, go up the esophagus and out through the mouth or nose, or crawl into the trachea and lungs, causing respiratory obstruction or lung abscesses. Downward migration can cause obstructive appendicitis.

Sample Collection

• The stool specimen is the primary sample for diagnosing intestinal ascariasis.
• Preserve the stool specimen in formalin or another fixative.
• Sputum or gastric aspirate can be collected to identify larvae during the pulmonary migration phase.
• Adult worms are occasionally passed in the stool or through the mouth or nose.
• Bile obtained by duodenal aspirates may contain eggs.

Laboratory Diagnosis

• Microscopic identification of eggs in the stool is the most common method for diagnosing intestinal ascariasis. Both fertilized and unfertilized eggs may be present.
• The recommended procedure involves: collecting a stool specimen, preserving it, concentrating it using the formalin–ethyl acetate sedimentation technique, and examining a wet mount of the sediment.
• Where concentration procedures are unavailable, a direct wet mount examination of the specimen is adequate for detecting moderate to heavy infections.
• For quantitative assessments of infection, methods like Kato-Katz or quantitative fecal flotation can be used.
• If very few eggs are present, concentration techniques are crucial.
• Identification of larvae in sputum or gastric aspirate during the pulmonary migration phase. Fixed organisms should be examined for morphology.
• Identification of adult worms passed in stool or through the mouth or nose based on their macroscopic characteristics (e.g., presence of three “lips”).
• Serodiagnosis: Detection of Ascaris antibodies using tests like the Indirect hemagglutination test (IHA), Immunofluorescence assay (IFA), and Enzyme-linked immunosorbent assay (ELISA). Serodiagnosis is helpful in extraintestinal ascariasis, like Loeffler’s syndrome.
• Blood examination: A complete blood count may show peripheral eosinophilia, especially during the larval migration through the lungs.
• X-ray, ultrasonography, and CT scan can be used in diagnosis, particularly for detecting complications or adult worms. Chest X-ray may show patchy pulmonary infiltrates during larval migration.

Treatment

• Anti-parasite medications are the first-line treatment. Common medications include:
• Albendazole (single dose).
• Mebendazole (for 1-3 days).
• Ivermectin (single dose).
• Pyrantel pamoate (single dose). Safe for pregnant women.
• Piperazine citrate. Can be used via nasogastric tube for partial intestinal obstruction.
• These medications kill the adult worms. Side effects are usually mild, such as abdominal pain or diarrhea.
• Complete intestinal obstruction requires immediate surgical intervention.

Prevention

• Preventing fecal contamination of soil.
• Wash hands with soap and water before handling food, and teach children the importance of handwashing.
• 
Wash, peel, or cook all raw vegetables and fruits before eating, especially those grown in soil fertilized with manure or 'night soil'.
• Not defecating outdoors.
• Effective sewage disposal systems.
• Proper composting of manure to ensure the destruction of eggs.
• Treatment of vegetables and garden crops with water containing iodine (200 ppm for 15 minutes) can kill eggs and larvae.
• Improvement of personal hygiene.
• Treatment of infected persons.