Ascariasis

Introduction and Etiology

• Definition: Ascariasis is a helminthic infection caused by Ascaris lumbricoides, the largest nematode (roundworm) parasitizing the human intestine.
• Morphology:
  • Adult worms are large, white or pinkish, and cylindrical.
  • Females measure 20–35 cm in length; males are smaller (15–30 cm) with a curved tail.
  • Reproductive Potential: A single gravid female can produce approximately 200,000 eggs per day.
• Eggs:
  • Fertilized eggs: Oval to round with a thick, mamillated (bumpy), bile-stained outer shell. They measure 45–70 µm by 35–50 µm.
  • Unfertilized eggs: Elongated and narrower.
  • Viability: Eggs are extremely hardy and resistant to desiccation, freezing, and chemical disinfectants. They can remain viable in the soil for years (7–10 years).

Epidemiology

• Global Burden: Ascariasis is the most prevalent helminthic infection worldwide, affecting an estimated 800 million to 1 billion people.
• Geographic Distribution: It is most common in tropical and subtropical regions, particularly in East Asia, Southeast Asia, the Indian subcontinent, Africa, and South America.
• Risk Factors:
  • Age: Prevalence and intensity of infection are highest in preschool and early school-age children (5–15 years).
  • Socioeconomic Status: Strongly associated with poverty, poor sanitation, and lack of clean water.
  • Behavioral: Pica (geophagia) and playing in contaminated soil increase risk in children.
  • Environmental: Use of human feces ("night soil") as fertilizer for crops.
• Transmission:
  • Fecal-Oral Route: Primarily through ingestion of infective embryonated eggs from soil-contaminated hands, food (raw vegetables/fruits), or water.
  • Pig Reservoirs: In some areas, pigs may serve as a reservoir for zoonotic Ascaris infection (A. suum), which can infect humans.

Life Cycle

The life cycle involves an intricate migration phase through the host's body before maturation in the intestine.

1. Ingestion: Infection begins when humans ingest embryonated eggs containing second-stage larvae.
2. Hatching and Invasion: Eggs hatch in the duodenum. Released larvae penetrate the intestinal mucosa.
3. Hepatic Migration: Larvae enter the portal circulation and are carried to the liver.
4. Pulmonary Migration: From the liver, larvae travel via the systemic circulation to the right heart and then to the lungs.
   • In the lungs, they break out of the capillaries into the alveolar spaces.
   • They migrate up the bronchi and trachea to the glottis.
5. Swallowing and Maturation: The larvae pass over the epiglottis, are swallowed, and return to the small intestine.
6. Adulthood: In the intestine, larvae undergo final molting and mature into adult worms.
   • Prepatent Period: The time from ingestion of eggs to the production of new eggs by adult females is approximately 8–10 weeks (or roughly 2 months).
   • Life Span: Adult worms live for approximately 1 year (6–18 months) and are then expelled.

Pathogenesis

Pathology is caused by both the migrating larvae and the adult worms.

Larval Phase (Migratory)

• Inflammatory Response: Migrating larvae provoke an inflammatory reaction characterized by eosinophilic infiltration.
• Lung Injury: Breaking through alveolar walls causes minute hemorrhages and pneumonitis.
• Immune Modulation: Larvae release antigens (ABA-1 allergen) and immunomodulatory glycosphingolipids that induce a Th2 immune response (high IgE) and inhibit Th1 responses. This mechanism is linked to Ascaris-associated asthma.

Adult Phase (Intestinal)

• Nutritional Impairment:
  • Adult worms compete with the host for nutrients.
  • They secrete peptides that inhibit host pancreatic enzymes (trypsin, chymotrypsin, elastase), leading to malabsorption of proteins, fat, and vitamin A.
  • Infection is associated with lactose intolerance and altered jejunal mucosal structure.
  • Chronic infection contributes to malnutrition, growth stunting, and cognitive deficits in children.
• Mechanical Effects: Large aggregates of worms can cause intestinal obstruction, volvulus, or intussusception, especially in young children with small intestinal lumens.
• Aberrant Migration: Adult worms are motile and may migrate into the biliary tree, pancreatic duct, or appendix, especially during fever, illness, or anesthesia.

Clinical Manifestations

The spectrum of disease ranges from asymptomatic carriage to life-threatening complications.

Pulmonary Ascariasis (Loeffler's Syndrome)

• Timing: Occurs 4–16 days after infection during larval migration.
• Symptoms: Cough (often non-productive), dyspnea, wheezing, fever, and chest pain.
• Signs: Rales or wheezing on auscultation.
• Seasonal Presentation: In endemic areas, this can present as seasonal pneumonia or asthma.

Intestinal Ascariasis

• General: Vague abdominal discomfort, distension, nausea, anorexia, and vomiting.
• Intestinal Obstruction:
  • Most common serious complication in children (estimated incidence 2 per 1000 infected children per year).
  • Caused by a bolus of tangled worms blocking the ileocecal valve or small intestine.
  • Presentation: Bilious vomiting, abdominal distension, obstipation, and signs of dehydration. Can progress to bowel ischemia, necrosis, and perforation.
• Malnutrition: Failure to thrive, vitamin A deficiency, and hypoalbuminemia in chronic heavy infections.

Hepatobiliary and Pancreatic Ascariasis (HPA)

• Mechanism: Migration of worms across the ampulla of Vater.
• Clinical Syndromes:
  • Biliary Colic: Severe right upper quadrant pain.
  • Ascending Cholangitis: Fever, jaundice, and pain.
  • Acalculous Cholecystitis.
  • Acute Pancreatitis.
  • Hepatic Abscess: Rare complication if worms enter the liver parenchyma.

Other Manifestations

• Allergic: Urticaria, skin rash.
• Ectopic: Worms may be vomited up, passed from the nose, or emerge from the umbilicus.

Diagnosis

Laboratory Identification

• Stool Microscopy: The gold standard. Direct saline smear or concentration techniques detect the characteristic mamillated eggs.
  • Note: Stool may be negative during the early migratory phase or if only male worms are present.
• Macroscopic: Identification of adult worms passed in stool, vomited, or emerging from the nose.
• Eosinophilia: Significant peripheral eosinophilia (5–12% or higher) is present, particularly during the pulmonary migration phase. It may subside in the chronic intestinal phase.
• Sputum/Gastric Aspirate: Larvae may occasionally be found in sputum during the pulmonary phase.

Imaging

• Abdominal Ultrasound: Highly sensitive for detecting adult worms in the biliary tree (appearing as long, linear echogenic structures without acoustic shadows) or pancreas. Can also visualize the "bull's eye" appearance of worms in the intestine.
• Abdominal X-ray: May show signs of intestinal obstruction or the "whirlpool" sign of worm masses. Barium studies can show linear filling defects.
• Chest X-ray: Transient, shifting, patchy pulmonary infiltrates (Loeffler's syndrome).

Management

Pharmacological Treatment

• Drug of Choice: Albendazole
  • Dose: 400 mg single oral dose (200 mg for children 12–24 months).
  • Mechanism: Inhibits tubulin polymerization, paralyzing the worm.
• Alternatives:
  • Mebendazole: 100 mg twice daily for 3 days OR 500 mg single dose.
  • Pyrantel Pamoate: 11 mg/kg (max 1 g) single dose. Safe in pregnancy.
  • Ivermectin: 150–200 µg/kg single dose.
  • Nitazoxanide: 100 mg BID (1–3 years), 200 mg BID (4–11 years), 500 mg BID (>12 years) for 3 days.
• Pulmonary Ascariasis: Anthelmintics are generally not effective against migratory larvae. Treatment is supportive (bronchodilators, corticosteroids) until worms reach the intestine, where they can be treated.

Management of Complications

• Intestinal Obstruction:
  • Conservative Management: Intravenous fluids, nasogastric suction, and electrolyte correction.
  • Piperazine Citrate: Sometimes used for obstruction as it causes flaccid paralysis (75 mg/kg/day for 2 days), aiding expulsion without agitating the worms. Note: Withdrawn in some markets.
  • Gastrografin: Hyperosmolar contrast enema can help untangle worm masses.
  • Surgery: Indicated for complete obstruction, volvulus, perforation, or failure of conservative therapy. Involves enterotomy to remove worms or resection of necrotic bowel.
• Biliary Ascariasis: Conservative management with fluids, antibiotics, and antispasmodics leads to spontaneous exit of the worm in most cases. ERCP may be needed for extraction if conservative therapy fails.

Prevention and Control

• Sanitation: Safe disposal of human excreta and prevention of soil contamination. Discontinuation of using night soil as fertilizer.
• Hygiene: Hand washing before eating and after defecation. Washing raw fruits and vegetables.
• Mass Drug Administration (MDA):
  • Periodic deworming (e.g., Albendazole 400 mg once or twice yearly) is recommended by WHO for preschool and school-age children in endemic areas (prevalence >20%).
  • Aims to reduce the overall worm burden in the community and prevent morbidity (growth stunting, cognitive impairment).