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Roundworm

629 wordsUpdated 03/03/2026
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Exam Tips

  • Classic viva lifecycle: ingestion of embryonated eggs -> duodenal hatch -> lung migration -> swallowed larvae -> adult worms in small bowel.
  • A negative early stool test does not exclude infection; eggs may be absent for several weeks after exposure.
  • In UK OSCEs, always ask travel/migration and sanitation history in unexplained eosinophilia or abdominal/respiratory symptom clusters.
  • Red flags needing same-day admission: acute abdomen, bowel obstruction, jaundice with fever/RUQ pain, or sepsis signs.
  • Children with heavy burden are at highest risk of malnutrition and growth/developmental effects.
  • Image memory aid: review a standard Ascaris lifecycle diagram (intestine-lung-intestine loop) in your parasitology text before exams.

Definition

Ascariasis is intestinal and systemic disease caused mainly by the nematode Ascaris lumbricoides, the commonest human helminth infection globally. It ranges from asymptomatic low-burden infection to heavy worm burden causing pulmonary larval syndromes and serious hepatobiliary or bowel complications, particularly in children and people exposed in areas with poor sanitation.

Pathophysiology

Infection follows ingestion of embryonated eggs from faecally contaminated soil, food, or water (soil-transmitted helminth). Larvae hatch in the duodenum, penetrate intestinal mucosa, migrate via bloodstream to the lungs, then ascend the bronchial tree and are swallowed back into the small bowel where they mature into adult worms. Pulmonary migration can trigger eosinophilic inflammation (Loffler syndrome) at about 10-14 days; high adult worm loads can cause mechanical obstruction, volvulus/intussusception, and migration into biliary or pancreatic ducts causing cholangitis, cholecystitis, or pancreatitis. Eggs are not immediately infective when passed in stool, so direct person-to-person spread does not occur without environmental maturation.

Risk Factors

  • Travel to, residence in, or migration from tropical/subtropical endemic regions with poor sanitation
  • Exposure to contaminated soil, untreated water, or inadequately washed/peeled/cooked produce
  • Poor hand hygiene after toileting, nappy changing, or soil/manure contact
  • Childhood (especially 5-15 years), associated with higher-intensity worm burden
  • Household or community settings using manure/wastewater in agriculture

Clinical Features

Symptoms

  • Often asymptomatic or mild non-specific abdominal discomfort
  • Abdominal pain, distension, nausea, diarrhoea, reduced appetite
  • Malaise, weakness, weight loss, and features of malnutrition
  • Cough, wheeze, dyspnoea, fever, or haemoptysis during larval lung migration
  • Biliary colic or acute severe abdominal pain if obstructive/hepatobiliary complications develop

Signs

  • Possible urticarial or transient rash
  • Wheeze or other abnormal breath sounds in eosinophilic pneumonitis
  • Abdominal tenderness/distension; signs of intestinal obstruction in heavy infection
  • Fever or sepsis physiology in complicated disease (for example cholangitis or peritonitis)
  • Growth faltering and developmental impact in heavily infected children

Investigations

Stool microscopy for ova and parasites:Ascaris eggs in stool; sensitivity improves by sending 3 specimens on different days
Timing consideration:Early infection can be stool-negative because egg production usually begins >40 days after infection
Full blood count:Peripheral eosinophilia may be present, especially in migratory/pulmonary phase
Chest X-ray (if respiratory features):Transient migratory pulmonary infiltrates consistent with Loffler syndrome
Abdominal X-ray (if acute abdomen/obstruction suspected):Features of bowel obstruction; escalate urgently
Targeted helminth screen in exposed patients with eosinophilia:Add Strongyloides serology (all tropical exposure); include urine microscopy and Schistosoma serology for sub-Saharan Africa exposure

Management

Lifestyle Modifications

  • Urgently refer/admit if intestinal or biliary obstruction, peritonitis, cholangitis, pancreatitis, or sepsis is suspected
  • Hand hygiene with soap and warm water before food handling/eating and after toilet use, nappy changes, or soil/manure contact
  • Wash, peel, or thoroughly cook vegetables and fruit, especially if grown in potentially contaminated soil
  • Provide patient education on reinfection risk and public-health prevention measures

Pharmacological Treatment

Benzimidazole anthelmintic

  • Mebendazole 100 mg orally twice daily for 3 days
  • Mebendazole 500 mg oral single dose (commonly used off-label regimen for ascariasis)

Use for confirmed uncomplicated stool-positive infection in primary care. Safety: mebendazole is generally avoided/unlicensed in pregnancy, breastfeeding, and children under 2 years for this indication; seek infectious diseases/tropical medicine advice for these groups. Check BNF/eMC for interactions, hepatic impairment cautions, and adverse effects.

Surgical / Interventional

  • Emergency surgical management for intestinal obstruction, volvulus, intussusception, perforation, or infarction
  • Urgent endoscopic/surgical biliary decompression if severe biliary obstruction or cholangitis

Complications

  • Loffler syndrome (eosinophilic pneumonitis)
  • Small bowel obstruction
  • Volvulus and intussusception
  • Peritonitis, bowel infarction, or perforation
  • Upper gastrointestinal bleeding
  • Biliary colic, acute cholecystitis, acute cholangitis
  • Acute pancreatitis
  • Sepsis secondary to complicated intra-abdominal or biliary infection
  • Nutritional deficiency (including vitamin A deficiency), growth and cognitive delay in children

Prognosis

Overall prognosis is excellent with treatment; most infections are mild or asymptomatic and cure rates with anthelmintics are high. Morbidity and mortality rise with untreated heavy worm burden, particularly when obstruction or biliary/peritoneal complications occur.

Sources & References

NICE Guidelines(1)

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