Intestinal nematodes: life cycles, clinical features, diagnosis and complete management

Learning objectives

• Identify the major intestinal nematodes by transmission route, morphology and life cycle.
• Link worm burden and tissue migration to the patient’s symptoms and complications.
• Select and interpret stool microscopy, concentration, culture, tape tests, serology and blood counts.
• Choose appropriate anthelmintic treatment, repeat dosing, contact management and follow-up.
• Recognise obstruction, severe anaemia and Strongyloides hyperinfection as emergencies.

Classification and transmission

Life cycles and pathophysiology

Ascaris

Eggs embryonate in warm moist soil. After ingestion, larvae hatch in the intestine, cross the mucosa, travel via portal circulation to the liver and then lungs, ascend the trachea, are swallowed and mature in the jejunum. Adult worms consume little host nutrition but compete for micronutrients, form boluses and migrate into the biliary tree or pancreatic duct.

Hookworms

Filariform larvae penetrate skin, enter blood, pass through lungs and are swallowed. Adults attach to duodenal and jejunal mucosa and feed on blood. Ongoing mucosal bleeding causes iron deficiency; A. duodenale may also cause substantial blood loss during tissue dormancy.

Trichuris

Eggs mature in soil and hatch after ingestion. Adults embed their thin anterior ends in colonic mucosa. Heavy infection produces epithelial inflammation, blood loss, protein-losing enteropathy and impaired growth.

Strongyloides

Parthenogenetic adult females in the mucosa produce larvae. Some pass in stool; others penetrate colonic mucosa or perianal skin and restart infection. Corticosteroids, HTLV-1, transplantation and severe immunosuppression accelerate autoinfection, causing thousands of migrating larvae and Gram-negative sepsis.

Risk factors and epidemiology

• Open defecation, contaminated soil or vegetables and unsafe water.
• Walking barefoot or occupational soil contact.
• Crowded households and inadequate hand hygiene, particularly for pinworm.
• Children, pregnancy, malnutrition and chronic blood loss increase consequences.
• Before steroids, chemotherapy or transplantation, screen for possible Strongyloides exposure even if stool tests are negative.

Clinical presentation

General symptoms

Many infections are asymptomatic. Possible features include abdominal pain, nausea, altered bowel habit, anorexia, bloating, fatigue, urticaria, cough during larval migration and eosinophilia.

Ascaris syndromes

Heavy infection can cause colicky pain, vomiting, abdominal distension and intestinal obstruction. Migrating worms produce biliary colic, cholangitis, pancreatitis or obstructive jaundice. Pulmonary migration may cause transient fever, wheeze and eosinophilic pneumonitis (Löffler syndrome).

Hookworm disease

Early itchy dermatitis occurs at the entry site. Later, patients develop fatigue, exertional dyspnoea, pallor, dizziness, pica, oedema from hypoalbuminaemia or cognitive and growth effects in children. Severe anaemia may precipitate heart failure.

Trichuriasis

Light infection is often silent. Heavy disease causes chronic mucoid or bloody diarrhoea, tenesmus, abdominal pain, anaemia, growth retardation and rectal prolapse.

Strongyloidiasis

Intermittent abdominal pain, diarrhoea, constipation, urticaria and rapidly moving linear rash (larva currens) may occur. Hyperinfection presents with fever, cough, dyspnoea, wheeze, abdominal pain, ileus, meningitis or sepsis; eosinophilia may disappear in severe disease.

Enterobiasis

Intense nocturnal perianal itching disturbs sleep. Excoriations, secondary infection, vulvovaginitis or rarely appendiceal/urinary symptoms may occur.

History and examination

1. Ask about onset, stool appearance, pruritus, weight change, fever, respiratory symptoms, jaundice and obstructive pain.
2. Document diet, pica, menstrual and pregnancy history, drug exposure, prior deworming and household symptoms.
3. Map residence, travel, sanitation, footwear, farming and contact with contaminated soil.
4. Examine hydration, nutrition, pallor, oedema, abdomen, perianal skin, lungs, jaundice and signs of heart failure.
5. In suspected hyperinfection, assess sepsis, oxygenation, meningism and ileus urgently.

Investigations

• Full blood count: eosinophilia supports tissue migration but may be absent in severe Strongyloides; assess haemoglobin and indices for iron deficiency.
• Stool ova and parasite microscopy on properly collected samples; concentration improves yield. Multiple samples are useful for intermittent shedding.
• Perianal adhesive tape test on three early mornings for Enterobius; routine stool examination is insensitive.
• Strongyloides stool culture or PCR where available; serology helps chronic infection but may be unreliable in immunosuppression.
• Chest radiograph during pulmonary migration; ultrasound/MRCP/ERCP for biliary obstruction; abdominal radiograph or CT for obstruction, perforation or abscess.
• Iron studies, albumin, renal/electrolyte profile and stool occult blood when anaemia or protein loss is suspected.

Differential diagnosis

Giardiasis, amoebiasis, inflammatory bowel disease, coeliac disease, bacterial dysentery, tuberculosis, appendicitis, biliary stones, peptic disease, malignancy, iron deficiency from other causes and eosinophilic gastrointestinal disease.

Management

Emergency complications

• Obstruction: nil by mouth, IV fluids, electrolyte correction, imaging, surgical review and nasogastric decompression when indicated. Do not give laxatives in suspected complete obstruction.
• Biliary or pancreatic migration: manage cholangitis/sepsis and arrange endoscopic or surgical extraction where required.
• Severe hookworm anaemia: assess haemodynamic compromise and heart failure; transfuse only when clinically indicated, give iron and eradicate infection.
• Strongyloides hyperinfection: isolation is not usually the key intervention; urgent ivermectin, broad sepsis management, search for Gram-negative bacteraemia and stop/reduce steroids where safe.
• Rectal prolapse: correct dehydration and anaemia, treat Trichuris, reduce prolapse and seek surgical review if persistent.

Follow-up and prevention

• Reassess symptoms, haemoglobin, weight and stool results after treatment according to parasite and local programme.
• Repeat Strongyloides testing after therapy in immunosuppressed patients and document cure before future steroids.
• Use latrines, safe water, handwashing, washing of produce and footwear; dispose of faeces safely.
• Community preventive chemotherapy should follow national school-age and at-risk population programmes.
• Iron, protein and vitamin support are essential when chronic infection caused anaemia or growth faltering.

Exam and OSCE pearls

• Nocturnal perianal itch plus household spread suggests pinworm; order a tape test, not routine stool microscopy.
• Marked anaemia with soil exposure and barefoot walking suggests hookworm.
• Rectal prolapse in a child with chronic dysentery suggests heavy Trichuris infection.
• Negative eosinophils do not reassure in Strongyloides hyperinfection.
• Albendazole is not a substitute for ivermectin in Strongyloides.

References

• SlideShare: Intestinal nematodes.
• WHO soil-transmitted helminth and strongyloidiasis guidance.
• Current Uganda Clinical Guidelines and local deworming protocols.

Safety note: Verify current national dosing, pregnancy restrictions, paediatric doses and specialist regimens for hyperinfection before prescribing.