Soil-transmitted nematodes acquired in tropical regions: hookworm causes iron-deficiency anemia; ascariasis causes pulmonary and obstructive GI disease.
Also known as: hookworm, Ancylostoma duodenale, Necator americanus, ascariasis, Ascaris lumbricoides, soil-transmitted helminths, STH
Overview
Soil-transmitted helminth (STH) infections caused by intestinal nematodes acquired by skin penetration (hookworm) or fecal-oral ingestion of embryonated eggs (Ascaris). Hookworm — Ancylostoma duodenale and Necator americanus — causes chronic iron-deficiency anemia. Ascaris lumbricoides causes pulmonary migration syndromes and intestinal/biliary obstruction.
Epidemiology
Among the most prevalent infections worldwide. WHO estimates 500 million people infected with hookworm and over 800 million with Ascaris, concentrated in tropical and subtropical regions with poor sanitation. School-age children carry the highest worm burden. The southeastern United States historically had endemic hookworm; sporadic cases persist.
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Question 1Infectious DiseaseMedium
A 9-year-old boy who recently immigrated from rural sub-Saharan Africa is brought in for fatigue, exertional dyspnea, and poor school performance. He often walked barefoot at home. Exam shows conspicuous pallor, glossitis, and spoon-shaped nails. CBC reveals a microcytic, hypochromic anemia with a low ferritin and low transferrin saturation; stool ovum and parasite exam shows thin-shelled oval eggs. Which of the following complications is most likely to develop if this infection remains untreated?
ABiliary obstruction from worm migration
BLoeffler syndrome from larval migration
CIntestinal obstruction from a worm bolus
DWorsening anemia with impaired growth
Reveal answer & full explanation
Correct answer: D — Worsening anemia with impaired growth
ABiliary obstruction from worm migration
BLoeffler syndrome from larval migration
CIntestinal obstruction from a worm bolus
DWorsening anemia with impaired growth✓
Why Worsening anemia with impaired growth is correct
The vignette describes hookworm (Ancylostoma duodenale or Necator americanus): barefoot soil exposure in an endemic region, pallor, glossitis, koilonychia, and a microcytic hypochromic anemia with low ferritin plus thin-shelled oval eggs on O&P.
Adult hookworms attach to the small-bowel mucosa and feed on blood (Ancylostoma ~0.2 mL/worm/day, Necator ~0.05 mL/worm/day), producing chronic gastrointestinal blood loss and iron depletion.
In children the dominant complication of untreated infection is progressive iron-deficiency anemia driving growth and cognitive delay; treatment is albendazole or mebendazole plus iron repletion continued 3-6 months.
Why the others are wrong
Biliary obstruction from worm migration — This is a complication of Ascaris lumbricoides, whose adult worms can migrate up the ampulla into the biliary tree and cause cholangitis or pancreatitis; hookworms stay anchored to small-bowel mucosa and do not invade the ducts.
Intestinal obstruction from a worm bolus — A classic Ascaris complication in heavily infected children, where the large 15-35 cm worms fill the lumen; hookworms are small and do not form an obstructing bolus.
Loeffler syndrome from larval migration — Transient migratory pulmonary infiltrates with eosinophilia during larval lung transit are most associated with the Ascaris migration phase and are an acute, self-limited event rather than the chronic complication driving this child's disease.
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Residence in or travel to tropical/subtropical regions with poor sanitation
Walking barefoot on contaminated soil (hookworm)
Ingestion of contaminated soil, food, or water (Ascaris)
Pica or geophagia in children (Ascaris)
Inadequate hand hygiene and waste management
Co-existing malnutrition amplifies anemia and growth effects
Pathophysiology
Hookworm: filariform larvae penetrate skin (often interdigital spaces of bare feet) → migrate via blood to lungs → ascend trachea → swallowed → mature in small intestine where adult worms attach to mucosa and feed on blood. Each adult Ancylostoma consumes ~0.2 mL/day, Necator ~0.05 mL/day — explaining chronic iron-deficiency anemia. Ascaris: ingested eggs hatch in small bowel → larvae migrate through portal circulation to lungs → ascend trachea → swallowed → mature into large adult worms (15-35 cm) in jejunum. Adults can obstruct lumen, migrate into bile ducts, or perforate bowel.
Clinical presentation
Symptoms
Hookworm — early: pruritic dermatitis at site of larval penetration (ground itch); pulmonary phase often mild
Hookworm — chronic: fatigue, dyspnea on exertion, pallor, glossitis, pica, growth and cognitive delays in children
Hookworm — heavy infection: protein-losing enteropathy, edema, hypoproteinemia
Ascariasis — intestinal: vague abdominal pain, intermittent diarrhea; heavy load can cause obstruction (especially in children) with vomiting, distension, ileus
Ascariasis — biliary/pancreatic: RUQ pain, cholangitis, pancreatitis from worm migration up the ampulla
Worms visible in stool or vomitus
Signs / physical exam
Hookworm: pallor, koilonychia, signs of iron deficiency
Ascariasis: abdominal distension, palpable mass in heavy infections, jaundice in biliary involvement
Wheezing or transient crackles during pulmonary phase
Edema with hypoalbuminemia in protein-losing enteropathy
Classic findings
Chronic iron-deficiency anemia with no apparent GI bleed in a patient from a tropical region — think hookworm. Large adult Ascaris worm passed in stool or coughed up. Pulmonary infiltrates with eosinophilia (Loeffler syndrome) during initial migration.
Differential diagnosis
Other causes of iron-deficiency anemia (GI bleed, menstrual loss, dietary) — Endoscopy, occult blood; geography and exposure for hookworm
Other intestinal helminths (Strongyloides, Trichuris) — O&P, eosinophilia; specific egg morphology
Acute bacterial pneumonia versus Loeffler syndrome — Eosinophilia, exposure history, transient infiltrates that resolve
Biliary disease (cholangitis, choledocholithiasis) versus Ascaris in biliary tree — Imaging may show worms in CBD/duct; ERCP
Mechanical small bowel obstruction (adhesions, tumor) — Imaging; Ascaris bolus in pediatric obstruction in endemic areas
Identification of eggs (or adult worms) on stool examination is definitive. Heavy infection may be quantified by egg-per-gram counts (Kato-Katz).
Labs
Stool ovum and parasite exam — hookworm thin-shelled oval eggs; Ascaris large mammillated bile-stained eggs
CBC: microcytic hypochromic anemia (hookworm); eosinophilia (variable, more prominent during migration)
Iron studies: low ferritin, low transferrin saturation
Albumin and total protein
LFTs and lipase if biliary/pancreatic involvement suspected
Imaging
Generally not required for diagnosis
Chest x-ray for pulmonary phase showing migratory infiltrates
Abdominal x-ray, ultrasound, or CT for suspected obstruction or biliary worms (Ascaris)
ERCP for biliary ascariasis (diagnostic and therapeutic — extract worms)
Treatment
First-line
Albendazole 400 mg PO single dose (Ascaris) or 400 mg PO daily x 3 days (heavy or hookworm)
Mebendazole 100 mg PO BID x 3 days OR 500 mg single dose
Hookworm: albendazole or mebendazole, plus iron replacement therapy; severe anemia may require transfusion
Ascariasis with intestinal obstruction: nasogastric decompression, IV fluids, mebendazole or albendazole, piperazine (paralyzes worms, helps clear bolus) where available; surgery for nonresolving obstruction or perforation
Biliary ascariasis: ERCP to extract worms; antihelminthic therapy
Pyrantel pamoate 11 mg/kg (max 1 g) is an alternative (safe in pregnancy, single dose for many STH)
Pregnancy: avoid albendazole and mebendazole in first trimester; pyrantel pamoate is preferred during pregnancy if treatment cannot be deferred
WHO recommends mass drug administration of albendazole or mebendazole to school-age children in endemic areas
Second-line / adjunct
Ivermectin 200 microg/kg has activity against Ascaris (and Strongyloides)
Iron supplementation must continue 3-6 months after antihelminthic to replenish stores
Combination therapy and re-treatment in heavily endemic settings or persistent infections
Complications
Hookworm: profound iron-deficiency anemia, hypoproteinemia, growth and cognitive delays in children, adverse pregnancy outcomes
Larval pulmonary phase can cause Loeffler syndrome with severe wheezing in atopic patients
Drug toxicity rare with short courses
PANCE pearls
Hookworm is a leading global cause of iron-deficiency anemia in tropical regions — consider in any traveler or immigrant with unexplained iron-deficiency anemia.
Ascariasis obstruction is a pediatric emergency in endemic areas — heavy worm burdens can fill the lumen.
Ascaris can migrate up the ampulla into the biliary tree or pancreatic duct, causing cholangitis or pancreatitis treatable with ERCP.
Albendazole and mebendazole are both effective for most soil-transmitted helminths; pyrantel pamoate is the safe pregnancy option.
Iron repletion must be initiated alongside antihelminthic therapy in hookworm-related anemia.
References
WHO 2017 — WHO Guideline: Preventive chemotherapy to control soil-transmitted helminth infections in at-risk population groups (WHO 2017)
CDC — CDC Parasites — Hookworm and Ascariasis: clinical guidance
ASTMH — ASTMH practice statements on soil-transmitted helminth infections
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