Infectious Disease · PANCE / PANRE

Hookworm and Ascariasis (Intestinal Helminths)

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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Risk factors

  • 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 — early (Loeffler syndrome): dry cough, wheezing, low-grade fever, transient pulmonary infiltrates, eosinophilia
  • 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
  • Allergic asthma — Atopy history; transient migratory infiltrates suggest helminthic etiology

Diagnostic workup

Diagnostic criteria

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
  • Ascariasis: intestinal obstruction (volvulus, intussusception), biliary obstruction, pancreatitis, appendicitis, bowel perforation
  • 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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