Hookworm - Complete Overview

1. Etiology (Causative Agents)

• A. caninum (dog hookworm) - causes eosinophilic enteritis (Australia) and cutaneous larva migrans
• A. braziliense (cat hookworm) - classic cause of cutaneous larva migrans
• Bunostomum phlebotomum, Uncinaria stenocephala - occasional CLM

2. Lifecycle

1. Egg stage: Adult female worms in the small intestine produce eggs that are passed out in feces (diagnostic stage - eggs are 40x60 μm, oval, thin-shelled)
2. Rhabditiform larva (L1/L2): In warm, moist soil (23-33°C), eggs hatch within 1-2 days into non-infective rhabditiform larvae, which undergo two molts over 5-10 days
3. Filariform larva (L3 - infective stage): Third-stage filariform larvae develop, migrate upward on grass blades, can survive in soil for up to 1 month
4. Skin penetration: Infective filariform larvae penetrate unprotected skin (usually feet/hands), triggering "ground itch"
   • A. duodenale can also be transmitted orally (ingested larvae survive and develop)
5. Migration: Larvae enter venous circulation → pulmonary vasculature → penetrate alveoli → ascend bronchial tree to larynx → swallowed
6. Intestinal development: In the small intestine, larvae molt twice more and mature into sexually mature adults
7. Prepatent period: 6-8 weeks from skin penetration to eggs in feces (can be longer with Ancylostoma spp.)

3. Pathogenesis

3a. Blood Loss - The Core Mechanism

• Adult worms attach to intestinal villi, aspirate a plug of tissue, secrete anticoagulant and antiplatelet enzymes, and ingest blood
• A. duodenale extracts ~0.2 mL blood/worm/day
• N. americanus extracts ~0.03 mL blood/worm/day
• Worms move frequently, leaving bleeding points at old attachment sites
• Accumulated blood loss in heavy/prolonged infection leads to iron-deficiency anemia and hypoalbuminemia

3b. Three Phases of Disease

• Pruritic erythematous maculopapular rash at site of larval penetration
• More common with N. americanus; typically between toes or on ankles
• Resolves spontaneously within days

• Dry cough, sore throat, wheezing, low-grade fever
• Less frequent and less severe than in ascariasis
• Transient eosinophilia
• Loeffler-like syndrome is uncommon

• Epigastric pain, abdominal bloating, abnormal peristalsis
• Chronic iron-deficiency anemia (hypochromic microcytic) - severity depends on worm burden, dietary iron intake, concurrent blood loss
• Hypoalbuminemia (protein-losing enteropathy) in heavy infections
• Fatigue, weakness, exertional dyspnea
• In children: growth retardation, cardiac failure (with severe anemia), kwashiorkor-like picture
• In pregnant women: increased maternal/fetal morbidity (~44 million pregnant women infected globally)

3c. Immune Response

• Elicits humoral antibody response and immediate hypersensitivity
• Peripheral eosinophilia and gut eosinophilia
• Eosinophils may play a role in worm destruction; however, evidence that immune responses significantly limit infection is lacking

4. Epidemiology

• Global burden: Over 400-700 million people infected worldwide (figures vary by source)
• Estimated 50,000-60,000 deaths/year; collectively extract over 1 million liters of blood/day from infected individuals
• Distributed between 45°N and 30°S latitude; greatest burden in sub-Saharan Africa, Asia, and rural Americas
• Transmission requires: feces-contaminated shady/moist soil + adequate rainfall + high temperature (23-33°C) + direct skin contact
• Risk factors: poverty, no footwear, use of human excrement as fertilizer, poor sanitation
• Prevalence increases through childhood, plateauing by age ~10 years; intensity peaks by age ~20 and may rise again in elderly
• Male sex more commonly infected; women and children more vulnerable to anemia/sequelae

5. Diagnosis

6. Treatment

• For cutaneous larva migrans (zoonotic hookworm): albendazole 400 mg/day x 3-5 days or ivermectin 200 μg/kg x 1-2 days
• Albendazole single dose has lower cure rates for N. americanus than 3-day regimens
• Treat symptomatic disease even when worm burden is light in vulnerable populations (pregnant women, children)

7. Important Points (High-Yield Summary)

1. "Hook" shape of worm = dorsally curved anterior end; name derives from this
2. Two cutting mechanisms: A. duodenale uses biting teeth (2 pairs), N. americanus uses cutting plates - both enable mucosal attachment and blood ingestion
3. Infective stage = filariform (L3) larva - the diagnostic stage in stool = eggs
4. A. duodenale is unique: larvae can also infect orally (swallowed, survive, develop directly)
5. Ground itch = pruritic rash at skin entry site, typically between toes, more common with N. americanus
6. A. duodenale extracts ~7x more blood per worm than N. americanus (0.2 vs 0.03 mL/day) - more anemia-inducing
7. Eggs in old/stale stool may hatch - must distinguish rhabditiform larvae from Strongyloides (S. stercoralis has a longer buccal cavity)
8. Cutaneous larva migrans = serpiginous, creeping track in skin from dog/cat hookworm larvae; a self-limited condition
   
9. Most infections are asymptomatic - disease develops only with heavy worm burden + prolonged infection + poor dietary iron
10. Pulmonary symptoms less severe than ascariasis - remember this distinction for exams
11. PCR for species differentiation - eggs are morphologically identical between species
12. WHO mass drug administration (MDA) targets school-age children in endemic areas using albendazole or mebendazole
13. Prevention: wearing footwear, sanitary disposal of feces, avoiding use of human feces as fertilizer
14. Hyperinfection does NOT occur with hookworm (unlike Strongyloides stercoralis) - key distinguishing feature in immunocompromised patients
15. Wakana disease (A. duodenale oral ingestion): nausea, vomiting, pharyngeal irritation, cough - follows oral ingestion of larvae