NEMATODES – DRACUNCULUS MEDINENSIS

**NEMATODES – DRACUNCULUS MEDINENSIS **

Definition – Dracunculus medinensis (Guinea‑worm) is a parasitic nematode causing dracunculiasis

Cause – Drinking water contaminated with copepods (Cyclops) that harbour infective third‑stage larvae

Types – No distinct varieties; disease is described as dracunculiasis (acute, chronic phases)

Pathogenesis

1. Ingestion → water containing infected copepods is swallowed
2. Copepod digestion → gastric acid kills copepod, releasing L3 larvae in gut lumen
3. Intestinal penetration → larvae penetrate intestinal wall within minutes
4. Hematogenous spread → larvae enter bloodstream, migrate to sub‑cutaneous tissues of lower limbs or trunk
5. Maturation → two months later larvae develop into adult male (≈20 cm) and female (up to 100 cm) worms; males die, females remain alive
6. Female migration → female worm moves toward skin surface, usually on distal extremities
7. Blister formation → a painful, erythematous vesicle appears on skin
8. Worm emergence → when blister contacts water, female creates a pore, releases thousands of L1 larvae into water, completing cycle

Morphology

• Adult female: long, thin, white, ribbon‑like, up to 100 cm, coiled in sub‑cutaneous tissue
• Adult male: much smaller (≈20 cm), shorter, dies after mating
• Larvae: L3 (infective) ≈1 mm, L1 (released in water) ≈0.5 mm

Clinical features

• Incubation 10‑14 months (time from infection to worm emergence)
• Early stage: usually asymptomatic
• Skin blister on lower limb, foot, or trunk, often on the dorsal surface
• Severe burning pain, swelling, edema, and itching around blister
• Worm visible as a white thread emerging from ulcer

Complications

• Secondary bacterial infection of ulcer (Staphylococcus, Streptococcus) → cellulitis, abscess
• Chronic ulceration, scar formation, disability due to repeated infections
• Lymphangitis, lymphadenitis in severe cases

Diagnosis

• Direct visualization of emerging female worm (≈10–30 cm) from skin ulcer
• History of drinking stagnant water in endemic area
• Microscopic identification of L1 larvae in water collected from blister

Management

• Gentle extraction of worm over 2‑3 days: soak affected limb in warm water (30‑35 °C) → worm emerges, pull slowly with a stick, rotate to avoid breakage
• Clean wound, apply antiseptic dressing, give antibiotics if secondary infection suspected
• Provide analgesics for pain relief
• Preventive measures: filter water (20 µm), treat water with chlorine or boil, educate community, use larvicidal agents in water bodies

Life cycle (step‑wise)

1. Adult female in sub‑cutaneous tissue → creates blister on skin
2. Blister contacts water → releases thousands of L1 larvae into water
3. Copepod (Cyclops) ingests L1 → larvae develop to infective L3 inside copepod (≈2 weeks)
4. Human drinks contaminated water → copepod is killed in stomach, L3 released
5. L3 penetrates intestinal wall → migrates to sub‑cutaneous tissue → matures → cycle repeats

Memory trick for life cycle – “B‑W‑C‑D‑M”
B = Blister releases larvae, W = Water, C = Copepod eats larvae, D = Drink contaminated water, M = Mature worm emerges

Memory trick for pathogenesis – “I‑P‑L‑M‑F‑E”
I = Ingestion, P = Penetration, L = Larval migration, M = Maturation, F = Female moves to skin, E = Emergence

These points cover Robbins, Harsh Mohan, Ananthanarayan & Paniker, Chatterjee and essential NCH highlights, and are formatted for MUHS/NCH exams.