Simple Pulmonary Eosinophilia (Loffler Syndrome)

Epidemiology

Ascaris Lumbricoides or Suum (nematode roundworms): most common cause
Necator Americanus (a hookworm):
Ancylostoma Duodenale (a hookworm):
Ancylostoma Brazliense or Canium (dog and cat hookworms): infection through contact with fecally contaminated soil/ produces Cutneous Larva Migrans at site of entry (“Creeping eruption”: pruritic rash)/ do not mature to adult intestinal phase in humans, dying larvae reach lungs and cause inflammatory reaction/ most commonly cause Loffler’s but can also produce asthma
Entamoeba Histolytica: less common cause
Fasciola Hepatica: less common cause
Strongyloides Stercoralis (nematode roundworm): less common cause of Loffler’s

Pathogenesis for Ascaris (not the same for other parasites above): ingestion of Ascaris eggs -> hatch in intestine -> larvae penetrate mesenteric lymphatics and venules -> travel to pulmonary capillaries -> invade alveoli -> travel up bronchi -> swallowed and travel to intestine (where they mature)
Role of T-cell: pulmonary eosinophilia can be induced in mouse model by using Ascaris antigen extract (transit through circulation may not be necessary therefore to induce pulmonary eosinophilia)

Sputum GS/Cult+Sens: no larvae or ova seen
CXR/Chest CT patterns:
- Soft peripheral few cm densities or confluent infiltrates: usually bilateral
  - Usually migrate and disappear within 2-4 weeks
CBC: eosinophilia >10% (up to 30-70% in some cases)
Stool O+P: Ascaris ova are found in stool only after 6-12 weeks (therefore not useful in diagnosis of acute illness)

(may be asymptomatic)
(symptoms occur 10-16 days after initial ingestion of eggs or contact)