Describe eosinophilia in helminth infection and the approach to a patient with eosinophilia.

The Basis of Helminth-associated Eosinophilia

• The response is a Th2 response — helminth antigens drive IL-5 (which is the specific eosinophil growth, differentiation and survival factor), together with IL-4 and IL-13 driving IgE production and mast cell activation
• Eosinophils kill helminths by antibody-dependent cellular cytotoxicity — they cannot phagocytose an organism far larger than themselves, so they bind to IgE- or IgG-coated larvae and degranulate onto the surface, releasing major basic protein, eosinophil cationic protein and peroxidase
• This is why worms provoke eosinophilia and protozoa do not — the response evolved against a target too big to swallow, and protozoa are dealt with by phagocytosis and cell-mediated killing instead

Approach to a Patient with Eosinophilia

• Confirm it is real and persistent with an absolute count, and repeat it; transient eosinophilia is common and often needs no pursuit
• The differential beyond parasites — remembered as "CHINA": Connective tissue disease (eosinophilic granulomatosis with polyangiitis, polyarteritis); Helminths; Idiopathic hypereosinophilic syndrome; Neoplasia (Hodgkin lymphoma, leukaemia, solid tumours); Allergy, Asthma, Atopy and Adrenal insufficiency. Also drugs — a very common cause and the first thing to review — and fungal disease (ABPA), skin disease and, among infections, Cystoisospora and the convalescent phase of scarlet fever
• Take a travel, residence, dietary and occupational history, which in practice narrows the parasitic possibilities faster than any test — raw fish, raw crab, undercooked pork, freshwater swimming, barefoot work, pets and pica
• Investigate — three stool specimens for ova and parasites; night blood for microfilariae; serology directed by the history (Strongyloides, Toxocara, Trichinella, hydatid, schistosomes, filaria); chest radiograph; total IgE; and imaging as indicated
• Remember that the stool is negative in several important ones — Toxocara (never matures), Trichinella (viviparous), filariasis, hydatid disease and tropical pulmonary eosinophilia. In these, serology is the only route
• Always exclude or empirically treat Strongyloides before corticosteroids in anyone with eosinophilia and any possible exposure

Applied Aspects

• Eosinophilia with a compatible history is an indication to look for a helminth, and its degree indicates the phase — the highest counts occur during larval migration, not in established infection
• A normal count does not exclude worms, particularly luminal ones, so stool examination is still worthwhile in a symptomatic patient
• Review the drug chart first; drug hypersensitivity is a commoner cause of eosinophilia in hospital practice than any parasite
• Persistent unexplained severe eosinophilia damages organs — eosinophil granule proteins cause endomyocardial fibrosis, neuropathy and thrombosis — so hypereosinophilic syndrome needs prompt haematological assessment rather than indefinite parasite hunting
• Tropical pulmonary eosinophilia responds dramatically to DEC, and the response is itself diagnostic; it should be considered in any Indian patient with nocturnal asthma-like symptoms and a very high count
• Empirical albendazole or ivermectin is reasonable in an appropriate setting where investigation is limited, particularly before immunosuppression — the drugs are cheap and safe, and the risk of missing Strongyloides is not