Eosinophilia & Helminthic Infections (Clinical)
From the eosinophil count to the worm — and the steroid trap
Eosinophilia: definitions and causes
Thresholds. An absolute eosinophil count above 500/µL is eosinophilia; above 1,500/µL is hypereosinophilia. Always calculate the absolute count rather than relying on the percentage. Persistent hypereosinophilia with eosinophil-mediated organ damage (heart, lungs, skin, nerves) and no secondary cause defines the hypereosinophilic syndrome (HES). The most dangerous complication is cardiac: endomyocardial fibrosis with mural thrombi (Loeffler endocarditis), leading to restrictive cardiomyopathy and emboli, so troponin and echocardiography are part of the evaluation.
| Category | Examples | Clues |
|---|---|---|
| Allergic | Asthma, allergic rhinitis, atopic dermatitis; ABPA | Most common US cause; ABPA = asthma, very high IgE, fleeting infiltrates, central bronchiectasis |
| Drugs | DRESS from anticonvulsants, allopurinol, sulfonamides, minocycline, vancomycin | 2–8 weeks after starting; fever, rash, facial edema, lymphadenopathy, hepatitis |
| Endocrine | Adrenal insufficiency | Hyponatremia, hyperkalemia, hypotension |
| Vasculitis | EGPA | Asthma, sinusitis, mononeuritis multiplex, MPO-ANCA |
| Neoplastic | Hodgkin lymphoma, T-cell lymphomas, myeloid neoplasms (FIP1L1-PDGFRA) | B symptoms, nodes; PDGFRA: splenomegaly, high tryptase, imatinib-responsive |
| Infectious | Tissue-invasive helminths | Leading cause worldwide; travel or immigration history |
Treatment clues. DRESS requires stopping the drug and usually systemic glucocorticoids. The FIP1L1-PDGFRA fusion kinase is exquisitely sensitive to imatinib, whereas idiopathic HES is treated with glucocorticoids, with mepolizumab (anti-IL-5) or hydroxyurea as steroid-sparing options. Cortisol normally suppresses eosinophils, which is why eosinophilia accompanies adrenal insufficiency.
Evaluating possible helminth infection
- Exposure historyCountry of origin and travel, diet (undercooked pork or game, raw fish), freshwater contact, barefoot soil contact, dogs and sheep.
- Stool ova and parasites ×3Collected on separate days; useful for intestinal-phase worms such as hookworm, but insensitive for Strongyloides and silent during tissue migration.
- Targeted serologyStrongyloides for anyone from an endemic area; Schistosoma after African freshwater exposure; others (cysticercosis, echinococcosis, trichinellosis) as the picture suggests.
- If no cause and count stays >1,500/µLAssess end organs, peripheral smear, flow cytometry, FIP1L1-PDGFRA testing and bone marrow examination.
Strongyloides stercoralis
Life cycle. Filariform larvae in soil penetrate bare skin in the tropics, subtropics and rural Appalachia, travel through the lungs and mature in the small intestine. Strongyloides can complete its life cycle inside the host (autoinfection), so infection persists for decades; immigrants and veterans who served in endemic regions remain at risk long after leaving.
Chronic infection. Most patients are asymptomatic or have intermittent abdominal pain, diarrhea and eosinophilia. The skin sign is larva currens, a rapidly moving (centimeters per hour), serpiginous, urticarial track over the buttocks, perineum and thighs. Serology is the best screening test; agar plate culture is more sensitive than routine stool exams. Ivermectin is the treatment of choice.
Hyperinfection and dissemination. Glucocorticoids (the most important trigger), HTLV-1 coinfection, transplantation and hematologic malignancy allow autoinfection to accelerate. Massive numbers of larvae cross the bowel wall carrying enteric flora, causing gram-negative bacteremia and meningitis, pneumonitis with alveolar hemorrhage, and ileus. Eosinophilia is often absent because steroids suppress it, and mortality is high. HIV infection is not a major risk factor.
Before high-dose or prolonged glucocorticoids, transplantation, chemotherapy or biologics, anyone from an endemic region should have Strongyloides serology or receive empiric ivermectin if steroids cannot wait. Hyperinfection requires daily ivermectin and reduction of immunosuppression. In patients from Central or West Africa, exclude heavy Loa loa microfilaremia first, because ivermectin can then provoke encephalopathy.
Tissue cestodes and the amebic abscess
Neurocysticercosis. Humans develop cysticercosis by swallowing Taenia solium eggs through fecal-oral contact with a tapeworm carrier; eating undercooked pork containing cysts instead produces the intestinal adult tapeworm (taeniasis). Larval cysts in the brain make neurocysticercosis a leading cause of acquired epilepsy worldwide, typically presenting as new seizures in an immigrant from Latin America, Asia or Africa. Imaging shows cysts with an eccentric scolex ("hole with a dot"), ring-enhancing degenerating cysts with edema, or punctate calcifications; serology supports the diagnosis.
Treatment by stage. Antiseizure drugs are given to every patient with seizures. Antiparasitic therapy (albendazole, adding praziquantel for more than two cysts) is used only for viable parenchymal cysts and always with corticosteroids, because dying cysts provoke inflammation and edema. Calcified lesions represent dead parasites and need no antiparasitic drug. Hydrocephalus or intraventricular cysts need neurosurgery first, and a fundoscopic exam excludes ocular cysts, which antiparasitic treatment could turn into a sight-threatening inflammatory reaction.
| Feature | Hydatid cyst | Amebic liver abscess |
|---|---|---|
| Organism | Echinococcus granulosus (helminth) | Entamoeba histolytica (protozoan) |
| Acquisition | Eggs from dog feces; sheep-raising regions | Fecal-oral cysts; endemic tropical regions |
| Presentation | Slow growth; often incidental; liver ~70%, then lung | Fever and RUQ pain over days to weeks; often no current diarrhea |
| Imaging | Daughter cysts, floating membrane ("water lily"), calcified wall | Usually single right-lobe abscess |
| Eosinophilia | Possible | Absent |
| Treatment | Albendazole + PAIR or surgery | Metronidazole, then paromomycin; drainage rarely |
Echinococcosis. Dogs are the definitive host and sheep the usual intermediate host; humans are accidental intermediate hosts, mostly in sheep-raising regions of the Mediterranean, Middle East, South America and Central Asia. PAIR means puncture, aspiration, injection of a scolicidal agent and reaspiration. Albendazole is given around any procedure, because rupture or careless aspiration spills antigenic fluid, causing anaphylaxis and seeding new cysts.
Amebic liver abscess. Typically a young man who lives in or has visited an endemic area presents with fever and right-upper-quadrant pain. Serology is positive and any aspirate is odorless "anchovy paste." Metronidazole (a tissue agent) is followed by paromomycin, a luminal agent that clears intestinal cysts. Drainage is reserved for diagnostic uncertainty, failure to respond, or large left-lobe abscesses at risk of rupture.
Trichinella, schistosomes and hookworm
Trichinellosis. Eating undercooked pork or wild game (bear, wild boar, walrus) releases Trichinella spiralis larvae that encyst in striated muscle. A brief diarrheal phase is followed by fever, myalgias, periorbital edema, subconjunctival and splinter hemorrhages, marked eosinophilia and elevated CK; myocarditis and encephalitis are the feared complications. Serology or muscle biopsy confirms the diagnosis. Treatment is albendazole (or mebendazole) plus corticosteroids for significant symptoms.
Schistosomiasis. Cercariae released by freshwater snails penetrate the skin (swimmer's itch). Acute schistosomiasis (Katayama fever) brings fever, urticaria, cough and eosinophilia weeks later. S. haematobium (Africa, Middle East) lives in the bladder venous plexus and causes terminal hematuria, bladder calcification, obstructive uropathy and squamous cell carcinoma of the bladder; its eggs, which bear a terminal spine, are found in midday urine. S. mansoni and S. japonicum live in mesenteric veins and cause periportal ("pipe-stem") fibrosis with presinusoidal portal hypertension, varices and splenomegaly, while liver synthetic function is preserved; S. mansoni eggs have a lateral spine. Praziquantel treats all species.
Hookworm. Necator americanus and Ancylostoma duodenale larvae penetrate bare feet (ground itch), migrate through the lungs (Löffler syndrome with cough and transient eosinophilic infiltrates) and attach to the small-bowel mucosa, consuming blood. The result is microcytic iron-deficiency anemia and hypoalbuminemia, especially in children. Eggs appear in stool; treat with albendazole and iron. Dog and cat hookworms (Ancylostoma braziliense) cannot mature in humans and instead cause cutaneous larva migrans, a slowly advancing creeping eruption treated with ivermectin or albendazole.