Strongyloides

**Organism & epidemiology** - Strongyloides stercoralis: nematode found in tropical/subtropical regions, rural Appalachia, and the southeastern US; also endemic in Southeast Asia, Latin America, and sub-Saharan Africa. - Transmission: filariform (L3, infective) larvae in contaminated soil penetrate intact skin (bare feet). No need to ingest eggs.

**Life cycle (high-yield)** 1. Filariform larvae penetrate skin, enter the venous circulation, and travel to the lungs. 2. They ascend the bronchial tree, are swallowed, and mature into adult females in the duodenum/jejunum. 3. Parthenogenetic females burrow into the mucosa and lay eggs. Eggs hatch in the gut, so **rhabditiform larvae (not eggs) are passed in stool**. 4. **Autoinfection:** rhabditiform larvae molt into filariform larvae in the gut and penetrate the colonic mucosa or perianal skin. This allows infection to persist for decades after leaving an endemic area (e.g., WWII veterans/POWs, refugees). - Mnemonic: "Strongyloides = **S**tool **l**arvae, not eggs"; the infection can be self-perpetuating.

**Clinical features** - Cutaneous: pruritic papular rash at the penetration site. **Larva currens** is a rapidly migrating (up to 5–10 cm/hr) serpiginous urticarial track, typically on the buttocks, perineum, and trunk from autoinfection. - Pulmonary (Löffler-like syndrome): cough, wheeze, transient pulmonary infiltrates during larval migration. - GI: epigastric pain, diarrhea, nausea, malabsorption. It can mimic peptic ulcer disease. - **Eosinophilia** is common in chronic infection but may be absent in hyperinfection, especially with corticosteroid use (a poor prognostic sign).

**Hyperinfection and disseminated strongyloidiasis** - Risk factors: corticosteroids (most important, even short courses), HTLV-1, hematologic malignancy, transplant, and other immunosuppression (e.g., TNF inhibitors, chemotherapy). **HIV alone is a weaker risk factor.** - Accelerated autoinfection leads to massive larval burden. Larvae disseminate to the lungs (ARDS, diffuse hemorrhage), CNS (meningitis), and other organs. - Gut flora are carried along with the larvae, causing **gram-negative bacteremia/sepsis and recurrent polymicrobial meningitis** (e.g., E. coli, Klebsiella, Enterococcus). - Mortality is high (often >50%) if untreated.

**Diagnosis** - Stool exam for rhabditiform larvae (low sensitivity per sample; repeat ×3 or use concentration methods). - **Agar plate culture** or Baermann technique increases sensitivity. - Serology (IgG ELISA) is useful for screening, though cross-reactivity with other helminths can occur. - In hyperinfection, larvae may be found in sputum, BAL fluid, or other fluids. - Duodenal aspirate/biopsy is rarely needed.

**Treatment** - **Ivermectin** is first line (binds glutamate-gated Cl⁻ channels, causing hyperpolarization and paralysis of the worm). Albendazole is less effective. - Hyperinfection: prolonged ivermectin until stool/sputum are negative for ≥2 weeks, plus broad-spectrum antibiotics for enteric bacteria, and reduction of immunosuppression if possible. - **Prevention/screening:** Screen or empirically treat patients from endemic regions before starting corticosteroids or other immunosuppression or before transplant. - Caution: In areas endemic for Loa loa, ivermectin can cause encephalopathy with high microfilarial loads.

**Board pearls** - Strongyloides is the helminth with **autoinfection**. Enterobius (pinworm) can also reinfect, but by the fecal-oral route. - Differentiate from hookworms (Ancylostoma/Necator): both penetrate skin and travel through the lungs. Hookworms cause **iron-deficiency anemia** and are diagnosed by **eggs** in stool. Strongyloides eggs are not usually seen in stool. - Classic vignette: immigrant or veteran from an endemic area develops gram-negative sepsis or meningitis, pulmonary infiltrates, and diarrhea after starting prednisone. Answer: disseminated strongyloidiasis, treated with ivermectin.