A family of six immigrated from Yemen to Switzerland on March 5, 2011. Presenting with painless macrohematuria and a blood eosinophilia of 16% (0.6 × 109/L), the 15-year-old son of the family was diagnosed with a Schistosoma haematobium–Schistosoma mansoni mixed infection by detection of parasite eggs in stool and urine. A serology screen of the five remaining asymptomatic family members indicated four had schistosomal infections (13-year-old son: eosinophils 1.1 × 109/L, adult-antigen enzyme-linked immunosorbent assay (ELISA) 1.85 OD, egg-antigen ELISA 1.45 OD, IFAT 640; 17-year-old son: eosinophils 2.9 × 109/L, adult-antigen ELISA 1.47, egg-antigen ELISA 1.51, IFAT 640; father: eosinophils 0.3 × 109/L, adult-antigen ELISA 1.22 OD, egg-antigen ELISA 0.79 OD, IFAT 320; mother: eosinophils 0.074 × 109/L, adult-antigen ELISA 0.69 OD, egg-antigen ELISA 0.31 OD, IFAT 160 [references: adult-antigen ELISA <0.15; egg-antigen ELISA <0.3; IFAT <80]). However, no eggs were found in subsequent urine and stool examinations. The last contact with potentially contaminated freshwater was late February 2011 in a lake close to Aden, Yemen. The patients were diagnosed by the end of July 2011. Praziquantel (PZQ; 60 mg/kg body weight) was administrated orally on August 10, 2011 to the parasitological-confirmed index patient and the four sero-positive family members. PZQ was well tolerated, except by the 17-year-old son about whom we report here (see above and Table 1 for baseline laboratory parameters). Within 24 hours of PZQ administration, the patient developed fatigue, fever, cough, and increasing dyspnoea. A physical examination revealed an impaired general condition including fever [38.7°C (tympanal)] with stable circulatory parameters (pulse rate 99/min, blood pressure 127/87 mmHg) but also marked broncho-pulmonary obstruction (wheeze) on auscultation and progressive signs of respiratory decompensation [respiratory rate 33/min, oxygen saturation 84% (by pulse oxymetry)]. The laboratory investigation showed a leukocytosis of 16.6 × 109/μL with an eosinophil fraction of 51% and an elevated C-reactive protein (Table 1). The chest X-ray was normal. Due to compromised respiratory function, the patient was admitted to the hospital for symptomatic treatment (oxygen supplementation and inhaled bronchodilators) and monitoring. Within 2 days the patient's respiratory function stabilized, and the patient was discharged. A follow-up examination 3 days later (August 16) at our outpatient department showed that the patient's general condition continued to improve (no fever, no dyspnoea). On the other hand, wheeze was still prominent on auscultation, and the pulmonary function test showed a persisting airflow obstruction [forced expiratory volume/1 s (FEV1) 54%; forced vital capacity (FVC) 48%]. Simultaneous blood investigation revealed a leukocytosis of 28.0 × 109/μL with an eosinophil fraction of 70.5% (Table 1). Additional laboratory investigation showed mildly elevated liver function tests [aspartate transaminase (AST) 47.5 U/L (<40), alanine transaminase (ALT) 58.4 U/L (<41), gamma-glutamyltransferase (γGT) 81.9 U/L (11–50), and alkaline phosphatase (AP) 237 U/L (<270)]. Under the tentative diagnosis of an acute systemic allergic reaction, we initiated symptomatic treatment with oral prednisolone (1.5 mg/kg body weight OD) and inhaled budesonide/formoterol (200/6 µg BID). Under this treatment the respiratory symptoms improved, the laboratory parameters normalized, and it was possible to taper down and finally discontinue oral prednisolone on August 29. Inhaled budesonide/formoterol was stopped on September 12 when the patient indicated complete resolution of all symptoms. A follow-up spirometry on October 11 was normal.