A 67-year-old man was diagnosed with metastatic (bone, adrenal glands, brain) lung mixed adeno and squamous cell carcinoma in December 2004. The patient started chemotherapy with cis-platin and gemcitabine for 3 cycles and Zoledronic acid. From February 2005 acetate cortisone and low-dose dexametazone was prescribed because of the evidence of adrenal glands deficiency. Early after the third cycle he presented gastrointestinal symptoms (nausea, vomiting), worsening in general conditions, dry cough, dyspnea, and hemophtoe without fever. Routine hematologic laboratory analysis was unremarkable. An otorhynolaringology examination excluded bleeding signs from the upper airways and a bronchoscopy did not reveal pathologic findings on the bronchial mucosa. Furthermore, a bronchial washing performed for both microbiological and cytologic study revealed a bloody lavage fluid. Chest computed tomography (CT) scan showed a diffuse, bilateral ground-glass interstitial and alveolar involvement mainly at right upper lobe and at left low lobe, initially suggesting a pulmonary hemorrhagic disease or a Pneumocystis carinii infection (Fig. 1A). At cytology, bronchioalveolar lavages (BAL) showed several rhabditiform larvae of Strongyloides stercoralis (SS) (Fig. 1B), while special stains (grocott, PAS, Ziehl-Neelsen) did not evidence other microorganisms. SS was also isolated in cultures of the BAL. Two stool specimens (before starting treatment and after 2 days) were both negative for SS. HIV test was negative. Thus, the patient was diagnosed as having pulmonary strongyloidiasis. Treatment with thiabendazole was instituted and patient symptoms resolved in one week. Sputum cytology (performed after 4 days) didn’t show the presence of the parasite. After a follow-up of 4 months the patient died for cancer progression. SS is an intestinal nematode worldwide distributed that harbor within a host for prolonged periods of time but may cause fatal opportunistic infections in immunocompromised patients. Human infection begins with the penetration of skin by filariform larvae that migrate hematogenously to the lung. Larvae then ascend the airway, are swallowed, and mature in the gut. SS completes its life cycle within the host through an asexual autoinfective cycle, allowing the infection to persist in the host indefinitely. In the immunocompromised host, hyperinfections and wide dissemination of larvae may lead to hemorragic pneumonitis (because of larva-induced mucosal injury during larval migration in the hyperinfection syndrome), enteritis, septicemia (gram-negative bacteriemia is common) and death. It tend to disseminate once immunity is suppressed and commonest causes of “cell-mediated” immunodeficiency-related strongyloidiasis include malnutrition, immunosuppressive drug therapy (mainly steroids), transplants, hematologic malignancies, HIV infection. Although it is uncommon among patients receiving therapy for solid cancer, in this case the association of chemotherapy and corticosteoids may have played a crucial role. Mortality from disseminated strongyloidiasis approaches 80%; early diagnosis together with prompt initiation of thiabendazole therapy provides the greatest survival opportunity for patient with SS infestation. This case underlines the possibility that cancer management may create an immunosuppression condition that increase the susceptibility not only to common infectious agents but also to more “exotic” pathogens, such as SS. Before starting an immunosuppressive therapy, especially for patients from the endemic area, routine stools screening should be considered.