Answer to February 2015 Photo Quiz

Answer: Strongyloides stercoralis hyperinfection syndrome. The blood agar plates demonstrated serpiginous bacterial growth suspicious for Strongyloides stercoralis infection (as the larvae crawl over the agar, they carry bacteria with them, creating visible tracks). Review of the Gram stain of bronchoalveolar lavage (BAL) fluid showed rare filariform larvae of Strongyloides stercoralis (see Fig. S1 in the supplemental material). Biopsy of the purpuric abdominal rash also revealed filariform larvae.

Infection with S. stercoralis is most commonly acquired from the soil where the infective filariform larvae penetrate the skin and migrate to the small intestine, classically via the pulmonary route. In immunocompetent patients, infectious signs and symptoms can range from asymptomatic eosinophilia to intermittent gastrointestinal symptoms and malabsorption (1). However, S. stercoralis is unique among the geohelminths in that it can multiply within the gastrointestinal tract and autoinfect the host (2). In the setting of immunosuppression, particularly the use of glucocorticosteroids, widespread dissemination may occur, causing adult respiratory distress syndrome, pulmonary hemorrhage, meningoencephalitis, hepatitis, and characteristic skin lesions consisting of widespread petechiae and purpura (1, 2). A frequent complication of hyperinfection syndrome is bacteremia, usually with enteric Gram-negative bacteria, caused by larvae migrating through the bowel lumen, but other organisms have also been described, including Streptococcus bovis, Streptococcus pneumoniae, Enterococcus faecalis, Pseudomonas, and coagulase-negative staphylococci (1). Mortality is high (>50%) among immunosuppressed patients, and diagnostic clues such as eosinophilia are frequently absent.

Parasitologic diagnosis of hyperinfection syndrome is often straightforward because of the increased larval burden in stool as well as in samples obtained from sites of larval migration, including sputum, bronchoalveolar lavage fluid, ascites, urine, or cerebrospinal fluid. The real challenge is to identify and screen patients at risk for disseminated strongyloidiasis prior to initiation of immunosuppressive therapy. S. stercoralis is endemic in tropical and subtropical areas of the world, and patients from an area of endemicity or patients with eosinophilia should have Strongyloides IgG enzyme-linked immunosorbent assay (ELISA) antibody testing before initiation of immunosuppressive therapy or solid-organ or hematopoietic transplantation (3). Alternatively, stool screening (at least 3 stool ova and parasite examinations) should be performed when serological testing is unavailable or results are negative for a patient with significant gastrointestinal symptoms, human T-cell leukemia virus type 1 (HTLV-1) infection, eosinophilia, and a history of exposure. Treatment with ivermectin should be initiated before immunosuppression if possible. Treatment of the hyperinfection syndrome is with prolonged courses of ivermectin for at least 2 weeks and until documented clearance of larvae from stool culture and/or sputum or BAL specimens (1, 3). The patient was started on ivermectin on hospital day 2, but because of clinical instability and worsening thrombocytopenia, lumbar puncture could not be performed. Despite aggressive treatment, his condition deteriorated and he expired on day 4.

(See page 369 in this issue [doi:10.1128/JCM.01084-13] for photo quiz case presentation.)