A 37-year-old male from Honduras with a history of brainstem glioblastoma treated with radiation, bevacizumab, temozolomide, and dexamethasone presented with sudden onset of dyspnea, pleuritic chest pain, and hoarseness. He also complained of a pruritic abdominal rash and painful swallowing. Physical examination revealed a temperature of 36.9°C; expiratory wheezing; and maculopapular rash on the chest, abdomen, and thighs. Laboratory results, including severe lymphopenia, a mildly elevated lactate dehydrogenase level, and sterile blood cultures, were significant for pancytopenia. Echocardiogram was normal, but computed tomography angiography of the chest showed diffuse ground glass opacities. Empiric antibiotic therapy with piperacillin-tazobactam and azithromycin was initiated. Bronchoalveolar lavage revealed larvae consistent with Strongyloides stercoralis (Figure); the fluid was also positive for rhinovirus by polymerase chain reaction but was negative for Pneumocystis jiroveci antigen. Treatment with ivermectin was initiated.
On hospital day seven, the patient developed acute respiratory failure and septic shock requiring intubation and mechanical ventilation, vasopressors, and a broader spectrum of antibiotics. Repeat chest imaging showed increased diffuse micronodularity; respiratory and blood cultures were positive for Escherichia coli. Antibiotics were de-escalated to ceftriaxone, and the patient completed 12 days of ivermectin therapy prior to discharge.
S stercoralis is a parasitic roundworm endemic to tropical and subtropical regions. Infection occurs when the filariform larva penetrates intact skin. The patient in this case presumably became infected with Strongyloideswhile residing in Honduras and had asymptomatic chronic infection. His acquired immunocompromised state triggered an acceleration of parasitic autoinfection, whereby an increased number of larvae carrying enteric gram-negative bacteria migrate from the gastrointestinal tract to the respiratory tract via the bloodstream. The patient’s symptoms on presentation were due to migrating larvae.
There is an established association between corticosteroids and Strongyloides hyperinfection syndrome. However, other immunosuppressive drugs may potentially also stimulate hyperinfection in patients infected with Strongyloides. Individuals who have traveled or resided in endemic areas should be evaluated for strongyloidiasis prior to the initiation of immunosuppression therapies.
The gold standard for diagnosing strongyloidiasis is the detection of larvae in stool; however, serial stool samples are required for increased diagnostic sensitivity. Serology may not be a viable means of diagnosis in immunosuppressed patients given the inability to mount an immune response. In addition, S stercoralis serology can be falsely positive as a result of cross-reactivity with other active parasitic infections.1
There may be higher diagnostic yield in respiratory specimens given the increased larvae burden that is characteristic of hyperinfection syndrome. S stercoralis has been diagnosed by the identification of larvae in sputum and bronchial brushing.2 Strongyloides hyperinfection can also be readily diagnosed by bronchoalveolar lavage, as demonstrated in this case. Bronchoalveolar lavage is beneficial for easy and early diagnosis when there is clinical suspicion of Strongyloides hyperinfection.
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-Rhonda Dillon, MD, David J. Riedel, MD
This article originally appeared in the October issue of The American Journal of Medicine.
