Abstract Strongyloides stercoralis is a unique nematode capable of persisting for decades via an autoinfective cycle. In immunocompromised hosts, this can escalate into a hyperinfection syndrome, where massive larval replication leads to dissemination beyond the gastrointestinal tract, often with fatal consequences. While corticosteroid use and HTLV-1 infection are well-established risk factors for dissemination, the role of HIV is paradoxical. Despite causing profound cellular immunodeficiency, HIV primarily impairs Th1 immunity, while the Th2 response is critical for controlling helminthic infections and may remain relatively intact. This may explain the surprising rarity of disseminated strongyloidiasis in AIDS patients, making cases like this particularly noteworthy. A 44-year-old man with untreated HIV (CD4 count 43 cells/µL) presented with a 10-day history of nausea, vomiting, hematemesis, melena, abdominal pain, productive cough, and constitutional symptoms. Initially critical with hyponatremia and anemia, his condition deteriorated rapidly. He developed severe acute respiratory distress syndrome from pneumocystis jirovecii pneumonia (PCP), Fig.1, requiring mechanical ventilation. His course was complicated by septic and hemorrhagic shock, necessitating dual vasopressor support, and worsening metabolic acidosis with hyperkalemia, mandating continuous renal replacement therapy (CRRT). The pivotal diagnostic finding came from a small bowel biopsy, which revealed the presence of both strongyloides stercoralis and cytomegalovirus (CMV). This confirmed the diagnosis of disseminated strongyloidiasis, a hyperinfection syndrome likely triggered by the administration of steroids for his PCP pneumonia. This condition also explained his gram-negative bacteremia (Klebsiella pneumoniae) and ongoing gastrointestinal hemorrhage. Concurrently, he was diagnosed with CMV colitis and CMV encephalitis, evidenced by CSF pleocytosis and a positive meningoencephalitis panel. Management involved a multi-pronged approach. Intravenous (IV) bactrim and steroids for PCP, oral ivermectin for strongyloidiasis, and IV ganciclovir and foscarnet for CMV disease. Antiretroviral therapy was deliberately withheld due to the high risk of immune reconstitution inflammatory syndrome (IRIS). Maximal therapeutic efforts failed to reverse his course, which was marked by progressive multiorgan failure and severe encephalopathy. Following family discussions, care was withdrawn to focus on comfort, and the patient died. This tragic outcome highlights the fatal risk of strongyloides hyperinfection triggered by corticosteroids in immunocompromised individuals. While HIV alone is an uncommon trigger for dissemination, the concomitant use of corticosteroids, even for legitimate indications like PCP, can precipitate a fatal hyperinfection cascade. It highlights the critical need to screen and pre-emptively treat for strongyloides in at-risk patients with advanced HIV before initiating immunosuppressive therapy. This abstract is funded by: none
G et al. (Fri,) studied this question.