Abstract
Pneumocystis jirovecii pneumonia (PJP), an opportunistic fungal infection, typically occurs in immunocompromised patients, such as those with human immunodeficiency virus (HIV) infection or those receiving prolonged immunosuppressive therapy. Recently, PJP in non-HIV patients treated with novel immunomodulatory agents, including Janus kinase (JAK) inhibitors, has been increasingly reported. Here, we report a case of PJP in a 53-year-old HIV-negative Japanese man with no recognized immunosuppressive comorbidities. The patient, a veterinarian, had been self-administering oclacitinib (16-64 mg/day), a selective JAK1 inhibitor approved for the treatment of atopic dermatitis in dogs, daily for approximately 2 years to manage atopic dermatitis. He presented with progressive exertional dyspnea and fever. Chest computed tomography revealed bilateral ground-glass opacities with patchy consolidations. The diagnosis of PJP was confirmed by polymerase chain reaction of bronchoalveolar lavage fluid and Grocott's methenamine silver staining of transbronchial lung biopsy specimens. He was initially treated with trimethoprim-sulfamethoxazole and corticosteroids; however, the regimen was switched to atovaquone owing to hepatotoxicity. The patient recovered fully and remained recurrence-free at 1-year follow-up. No other causes of immunosuppression were identified, and oclacitinib use was considered the likely precipitating factor. To our knowledge, this is the first reported case of PJP associated with oclacitinib use in humans. As JAK inhibitors are increasingly being used, clinicians should be aware of their potential to cause opportunistic infections, even with veterinary formulations without approved human indications.