B72-32 Pneumocystis Jirovecii Pneumonia in a Patient Receiving Teclistamab for Multiple Myeloma

Abstract Introduction Multiple myeloma is increasingly treated with targeted immunotherapies, including bispecific T-cell engagers such as Teclistamab, which binds BCMA on plasma cells and CD3 on T cells. While these agents improve survival in relapsed or refractory disease, they can cause T-cell dysfunction and hypogammaglobulinemia, predisposing patients to opportunistic infections. Pneumocystis jirovecii Pneumonia (PJP) is a life-threatening fungal infection classically seen in severely immunocompromised hosts but is now reported in non-HIV patients receiving novel immunotherapies. Case Presentation A 72-year-old female with relapsed IgG-kappa multiple myeloma, atrial fibrillation, hypertension, and thrombocytopenia presented with flu-like symptoms and hypotension. She had recently started Teclistamab, her last dose was two weeks earlier, complicated by cytokine-release syndrome with rash, and received dexamethasone 20 mg with transfusions. Initial chest x-ray showed bronchial wall thickening without consolidation, and she was discharged. She returned the next day with worsening dyspnea, cough, and fever of 100.4 °F. She was tachycardic, hypotensive, and developed acute hypoxic respiratory failure requiring 11 L/min oxygen. Labs showed pancytopenia (WBC 2.4 × 109/L, Hgb 9 g/dL, Plt 110 × 109/L), elevated LDH, and positive β-D-glucan. High-resolution CT (Figure 1) revealed bilateral ground-glass opacities with interlobular septal thickening. Repeat CT showed worsening bilateral ground glass opacities. Empiric antibiotics were stopped after negative cultures, and intravenous trimethoprim-sulfamethoxazole was started for presumed PJP. Her clinical improvement, along with decreased oxygen requirements, further supported the diagnosis. Discussion eclistamab, a BCMA-directed bispecific antibody, has revolutionized the treatment of relapsed or refractory multiple myeloma but carries a substantial infectious risk due to T-cell depletion. In pivotal trials, grade ≥ 3 infections occurred in nearly half of patients, with Pneumocystis jiroveci Pneumonia (PJP) increasingly recognized. Hypogammaglobulinemia, corticosteroid exposure, and treatment-induced lymphopenia further heighten susceptibility.This patient developed presumed PJP shortly after initiating Teclistamab, consistent with early-onset cases reported with BCMA-targeted therapies. Diagnosis in non-HIV immunocompromised hosts remains challenging, as microbiologic confirmation is often limited and imaging findings are nonspecific. Elevated β-D-glucan in conjunction with compatible imaging should prompt empiric therapy, as demonstrated by this patient’s response to trimethoprim-sulfamethoxazole. Although current guidelines do not mandate PJP prophylaxis for patients receiving bispecific antibodies, emerging evidence supports its consideration in high-risk populations. Conclusion This case highlights diagnostic and therapeutic challenges of PJP in patients receiving Teclistamab. Given its nonspecific presentation and limited diagnostic confirmation, clinicians must maintain vigilance and initiate early empiric therapy. As bispecific T-cell engagers become more common, prophylaxis should be considered to mitigate opportunistic infection risk. This abstract is funded by: None