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In a 2018 review of 196 case reports of drug-induced eosinophilic pneumonia, daptomycin was the leading cause.[2] Daptomycin-associated pulmonary toxicity has predominantly been described in hosts without underlying immunosuppression and is typically associated with eosinophilia.[[3], [5]] Although the use of daptomycin in the neutropenic and HCT patient population is now commonplace,[[6], [8]] there have been no published cases of daptomycin-associated pulmonary toxicity in this population. Additional research to clarify the pathophysiology of daptomycin-associated pulmonary toxicity is needed, as well as additional data on the safety and toxicity profile of daptomycin in HCT recipients. Daptomycin-associated pulmonary toxicity sans eosinophilia in a hematopoietic cell transplant recipient with profound leukopenia Keywords: daptomycin; eosinophilic pneumonia; hematopoietic stem cell transplant recipient; pulmonary toxicity EN daptomycin eosinophilic pneumonia hematopoietic stem cell transplant recipient pulmonary toxicity 1 3 3 06/19/23 20230601 NES 230601 To The Editor, A 44-year-old woman with relapsed high-risk myelodysplastic syndrome following allogeneic hematopoietic cell transplant (HCT) in October 2021, with subsequent transformation to acute myelogenous leukemia was admitted to the hospital for fever, hypotension, and dry cough. [Extracted from the article]

Hepatitis B virus (HBV) can be transmitted from organ donor to recipient, but details of transmission events are not widely published. The Disease Transmission Advisory Committee (DTAC) evaluated 105 cases of potential donor derived transmission events of HBV between 2009‐2017. Proven, probable or possible transmission of HBV occurred in 25 (23.8%) cases. Recipients of liver grafts were most commonly infected (20 of 21 exposed recipients) compared to 9 of 21 exposed non‐hepatic recipients. Eleven of 25 donors were HBV core antibody (HBcAb) positive/HBV surface antigen (HBsAg) negative and infected 8/20 recipients. Of the 10 liver recipients and 1 liver‐kidney recipient who received organs from these donors: six were not given antiviral prophylaxis, two developed infection after antiviral prophylaxis was discontinued, two developed HBV while on lamivudine prophylaxis, one was on antiviral prophylaxis and did not develop HBV viremia or antigenemia. One recipient of a HBcAb positive/HBsAg negative kidney developed active HBV infection. Unexpected donor‐derived transmission of HBV was a rare event in reports to DTAC, but was often detected in the recipient late post‐transplant. Six of 11 recipients (54.5%) of a liver from a HBcAb positive donor did not receive prophylaxis; all of these were potentially preventable with the use of anti‐viral prophylaxis. [ABSTRACT FROM AUTHOR]

Trimethoprim‐sulfamethoxazole (TMP‐SMX) is the first‐line agent for Pneumocystis jiroveci pneumonia (PJP) prophylaxis for solid organ transplant (SOT) recipients because of its efficacy for this indication, extended antimicrobial coverage, and favorable cost. Reported sulfonamide allergy is not uncommon and often results in TMP‐SMX avoidance. Desensitization offers an efficacious and cost‐effective alternative to TMP‐SMX avoidance. Herein, we reviewed our experience with desensitization during the index transplant hospitalization among 52 SOT recipients with history of a non‐anaphylactic sulfonamide allergy. Of those enrolled in the desensitization protocol, 92% (48/52) completed the protocol, with nearly 80% (41/52) still on TMP‐SMX at 3 months without adverse reaction. Eleven patients discontinued TMP‐SMX (7 for allergic reactions and 4 for non‐allergic reasons) and switched to pentamidine. A cost savings of $575 per desensitization was calculated based on annual wholesale drug prices, for a total savings of $23 575. Additionally, the protocol did not delay discharge in any patient nor was it associated with any severe allergic reactions. These findings suggest TMP‐SMX desensitization is safe and effective in SOT recipients with a history of non‐anaphylactic, non‐life‐threatening sulfonamide hypersensitivity. [ABSTRACT FROM AUTHOR]