A Case of Daptomycin Induced Acute Eosinophilic Pneumonia in a Patient with Septic Arthritis

Introduction-Daptomycin is a unique lipopeptide antibiotic that exerts bactericidal action by cell membrane action potential disruption. It is used in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin resistant gram-positive organisms. However, acute eosinophilic pneumonitis (AEP) remains a rare life-threatening adverse effect of daptomycin therapy. Case-A 65-year-old gentleman with a history of diabetes mellitus presented with palpitations, dyspnea, and lethargy for four days. He did not have any fever but noted occasional nonproductive cough. He was discharged a week prior after a two-week hospitalization where he underwent treatment for MRSA septic knee arthritis, which was complicated by MRSA bacteremia and COVID-19 pneumonia. He was discharged on daptomycin and ceftaroline maintenance therapy. He was afebrile, but had tachycardia, tachypnea, and was hypoxic to 88% on room air. Pulmonary examination revealed bibasal decreased breath sounds. Investigations were notable for leukocytosis with peripheral eosinophilia of 27%. COVID-19 testing was negative twice. His chest-Xray revealed patchy bilateral opacities (Fig-1A), similar to his prior admission (Fig-1B). A computed tomography pulmonary angiogram showed bilateral, multifocal, irregular opacities (Fig-1C). Supplemental oxygen was started and daptomycin was promptly discontinued. Intravenous methylprednisolone was also initiated. Over the next two days, the patient improved significantly, was weaned off supplemental oxygen, and peripheral eosinophilia also improved. He was discharged after four days, on a prednisone taper and only ceftaroline was completed for a total of eight weeks. Discussion-Daptomycin induced AEP may present with dyspnea, fever, peripheral eosinophilia and bilateral multifocal pulmonary infiltrates, commonly within two to four weeks of drug exposure. 25% or more eosinophilia on bronchoalveolar lavage specimen is very specific. This adverse effect of daptomycin appears to be more time-dependent than dose-dependent. Daptomycin is inactivated by pulmonary surfactant, and this altered lipid biochemistry may precipitate T-helper-2 cell-mediated interleukin-5 elaboration. This triggers eosinophil recruitment and their pulmonary migration, resulting in the characteristic pulmonary inflammatory response. However, the exact mechanism remains unclear. We considered other differentials, including fungal or parasitic infections, recent COVID-19 pneumonia, and vasculitides;however, considering our patient's compatible presentation, and with a Naranjo algorithm score of six, daptomycin induced AEP was hypothesized to be the probable etiology. Management involves early recognition and discontinuation of daptomycin, with corticosteroids being used often to augment clinical recovery. The rarity of the presentation necessitates awareness and vigilance, as early discontinuation often results in an excellent prognosis and leads to future avoidance of daptomycin, whereas a missed diagnosis may be life-threatening.