Abstract Introduction Cytomegalovirus (CMV) infection remains a leading cause of morbidity and mortality in lung transplant recipients, particularly in donor-positive/recipient-negative (D+/R-) mismatches. The interplay between immunosuppression, antiviral resistance, and end-organ dysfunction can lead to multiorgan failure. This case illustrates refractory CMV viremia complicated by pneumonitis, colitis, aseptic meningitis, Bell’s palsy, and ischemic stroke in a D+/R- lung transplant recipient. Case Description A 66-year-old man, 11 months after bilateral lung transplantation for end-stage lung disease, presented with chronic fatigue and headache. He was maintained on valganciclovir prophylaxis but was found to have recurrent CMV viremia. Antiviral therapy was escalated to intravenous ganciclovir, later transitioned to foscarnet and CMV immune globulin (Cytogam) after resistance testing revealed ganciclovir and cidofovir resistance but preserved sensitivity to foscarnet, maribavir, and letermovir. Chest CT showed bilateral lower-lobe predominant nodular ground-glass opacities consistent with CMV pneumonitis (Figure 1A). Despite treatment, he developed worsening abdominal pain, and imaging revealed colonic perforation requiring surgical intervention (Figure 1B). During recovery, he developed new-onset Bell’s palsy and recurrent headaches. Cerebrospinal fluid analysis showed aseptic meningitis, hypothesized to be immune-mediated due to cytogam exposure. Shortly thereafter, he suffered a fatal ischemic stroke. Persistent viremia and widespread CMV-related endothelial injury were considered the unifying etiology. Discussion This case highlights the complex, multisystem consequences of refractory CMV infection in immunosuppressed lung transplant recipients. D+/R- serostatus is a major risk factor for high viral load, resistance development, and severe end-organ involvement. CMV infection can cause vasculitis, thrombosis, and ischemic injury through endothelial inflammation, compounding the effects of immunosuppressive therapy. Therapeutic resistance necessitates early use of alternative antivirals such as foscarnet or maribavir and consideration of CMV-specific immunoglobulin. Continuous viral load monitoring, aggressive multidisciplinary management, and vigilance for neurologic and gastrointestinal complications are essential. This case underscores the importance of individualized antiviral stewardship and close follow-up to mitigate life-threatening CMV sequelae in lung transplant patients. This abstract is funded by: None
Kerns et al. (Fri,) studied this question.