Allograft infection after lung transplantation has a significant impact on the outcome and can be a diagnostic challenge. The increased susceptibility of the pulmonary allograft to infection is due to its direct contact with environmental microbes by inhalation, concurrent immunosuppression, and the impaired clearance mechanisms after denervation of the transplanted lung. The possible spectrum of microorganisms infecting the allograft after lung transplantation is broad, but commonly includes Pseudomonas aeruginosa, cytomegalovirus, community-acquired respiratory viruses, and Aspergillus species. Prophylactic antimicrobial treatment regimens after surgery reduced the incidence of infections. However, preventive strategies for reducing infectious complications used by different transplant centers are still heterogeneous, and many questions regarding efficacy remain unanswered.

This case demonstrates a possible direct aetiological link between rifampicin and RS3PE.

Chronic allograft dysfunction in form of bronchiolitis obliterans is the most important hurdle to improved longterm survival after clinical lung transplantation to date. Recently, it was observed that the progression of bronchiolitis obliterans in lung transplant recipients might be inhibited by macrolide antibiotics. The authors therefore tested whether macrolide therapy can attenuate fibrous obliteration of airways in an animal model of bronchiolitis obliterans. Rats with heterotopic tracheal allografts were treated intraperitoneally with clarithromycin and compared to untreated transplanted animals with respect to allograft histology and expression of selected cytokines. At day 21 after transplantation, the tracheal allografts of treated animals were free of fibrous material or partially occluded dependent of clarithromycin dosage. Untreated animals had completely obliterated allografts. In treated animals, tumor necrosis factor alpha (TNF-alpha) was down-regulated early (5 days) and late (21 days) post transplant, whereas interferon gamma (IFN-gamma) expression was decreased only early after transplantation. Transforming growth factor beta (TGF-beta) expression was not affected. Therapy with low-dose macrolides in post-transplant obliterative bronchiolitis is based on their immunomodulatory rather than antimicrobial properties. In the setting of lung transplantation, macrolides primarily act as modulators of the early inflammatory response to stressed, damaged, or infected cells.

Ciprofloxacin attenuates airway rejection after tracheal transplantation. Genetic expression of mediators that are known to play an important role in mediating rejection in this model supports an immunomodulatory and antifibrotic role of ciprofloxacin. These findings suggest that further clinical studies are needed to investigate whether ciprofloxacin in addition to its bactericidal effect might be beneficial in the treatment of human posttransplant bronchiolitis obliterans.