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Review
. 2013 Jan;18(1):22-38.
doi: 10.1111/j.1440-1843.2012.02196.x.

Lung transplant infection

Affiliations
Review

Lung transplant infection

Sergio R Burguete et al. Respirology. 2013 Jan.

Abstract

Lung transplantation has become an accepted therapeutic procedure for the treatment of end-stage pulmonary parenchymal and vascular disease. Despite improved survival rates over the decades, lung transplant recipients have lower survival rates than other solid organ transplant recipients. The morbidity and mortality following lung transplantation is largely due to infection- and rejection-related complications. This article will review the common infections that develop in the lung transplant recipient, including the general risk factors for infection in this population, and the most frequent bacterial, viral, fungal and other less frequent opportunistic infections. The epidemiology, diagnosis, prophylaxis, treatment and outcomes for the different microbial pathogens will be reviewed. The effects of infection on lung transplant rejection will also be discussed.

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Figures

Figure 1
Figure 1
Infectious and non‐infectious complications after lung transplantation and the typical time frame in which they occur. Modified with permission from Levine. 4 BOS, bronchiolitis obliterans syndrome; CAP, community‐acquired pneumonia; CARV, community‐acquired respiratory virus; CMV, cytomegalovirus; EBV, Epstein–Barr virus; HCAP, health care‐associated pneumonia; PJP, Pneumocystis jiroveci pneumonia; PNA, pneumonia; PTLD, post‐transplant lymphoproliferative disorder.
Figure 2
Figure 2
A schematic overview of the mechanisms of action of medications used for immunosuppression. IL‐2 is required for the activation of the mTOR pathway and progression of the T cell cycle. Both CsA and tacrolimus reduce the activation of NFAT, which in turn results in a decreased production of IL‐2. Basiliximab is a monoclonal antibody that inhibits the IL‐2 receptor. Sirolimus and everolimus inhibit the mTOR pathway through inhibition of specific enzymes. Alemtuzumab targets protein CD52 causing T cell dysfunction. Both MMF and AZA disrupt key elements of the deoxyribonucleic acid synthesis affecting the progression of the T cell cycle. AZA, azathioprine; Csa, cyclosporine A; FKBP12, FK‐binding protein 12; IMPDH,inosine‐50‐monophosphate dehydrogenase; IL‐2, interleukin‐2; IL‐2R, IL‐2 receptor; MMF, mycophenolate mofetil; mTOR, mammalian target of rapamycin; NFAT, nuclear factor of activated T‐lymphocytes.

References

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