451: Epidemiology of late bacterial pneumonia in a prospective cohort of lung transplant recipients (LTRs)

451: Epidemiology of late bacterial pneumonia in a prospective cohort of lung transplant recipients (LTRs)

The Journal of Heart and Lung Transplantation Volume 26, Number 2S 451 EPIDEMIOLOGY OF LATE BACTERIAL PNEUMONIA IN A PROSPECTIVE COHORT OF LUNG TRANS...

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The Journal of Heart and Lung Transplantation Volume 26, Number 2S

451 EPIDEMIOLOGY OF LATE BACTERIAL PNEUMONIA IN A PROSPECTIVE COHORT OF LUNG TRANSPLANT RECIPIENTS (LTRS) K. Raza,1 S. Studer,2 D.L. Paterson,1 M. Crespo,2 D.L. Pakstis,1 M.E. Carey,1 A. Zeevi,3 J. Pilewski,2 K.R. McCurry,3 S. Husain,1 1Div of Infect Dis, Univ of Pitt, Pittsburgh, PA; 2Div of Pulm & Crit Care, Univ of Pitt, Pittsburgh, PA; 3Dept of Surgery, Univ of Pitt, Pittsburgh, PA Purpose: LTRs experience a higher risk of graft infection compared to other solid organ transplant recipients. However, the epidemiology and outcome of late onset bacterial pneumonia in this population has not been prospectively studied. Methods and Materials: We collected infection data affecting all LTRs at our institution from 2002 until present (n⫽222). All infectious episodes were prospectively identified using standardized criteria. Late onset pneumonia was defined as pneumonia occurring ⬎30 days after transplant. Results: Of the 222 LTRs enrolled over the study period, 30 episodes of pneumonia were recorded in 28 LTRs yielding an overall pneumonia rate of 12.6% (28/222). Most of these pneumonias [86.6% (26/30)] occurred ⬎180 days after transplantation. 10% (3/30) of episodes occurred between 30-100 days, and 3.3% (1/30) between 100-180 days. Health care associated pneumonia (HCAP) was observed in 73.3% (22/30) of episodes, while 26.6% (8/30) were classified as hospital acquired pneumonia (HAP). 40.9% (9/22) of HCAP and 62.5% (5/8) of HAP involved multi-drug resistant pathogens (MDRs) (p⫽NS). The majority of isolates [76.3% (29/38)] were gram-negative bacteria. More than half of isolates [55.2% (21/38)] were MDRs. Pseudomonas aeruginosa was the most common bacterial pathogen, [60.5% (23/38)]. No difference in the rate of bacterial pneumonia was noted between various underlying diseases in LTRs. However, 91.6% (11/12) isolates from cystic fibrosis patients were MDRs, while none of the isolates (n⫽6) from Alpha-1 Antitrypsin deficiency patients were MDR. 30-day mortality in our cohort was only 3.3% (1/30). Conclusions: The majority of late onset bacterial pneumonias in this cohort of LTRs were HCAPs, which occurred more than 6 months following lung transplantation. Pathogens were most frequently gramnegative and more than half of all microbial isolates were MDRs. Pre-transplant pulmonary diagnosis did not affect pneumonia frequency but impacted risk for MDR pathogen infection. The 30-day mortality from late pneumonia in this cohort was low (3.3%). 452 EFFECTIVENESS AND SAFETY OF EPSTEIN-BARR VIRUS DNALOAD GUIDED REDUCTION OF IMMUNOSUPPRESSION LATE AFTER LUNG TRANSPLANTATION N.A. Bakker,1 E.A.M. Verschuuren,2 M.E. Erasmus,3 B.G. Hepkema,4 N.J.G.M. Veeger,5 C.G.M. Kallenberg,6 W. van der Bij,2 1Hematology, University Medical Center, Groningen, Netherlands; 2Pulmonary Diseases, University Medical Center, Groningen, Netherlands; 3 Cardiothoracic Surgery, University Medical Center, Groningen, Netherlands; 4Pathology and Laboratory Medicine, University Medical Center, Groningen, Netherlands; 5Clinical Epidemiology, University Medical Center, Groningen, Netherlands; 6Clinical Immunology, University Medical Center, Groningen, Netherlands Purpose: Posttransplant lymphoproliferative disease (PTLD) is a serious complication after lung transplantation and its relation with EpsteinBarr virus (EBV) is well recognized. In June 2001 pre-emptive reduction of immunosuppression guided by EBV-DNA load was routinely intro-

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duced in our lung transplant program. In this report, we describe the effectiveness of this approach in terms of PTLD prevention and safety with regard to acute as well as chronic allograft rejection in 75 lung transplant recipients transplanted between 1990 and June 2001. Methods and Materials: From all patients visiting our outpatient clinic, EBV-DNA load was measured at least twice a year from June 1, 2001 onwards. In patients with positive results, measurements were repeated every 2 to 4 weeks. EBV reactivation was defined as two consecutive EBV-DNA load measurements with a rising trend; with the last measurement exceeding 10.000 copies/ml under stable immunosuppression. In such case, immunosuppression was stepwise reduced. Results: EBV reactivation was observed in 26/75 patients (35%). Immunosuppression was reduced in 19 patients. One (1.5%) of the 75 patients developed PTLD. No acute rejection was observed after reduction of immunosuppression. EBV-reactivation and subsequent reduction of immunosuppression was not associated with a worse survival or acceleration of BOS progression. Conclusions: These findings demonstrate that EBV reactivation after lung transplantation is a frequent event, also late after transplantation. Reduction of immunosuppression in patients with an EBV reactivation might prevent PTLD development. This approach was safe with respect to acute as well as progression of chronic allograft rejection and survival.

453 USEFULNESS OF POLYMERASE CHAIN REACTION STRATEGIES FOR EARLY DIAGNOSIS OF CHAGAS DISEASE REACTIVATION AND TREATMENT FOLLOW-UP IN HEART TRANSPLANTATION M. Diez,1 L. Favaloro,1 J.M. Burgos,2 M. Peradejordi Lastras,1 A. Bertolotti,1 C. Vigliano,1 A.G. Schijman,1 R.R. Favaloro,1 1 Intrathoracic Transplant Unit, Fundacion Favaloro, Buenos Aires, Argentina; 2Laboratorio de Biologia Molecular de la Enfermedad de Chagas, INGEBI-CONICET, Buenos Aires, Argentina Purpose: Reactivation (R) of Chagas disease is one of the main complications in chagasic patients after heart transplant (HTx).The sensitivity of parasitological methods is low; therefore more sensitive methods are needed. We evaluated the usefulness of two different PCR methods for early diagnosis of R and follow-up of treatment response. Methods and Materials: Thirteen out of 234 patients (pts) undergoing HTx had Chagasic cardiomyopathy. Parasitemia was determined using the Strout method. To detect T.cruzi DNA, two PCR strategies were carried out: 1) the amplification of the highly repetitive 330bp minicircle variable region of the kinetoplastid genome (kDNA) with an analytical sensitivity of 5 fgr of total T cruzi DNA (1 parasite cell in 10 ml of blood) and 2) the amplification of the intergenic spacer of the spliced leader genes (SL-DNA) which presented an analytical sensitivity of around 1pg of total T.cruzi DNA (200 parasite cells/10mL blood). Results: Five pts showed 6 R episodes during follow-up (mean 689 ⫾673 days(d)). The mean time to clinical R was 71d (range 38-92); Out of 6 R episodes, only 4 showed positive Strout. Nine pts had positive kDNA and 6 became SL-DNA positive later. Five of them developed clinical R. kDNA-PCR was positive 59 d before clinical reactivation, whereas SL-DNA was positive 7 to 23 d later than k DNA-PCR , revealing the enhancement of parasitic load after HTx. Only one PCR positive pt who did not reactivate showed a slower increase of his parasitic load. This pt. turned negative after switching MMF to AZA. All R were successfully treated with benznidazole; treatment outcome was accompanied by PCR negative findings.The decrease of parasite DNA was detected earlier by means of SL-DNA PCR and later using the more sensitive kDNA PCR test.