scholarly journals ECIL guidelines for preventing Pneumocystis jirovecii pneumonia in patients with haematological malignancies and stem cell transplant recipients

2016 ◽  
Vol 71 (9) ◽  
pp. 2397-2404 ◽  
Author(s):  
Johan Maertens ◽  
Simone Cesaro ◽  
Georg Maschmeyer ◽  
Hermann Einsele ◽  
J. Peter Donnelly ◽  
...  
Keyword(s):  
Stem Cell Transplant ◽  
Primary Prophylaxis ◽  
Pneumocystis Jirovecii ◽  
Pneumocystis Jirovecii Pneumonia ◽  
Evidence Based ◽  
Cell Transplant ◽  
Transplant Recipients ◽  
Allogeneic Hsct ◽  
Drug Of Choice ◽  
Immune Deficiencies

AbstractThe 5th European Conference on Infections in Leukaemia (ECIL-5) meeting aimed to establish evidence-based recommendations for the prophylaxis of Pneumocystis jirovecii pneumonia (PCP) in non-HIV-infected patients with an underlying haematological condition, including allogeneic HSCT recipients. Recommendations were based on the grading system of the IDSA. Trimethoprim/sulfamethoxazole given 2–3 times weekly is the drug of choice for the primary prophylaxis of PCP in adults (A-II) and children (A-I) and should be given during the entire period at risk. Recent data indicate that children may benefit equally from a once-weekly regimen (B-II). All other drugs, including pentamidine, atovaquone and dapsone, are considered second-line alternatives when trimethoprim/sulfamethoxazole is poorly tolerated or contraindicated. The main indications of PCP prophylaxis are ALL, allogeneic HSCT, treatment with alemtuzumab, fludarabine/cyclophosphamide/rituximab combinations, >4 weeks of treatment with corticosteroids and well-defined primary immune deficiencies in children. Additional indications are proposed depending on the treatment regimen.

scholarly journals Pneumocystis jirovecii pneumonia: still a concern in patients with haematological malignancies and stem cell transplant recipients

2016 ◽  
Vol 71 (9) ◽  
pp. 2379-2385 ◽  
Author(s):  
Catherine Cordonnier ◽  
Simone Cesaro ◽  
Georg Maschmeyer ◽  
Hermann Einsele ◽  
J. Peter Donnelly ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplant ◽  
Laboratory Diagnosis ◽  
Pneumocystis Jirovecii ◽  
Pneumocystis Jirovecii Pneumonia ◽  
Cell Transplant ◽  
Haematological Malignancies ◽  
Transplant Recipients ◽  
Allogeneic Hsct ◽  
Prevention And Treatment

The risk of patients with ALL and recipients of an allogeneic HSCT developing Pneumocystis jirovecii pneumonia is sufficiently high to warrant guidelines for the laboratory diagnosis, prevention and treatment of the disease. In this issue, the European Conference on Infections in Leukemia (ECIL) presents its recommendations in three companion papers.

scholarly journals 2695. Pneumocystis jirovecii Pneumonia in the Era of Effective Prophylaxis Following Hematopoietic Stem Cell Transplant

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S947-S948
Author(s):  
Alexander Christian Drelick ◽  
Priya Kodiyanplakkal ◽  
Markus Plate ◽  
Michael J Satlin ◽  
Rosemary Soave ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Clinical Symptoms ◽  
Quantitative Polymerase Chain Reaction ◽  
Case Series ◽  
Pneumocystis Jirovecii ◽  
Pneumocystis Jirovecii Pneumonia ◽  
Cell Transplant ◽  
Hematopoietic Stem ◽  
Allogeneic Hsct

Abstract Background Pneumocystis jirovecii pneumonia is an uncommon and life-threatening disease that can occur following hematopoietic stem cell transplantation (HSCT). Trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis greatly reduces the incidence of PJP. We aim to determine what factors contribute to the development of PJP following HSCT where TMP-SMX prophylaxis is widely used. Methods We performed a single-center, retrospective case series of HSCT recipients from January 1, 2012 to December 31, 2018. Subjects had clinical symptoms and radiographic evidence for PJP along with at least one positive Pneumocystis test obtained from bronchoalveolar lavage (BAL) including direct fluorescence antibody (DFA), quantitative polymerase chain reaction (qPCR), cytology, and pathology. Results 1111 subjects underwent HSCT; of whom, 25 (2.2%) met inclusion criteria and were treated for PJP. 6 were autologous and 19 were allogeneic HSCT recipients (1.23% and 3.05% of total autologous and allogeneic HSCT, respectively). All allogeneic HSCT recipients received in-vivo T-cell depletion. Median duration from autologous and allogeneic HSCT to PJP diagnosis were 138 days (range 20 to 348) and 346 days (range 41 to 771), respectively. PJP qPCR was positive in all samples tested (n = 20, range < 84 to 14900). DFA was positive in 6 (28%). Death from pneumonia occurred in 2 subjects; 11 (44%) required ICU stay, and 7 (27%) required intubation. At diagnosis, 3 subjects had relapse of underlying disease and 10 were on immunosuppression. 12 were on PJP prophylaxis (autologous HSCT n = 3), the most common of which was atovaquone (n = 5); only 2 subjects were on TMP-SMX. Cytomegalovirus (CMV) viremia was detected in 9 subjects (36%) prior to PJP diagnosis; 4 had pulmonary CMV coinfection. In total, 17 subjects (68%) had one of the above risk factors for PJP. Median total lymphocyte count and % lymphocytes were 5.1 × 103 cells/μL (range 1.4 to 38.5 × 103 cells/μL) and 9.6% (range 1.1 to 29.5%), respectively. Conclusion PJP is an uncommon (2.2% of the study population) complication of HSCT while receiving PJP prophylaxis and in the absence of disease relapse, CMV reactivation, or ongoing immunosuppression. Presentation is often delayed in this population; a high degree of clinical suspicion should prompt diagnostic evaluation using a combination of laboratory tests on BAL fluid. Disclosures All authors: No reported disclosures.

Evaluation of Human Polyomavirus (BKV)–Specific T Cell Immune Reconstitution in Allogeneic Haematopoietic Stem Cell Transplant Recipients,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3223-3223
Author(s):  
Francesca Lorraine Wei Inng Lim ◽  
Ai Ling Teo ◽  
Yvonne SM Loh ◽  
William YK Hwang ◽  
Yeow-Tee Goh ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Reconstitution ◽  
Stem Cell Transplant ◽  
Haematopoietic Stem Cell ◽  
Human Polyomavirus ◽  
Cell Transplant ◽  
Transplant Recipients ◽  
Urothelial Cells ◽  
Blood Samples ◽  
Allogeneic Hsct

Abstract Abstract 3223 Abstract The human polyomavirus type 1, better known as “BK virus” (BKV), persists in a latent state in more than 90% of the world's population. It is infamous as a pathogen in kidney transplant recipients by causing BKV-associated nephropathy (BKVN) often resulting in allograft dysfunction and loss. BKV has also been associated with hemorrhagic cystitis (HC) in haematopoietic stem cell transplant (HSCT) recipients. However, treatment for this condition remains challenging, as the mechanism through which BKV reactivation causes HC in HSCT recipients is not known. In addition, there is currently little data about the reconstitution of BKV-specific immunity after HSCT and its relationship to HC. It is still unclear whether the BKV-specific T cell response helps to prevent and bring about the resolution of HC, or if HC is an immunopathology and the BKV specific immunity damages the bladder mucosa in the process of attacking BKV-infected urothelial cells. We hypothesized that BKV-associated HC is initiated by an imbalance between immune surveillance and BKV reactivation, followed by eventual rebound of BKV- specific T immunity causing an immunopathological reaction towards BKV-infected urothelial cells that ultimately lead to cystitis after HSCT. We aim to correlate BKV titre levels in the urine and blood with BKV- specific T cells. This is a novel prospective study that describes the immune reconstitution of BKV specific T cells immunity after allogeneic HSCT and uses the clinical manifestation of HC as a maker to analyze reconstitution of the immune system post HSCT. This study was approved by the institutional review board. Ten patients undergoing allogeneic HSCT were recruited over a 1 year period. The clinical data collected included conditioning regime, indication for transplant, presence of GVHD and development of HC. Patient's blood samples were collected prior to conditioning and at 4 weekly intervals for 24 weeks. Peripheral blood mononuclear cells (PBMCs) isolated from these whole blood samples were then stimulated with overlapping peptide mixes of BK LT and VP1. Quantification of BKV-specific T cells were accomplished by flow cytometry. Results revealed higher levels of CD3+IL-17+BKV specific T cells (p<0.05) in subjects who developed HC compared to those who did not. Peak levels of CD3+IL-17+BKV specific T cells were observed just before or just after the presentation of HC. Both CD4+IL-17+ (p<0.01) and CD8+IL-17+ (p=0.05) BKV specific T cells were significantly higher in patients who developed HC compared to those who did not. This increment of IL-17+ BKV-specific T immune cells coincided with high levels of BKV detected in the urine. These preliminary results strongly suggest that BKV-associated HC is an immunopathology caused by IL-17 secreting BKV-specific T cells. Though our cohort of patients is small however in view of the promising results; we plan to extend the study to a larger cohort of patient. The demonstration of an immunological basis of HC will provide a theoretical framework for the development of potential immunotherapeutic interventions in the prevention and treatment of HC. Disclosures: No relevant conflicts of interest to declare.

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