Infection in Organ Transplantation: Risk Factors and Evolving Patterns of Infection

Fishman, Jay A.; Issa, Nicolas C.

doi:10.1016/j.idc.2010.01.005

Cited by 148 publications

(111 citation statements)

References 68 publications

(48 reference statements)

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“…Preventing acute rejection has been the principal aim in transplantation medicine for several decades, and the success of transplantation was, to a significant extent, related to the development of effective immunosuppressive therapy (1). However, intense immunosuppression inevitably increases susceptibility to infections and malignancies, some of which are infection triggered (2)(3)(4). As a result, the relevance of infection episodes and infection-associated allograft failures progressively increased in the last decades, and balancing the beneficial and deleterious effects of immunosuppressive therapy emerged as a critical aim in the modern transplantation era (5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Risk Stratification for Rejection and Infection after Kidney Transplantation

Cippà¹,

Schiesser²,

Ekberg

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Definition of individual risk profile is the first step to implement strategies to keep the delicate balance between under-and overimmunosuppression after kidney transplantation. Results Despite different temporal dynamics, rejections and severe infections had similar overall incidences in the first year after transplantation (23.4% and 25.5%, respectively), and infections were the principal cause of death (43.2% of all deaths). Recipient older age, deceased donor, higher number of HLA mismatches, and high risk for cytomegalovirus disease were associated with infection; deceased donor, higher number of HLA mismatches, and immunosuppressive therapy including cyclosporin A (compared with tacrolimus), with rejection. These factors were integrated into a two-dimensional risk stratification model, which defined four risk groups: low risk for infection and rejection (30.8%), isolated risk for rejection (36.1%), isolated risk for infection (7.0%), and high risk for infection and rejection (26.1%). In internal validation, this model significantly discriminated the subgroups in terms of composite end point (low risk for infection/rejection, 24.4%; isolated risk for rejection and isolated risk for infection, 31.3%; high risk for infection/rejection, 54.4%; P,0.001), rejection episodes (isolated risk for infection and low risk for infection/rejection, 13.0%; isolated risk for rejection and high risk for infection/ rejection, 24.2%; P=0.001), and infection episodes (low risk for infection/rejection and isolated risk for rejection, 12.0%; isolated risk for infection and high risk for infection/rejection, 37.6%; P,0.001). External validation confirmed the applicability of the model to an independent cohort.Conclusions We propose a two-dimensional risk stratification model able to disentangle the individual risk for rejection and infection in the first year after kidney transplantation. This concept can be applied to implement a personalized immunosuppressive and antimicrobial treatment approach.

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“…After the first month, viral infections predominate. Tardive infections may include: Mycobacterium tuberculosis, Trypanosoma cruzi, Leishmania species, Strongyloides stercoralis, Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides and species of Paracoccidioides 6,7,8,9 . …”

Section: Central Nervous System Infectionsmentioning

confidence: 99%

Neurological complications of solid organ transplantation

Pedroso

Dutra

Braga‐Neto

et al. 2017

Arq. Neuro-Psiquiatr.

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Solid organ transplantation is a significant development in the treatment of chronic kidney, liver, heart and lung diseases. This therapeutic approach has increased patient survival and improved quality of life. New surgical techniques and immunosuppressive drugs have been developed to achieve better outcomes. However, the variety of neurological complications following solid organ transplantation is broad and carries prognostic significance. Patients may have involvement of the central or peripheral nervous system due to multiple causes that can vary depending on time of onset after the surgical procedure, the transplanted organ, and the intensity and type of immunosuppressive therapy. Neurological manifestations following solid organ transplantation pose a diagnostic challenge to medical specialists despite extensive investigation. This review aimed to provide a practical approach to help neurologists and clinicians assess and manage solid organ transplant patients presenting with acute or chronic neurological manifestations.Keywords: organ transplantation; neurological manifestations; central nervous system; peripheral nervous system. RESUMO O transplante de órgãos sólidos é um importante avanço no tratamento de doenças crônicas renal, hepática e cardíaca. Esta terapia tem aumentado a sobrevida e melhorado a qualidade de vida dos pacientes. Novas técnicas cirúrgicas e imunossupressores tem sido desenvolvidos para alcançar melhores desfechos. Entretanto, a variedade de complicações neurológicas que acompanham o transplante de órgãos sólidos é ampla, e carrega significado prognóstico. Pacientes podem ter acometimento do sistema nervoso central ou periférico devido a múltiplas causas que podem variar conforme o tempo após a realização da cirurgia, órgão transplantado e grau e tipo de terapia de imunossupressão. Manifestações neurológicas após o transplante de órgãos sólidos representam um desafio diagnóstico para médicos especialistas apesar de extensa investigação. O objetivo desta revisão é oferecer uma abordagem prática para ajudar neurologistas e clínicos a avaliar e manejar pacientes com transplante de órgãos sólidos que se apresentem com manifestações neurológicas agudas ou crônicas.Palavras-chave: transplante de órgãos; manifestações neurológicas; sistema nervoso central; sistema nervoso periférico.

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“…4 In addition, conditions attendant to end-stage liver disease in the immediate perioperative period may render a recipient vulnerable to infection and include: neutropenia, deficits in mucocutaneous barrier integrity, presence of necrotic tissue, ischemia, diabetes mellitus, immunomodulating viruses, uremia, and protein-calorie malnutrition. 5 Infectious exposures come from many sources post liver transplant including: de novo (acquired acute) in the recipient, reactivation in the recipient, the donor organ, and nosocomial and time from transplant may provide clues to etiology (Figure 1).…”

Section: Nfection After Orthotopic Liver Transplantation (Olt) Ismentioning

confidence: 99%

Infections After Orthotopic Liver Transplantation

Pedersen

Seetharam

2014

Journal of Clinical and Experimental Hepatology

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Opportunistic infections are a leading cause of morbidity and mortality after orthotopic liver transplantation. Systemic immunosuppression renders the liver recipient susceptible to de novo infection with bacteria, viruses and fungi post-transplantation as well to reactivation of pre-existing, latent disease. Pathogens are also transmissible via the donor organ. The time from transplantation and degree of immunosuppression may guide the differential diagnosis of potential infectious agents. However, typical systemic signs and symptoms of infection are often absent or blunted after transplant and a high index of suspicion is needed. Invasive procedures are often required to procure tissue for culture and guide antimicrobial therapy. Antimicrobial prophylaxis reduces the incidence of opportunistic infections and is routinely employed in the care of patients after liver transplant. In this review, we survey common bacterial, fungal, and viral infections after orthotopic liver transplantation and highlight recent developments in their diagnosis and management. ( J CLIN EXP HEPATOL 2014;4:347-360) I nfection after orthotopic liver transplantation (OLT) is a major cause of morbidity and mortality. Infection is estimated to occur in upto 80% of organ recipients. Bacterial infections are most frequent (70%), followed by viral (20%) and fungal infections (8%). 1,2,3 In addition to direct effects of infection and end-organ inflammation, pathogens may have a number of indirect effects that result in allograft injury, rejection and opportunistic superinfection.The risk of infection in liver transplant recipients is determined by the intensity of exposure to infectious agents and the overall level of immunosuppression. 4 In addition, conditions attendant to end-stage liver disease in the immediate perioperative period may render a recipient vulnerable to infection and include: neutropenia, deficits in mucocutaneous barrier integrity, presence of necrotic tissue, ischemia, diabetes mellitus, immunomodulating viruses, uremia, and protein-calorie malnutrition. 5 Infectious exposures come from many sources post liver transplant including: de novo (acquired acute) in the recipient, reactivation in the recipient, the donor organ, and nosocomial and time from transplant may provide clues to etiology (Figure 1). The overall level of immunosuppression is dependent upon the dose, duration, and choice of immunosuppression as well as underlying immune deficiencies. 6 Inflammatory responses to invading pathogens are often blunted by immunosuppressive therapy, and as a result, the classic signs or symptoms of infection may be absent. A high index of suspicion is need in the liver recipient, and a low threshold to perform invasive diagnostic procedures is often required. It is critical to identify clinical factors that predispose recipients to infection and much interest centers on identifying risk factors for infection after liver transplant. GENETIC POLYMORPHISMS IN THE INNATE IMMUNE SYSTEMIn addition to clinical factors that promote ...

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“…Pneumonia that occurs in the late posttransplant period (ie, the sixth month) is usually community acquired. 8,9 In the present study, we aimed to identify pneumonia episodes in renal transplant recipients followed in our center to determine the prevalence, risk factors, cause, and prognosis of pneumonia in this patient population.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Kara

Şen²,

Kurşun³

et al. 2018

Exp Clin Transplant

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Objectives: Pulmonary infections are a significant cause of morbidity and mortality in solid-organ transplant recipients despite enhanced facilities for perioperative care. The aim of this study was to evaluate the demographic characteristics, clinical course, and outcomes of renal transplant recipients with pneumonia. Materials and Methods:The medical records of all renal transplant recipients from January 2010 to December 2014 were retrospectively reviewed, and patients diagnosed with pneumonia according to Centers for Disease Control and Prevention criteria were evaluated. Pneumonia was classified as community acquired or nosocomial. Patient demographics, microbiologic findings, need for intensive care/mechanical ventilation over the course of treatment, and information about clinical follow-up and mortality were all recorded. Results: Eighteen (13.4%) of 134 renal transplant recipients had 25 pneumonia episodes within the study period. More than half (56%) of the pneumonia episodes developed within the first 6 months of transplant, whereas 44% developed after 6 months (all > 1 year). Eight cases (32%) were considered nosocomial pneumonia, and 17 (68%) were considered community-acquired pneumonia. Bacteria were the most common cause of pneumonia (28%), and fungi ranked second (8%). No viral or mycobacterial agents were detected. No patients required prolonged mechanical ventilation. No statistically significant difference was found in the need for intensive care or regarding mortality between patients with nosocomial and community-acquired pneumonia.Two patients (11%) died, and all remaining patients recovered.Conclusions: The present study confirmed that pneumonia after renal transplant is not a rare complication but a significant cause of morbidity. Long-term and close follow-up for pneumonia is necessary after renal transplant. Key words: Complications, Outcome, Renal transplantation IntroductionThe incidence of pulmonary infection after solidorgan transplant (SOT) has decreased with the development of effective prophylactic strategies and improved immunosuppressive treatment regimens. Nevertheless, lower respiratory tract infection remains a life-threatening complication. Approximately two-thirds of pulmonary infiltrations in this group are infectious. 1,2 The incidence of pneumonia in renal transplant recipients reportedly ranges from 8.8% to 20.0%. [3][4][5][6] The mortality rate in this group ranges from 10% to 30% depending on the type of transplant and study duration. 7 Infectious complications vary according to the individual patient's degree of immunosuppression and epidemiologic exposure. Opportunistic infections usually do not occur in the first month after transplant because not all effects of immunosuppression have manifested. Patients waiting for transplant may be colonized with nosocomial microorganisms due to frequent hospital stays, and pulmonary infections in the first month after transplant usually appear as nosocomial pneumonia caused by these microorganisms. Opportunistic pulmon...

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“…Post-transplant infection constitutes a major source of morbidity and mortality after kidney transplantation (KT) [1]. The application of immune monitoring strategies has been proposed as an approach to minimize the risk of such complication by tailoring immunosuppressive therapy to individual needs [2].…”

Section: Introductionmentioning

confidence: 99%

Monitoring of intracellular adenosine triphosphate in CD4⁺T cells to predict the occurrence of cytomegalovirus disease in kidney transplant recipients

et al. 2016

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SUMMARYThe measurement of intracellular concentrations of adenosine triphosphate (iATP) in phytohemagglutinin-stimulated CD4 + T cells constitutes a surrogate marker for post-transplant cell-mediated immunity (CMI). This assay has shown suboptimal accuracy for predicting infection after kidney transplantation (KT). We hypothesize that its predictive capacity depends on the specific contribution of the CMI to host-pathogen interactions. We assessed iATP levels in 100 KT recipients at baseline and months 1, 3, and 6 (363 measurements). No association was found between iATP at month 1 and the risk for overall or bacterial infection, although such association was evident for cytomegalovirus (CMV) disease (multivariate-adjusted hazard ratio [per 50-unit increment]: 0.83; Pvalue = 0.048). There were no significant differences in mean iATP between stable patients (319.4 ng/ml) and those developing overall (304.1 ng/ml) or bacterial infection (346.9 ng/ml) over the 45 days following monitoring. However, iATP was significantly lower in patients who developed CMV disease (223.5 ng/ml; P-values <0.002). The optimal cutoff (265 ng/ml) for predicting CMV disease in patients not receiving antiviral prophylaxis yielded sensitivity, specificity, positive, and negative predictive values of 85.7%, 68.3%, 15.2%, and 98.6%, respectively. In conclusion, a non-pathogen-specific monitoring of CMI by means of iATP informs the risk of CMV disease in KT recipients.

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Infection in Organ Transplantation: Risk Factors and Evolving Patterns of Infection

Cited by 148 publications

References 68 publications

Risk Stratification for Rejection and Infection after Kidney Transplantation

Neurological complications of solid organ transplantation

Infections After Orthotopic Liver Transplantation

Untitled

Monitoring of intracellular adenosine triphosphate in CD4⁺T cells to predict the occurrence of cytomegalovirus disease in kidney transplant recipients

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Infection in Organ Transplantation: Risk Factors and Evolving Patterns of Infection

Cited by 148 publications

References 68 publications

Risk Stratification for Rejection and Infection after Kidney Transplantation

Neurological complications of solid organ transplantation

Infections After Orthotopic Liver Transplantation

Untitled

Monitoring of intracellular adenosine triphosphate in CD4+T cells to predict the occurrence of cytomegalovirus disease in kidney transplant recipients

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Monitoring of intracellular adenosine triphosphate in CD4⁺T cells to predict the occurrence of cytomegalovirus disease in kidney transplant recipients