A Review of Critical Periods for Opportunistic Infection in the New Transplantation Era

Abstract

Our data suggest that in some high-risk patients, the critical period of risk for OI must be expanded beyond the first six months after transplant.

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

“…Cumulative incidence curves were constructed for study outcomes (overall and bacterial infection and CMV diseases) with death treated as a competing risk, and differences between groups were compared with the log-rank test. Uni-and multivariate Cox regression models were used to evaluate the association between iATP categories at each point (baseline and months 1 and 6 after transplantation) and outcomes throughout the following periods (early [first month], intermediate [months [1][2][3][4][5][6], and late periods [months [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24], respectively) [1]. Associations were expressed as hazard ratios (HRs) and 95% confidence intervals (CIs).…”

“…A detailed description of the 13 cases of CMV disease diagnosed in the intermediate period in which iATP levels at month 1 were available is provided as Supporting Information (Table S2). Finally, there were no significant differences in the incidence of infection at the end of the late period (i.e., months [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] according to the CMI response at month 6.…”

“…Episodes of asymptomatic bacteriuria and lower urinary tract infection were excluded from the definition of bacterial infection. Opportunistic infection was defined as that due to predominantly intracellular bacteria (i.e., mycobacteria), herpesviruses, yeasts, and molds [3,21]. CMV disease included viral syndrome and end-organ disease [22].…”

The Brain and the Kidney – Organ Cross Talk and Interactions

“…Some of the monoclonal antibody immunosuppressant agents which target lymphocytes, including OKT3, anti-CD25 and CAMPATH-1, by causing cytokine release can also precipitate encephalopathy and/or aseptic meningism. During the first 3 months following transplantation when immunosuppressant doses are at their highest, patients can develop opportunistic infections by reactivating dormant viruses, bacteria, metazoan and protozoan parasites or contracting de-novo infections, such as Listeria monocytogenes and invasive fungal infections [49] . Reactivation of the JC polyoma virus leads to a progressive multi-focal leukoencephalopathy, which can lead to a rapid downhill clinical course with dementia and ataxia, leading to a vegetative state [50] .…”

Low Immunogenic Potential of Human Neural Stem Cells

“…The major roadblock to their procurement from an autologous tissue source can be currently circumvented by their derivation from the fetal human brain, while the requirement for immunosuppression to prevent transplant rejection remains object of conflicting debates. Above all the disavantages of using immunosuppressive treatment during stem cells therapies include an increased risk for opportunistic infections (Garrido et al 2006), toxic side effects (Rezzani 2006) and potential negative effects on donor cells as recently described (Guo et al 2007) for cyclosporin treatment able to reduce cell proliferation and affect differentiation of rat NSCs in vitro. In this manuscript we will discuss about NSC immunogenic potential and the exploitation of -mild-and/or transient immune suppressive protocols after NSC transplantation.…”