Tuberculosis is a serious opportunistic infection that may affect transplant recipients. The incidence of tuberculosis among such persons is 20-74 times higher than that for the general population, with a mortality rate of up to 30%. The most common form of acquisition of tuberculosis after transplantation is the reactivation of latent tuberculosis in patients with previous exposure. Clinical presentation is frequently atypical and diverse, with unsuspected and elusive sites of affection. Manifestations include fever of unknown origin and allograft dysfunction. Coinfection with other pathogens is not uncommon. New techniques, such as PCR and quantification of interferon-g, have been developed to achieve more-rapid and -accurate diagnoses. Treatment requires control of interactions between antituberculous drugs and immunosuppressive therapy. Prophylaxis against latent tuberculosis is the main approach to treatment, but many issues remain unsolved, because of the difficulty in identifying patients at risk (such as those with nonreactive purified protein derivative test results) and the toxicity of therapy.Tuberculosis tends to behave as an opportunistic infection in patients with solid organ transplants (SOTs). The incidence of infection among such patients is estimated to be 20-74 times that for the general population [1][2][3]. Because of the atypical clinical presentation in transplant recipients, diagnosis is frequently challenging. Furthermore, treatment presents special problems because interactions between immunosuppressive drugs and antituberculous therapy are very important and may lead to graft rejection.Tuberculosis may directly contribute to graft dysfunction, and it is associated with a high mortality rate. Prophylaxis remains the best therapeutic approach, but it is still hindered by the difficulty of identifying proper candidates for treatment and by the potential toxicity of isoniazid, particularly in liver transplant recipients.Our objective was to review the available information about tuberculosis in SOT recipients. With the exception of 2 large series [1,4], this data is scattered among reports of individual cases from many different sources.

The study was designed to identify a subset of heart transplant (HT) recipients who could benefit from the administration of targeted antifungal prophylaxis and to evaluate the efficacy of oral itraconazole as the preventive drug. We have analyzed the risk factors for invasive aspergillosis (IA) in our entire population of HT recipients (1988)(1989)(1990)(1991)(1992)(1993)(1994)(1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002) and also the role of oral itraconazole prophylaxis that was provided to all patients since 1995 [400 mg q.d. of itraconazole oral (PO) for 3-6 months]. There were 24 cases of IA. Our main results indicate that the independent risk factors for IA after heart transplantation are: re-operation (RR 5.8; 95% CI 1.8-18, p = = 0.002), cytomegalovirus (CMV) disease (RR 5.2; 95% CI 2-13.9, p = = 0.001), post-transplant hemodialysis (RR 4.9; 95% CI 1.2-18, p = = 0.02), and the existence of an episode of IA in the HT program 2 months before or after the transplantation date (RR 4.6; 95% CI 1.5-14.4, p = = 0.007). Itraconazole prophylaxis showed an independent protective value against developing IA (RR 0.2; 95% CI 0.07-0.9, p = = 0.03) and also determined a significantly prolonged 1-year survival (RR 0.5; 95% CI 0.3-0.8, p = = 0.01). We believe that antifungal prophylaxis in heart transplant patients should be offered at least to patients with one or more of these predisposing conditions.

BSIs have decreased in HT recipients, but still contribute to mortality, mainly if related to pneumonia or polymicrobial infections. Reduction of early postoperative complications and viral infections are amenable goals that may further reduce BSI in this population.

Data suggest that early immune monitoring including C3, IgG2, and NK cell testing in addition to IgG concentrations is useful when attempting to identify the risk of infection in heart transplant recipients.

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