Chagas Disease Infection Reactivation after Heart Transplant

Abstract

<jats:p>Chagas disease, caused by a Trypanosona cruzi infection, is one of the main causes of heart failure in Latin America. It was originally a health problem endemic to South America, predominantly affecting residents of poor rural areas. With globalization and increasing migratory flows from these areas to large cities, the immigration of T. cruzi chronically-infected people to developed, non-endemic countries has occurred. This issue has emerged as an important consideration for heart transplant professionals. Currently, Chagas patients with end-stage heart failure may need a heart transplantation (HTx). This implies that in post-transplant immunosuppression therapy to avoid rejection in the recipient, there is the possibility of T. cruzi infection reactivation, increasing the morbidity and mortality rates. The management of heart transplant recipients due to Chagas disease requires awareness for early recognition and parasitic treatment of T. cruzi infection reactivation. This issue poses challenges for heart transplant professionals, especially regarding the differential diagnosis between rejection and reactivation episodes. The aim of this review is to discuss the complexity of the Chagas disease reactivation phenomenon in patients submitted to HTx for end-stage chagasic cardiomyopathy.</jats:p>

Benznidazole as Prophylaxis for Chagas Disease Infection Reactivation in Heart Transplant Patients: A Case Series in Brazil

“…It is important to highlight that due to immunosuppression, the recipients with CD can develop CDR, and the reactivation rate of CD after HTx for CC is variable, with an incidence of 21–45% [ 5 ]. In the literature, the degree of immunosuppression was often correlated with reactivation [ 6 , 7 ]. At our institution, reactivation occurred in 34.6% of patients with CC.…”

“…Nevertheless, CDR can cause both cardiac and noncardiac (skin lesions) manifestations. The cardiac manifestations of CDR include new conduction blocks that may require pacemaker placement, valvular regurgitation, and most seriously, allograft dysfunction that can progress to cardiogenic shock and death [ 5 , 7 ]. In the setting of CDR after HTx, we found great clinical variability, from patients with no symptoms to patients with heart failure.…”

“…In patients with CC who are treated with corticoids, Rassi [ 9 ] demonstrated that for many reasons, benznidazole used as a primary chemoprophylaxis prevented increased parasitemia (evaluated by xenodiagnoses) and suggested that in immunocompromised patients with chronic CD, the use of this drug could be useful. Importantly, the myocarditis of an acute CDR patient can be easily mistaken for allograft rejection [ 14 ], and treatment with intensified immunosuppression can lead to more severe T. cruzi infection [ 7 ]. Unfortunately, due to a lack of raw materials or difficulty obtaining the medication for prophylactic use, BZ was unavailable for some of the study period, making it impossible to carry out a randomized study in our center.…”

“…Thus, PCR is a precious tool which guides physicians to decide whether patients should begin receiving anti-parasite drugs or changes in the immunosuppression regimen. Today, the concept of reactivation must be redefined even if the patient is asymptomatic and includes an increase in parasitemia, detected either by direct parasitological techniques or by PCR [ 7 ].…”

“…Only two drugs (benznidazole (BZ) and nifurtimox) have been shown to be effective enough to warrant widespread use in acute CD treatment [ 7 ]. Data validating the use of prophylactic therapy with BZ in patients with CD who underwent heart transplantation are lacking in the literature.…”