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Trypanosoma cruzi
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Paula Andrea Jiménez, Jesus Eduardo Jaimes, Juan David Ramírez
The etiologic treatment is performed with benzonidazole or nifurtimox, except if it is a pregnant patient, with renal or hepatic failure. There are no benefits in patients with Chagas cardiomyopathy with severe cardiac failure or in those with megacolon with great affectation to ingest food. Additionally, in the latter, there is no evidence that drug administration prevents or improves the progression of gastrointestinal disease [71]. In contrast, in patients in the acute phase and patients in the early indeterminate phase (children under 18 years), it has been observed that the drugs are highly effective, eliminating the parasite and producing serological negativization [46,71–73]. In the chronic phase, little is known about the efficacy of these drugs, since the only criterion of cure is the serological negativization, which occurs many years after the treatment in these patients. For this reason, the PCR technique has recently been used to perform posttreatment follow-up, showing that benzonidazole treatment in chronic phase produces a decrease in PCR positivity between 66.3% and 95.0% [74].
Benznidazole
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Ralph K. Junckerstorff, Ronan J. Murray
An eagerly anticipated multicenter randomized controlled trial studying the utility of benznidazole in chronic Chagas cardiomyopathy has recently been published. 2854 patients from a number of South American countries (Argentina, Bolivia, Brazil, Colombia, and El Salvador) with Chagas cardiomyopathy were randomized to receive either benznidazole or placebo for a period of 40–80 days. Although initially dosed at 5 mg/kg/day, due to issues with drug production and availability, benznidazole dosing was modified in 2009 to a fixed dose of 300 mg per day. Of the 1896 patients tested at baseline, 60.5% had T. cruzi kinetoplast DNA detected in their blood via PCR. Patients treated with benznidazole demonstrated significantly increased rates of conversion from positive to negative T. cruzi PCR but unfortunately this did not significantly reduce cardiac sequelae during the minimum 5-year follow-up period (Morillo et al., 2015).
The management of Babesia, amoeba and other zoonotic diseases provoked by protozoa
Published in Expert Opinion on Therapeutic Patents, 2023
Clemente Capasso, Claudiu T. Supuran
The parasite Trypanosoma cruzi causes Chagas’ disease (CD), also known as American trypanosomiasis, which is spread via the bites of hematophagous triatomine insects, such as the vectors belonging to the genera Triatoma, Rhodnius, and Panstrongylus [5,82–84]. Although the disease is widespread in Latin America, it has spread to other parts of the world through a variety of channels, including migration, transfusions, organ transplants, congenital infection, and food-borne transmission, making it a problem even in non-endemic areas like North America, Europe, Japan, and Australia [5,85,86]. No vaccine or medication protects against CD [84]. Thus, vector control, blood and organ screening, and food safety are crucial in CD prevention [87,88]. Blood donor surveillance and CD screening questions have likely reduced acute transfusion-associated cases, as well as prenatal diagnosis and treatment prevent congenital transmission in women [84,87]. Challenges remain in more endemic locations and with widespread wild infection, such as Gran Chaco and the Amazon Basin, despite progress made in managing domestic vector infestation since 1991 [89]. Although the prevention campaign, CD remains a global public health issue due to the illness’s asymptomatic nature, widespread immigration, and many vectors and reservoirs [84]. Moreover, the disease manifests in chronic Chagas cardiomyopathy (CCC), which can develop years or decades after the initial infection [90].
Why hasn’t there been more progress in new Chagas disease drug discovery?
Published in Expert Opinion on Drug Discovery, 2020
Alane Beatriz Vermelho, Giseli Capaci Rodrigues, Claudiu T. Supuran
Morillo et al. [34] designed the Benznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial to evaluate the efficacy and safety of benznidazole. The project was done as a multicenter, randomized study with 2,854 Chagas patients with cardiomyopathy who received benznidazole or placebo for up to 80 days and were followed up for a mean of 5.4 years. The study concluded that BZN reduced serum parasite detection significantly but did not reduce cardiac clinical deterioration significantly through the 5-year follow-up. The BENEFIT trial also found that 17%–18% of both BZN treated and placebo patients died over this five-year period; most of them from cardiac complications. Although these results are not positive for patients with established Chagas’ cardiomyopathy, they brought further confirmation of the need to discover new drugs or drug combinations for a complete CD treatment [35,36].
An evaluation of benznidazole as a Chagas disease therapeutic
Published in Expert Opinion on Pharmacotherapy, 2019
Ivo S. Caldas, Elda G. Santos, Rômulo D. Novaes
Chronic Chagas cardiomyopathy (CCC) is the most severe and incapacitating manifestation of Chagas disease that occurs years or decades after acute infection [5,10]. CCC develops as a dilated cardiomyopathy in response to extensive heart microstructural remodeling associated with cardiomyocyte parasitism, autonomic denervation, persistent low-grade inflammation, redox imbalance and oxidative stress, thromboembolic events, necrotizing arteriolitis, cardiomyocytolysis, myonecrosis, and progressive myocardial fibrosis [10,13]. As a functional consequence, Chagasic patients develop potentially fatal electromechanical cardiac abnormalities, mainly characterized by conduction defects, frequent and complex ventricular arrhythmias and systolic ventricular dysfunction [1,10]. In Latin America, T. cruzi infection is the leading cause of non-ischemic cardiomyopathy and the third cause of indication for heart transplantation [5,14]. CCC is also associated with a worst prognosis and risk of death 2.48 times higher than noninfectious cardiomyopathies [5,15].