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Kissing Bugs
Published in Jerome Goddard, Public Health Entomology, 2022
Kissing bugs feed on a wide variety of small-to medium-sized mammals. One study showed that perhaps they feed on humans more than we know in areas not typically known for their presence.4 Other than nuisance biting and occasional reports of allergic reactions to their bites, kissing bugs are famous for their vectorial capacity for the agent of Chagas disease, Trypanosoma cruzi.1 Chagas disease is a zoonosis (originally a parasite of wild animals) mostly occurring in Mexico and Central and South America, but a few indigenous cases have been reported in Texas, Tennessee, Louisiana, and California.5–7 Further, there is serological evidence of T. cruzi in dogs, raccoons, opossums, and woodrats as far north as Oklahoma, Virginia, and Maryland.8,9 Some 8 million people are estimated to be infected with Chagas, with tens of millions of people at risk.10 Chagas disease has both acute and chronic forms, but is perhaps most well known for chronic sequelae (occurring years to decades later), such as myocardial damage with cardiac dilation, arrhythmias and major conduction abnormalities, and digestive tract involvement such as megaesophagus and megacolon.
Evidence for a Role of Infections in the Activation of Autoreactive T Cells and the Pathogenesis of Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
J. Ludovic Croxford, Stephen D. Miller
The A/J strain of mouse is susceptible to T. cruzi infection-induced myocarditis, and interestingly to both the CVB3 and MCMV-induced models of myocarditis. In addition, the C57B1/6 strain is resistant to all three pathogen-induced heart diseases. This suggests a common mechanism may be involved in all three models. Two main hypotheses have been used to explain the pathology observed in Chagas disease. The parasite persistence model suggests that disease severity, progression and perpetuation directly correlates to the presence of parasite DNA in muscle tissue.109 The immunosuppression of mice infected with T. cruzi leads to exacerbation of disease severity and infection,110,111 whereas alternatively, enhancing the anti-parasite response leads to a decreased severity of disease.112 This evidence supports the parasite presence hypothesis.
Chemical Hybridization Approaches Applied to Natural and Synthetic Compounds for the Discovery of Drugs Active Against Neglected Tropical Diseases
Published in Venkatesan Jayaprakash, Daniele Castagnolo, Yusuf Özkay, Medicinal Chemistry of Neglected and Tropical Diseases, 2019
Elena Petricci, Paolo Governa, Fabrizio Manetti
Chagas disease is a zoonotic disease caused by the protozoan parasite Trypanosoma cruzi that can be transmitted to humans by blood-sucking triatomine bugs (also known as the “kissing” bug) belonging to the genera Triatoma, Rhodnius, and Panstrongylus (Centers for Disease Control and Prevention 2018a). The parasite life cycle is divided in human (host) stages and triatomine bug stages. Chagas disease is currently treated with nifurtimox 1 and benznidazole 2 (Figure 1). Structure of active ingredients (nifurtimox and benznidazole) of drugs for Chagas disease.
Promiscuity in drug discovery on the verge of the structural revolution: recent advances and future chances
Published in Expert Opinion on Drug Discovery, 2023
Sarah Naomi Bolz, Michael Schroeder
Chagas disease is a potentially life-threatening infection caused by the protozoan parasite Trypanosoma cruzi that affects about 6–7 million people globally. It is recognized as a neglected tropical disease that primarily affects poor and marginalized populations in Latin America, leading to serious health consequences and socioeconomic burdens [96,97]. There are currently limited treatment options for Chagas disease, which have severe side effects and are only partially effective [98]. To identify novel medications, Adasme et al. performed a structure-based drug repositioning screening using interaction fingerprints [99]. They extracted the non-covalent protein–ligand interaction patterns from the available complex structures of 16 Chagas targets and screened the PDB to identify complexes with a similar binding mode. The screening yielded 38 top-hit compounds that showed high chemical diversity. Three of these repositioning candidates – ciprofloxacin, naproxen, and folic acid – displayed activity against the parasite when tested in vivo [99].
Thio- and selenosemicarbazones as antiprotozoal agents against Trypanosoma cruzi and Trichomonas vaginalis
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Alexandra Ibáñez-Escribano, Cristina Fonseca-Berzal, Mónica Martínez-Montiel, Manuel Álvarez-Márquez, María Gómez-Núñez, Manuel Lacueva-Arnedo, Teresa Espinosa-Buitrago, Tania Martín-Pérez, José Antonio Escario, Penélope Merino-Montiel, Sara Montiel-Smith, Alicia Gómez-Barrio, Óscar López, José G. Fernández-Bolaños
Herein, we have focussed our attention on Chagas disease and trichomoniasis. On the one hand, Chagas disease (aka American trypanosomiasis), discovered by the Brazilian physician Carlos R.J. das Chagas in 1909, is endemic in Latin America, where it affects roughly 7 million people12; nevertheless, it is also being spread to USA, Canada, Europe and Australia, because of human migrations13, and therefore, becoming a global health problem14. Chagas disease is caused by the haemoflagellate protozoan Trypanosoma cruzi, whose transmission to humans naturally takes place by contact with faeces or urine of infected triatomine insects. The infection can also be transmitted by non-vectorial routes, such as the iatrogenic and the congenital one12. The life-cycle of the parasite involves three stages: epimastigotes (extracellular and replicative form found in the intestine of the vector), amastigotes (intracellular and proliferative form of the vertebrate host) and trypomastigotes (extracellular and non-replicative state found in the bloodstream)15,16. Currently, there are only two available drugs for the specific treatment of Chagas disease: benznidazole (BZ), a nitroimidazole, and nifurtimox, a nitrofurane both showing some disadvantages (e.g., low efficacy in the chronic phase, adverse effects and parasite drug resistance) that constitute one of the main drawbacks of this parasitosis17.
Signal peptide peptidase: a potential therapeutic target for parasitic and viral infections
Published in Expert Opinion on Therapeutic Targets, 2022
Christopher Schwake, Michael Hyon, Athar H. Chishti
Trypanosoma cruzi is the etiologic agent of Chagas’ disease and Trypanosoma brucei rhodesiense and gambiense are the etiologic agents of African sleeping sickness (Human African Trypanosomiasis, HAT). Both diseases present high mortality throughout their geographic regions. Chagas’ disease is transmitted by a triatomine vector, known by those in endemic regions as the kissing bug. Worldwide, Chagas’ affects 6 million people mainly in Latin-American countries as well as 300,000 people living in the US [44]. Triatomine bugs have established populations in the Southern United States, some of which are infected with T. cruzi [45]. The extent to which endemic transmission occurs in the US is unknown due to the low incidence of testing and diagnostic assays, but there has been reports of locally acquired Chagas’ disease in the past [46,47]. Disease can progress to a chronic infection resulting in serious heart inflammation and intestinal problems in those afflicted [48]. Chagas’ disease has very few treatment options with only two currently available drugs, benznidazole and nifurtimox. However, both compounds exhibit low efficacy toward the chronic form of the disease and deleterious side effects over a long treatment period can lead to noncompliance [48].