Rassi A, Rassi A, Marin-Neto JA, 2010. Chagas disease. Lancet 375: 1388–1402.
World Health Organization , 2008. Chagas Disease (American trypanosomiasis) Factsheet. Geneva, Switzerland: WHO.
Coura JR, Dias JCP, 2009. Epidemiology, control and surveillance of Chagas disease: 100 years after its discovery. Mem Inst Oswaldo Cruz 104: 31–40.
Coura JR et al., 2002. Control of Chagas Disease. Geneva, Switzerland: World Health Organization—Technical Report Series, 1–99.
Longo DL, Bern C, 2015. Chagas’ disease. N Engl J Med 373: 456–466.
Bern C, Martin DL, Gilman RH, 2011. Acute and Congenital Chagas Disease, 1st ed., Vol. 75. Advances in Parasitology. Atlanta, GA: Elsevier Ltd., 19–47.
Moscatelli G et al., 2015. Prevention of congenital Chagas through treatment of girls and women of childbearing age. Mem Inst Oswaldo Cruz 110: 507–509.
Kaplinski M et al., 2015. Sustained domestic vector exposure is associated with increased Chagas cardiomyopathy risk but decreased parasitemia and congenital transmission risk among young women in Bolivia. Clin Infect Dis 61: 918–926.
Carlier Y, Sosa-Estani S, Luquetti AO, Buekens P, 2015. Congenital Chagas disease: an update. Mem Inst Oswaldo Cruz 110: 363–368.
Salas NA et al., 2007. Risk factors and consequences of congenital Chagas disease in Yacuiba, south Bolivia. Trop Med Int Health 12: 1498–1505.
Espinoza N, Borrás R, Abad-Franch F, 2014. Chagas disease vector control in a hyperendemic setting: the first 11 years of intervention in Cochabamba, Bolivia. PLoS Negl Trop Dis 8: e2782.
Mora MC et al., 2005. Early diagnosis of congenital Trypanosoma cruzi infection using PCR, hemoculture, and capillary concentration, as compared with delayed serology. J Parasitol 91: 1468–1473.
Bern C et al., 2009. Congenital Trypanosoma cruzi transmission in Santa Cruz, Bolivia. Clin Infect Dis 49: 1667–1674.
Rendell VR et al., 2015. Trypanosoma cruzi-infected pregnant women without vector exposure have higher parasitemia levels: implications for congenital transmission risk. PLoS One 10: e0119527.
Kirchhoff LV, Votava JR, Ochs DE, Moser DR, 1996. Comparison of PCR and microscopic methods for detecting Trypanosoma cruzi. J Clin Microbiol 34: 1171–1175.
Virreira M et al., 2003. Comparison of polymerase chain reaction methods for reliable and easy detection of congenital Trypanosoma cruzi infection. Am J Trop Med Hyg 68: 574–582.
Brasil PEAA, De Castro L, Hasslocher-Moreno AM, Sangenis LHC, Braga JU, 2010. ELISA versus PCR for diagnosis of chronic Chagas disease: systematic review and meta-analysis. BMC Infect Dis 10: 337.
Centers for Disease Control and Prevention , 2014. Parasites—American Trypanosomiasis (also known as Chagas Disease). Atlanta, GA: CDC.
Junqueira AC et al., 1996. Immunoblot assay using excreted-secreted antigens of Trypanosoma cruzi in serodiagnosis of congenital, acute, and chronic Chagas’ disease. Acute 34: 2143–2147.
Duffy T et al., 2009. Accurate real-time PCR strategy for monitoring bloodstream parasitic loads in Chagas disease patients. PLoS Negl Trop Dis 3: e419.
Ramírez JC et al., 2015. Analytical validation of quantitative real-time PCR methods for quantification of Trypanosoma cruzi DNA in blood samples from Chagas disease patients. J Mol Diagn JMD 17: 605–615.
Ramanakumar AV, Thomann P, Candeias JM, Ferreira S, Villa LL, Franco EL, 2010. Use of the normalized absorbance ratio as an internal standardization approach to minimize measurement error in enzyme-linked immunosorbent assays for diagnosis of human papillomavirus infection. J Clin Microbiol 48: 791–796.
Carlier Y et al., 2011. Congenital Chagas disease: recommendations for diagnosis, treatment and control of newborns, siblings and pregnant women. PLoS Negl Trop Dis 5: 4–6.
Torrico MC et al., 2005. Estimation of the parasitemia in Trypanosoma cruzi human infection: high parasitemias are associated with severe and fatal congenital Chagas disease. Rev Soc Bras Med Trop 38: 58–61.
Balouz V, Buscaglia CA, Aires B, 2017. Chagas disease diagnostic applications: present knowledge and future steps. Adv Parasitol 97: 1–45.
Viotti R et al., 2014. Towards a paradigm shift in the treatment of chronic Chagas disease. Antimicrob Agents Chemother 58: 635–639.
Georg I, Hasslocher-moreno AM, Xavier SS, Holanda T De, Roma EH, Bonecini-almeida MG, 2017. Evolution of anti-Trypanosoma cruzi antibody production in patients with chronic Chagas disease: correlation between antibody titers and development of cardiac disease severity. PLoS Negl Trop Dis 11: e0005796.
Vidarsson G, Dekkers G, Rispens T, 2014. IgG subclasses and allotypes: from structure to effector functions. Front Immunol 5: 1–17.
Chakraborty R et al., 2008. HIV-1 drug resistance in HIV-1-infected children in the United Kingdom from 1998 to 2004. Pediatr Infect Dis J 27: 457–459.
Stefani MMA, Takehara HA, Mota I, 1983. Isotype of antibodies responsible for immune lysis in Trypanosoma cruzi infected mice. Immunol Lett 7: 91–97.
Chandra RK, 2004. Impact of nutritional status and nutrient supplements on immune responses and incidence of infection in older individuals. Ageing Res Rev 3: 91–104.
Noazin S et al., 2019. Trypomastigote excretory secretory antigen blot is associated with Trypanosoma cruzi load and detects congenital T. cruzi infection in neonates, using anti–shed acute phase antigen immunoglobulin M. J Infect Dis 219: 609–618.
Howard EJ, Xiong X, Carlier Y, Sosa-Estani S, Buekens P, 2014. Frequency of the congenital transmission of Trypanosoma cruzi: a systematic review and meta-analysis. BJOG 121: 22–33.
|Past two years||Past Year||Past 30 Days|
|Full Text Views||136||62||21|
The mechanism of vertical transmission of Trypanosoma cruzi is poorly understood. In this study, we evaluated the role of IgG subclasses in the congenital transmission of Chagas disease. We conducted a case-control study in a public maternity hospital in Santa Cruz, Bolivia, enrolling women at delivery. Thirty women who transmitted T. cruzi to their newborns (cases), and 51 women who did not (controls) were randomly selected from 676 total seropositive women. Trypanosoma cruzi–specific IgG1, IgG2, and IgG3 levels were measured by in-house ELISA. The IgG4 levels were unmeasurable as a result of low levels in all participants. Quantitative polymerase chain reaction results and demographic factors were also analyzed. One-unit increases in normalized absorbance ratio of IgG1 or IgG2 levels increased the odds of congenital T. cruzi transmission in Chagas-seropositive women by 2.0 (95% CI: 1.1–3.6) and 2.27 (95% CI: 0.9–5.7), adjusted for age and previous blood transfusion. Odds of congenital transmission were 7.0 times higher in parasitemic mothers (95% CI: 2.3–21.3, P < 0.01) compared with nonparasitemic mothers. We observed that all mothers with IgG1 ≥ 4 were transmitters (sensitivity = 20%, specificity = 100%). Additionally, no mothers with IgG2 < 1.13 were transmitters (sensitivity = 100%, specificity = 21.6%). We demonstrated that IgG subclasses and parasite presence in blood are associated with vertical transmission of T. cruzi and could identify women at increased risk for congenital transmission by measuring IgG subclasses. These measures have potential as objective screening tests to predict the congenital transmission of Chagas.
Working group of Congenital Chagas in Bolivia and Peru: Federico Urquizu, Angela Giovana Vidal, Cynthia Paola Espinoza, Alejandra Pando, Celia Espinoza, Clariza Chavez, Jean Karla Velarde, Victoria Serrudo, Roberto Araya, Mirko Gorena, German Toledo.
Financial support: This work was supported by the Fogarty International Center at the National Institute of Health [5D43TW010074-04 to R.H.G]. This article will be published in PubMed Central for 12 months after publication in the Journal.
Authors’ addresses: Cristian Roca, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, and Laboratorio de Investigación de Enfermedades Infecciosas, Departamento de Ciencias Celulares y Moleculares, Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima, Peru, E-mail: email@example.com. Edith S. Málaga-Machaca, Manuela R. Verastegui, and Edward Valencia-Ayala, Laboratorio de Investigación de Enfermedades Infecciosas, Departamento de Ciencias Celulares y Moleculares, Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima, Peru, E-mails: firstname.lastname@example.org, email@example.com, and firstname.lastname@example.org. Billy Scola, Miller School of Medicine, University of Miami, Miami, FL, Email: email@example.com. Maria del Carmen Menduiña, Maternal Hospital Dr. Percy Boland, Santa Cruz, Bolivia, E-mail: firstname.lastname@example.org. Sassan Noazin, Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, E-mail: email@example.com. Natalie M. Bowman, Department of Medicine, Division of Infectious Diseases, University of North Carolina at Chapel Hill, Chapel Hill, NC, E-mail: firstname.lastname@example.org. Freddy Tinajeros, Asociación Benéfica PRISMA, Lima, Perú, E-mail: email@example.com. Robert H. Gilman, Laboratorio de Investigación de Enfermedades Infecciosas, Departamento de Ciencias Celulares y Moleculares, Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima, Peru, Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, and Asociación Benéfica PRISMA, Lima, Perú, E-mail: firstname.lastname@example.org.