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Previous hookworm infection attenuates the immune response to a subsequent Schistosoma mansoni infection in an experimental model

Published online by Cambridge University Press:  10 February 2025

L.F.V. Furtado*
Affiliation:
Universidade Federal de Minas Gerais, Faculdade de Farmácia, Departamento de Análises Clínicas e Toxicológicas, Avenida Presidente Antônio Carlos, 6627, Pampulha, CEP 31270-901, Belo Horizonte, Minas Gerais, Brazil
L.R. Serafim
Affiliation:
Universidade Federal de Minas Gerais, Instituto de Ciências Biológicas, Departamento de Parasitologia, Avenida Presidente Antônio Carlos, 6627, Pampulha, CEP 31270-901, Belo Horizonte, Minas Gerais, Brazil
V.J. da Silva
Affiliation:
Prefeitura Municipal de Sabará, Centro de Controle de Zoonoses, Avenida Charles Gonort, CEP: 34505-620, Rosario I, Sabará, Minas Gerais, Brazil
S.R.C. Dias
Affiliation:
Universidade do Estado de Minas Gerais, Unidade Carangola, Departamento de Ciências Biológicas, Praça dos Estudantes, 23, CEP 36800-000, Santa Emília, Carangola, Minas Gerais, Brazil
N.C.N. de Paiva
Affiliation:
Universidade Federal de Ouro Preto, Campus Universitário Morro do Cruzeiro, CEP 35400-000, Bauxita, Ouro Preto, Minas Gerais, Brazil
C.M. Carneiro
Affiliation:
Universidade Federal de Ouro Preto, Campus Universitário Morro do Cruzeiro, CEP 35400-000, Bauxita, Ouro Preto, Minas Gerais, Brazil
É.M.L. Rabelo
Affiliation:
Universidade Federal de Minas Gerais, Instituto de Ciências Biológicas, Departamento de Parasitologia, Avenida Presidente Antônio Carlos, 6627, Pampulha, CEP 31270-901, Belo Horizonte, Minas Gerais, Brazil
*
Corresponding author: L.F.V. Furtado; Email: [email protected]

Abstract

This study investigated the co-infection dynamics of Schistosoma mansoni and Ancylostoma ceylanicum in an experimental model. Two experiments were conducted to investigate varying infection orders. In experimental group 1, subjects were initially infected with A. ceylanicum, followed by S. mansoni infection. In group 2, subjects were first infected with S. mansoni, followed by A. ceylanicum infection. The co-infected groups were compared to mono-infected groups for further analysis. Parameters assessed included weight, fecal egg elimination, blood cell counts, IgG response, histopathological analysis, and granuloma morphometry. Results indicated that the timing of infections influenced weight loss. Co-infected animals lost weight similarly to A. ceylanicum-infected animals when A. ceylanicum preceded S. mansoni. The co-infected groups did not experience worsened anemia, despite both parasites being hematophagous. No linear correlation was found between S. mansoni egg counts and anti-SEA IgG production. The response to the S. mansoni adult worm antigen was significantly higher in the S. mansoni mono-infected group compared to the group previously infected with hookworm. Co-infection with A. ceylanicum after S. mansoni infection also interfered with the host response. It caused a delay in the peak of S. mansoni egg elimination compared to the S. mansoni monoinfected group. Additionally, fewer eggs were retained in the liver compared to single infections. These findings help elucidate the interactions between different parasites and their hosts in the same endemic area, providing valuable information to enhance strategies for disease control and management.

Type
Research Paper
Copyright
© The Author(s), 2025. Published by Cambridge University Press

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