RESUMO
Chagas disease (CD) is caused by the protozoan Trypanosoma cruzi, which leads to a spectrum of clinical presentations that range from asymptomatic to severe cardiac involvement. The host immune response plays a pivotal role in disease progression. Ig isotypes may contribute to disease pathogenesis. Investigating these components can provide insights into the immunopathogenic mechanisms underlying CD. This cross-sectional study aims to establish a correlation between the Ig profile of individuals infected with T. cruzi with the clinical forms of chronic CD. Serum samples were collected from partner institutions in different states of Brazil. Individuals diagnosed with chronic CD were categorized based on the clinical form of the disease. The indirect ELISA method using the recombinant chimeric Molecular Biology Institute of Paraná membrane protein 8.4 as the antigen was used to determine the Ig profile, including total IgG, IgG1, IgG2, IgG3, and IgG4. Ninety-seven serum samples from patients classified as negative (NEG, n = 38), indeterminate (IND, n = 24), mild cardiac (MC, n = 20), and severe cardiac (SC, n = 15) forms were analyzed. IgG1 exhibited greater levels compared with the other isotypes, showing a significant difference between the MC and IND groups. IgG3 levels were greater in individuals from the MC group compared with the SC group. IgG1 and IgG3 isotypes can serve as biomarkers to evaluate the progression of CD because they exhibit variations across clinical groups. Additional longitudinal studies are necessary to explore the relationship between antibody kinetics and the development of tissue damage.
Assuntos
Doença de Chagas , Trypanosoma cruzi , Humanos , Trypanosoma cruzi/genética , Proteínas Recombinantes de Fusão , Estudos Transversais , Antígenos de Protozoários , Doença de Chagas/diagnóstico , Imunoglobulina G , Anticorpos AntiprotozoáriosRESUMO
Although leptospirosis has been considered a major concern in urban areas, no study to date has spatially and simultaneously compared both owner and dog serology in households of major cities. Accordingly, the aim of the present study was to assess the seroprevalence of Leptospira antibodies, evaluate associated risk factors and conduct spatial analyses in 565 randomly selected households, which included 597 dog owners and 729 dogs in Londrina, Southern Brazil. Seropositivity by MAT were detected in in 11/597 (1.84%) owners and in 155/729 (21.26%) dogs. The risk factors were evaluated with logistic regression analysis and spatial factors and case distribution were evaluated with kernel density analyses. The sera of 14/155 (9.03%) dogs reacted for more than one serovar with the same titer. Canicola was the most frequent serogroup, detected in 3/11 (27.27%) owners and 76/155 (49.03%) dogs. The highest titer among the owners was 1:3,200 and was detected in the same household with a titer of 1:800 in the dog. Simultaneous owner-dog seropositivity was found in 7/565 (1.23%) households, with three reacted against serogroup Canicola. Positive owners were detected in 4/565 (0.70%) households and positive dogs were detected in 141/565 (24.95%) households. The associated risks of infection for dogs were different from those associated with infection in owners. Risk analyses for Canicola also identified specific factors of infection. Regardless of owner and dog cases were not statistically clustered, the kernel map has shown dog positivity occurrence in the same hot locations and near positive owners. The dependent variable analysis and logit model suggested a greater likelihood of peri-domiciliary contact with Leptospira. In conclusion, exposure to Leptospira infection was significantly higher in dogs than in their owners and human cases spatially overlapped dog cases, implicating dogs as potential environmental sentinels for this disease. In addition, the associated risk may vary according to serogroup, and the observed simultaneous Canicola seropositivity of owner and dog has suggested intradomicile-transmitted infection.