Leprosy remains a significant public health challenge in endemic regions, particularly among vulnerable populations. Immune dysregulation and community health factors, including environmental conditions and socio-economic status, may play a crucial role in the transmission and progression of the disease. This study aims to estimate the magnitude of the effects of immune dysregulation and community health status on the occurrence of leprosy among mothers and children in endemic areas.
A cross-sectional study was conducted. This study collected patient data from mothers and children with leprosy in endemic regions and non-leprosy subjects in endemic and non-endemic areas. This involved assessing immune dysregulation, focusing on T helper 1 (Th1; interferon-γ [IFN-γ]), T helper 2 (Th2; interleukin-4 [IL-4]), regulatory T cells (Treg; forkhead box P3 [FoxP3+]), and T helper 17 (Th17; interleukin-17 [IL-17]) markers. Because immune parameters were available only in a sub-sample, these variables were incorporated into the structural equation modelling as exploratory immune constructs. Community health status was evaluated through maternal nutrition, household environment, family education, economic status, household smoking habits, village endemicity, presence of Bacille Calmette–Guérin (BCG) scars in children, access to healthcare, and perinatal risk factors. The results were analysed using IBM SPSS Statistics for Windows (version 26.0, IBM Corp., Armonk, NY, USA), and SmartPLS 4 (SmartPLS GmbH, Bönningstedt, Germany).
One hundred six subjects were included in this study. Path analysis revealed significant effects within the studied factors. The health environment had a significant negative impact on village endemicity (β=-0.294; P<0.001). Leprosy in the family was significantly influenced by health environment (β=0.146; P<0.001), family education (β=-0.289; P<0.001), family economic status (β=-0.237; P<0.001), smoking in the family (β=0.191; P<0.001), access to health facilities (β=-0.051; P<0.001), and village endemicity (β=0.305; P<0.001). Mother immunity was significantly influenced by village endemicity (β=0.138; P<0.001), leprosy in the family (β=-0.554; P<0.001), maternal nutritional status (β=0.191; P<0.001), and maternal BCG scar (β=-0.149; P<0.001), which was noteworthy but should be interpreted cautiously. Child immunity was significantly affected by village endemicity (β=-0.148; P<0.001), leprosy in the family (β=-0.280; P<0.001), mother immunity (β=-0.156; P<0.001), child BCG scar (β=-0.021; P<0.001), perinatal risk (β=0.067; P<0.001), and mother leprosy (β=0.429; P<0.001). Maternal leprosy was significantly influenced by maternal immunity (β=-0.208; P<0.001). Finally, Child leprosy was significantly affected by mother immunity (β=0.441; P<0.001), child immunity (β=-0.374; P<0.001), and mother leprosy (β=-0.165; P<0.001).
This study highlights the intricate interplay between immune dysregulation and community health factors in the occurrence of leprosy. These findings underscore the need for targeted interventions to address these factors and reduce leprosy prevalence.
a2093-2340, 2092-6448