Objective: Interactions between iron nutrition and infectious disease (ID) may vary tremendously across environments. Iron deficiency may result from ID processes and contribute to ID susceptibility in complex ways, complicating interpretation of associations between iron status and prevalent ID. We evaluated associations between iron status and prevalent and incident ID in Kilimanjaro, Tanzania, a particularly intense and diverse ID ecology.
Methods: Iron status was evaluated among a random sample of 224 2-7 year old children through hemoglobin and transferrin receptor. Prevalent ID were identified through biomarkers of inflammation (C-reactive protein and a1-acid glycoprotein), morbidity history interviews, and physicians diagnoses. Incident ID were identified through physicians diagnoses (the entire sample participated in passive monitoring; a subsample underwent additional active monitoring). Associations between iron status and ID were assessed with logistic regression and Cox proportional hazard models.
Results: 30.36% of children exhibited iron deficiency without anemia, iron deficient erythropoiesis (IDE); 12.50% exhibited iron deficient anemia (IDA). ID prevalence was higher among children with IDAboth physician-diagnosed (OR: 2.54; 95% CI: 0.91, 7.17) and those identified by biomarkers of inflammation (OR: 2.68; 95% CI: 1.17, 6.15); this pattern was pronounced for malaria (OR: 3.47; 95% CI: 0.94, 12.85) and not apparent for respiratory infections. By contrast, ID incidence was lower among children with IDE (HR: 0.61; 95% CI: 0.32, 1.17), particularly respiratory infections (HR: 0.26; 95% CI: 0.07, 0.92), but not malaria.
Conclusions: Among Kilimanjaro children, IDA my result from some ID (such as malaria), while IDE may reduce risk for others.