Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections.

Abstract

Vitamin A deficiency (A(-)) remains a public health concern in developing countries and is associated with increased susceptibility to infection. Citrobacter rodentium was used to model human Escherichia coli infections. A(-) mice developed a severe and lethal (40%) infection. Vitamin A-sufficient (A(+)) mice survived and cleared the infection by day 25. Retinoic acid treatment of A(-) mice at the peak of the infection eliminated C. rodentium within 16 days. Inflammation levels were not different between A(+) and A(-) mouse colons, although the A(-) mice were still infected at day 37. Increased mortality of A(-) mice was not due to systemic cytokine production, an inability to clear systemic C. rodentium, or increased pathogenicity. Instead, A(-) mice developed a severe gut infection with most of the A(-) mice surviving and resolving inflammation but not eliminating the infection. Improvements in vitamin A status might decrease susceptibility to enteric pathogens and prevent potential carriers from spreading infection to susceptible populations.