Summary Antibiotic-resistant infections annually claim hundreds of thousands of lives worldwide. This problem is exacerbated by resistance gene exchange between pathogens and benign microbes from diverse habitats. Mapping resistance gene dissemination between humans and their environment is a public health priority. We characterized the bacterial community structure and resistance exchange networks of hundreds of interconnected human fecal and environmental samples from two low-income Latin American communities. We found that resistomes across habitats are generally structured by bacterial phylogeny along ecological gradients, but identified key resistance genes that cross habitat boundaries and determined their association with mobile genetic elements. We also assessed the effectiveness of widely-used excreta management strategies in reducing fecal bacteria and resistance genes in these settings representative of low- and middle-income countries. Our results lay the foundation for quantitative risk assessment and surveillance of resistance dissemination across interconnected habitats in settings representing over two-thirds of the world’s population.

To determine whether clinical manifestations are associated with genotypes or subtypes of Cryptosporidium spp., we studied a 4-year longitudinal birth cohort of 533 children in Peru. A total of 156 infection episodes were found in 109 children. Data from fi rst infections showed that C. hominis was associated with diarrhea, nausea, vomiting, general malaise, and increased oocyst shedding intensity and duration. In contrast, C. parvum, C. meleagridis, C. canis, and C. felis were associated with diarrhea only. C. hominis subtype families were identifi ed (Ia, Ib, Id, and Ie); all were associated with diarrhea. Ib was also associated with nausea, vomiting, and general malaise. All C. parvum specimens belonged to subtype family IIc. Analysis of risk factors did not show associations with specifi c Cryptosporidium spp. genotypes or subtypes. These fi ndings strongly suggest that Cryptosporidium spp. and subtypes are linked to different clinical manifestations in children.

Serial norovirus infections with multiple genotypes were found among a Peruvian birth cohort early in infancy. Protection against the subsequent infection was genotype specific, suggesting that norovirus vaccines may need to target multiple genotypes.

The authors conducted a 2-year (1989-1991) community-based longitudinal study in a shantytown in Lima, Peru, to examine the effect of Cryptosporidium parvum infection on child growth during the year following the onset of infection. A cohort of children, aged 0-3 months at recruitment, was followed monthly for anthropometrics, weekly for stool samples, and daily for diarrheal status. Data from 185 children in the cohort permitted a comparison of growth in C. parvum-infected and noninfected children. The analyses fitted smooth, flexible curves with a linear random-effects model to estimate growth differences between C. parvum-infected and noninfected children. Children infected with C. parvum experienced growth faltering, both in weight and in height, for several months after the onset of infection, followed by a period of catch-up growth. Younger children took longer to catch up in weight than did older children. Catch-up growth, however, did not occur in children infected between ages 0 and 5 months. These children did not catch up in height, and one year after infection they exhibited an average deficit of 0.95 cm (95% confidence interval (CI) 0.38-1.53) relative to noninfected children of similar age. Stunted children who became infected also did not catch up in either weight or height, and one year after infection they exhibited a height deficit of 1.05 cm (95% CI 0.46-1.66) relative to noninfected, stunted children of similar age. These results indicate that Cryptosporidium parvum has a lasting adverse effect on linear (height) growth, especially when acquired during infancy and when children are stunted before they become infected.

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