Urbanization spreads antimicrobial resistant enteric pathogens in wild bird microbiomes

Abstract

Human behaviour is dramatically changing global ecology. Nowhere is this more apparent than in urbanization, where novel high human density habitats are disrupting long established ecotones. Resultant changes to the transitional areas between organisms, especially enhanced contact between humans and wild animals, provides new opportunities for the spread of zoonotic pathogens, posing a serious threat to global public health. Here, by studying the multi-host enteric pathogenCampylobacter jejuniisolated from the gut of 30 bird species in 8 countries, we investigated how proximity to urbanization influenced the spread of antimicrobial resistant (AMR) strains. Generalized linear models compared multiple behavioural and ecological traits and confirmed a positive correlation between proximity to urbanization and the number ofC. jejunigenotypes and AMR genes in wild bird hosts. Wild birds from highly urban areas harboured up to four times moreC. jejunigenotypes and six times more AMR genes. This is consistent with increased frequency of transition events. Quantifying zoonotic transmission and gene pool spread is essential for quantitative one health surveillance and control measures against future zoonosis emergences.

Evidence of potential Campylobacter jejuni zooanthroponosis in captive macaque populations

“…A very high proportion of monkey isolates (95.4 %) were putatively resistant to ciprofloxacin. This is comparable to the levels observed among isolates from human infections in Taiwan (2016-2019; 91.1 %) [71] and Beijing (2017-2018; 94.50 %) [65], and livestock animals in China [30], Europe, and many other countries [72].…”

“…This host segregating genetic variation is the basis for attributing the source of isolates spread from reservoir hosts to humans [24, 64]. Consistent with this, it is possible that captive macaques could harbour host specialist lineages similar to those described for chickens, cattle and wild birds [20, 65–67]. However, several lines of evidence suggest that the strains isolated from macaques in our study represent infection either from humans or from a common human–monkey infection source.…”