Most people – both researchers and residents alike – are quickly coming to appreciate that wildlife are increasingly common in cities, and here to stay. Some species are generally considered a welcomed part of the tapestry of an urban environment (think peregrine falcons). Rats clearly fall on the other extreme of the spectrum, maligned for the zoonotic diseases they can harbor, the damage their gnawing and burrowing can cause (to the point of cities having to close entire parks), and for the general ‘ick’ factor they evoke when people see them scurrying about.
Because of this near-universal aversion to rats, and the very real risk they pose to public health, most cities implement some form of rodent control intervention to reduce their numbers. The consistency and thoroughness of these interventions range widely, but generally consist of short-term rodenticide poison application. Studies have indicated that these rodenticide-only campaigns often do reduce rat numbers in the short-term. But these reductions are often followed by rapid rebounds in population size – termed the ‘boomerang effect’ – due to reduced competition or reinvasion from untreated areas.
One thing that has never been evaluated (that we know of) is how these rapid bottlenecks in rat numbers impact the genetics of rat populations – or other pests targeted for lethal control. That’s what we did in our new study out this week, looking at how a major coordinated ‘eradication’ campaign in Salvador, Brazil impacted the population genetic characteristics of Rattus norvegicus rats.
For some context, Salvador is the third-largest city in Brazil, and suffers from high levels of leptospirosis bacterial infection in people, a potentially debilitating and lethal disease. Specifically, residents of several favela communities suffer from regular seasonal outbreaks of leptospirosis during the wet season, where standing water creates environmental reservoirs for the bacteria to persist until drier weather returns. Our team has studied the epidemiology of this disease for more than 20 years, incorporating genetic approaches more recently. So the overarching goals of our new study were to evaluate how an eradication campaign changes the genetics of the target population.
For this project, we sampled and genotyped 250 rats from 3 neighborhoods at 3 time points – immediately before, immediately after, and then 7 months following an intense city-run lethal control campaign in 2015. In our analyses we found that:
1.) There was a 54% reduction in rat infestation, meaning the campaign was effective at reducing rat numbers (but not eradicating them, which is probably impossible in cities).
2.) Genetic population size was reduced by 85-91% across the 3 sites after the campaign, demonstrating that a severe genetic bottleneck event had occurred.
3.) Rare alleles were lost from the population, presumably via drift. The average allele frequency across all loci was ~16%, whereas the average frequency of alleles present in the first sample period but not the second two was only 3.7%. This is consistent with evolutionary theory suggesting that alleles are lost at a rate proportional to their frequency in the population.
4.) There was a large shift in the population genetic structure of the rats after the campaign, illustrated in the figure below. This shift was nearly identical at each of the 3 neighborhood sites.
5.) The level of relatedness among rats increased after the campaign in each valley, significantly so in 2 of the 3 neighborhoods. This suggests that rat colonies may have been affected unequally across the area, or that campaigns disrupt the social structure of colonies.
The huge genetic impacts seen with this lethal-control campaign of rats in Salvador bring up some important new questions. First, given that urban rat populations are subject to repeated lethal-control efforts, how are they persisting over time if they experience numerous genetic bottlenecking events? There is a wealth of evolutionary theory suggesting that this repeated loss of genetic variation should erode the fitness/viability of these rat populations.
Alternatively, are these campaigns acting as intensive ‘natural’ selection events where only the incredibly fit rats/genotypes persist? In other words, are we creating ‘super rats’ with each subsequent campaign to remove them? We do know that alleles exist for certain genes like Vkorc1 that do not allow the rodenticides to antagonistically bind receptors and block vitamin K production (vitamin K being a key component of blood coagulation, hence why rodenticides are often described as ‘anticoagulants’ that cause excessive lethal bleeding). These Vkorc1 alleles have been documented in some populations of rodents around the world, but not yet in Salvador or surrounding cities.
Lastly, severely reducing the genetic variation of rat populations (or any ‘pest’ species) may be an additional facet of integrated pest management (IPM). Currently, long-term genetic viability is not generally considered with IPM strategies, but could be a valuable additional target response to incorporate beyond the standard poison, trash, harborage, and education components. This is particularly important with predictions that urbanization and climate change may increase rat numbers and their associated risks to humans in Salvador and elsewhere.
Referenced article:
Richardson, J.L., G. Silveira, I. Soto Medrano, A.Z. Arietta, C. Mariani, A.C. Pertile, T. Carvalho Pereira, J. Childs, A.I. Ko, F. Costa, A. Caccone. 2019. Significant genetic impacts accompany an urban rat control campaign in Salvador, Brazil. Frontiers in Ecology & Evolution 7:115. (doi:10.3389/fevo.2019.00115)
Featured image: Norway rat (Rattus norvegicus) in stream (credit: Sciadopitys from UK – CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=20413572)
- Urban Rodent Control has Big Genetic Impacts for Rats in Brazil - June 21, 2019