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Lyme Disease in Urban Environments

Most people associate Lyme disease with thick forests, dense wildlife populations, and other components of the great outdoors. We are often warned that our risk of contracting Lyme disease is heavily influenced by the amount of time we spend in the woods or how much contact we have with pets or wildlife. So how about people living in urban areas? Are people living in concrete cities also at risk for Lyme disease? How is urbanization affecting this disease and its transmission, prevalence, and incidence? This blog will focus on the effects of urbanization on Lyme disease and explore how the risk of contracting this disease may (or may not) be different for those living in cities.

Urbanization can significantly reduce biodiversity. This is especially true for species diversity within the actual urban areas. By reducing the biodiversity of urban wildlife, urbanization can strongly influence the transmission of several vector-borne diseases such as Lyme disease. This link is explained by the ‘dilution effect’ (Bradley and Altizer, 2007). In this process, a low host species richness (low wildlife biodiversity) can increase parasite transmission if it causes an increased proportional abundance of competent reservoir hosts. In the case of Lyme disease, this would mean an increased proportional abundance of white-footed mice compared to other urban wildlife species. In a way, the loss of biodiversity is removing the less competent hosts, thereby helping the pathogen’s amplification by increasing its chances of coming into contact with competent hosts (Brunner and Ostfeld, 2008). Nupp and Swihart (1998) confirmed that white-footed mice tend to reach higher abundances in species-poor communities, such as urban areas. Additionally, other studies verified that a greater proportional abundance of white-footed mice is linked with an increased infection prevalence in ticks, mice, and humans (Allan et al. 2003; LoGiudice et al. 2003). This would suggest that people living in these urban areas would have a greater risk of contracting Lyme disease than people living in rural forested areas! However, this depends on whether or not the decrease in urban wildlife biodiversity truly increases the proportional abundance of this competent reservoir host. For example, if there is no increase in the proportional abundance of white-footed mice in urban areas, then the risk of contracting Lyme disease would not be expected to go up.

Most urban areas retain a few small areas of “forest” in the form of city parks. Researchers from different areas of the world found that Lyme disease may be acquired in these parks (Pokorny 1990; Guy and Farquhar, 1991; Schwartz et al. 1991; Magnarelli et al. 1995). Matuschka et al (1996) found that the Norwegian rat (Rattus norvegicus) was a very competent reservoir host for Lyme disease in city parks located in Magdeburg, Germany. All of the rats sampled were heavily infested with both larval and nymphal Ixodes scapularis, and they had a larvae: nymph ratio of 6:1. When assessing the rats’ seropositivity for Borrelia burgdorferi, they found that all rats produced infected ticks. Similar results were later found for black rats (Rattus rattus; Matuschka et al. 1997). Rats fulfill several criteria for being competent reservoir hosts for B. burgdorferi: they are comparatively long-lived (~2 years), they remain persistently competent, they are frequently parasitized by both nymphal and larval I. scapularis, and they forage relatively far from their nests. Since rats are a common urban species, these findings may suggest an increased risk of contracting Lyme disease for people who visit urban parks.

Another side-effect of urbanization is habitat fragmentation. While habitat fragmentation affects many wildlife species in several different ways, one important result of this process is increased interspersion of wild and populated areas which leads to an amplified edge-effect. Jackson et al (2006) found that landscapes with a large percentage of forest-herbaceous edge are associated with higher Lyme disease rates. This positive correlation was also found by Das et al (2002). Two important reservoirs of B. burgdorferi, the white-footed mouse and white-tailed deer, thrive in edge habitats. As stated in previous blogs, the abundance of I. scapularis is highly correlated with the abundance of these two wildlife species. Edge habitats are therefore expected to harbor more potentially infected ticks, which leads to an increased risk of Lyme disease for people living near these habitats. Another important component of habitat fragmentation is the creation of patches. The size of these remaining forested patches can have serious effects on both wildlife biodiversity and disease transmission. Allan et al (2003) found that Lyme disease risk is inversely related to forest patch area. He found that patches that were smaller than 1-2 hectares had a greater Lyme disease risk due to these areas having higher densities of infected nymphal ticks. A potential reason for these findings is that small patches contain relatively larger populations of white-footed mice. Due to this reservoir’s high prevalence and infectivity rate, most ticks in smaller patches are therefore expected to become infected with B. burgdorferi.

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Allan, B.F., Keesing, F., Ostfeld, R.S. 2003. Effect of forest fragmentation on Lyme disease risk. Conservation Biology 17: 267-272.

Bradley, C.A., Altizer, S. 2007. Urbanization and the ecology of wildlife diseases. Trends in Ecology & Evolution 22: 95-102.

Brunner, J.L., Ostfeld, R.S. 2008. Multiple causes of variable tick burdens on small-mammal hosts. Ecology 89: 2259-2272.

Das, A., Lele, S.R., Glass, G.E., Shields, T., Patz, J. 2002. Modelling a discrete spatial response using generalized linear mixed models: application to Lyme disease vectors. International Journal of Geographical Information Science 16: 151-166.

Guy, E.C., Farquhar, R.G. 1991. Borrelia burgdorferi in urban parks. Lancet 338: 253.

Jackson, L.E., Hilborn, E.D., Thomas, J.C. 2006. Towards landscape design guidelines for reducing Lyme disease risk. International Journal of Epidemiology 35: 315-322.

LoGiudice, K., Ostfeld, R.S., Schmidt, K.A., Keesing, F. 2003. The ecology of infectious disease: effects of host diversity and community composition on Lyme disease risk. Proceedings of the National Academy of Sciences USA 100: 567-571.

Magnarelli, L.A., Denicola, A., Stafford, K.C., Anderson, J.F. 1995. Borrelia burgdorferi in an urban environment: white-tailed deer with infected ticks and antibodies. Journal of Clinical Microbiology 33: 541-544.

Matuschka, F.R., Endepols, S., Richter, D., Ohlenbusch, A., Eiffert, H., Spielman, A. 1996. Risk of urban Lyme disease enhanced by the presence of rats. The Journal of Infectious Diseases 174: 1108-1111.

Matuschka, F.R., Endepols, S., Richter, D., Spielman, A. 1997. Competence of urban rats as reservoir hosts for Lyme disease spirochetes. Journal of Medical Entomology 34: 489-493.

Nupp, T.E., Swihart, R.K. 1998. Effects of forest fragmentation on population attributes of white-footed mice and eastern chipmunks. Journal of Mammalogy 79: 1234-1243.

Pokorny, P. 1990. Borrelia sp. in ticks (Ixodes ricinus) on the territory of the capital of Prague. Ceskoslovenska Epidemiologie, Mikrobiologie, Imunologie 39: 32-38.

Schwartz, B.S., Hofmeister, E., Glass, G.E., Arthur, R.R., Childs, J.E., Cranfield, M.R. 1991. Lyme borreliosis in an inner-city park in Baltimore. American Journal of Public Health 81: 803-804.