Lyme disease risk not amplified in a species-poor vertebrate community: similar Borrelia burgdorferi tick infection prevalence and OspC genotype frequencies.
The effect of biodiversity declines on human health is currently debated, but empirical assessments are lacking. Lyme disease provides a model system to assess relationships between biodiversity and human disease because the etiologic agent, Borrelia burgdorferi, is transmitted in the United States by the generalist black-legged tick (Ixodes scapularis) among a wide range of mammalian and avian hosts. The 'dilution effect' hypothesis predicts that species-poor host communities dominated by white-footed mice (Peromyscus leucopus) will pose the greatest human risk because P. leucopus infects the largest numbers of ticks, resulting in higher human exposure to infected I. scapularis ticks. P. leucopus-dominated communities are also expected to maintain a higher frequency of those B. burgdorferi outer surface protein C (ospC) genotypes that this host species more efficiently transmits ('multiple niche polymorphism' hypothesis). Because some of these genotypes are human invasive, an additive increase in human disease risk is expected in species-poor settings. We assessed these theoretical predictions by comparing I. scapularis nymphal infection prevalence, density of infected nymphs and B. burgdorferi genotype diversity at sites on Block Island, RI, where P. leucopus dominates the mammalian host community, to species-diverse sites in northeastern Connecticut. We found no support for the dilution effect hypothesis; B. burgdorferi nymphal infection prevalence was similar between island and mainland and the density of B. burgdorferi infected nymphs was higher on the mainland, contrary to what is predicted by the dilution effect hypothesis. Evidence for the multiple niche polymorphism hypothesis was mixed: there was lower ospC genotype diversity at island than mainland sites, but no overrepresentation of genotypes with higher fitness in P. leucopus or that are more invasive in humans. We conclude that other mechanisms explain similar nymphal infection prevalence in both communities and that high ospC genotype diversity can be maintained in both species-poor and species-rich communities.
Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA.
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Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA; University of Richmond, Department of Biology, 28 Westhampton Way, Richmond, VA 23173, USA; University of KwaZulu-Natal, School of Life Sciences, Pietermaritzburg, South Africa.
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Brinkerhoff
Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA.
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Carpi
Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA.
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Steeves
Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA; Audubon Connecticut, 185 East Flat Hill Rd., Southbury, CT 06488, USA.
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Folsom-O'Keefe
Yale School of Public Health, Department of Biostatistics, 60 College Street, New Haven, CT 06520, USA.
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DeVeaux
Yale School of Public Health, Department of Epidemiology of Microbial Diseases, 60 College Street, New Haven, CT 06520, USA. Electronic address: maria.diuk@yale.edu.
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Diuk-Wasser
D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics; D044822:Biodiversity; D025065:Borrelia burgdorferi / Q000235:genetics; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D007814:Larva; D008193:Lyme Disease / Q000453:epidemiology* / Q000635:transmission; D009758:Nymph; D015995:Prevalence; D012306:Risk; D013987:Ticks / Q000382:microbiology; D014714:Vertebrates
D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; C079616:OspC protein
Biodiversity; Borrelia burgdorferi; Dilution effect; Lyme disease; Multiple niche polymorphism; ospC