Effects of species diversity on disease risk
The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not surprisingly, then, the species diversity of ecological communities can potentially affect the prevalence of infectious diseases. Although a number of s...
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Published in | Ecology letters Vol. 9; no. 4; pp. 485 - 498 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Oxford, UK : Blackwell Publishing Ltd
01.04.2006
Blackwell Publishing Ltd |
Subjects | |
Online Access | Get full text |
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Abstract | The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not surprisingly, then, the species diversity of ecological communities can potentially affect the prevalence of infectious diseases. Although a number of studies have now identified effects of diversity on disease prevalence, the mechanisms underlying these effects remain unclear in many cases. Starting with simple epidemiological models, we describe a suite of mechanisms through which diversity could increase or decrease disease risk, and illustrate the potential applicability of these mechanisms for both vector-borne and non-vector-borne diseases, and for both specialist and generalist pathogens. We review examples of how these mechanisms may operate in specific disease systems. Because the effects of diversity on multi-host disease systems have been the subject of much recent research and controversy, we describe several recent efforts to delineate under what general conditions host diversity should increase or decrease disease prevalence, and illustrate these with examples. Both models and literature reviews suggest that high host diversity is more likely to decrease than increase disease risk. Reduced disease risk with increasing host diversity is especially likely when pathogen transmission is frequency-dependent, and when pathogen transmission is greater within species than between species, particularly when the most competent hosts are also relatively abundant and widespread. We conclude by identifying focal areas for future research, including (1) describing patterns of change in disease risk with changing diversity; (2) identifying the mechanisms responsible for observed changes in risk; (3) clarifying additional mechanisms in a wider range of epidemiological models; and (4) experimentally manipulating disease systems to assess the impact of proposed mechanisms. |
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AbstractList | The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not surprisingly, then, the species diversity of ecological communities can potentially affect the prevalence of infectious diseases. Although a number of studies have now identified effects of diversity on disease prevalence, the mechanisms underlying these effects remain unclear in many cases. Starting with simple epidemiological models, we describe a suite of mechanisms through which diversity could increase or decrease disease risk, and illustrate the potential applicability of these mechanisms for both vector‐borne and non‐vector‐borne diseases, and for both specialist and generalist pathogens. We review examples of how these mechanisms may operate in specific disease systems. Because the effects of diversity on multi‐host disease systems have been the subject of much recent research and controversy, we describe several recent efforts to delineate under what general conditions host diversity should increase or decrease disease prevalence, and illustrate these with examples. Both models and literature reviews suggest that high host diversity is more likely to decrease than increase disease risk. Reduced disease risk with increasing host diversity is especially likely when pathogen transmission is frequency‐dependent, and when pathogen transmission is greater within species than between species, particularly when the most competent hosts are also relatively abundant and widespread. We conclude by identifying focal areas for future research, including (1) describing patterns of change in disease risk with changing diversity; (2) identifying the mechanisms responsible for observed changes in risk; (3) clarifying additional mechanisms in a wider range of epidemiological models; and (4) experimentally manipulating disease systems to assess the impact of proposed mechanisms. The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not surprisingly, then, the species diversity of ecological communities can potentially affect the prevalence of infectious diseases. Although a number of studies have now identified effects of diversity on disease prevalence, the mechanisms underlying these effects remain unclear in many cases. Starting with simple epidemiological models, we describe a suite of mechanisms through which diversity could increase or decrease disease risk, and illustrate the potential applicability of these mechanisms for both vector-borne and non-vector-borne diseases, and for both specialist and generalist pathogens. We review examples of how these mechanisms may operate in specific disease systems. Because the effects of diversity on multi-host disease systems have been the subject of much recent research and controversy, we describe several recent efforts to delineate under what general conditions host diversity should increase or decrease disease prevalence, and illustrate these with examples. Both models and literature reviews suggest that high host diversity is more likely to decrease than increase disease risk. Reduced disease risk with increasing host diversity is especially likely when pathogen transmission is frequency-dependent, and when pathogen transmission is greater within species than between species, particularly when the most competent hosts are also relatively abundant and widespread. We conclude by identifying focal areas for future research, including (1) describing patterns of change in disease risk with changing diversity; (2) identifying the mechanisms responsible for observed changes in risk; (3) clarifying additional mechanisms in a wider range of epidemiological models; and (4) experimentally manipulating disease systems to assess the impact of proposed mechanisms.The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not surprisingly, then, the species diversity of ecological communities can potentially affect the prevalence of infectious diseases. Although a number of studies have now identified effects of diversity on disease prevalence, the mechanisms underlying these effects remain unclear in many cases. Starting with simple epidemiological models, we describe a suite of mechanisms through which diversity could increase or decrease disease risk, and illustrate the potential applicability of these mechanisms for both vector-borne and non-vector-borne diseases, and for both specialist and generalist pathogens. We review examples of how these mechanisms may operate in specific disease systems. Because the effects of diversity on multi-host disease systems have been the subject of much recent research and controversy, we describe several recent efforts to delineate under what general conditions host diversity should increase or decrease disease prevalence, and illustrate these with examples. Both models and literature reviews suggest that high host diversity is more likely to decrease than increase disease risk. Reduced disease risk with increasing host diversity is especially likely when pathogen transmission is frequency-dependent, and when pathogen transmission is greater within species than between species, particularly when the most competent hosts are also relatively abundant and widespread. We conclude by identifying focal areas for future research, including (1) describing patterns of change in disease risk with changing diversity; (2) identifying the mechanisms responsible for observed changes in risk; (3) clarifying additional mechanisms in a wider range of epidemiological models; and (4) experimentally manipulating disease systems to assess the impact of proposed mechanisms. |
Author | Holt, R. D. Keesing, F. Ostfeld, R. S. |
Author_xml | – sequence: 1 fullname: Keesing, F – sequence: 2 fullname: Holt, R.D – sequence: 3 fullname: Ostfeld, R.S |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16623733$$D View this record in MEDLINE/PubMed |
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Effects of intersowing with beans on the spread of groundnut rosette virus by Aphis craccivora Koch (Hemiptera, Ahpididae) in Malawi. Bull. Entom. Res., 66, 331-333. Power, A.G. & Mitchell, C.E. (2004). Pathogen spillover in disease epidemics. Am. Nat., 164, S79-S89. Hochberg, M.E. (1991). Non-linear transmission rates and the dynamics of infectious disease. J. Theor. Biol., 153, 301-321. Rhodes, C.J., Atkinson, R.P.D., Anderson, R.M. & Macdonald, D.W. (1998). Rabies in Zimbabwe: Reservoir Dogs and the Implications for Disease Control. 353, 999-1010. Schmidt, K.A., Ostfeld, R.S. & Schauber, E.M. (1999). Infestation of Peromyscus leucopus and Tamias striatus by Ixodes scapularis (Acari: Ixodidae) in relation to the abundance of hosts and parasites. J. Med. Entomol., 36, 749-757. Hudson, P. & Greenman, J. (1998). Competition mediated by parasites: biological and theoretical progress. TREE, 13, 387-390. Schmidt, K.A. & Ostfeld, R.S. (2001). 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Krohne, D.T. & Hoch, G.A. (1999). Demography of Peromyscus leucopus populations on habitat patches: the role of dispersal. Can. J. Zool., 77, 1247-1253. Ostfeld, R.S. & Holt, R.D. (2004). Are predators good for your health? Evaluating evidence for top-down regulation of zoonotic disease reservoirs. Front. Ecol. Evol., 2, 13-20. Antonovics, J., Iwasa, Y. & Hassell, M.P. (1995). A generalized model of parasitoid, venereal, and vector-based transmission processes. Am. Nat., 145, 661-675. Power, A.G. (1987). Plant community diversity, he 1991; 153 2004; 164 1979; 79 2005; 130 1976; 66 2004; 29 2002; 12 1996; 74 1985; 126 2003; 17 2004; 2 1999; 200 2000a; 14 1998; 353 1998; 88 1978 1986; 1 2001; 294 1990; 136 1997; 11 2002; 83 2001; 292 2003; 6 1982; 20 2003; 9 2003; 2 1996; 63 1970; 63 1982 2000; 287 2003; 84 1991; 148 1998; 58 1998; 13 2001; 70 2004; 41 2000; 20 1997 1995 1999; 141 1969; 59 1999; 2 1999; 266 2002 2003; 72 1958 1957 1993; 142 1995; 5 1992; 73 2001; 65 2000b; 78 1987; 68 1981; 291 2001; 82 1994; 169 1991; 25 1983; 121 2005; 166 1999; 36 2003; 68 1992; 139 1999; 77 1963 1995; 145 2003; 224 2003; 421 2003; 100 e_1_2_7_5_1 e_1_2_7_9_1 e_1_2_7_19_1 Ostfeld R.S. (e_1_2_7_53_1) e_1_2_7_17_1 e_1_2_7_62_1 World Health Organization (e_1_2_7_78_1) 1982 e_1_2_7_15_1 e_1_2_7_41_1 e_1_2_7_64_1 Ruedas L.A. (e_1_2_7_67_1) 2004; 29 e_1_2_7_13_1 e_1_2_7_66_1 e_1_2_7_11_1 e_1_2_7_45_1 e_1_2_7_68_1 e_1_2_7_47_1 e_1_2_7_26_1 e_1_2_7_49_1 e_1_2_7_28_1 e_1_2_7_73_1 e_1_2_7_50_1 e_1_2_7_71_1 e_1_2_7_25_1 e_1_2_7_52_1 Ostfeld R.S. (e_1_2_7_54_1) e_1_2_7_77_1 e_1_2_7_23_1 e_1_2_7_33_1 e_1_2_7_75_1 e_1_2_7_21_1 e_1_2_7_35_1 e_1_2_7_56_1 e_1_2_7_37_1 e_1_2_7_79_1 e_1_2_7_39_1 e_1_2_7_4_1 Holt R.D. (e_1_2_7_31_1) 1997 Grenfell B.T. (e_1_2_7_27_1) 2002 e_1_2_7_8_1 Barrett J.A. (e_1_2_7_6_1) 1978 e_1_2_7_18_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_61_1 e_1_2_7_2_1 e_1_2_7_14_1 e_1_2_7_42_1 e_1_2_7_44_1 e_1_2_7_65_1 e_1_2_7_10_1 e_1_2_7_46_1 e_1_2_7_48_1 e_1_2_7_69_1 e_1_2_7_29_1 Anderson R.M. (e_1_2_7_3_1) 1982 Van Der Plank J.E. (e_1_2_7_58_1) 1963 Macdonald G. (e_1_2_7_43_1) 1957 e_1_2_7_72_1 e_1_2_7_51_1 e_1_2_7_70_1 e_1_2_7_30_1 e_1_2_7_76_1 Power A.G. (e_1_2_7_60_1) e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_55_1 e_1_2_7_74_1 e_1_2_7_22_1 e_1_2_7_34_1 e_1_2_7_57_1 e_1_2_7_20_1 e_1_2_7_36_1 e_1_2_7_59_1 Boudreau M.A. (e_1_2_7_12_1) 1997 e_1_2_7_38_1 Rhodes C.J. (e_1_2_7_63_1) 1998 Begon M. (e_1_2_7_7_1) |
References_xml | – reference: Anderson, R.M. & May, R.M. (1981). The population dynamics of microparasites and their invertebrate hosts. Philos. Trans. R. Soc. Lond. Ser. B, 291, 451-524. – reference: Power, A.G. & Mitchell, C.E. (2004). Pathogen spillover in disease epidemics. Am. Nat., 164, S79-S89. – reference: Finckh, M.R., Gacek, E.S., Goyeau, H., Lannou, C., Merz, U., Mundt, C.C. et al. (2000). Cereal variety and species mixtures in practice, with emphasis on disease resistance. Agronomie, 20, 813-837. – reference: Begon, M. & Bowers, R.G. (1994). Host-host-pathogen models and microbial pest control: the effect of host self-regulation. J. Theor. Biol., 169, 275-287. – reference: Rhodes, C.J., Atkinson, R.P.D., Anderson, R.M. & Macdonald, D.W. (1998). Rabies in Zimbabwe: Reservoir Dogs and the Implications for Disease Control. 353, 999-1010. – reference: Craig, L.E., Norris, D.E., Sanders, M.L., Glass, G.E. & Schwartz, B.S. (1996). 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Biol., 200, 111-118. – reference: Mills, J.N., Johnson, J.M., Ksiazek, T.G. et al. (1998). A survey of hantavirus antibody in small-mammal populations in selected United States National Parks. Am. J. Trop. Med. Hyg., 58, 525-532. – reference: Antonovics, J., Iwasa, Y. & Hassell, M.P. (1995). A generalized model of parasitoid, venereal, and vector-based transmission processes. Am. Nat., 145, 661-675. – reference: Elton, C.S. (1958). The Ecology of Invasions by Animals and Plants. Methuen & Co., London. – reference: Thrall, P.H., Antonovics, J. & Hall, D.W. (1993). Host and pathogen coexistence in vector-borne and venereal diseases characterized by frequency-dependent disease transmission. Am. Nat., 142, 543-552. – reference: Holt, R.D., Dobson, A.P., Begon, M., Bowers, R.G. & Schauber, E.M. (2003). Parasite establishment in host communities. Ecol. Lett., 6, 837-842. – reference: Service, M.W. (1991). Agricultural development and arthropod-borne diseases: a review. Rev. 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Multiline cultivars as a means of disease control. Ann. Rev. Phytopath., 59, 355-382. – reference: 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. Proc. Natl. Acad. Sci., 100, 567-571. – reference: Mitchell, C.A., Tilman, D. & Groth, J.V. (2002). Effects of grassland plant species diversity, abundance, and composition on foliar fungal disease. Ecology, 83, 1713-1726. – reference: Daszak, P., Cunningham, A.A. & Hyatt, A.D. (2000). Emerging infectious diseases of wildlife: threats to biodiversity and human health. Science, 287, 443-449. – reference: Ruedas, L.A., Salazar-Bravo, J., Tinnin, D.S., Armién, B., Cáceres, L., García, A. et al. (2004). Community ecology of small mammal populations in Panamá following an outbreak of Hantavirus pulmonary syndrome. J. Vector Ecol., 29, 177-191. – reference: Mitchell, C.A., Reich, P.B., Tilman, D. & Groth, J.V. (2003). 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Trophically transmitted parasites and the conservation of small populations: Raccoon roundworm and the imperiled Allegheny woodrat. Conserv. Biol., 17, 258-266. – reference: Macdonald, G. (1957). The Epidemiology and Control of Malaria. Oxford University Press, London. – reference: Rosà, R., Pugliese, A., Norman, R. & Hudson, P.J. (2003). Thresholds for disease persistence in models for tick-borne infections including non-viraemic transmission, extended feeding and tick aggregation. J. Theor. Biol., 224, 359-376. – reference: Allan, B.F., Keesing, F. & Ostfeld, R.S. (2003). Effects of habitat fragmentation on Lyme disease risk. Cons. Biol., 17, 267-272. – reference: Dobson, A.P. & Hudson P.J. (1986). Parasites disease and the structure of ecological communities. TREE, 1, 11-15. – reference: Randolph, S.E. (1979). Population regulation in ticks: the role of acquired resistance in natural and unnatural hosts. Parasitology, 79, 141-156. – reference: Schmidt, K.A. & Ostfeld, R.S. (2001). Biodiversity and the dilution effect in disease ecology. Ecology, 82, 609-619. – reference: Gilbert, L., Norman, R., Laurenson, K., Reid, H.W. & Hudson, P.J. (2001). Disease persistence and apparent competition in a three-host community: an empirical and analytical study of large-scale,wild populations. J. Anim. Ecol., 70, 1053-1061. – reference: Ostfeld, R.S. & Keesing, F. (2000a). Biodiversity and disease risk: the case of Lyme disease. Conserv. Biol., 14, 722-728. – reference: Knops, J.M.H., Tilman, D., Haddad, N.M., Naeem, S., Mitchell, C.E., Haarstad, J. et al. (1999). Effects of plant species richness on invasion dynamics, disease outbreaks, insect abundances and diversity. Ecol. Lett., 2, 286-293. – reference: Ostfeld, R.S. & LoGiudice, K. (2003). Community disassembly, biodiversity loss, and the erosion of an ecosystem service. Ecology, 84, 1421-1427. – reference: Farrell, J.A.K. (1976). 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SubjectTerms | Animals Biodiversity Communicable Diseases - epidemiology Communicable Diseases - transmission dilution effect disease ecology disease prevalence disease transmission Disease Vectors diversity Ecology ecosystem function host hosts Humans infectious diseases Models, Theoretical pathogen pathogens Population Density Prevalence risk Risk Factors species diversity |
Title | Effects of species diversity on disease risk |
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