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 inEcology letters Vol. 9; no. 4; pp. 485 - 498
Main Authors Keesing, F, Holt, R.D, Ostfeld, R.S
Format Journal Article
LanguageEnglish
Published Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.04.2006
Blackwell Publishing Ltd
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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.
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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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
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– 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.
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– reference: Hudson, P. & Greenman, J. (1998). Competition mediated by parasites: biological and theoretical progress. TREE, 13, 387-390.
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– 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. Saude Pública, 25, 167-178.
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– reference: Cecere, M.C., Gürtler, R.E., Chuit, R. & Cohen, J. (1997). Effects of chickens on the prevalence of infestation and population density of Triatoma infestans in rural houses of northwest Argentina. Med. Vet. Entomol., 11, 383-388.
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– 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.
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– reference: Caley, P.J. & Hone, J. (2004). Disease transmission between and within species, and the implications for disease control. J. Appl. Ecol., 41, 94-104.
– reference: Yahnke, C.J., Meserve, P.L., Ksiazek, T.G. & Mills, J.N. (2001). Patterns of infection with Laguna Negra virus in wild populations of Calomys laucha in the central Paraguayan chaco. Am. J. Trop. Med. Hyg., 65, 768-776.
– reference: Grosholz, E.D. (1992). Interactions of intraspecific, interspecific, and apparent competition with host-pathogen population dynamics. Ecology, 73, 507-514.
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Snippet The transmission of infectious diseases is an inherently ecological process involving interactions among at least two, and often many, species. Not...
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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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Volume 9
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