Abstract
Habitat loss is one of the leading causes of declines of wild animal populations.17 In the last 20 yr, it has become clear that disease poses a serious threat to natural populations, especially those that are endangered, occasionally leading to significant declines or extinctions.13,18,19 Disease in wild animal populations has also been recognized as playing an important role in natural systems, often altering ecological communities.1,3,6,8 Currently, the literature reflects numerous examples of disease causing significant declines in wild animal populations.1,10,11,18-21 Among birds alone, avian malaria and pox in Hawaii, and West Nile virus and Mycoplasma conjunctivitis in North America, have caused significant population effects in susceptible species.2,12,19-21 Extinction resulting from habitat loss/fragmentation is well documented, and such land-use changes have also been shown to result in the creation of new and different host-pathogen relationships.1,5-7,14
A growing area of research within the field of disease ecology is aimed at understanding the direct relationship between disease and anthropogenic activity, which we now understand to play a significant role in wildlife health and its conservation.7 A variety of mechanisms have been proposed for this relationship, including 1) the introduction of pathogens into new geographic areas, 2) the alteration of habitat which changes the ecology and/or range of a pathogen or its vector, 3) alterations in habitat that have increased the contact between wildlife and domestic animals, or 4) alterations to climate that affect either the pathogen virulence or the host’s immune response.4-6,12,15,16 However, to date, there are few examples where avian biodiversity declines due to disease were investigated in the context of habitat change.9,18
The overall goal of our long-term project is to investigate how specific land use changes affect the health status of avian communities in a rural region of Ecuador. We are testing the hypothesis that anthropogenically affected habitats can change the susceptibility of a host to infection (through an increase in physiologic stress to the individual host, or through diminishing genetic heterogeneity in a population), the exposure of a host to a pathogen (through an increase of the contact rate between humans/domestic animals and wild birds, introduction of novel anthropogenic pathogens or increasing the range of vectors that transmit disease through microclimatic changes) or change the transmission potential of a pathogen (through the addition of bacterial genetic material in an environment that facilitates a change in virulence for bacteria). In Ecuador, a recent increase in the extent of human encroachment in the region surrounding the Maquipucuna Reserve has led to the degradation of forests, the introduction of domestic animals (including free-roaming chickens) and mismanagement of human/animal waste. For these reasons, we have chosen this area as our study site.
Backyard chickens may serve as potential pathogen reservoirs for wild birds in Maquipucuna. Our pilot study aimed to survey for avian pathogens present in the ecosystem by assessing the health of backyard chicken flocks. Ten flock owners living around the edge of Maquipucuna Reserve were interviewed to obtain information on flock management and husbandry. The mean flock size was 20 birds, and most birds were kept for eggs and meat, for either domestic consumption or local sale. Chickens were either sold at 24 mo or slaughtered at 36 mo. Vaccination rates were low, with most owners not vaccinating at all, and some vaccinating with one product either sporadically or annually. No owners deparasitized their animals. Mortality rates of offspring were reported as high as 50%, often associated with diseases causing neurologic signs, sudden death or respiratory problems. In addition, most owners reported observing epizootics of skin lesions consistent with avian pox. Most owners complained of their lack of knowledge about diseases affecting their chickens and lack of veterinary advice.
We conducted physical examinations and collected blood and ectoparasite samples from 100 randomly selected birds from 10 flocks. Commercial enzyme-linked immunosorbent assays (ELISA) on all sera revealed that the backyard chicken population showed evidence of exposure to the following avian pathogens: infectious bursal disease virus (100%), avian encephalomyelitis virus (92%), chicken anemia virus (90%), infectious bronchitis virus (85%), Newcastle disease (97%), Mycoplasma gallisepticum (73%), and M. synoviae (68%). Twenty percent of animals were reported positive for avian influenza; however, testing artifact might account for these results. Necropsy and limited fecal examinations found low levels of internal parasitism, with cestodes and ascarids identified as the most prevalent endoparasites. Ectoparasites were noted on all animals and identified as Dermanyssus gallinae and Ornithonyssus bursa. Most of the animals (90%) had mild-moderate feather mite infestations.
The poultry diseases to which sampled chickens had been exposed are likely the cause for the high mortalities reported by local flock owners. Because wild birds are susceptible to some poultry diseases, free-roaming chickens might be potential vectors of pathogens that could affect wild birds. Subsequent to this pilot study, we will examine the disease prevalence and diversity of distinct avian communities inhabiting four land use types (“eco-friendly” agricultural land, traditional agricultural land, secondary growth and primary growth forests). Specifically, this project will examine a variety of indices to generate a “health score” for these avian communities, in order to correlate their health status with the degree of anthropogenic disturbance.
Acknowledgments
The authors would like to thank the Maquipucuna Foundation for logistic support of this project and the following sponsors for providing financial support: Neurocare Consultants, Palm Beach, Florida; Bankers Equity, Athens, Georgia; Centurion Poultry, Athens, Georgia; HOPE Animal Medical Center, Athens, Georgia; Jittery Joe’s, Athens, Georgia; and Sigma XI Grants-In-Training. We would particularly like to acknowledge the chicken owners and the Santa Marianita community; without their trust and enthusiasm, this project could not have been realized. We would also like to thank Dr. Bolivar Valencia, who provided us with further logistic support in Ecuador.
Literature Cited
1. Altizer S., W.M. Hochachaka and A. Dhondt. 2004. Seasonal dynamics of Mycoplasma conjunctivitis in eastern North American house finches. J. Anim. Ecol. 73:309–322.
2. Altizer S. et al. 2003. Rapid evolutionary dynamics and disease threats to biodiversity. Trends Ecol. Evol. 18(11):589–596.
3. Anderson R.M., and R.M. May. 1978. Regulation and stability of host-parasite population interactions: I, Regulatory processes. J. Anim. Ecol. 47:219–247.
4. Blaustein, A. 2003. Diversity and Distributions. 9(2):123–141.
5. Cleaveland S. 1996. Canine distemper and rabies infection in wildlife in the Serengeti National Park. IUCN/SSC Vet. Spec. Group Newsl. 12:2–4.
6. Dasak P. et al. 2000. Emerging infectious diseases of wildlife-threats to biodiversity and human health. Science. 287:443–449.
7. Deem S.L., W.B. Karesh, and W. Weisman. 2001. Putting theory into practice: wildlife health in conservation. Conserv. Biol. 15:1224–1232.
8. Dobson, A.P., and B.T. Grenfell. 1995. Introduction. In: Ecology of Infectious Diseases in Natural Populations. B.T. Grenfell and A.P. Dobson (eds.). Publication of the Newton Institute, University of Cambridge.
9. Ford, H. 2001. Why have birds in the woodlands of southern Australia declined? Biol. Conserv. 97(1):71–88.
10. Jacobson, E.R. 1994. Causes of mortality and diseases in tortoises-a review. J. Zoo Wildl. Med. 25:2–17.
11. Laurance, W.F., K.R. McDonald, and R. Speare. 1996. Epidemic disease and the catastrophic decline of Australian rain forest frogs. Conserv. Biol. 10:406–413.
12. Marra, P.P., S. Griffin, C. Caffrey, A.M. Kilpatrick, R. McLean. C. Brand, E. Saito, A. Dupuis, L. Kramer, and R. Novak. 2004. West Nile virus and wildlife. BioScience. 54(5):393–402.
13. May, R.M. 1988. Conservation and disease. Conserv. Biol. 2:28–30.
14. McCallum, H. et al. 2002. Disease, habitat fragmentation and conservation. Proc. R. Soc. Lond., Ser. B: Biol. Sci. Vol 269(1504):2041–2049.
15. Molyneux, D. 2002. Vector-borne infections and health related to landscape changes. In: Aguirre A. et al. (eds.) Conservation Medicine: Ecological Health in Practice. Oxford University Press, New York, New York.
16. Ostfeld, R.S., and R.D. Holt. Are predators good for your health? Evaluating evidence for top-down regulations of zoonotic disease reservoirs. Frontiers Ecol. Environ. 2:13–20.
17. Sih, A., B.G. Johnson, and G. Luikart. 2000. Habitat loss: ecological, evolutionary and genetic consequences. Trends Evol. Ecol. 15:132–143.
18. Smith, G.R. 1982. Animal disease and conservation. Nature, Lond. 295:16.
19. Van Ripper, C. III, S.G. Van Riper, M.L. Goff and M. Laird. 1986. The epizootiology and ecological significance of malaria in Hawaiian land birds. Ecol. Monogr. 56:327–344.
20. Van Ripper, C. et al. 2002. Epizootiology and effect of avian pox on Hawaiian forest birds. The Auk. 119(4):929–942.
21. Woodroffe, R. 1999. Managing disease threats to wild mammals. Anim. Conserv. 2:185–193.