During the past 60 years, the number of emerging pathogens affecting humans has substantially increased (1
). Of these emerging infectious diseases, 62% are zoonotic (2
), meaning they are naturally hosted by, and persist in, wildlife but also affect human populations. The ecological factors associated with zoonotic disease emergence are likely complex and are poorly understood. Most often, because of limited time, resources, and the exigencies of the situation, outbreak investigations of emerging diseases seek only to discover the pathogen responsible for the disease in humans. But ecological studies are of critical importance to long-term containment of zoonotic disease emergence; they are the only way to ascertain the wildlife source of the disease, the dynamics of the host–pathogen relationship, and the ecological factors associated with an outbreak. Knowledge of all these factors is needed to proactively protect the public from zoonotic diseases; without this knowledge, new diseases will continue to emerge. The worldwide distribution of these largely zoonotic diseases suggests a globally distributed mechanism for their emergence.
Anthropogenic factors—including pollution, land-use conversions, and climate change—likely contribute to disease emergence by several mechanisms (3
), one of which has been hypothesized to be decreased species diversity. The number of species currently being lost, as well as the rate of species loss, is unprecedented (4
); these losses generally have negative effects on ecosystem functioning (5
). It likely is not coincidental that areas where many zoonoses are emerging among humans are the same areas where loss of species is accelerating, e.g., Central Africa (Ebola, monkeypox, Marburg virus), West Africa (Lassa virus, HIV-2), Southeast Asia (Nipah virus, severe acute respiratory syndrome, avian influenza), and South America (dozens of strains of hantaviruses and arenaviruses).
Lyme disease, a vector-borne zoonosis, is affected by loss of species by a process known as the dilution effect (7
), whereby increasing species diversity decreases disease prevalence by diluting the availability of competent hosts with increased numbers of noncompetent hosts. Little research on the dilution effect has been carried out beyond its effect on Lyme disease (8
), yet the global implications of the phenomenon—if the effects are applicable to other types of diseases and transmission dynamics—could have substantial and enduring effects on human health and conservation.
Hantaviruses provide a model system in which to test the dilution effect in directly transmitted zoonoses. Since their initial discovery in the Western Hemisphere in 1982, several dozen hantavirus strains have been found, each hosted by a unique rodent species (9
); novel hantaviruses have recently been discovered in shrews (10
). Natural hosts are asymptomatic and chronically infected; intraspecies spread is hypothesized to be through bites (12
). Humans become infected with hantavirus by inhaling aerosolized excreta from infected rodents (13
). Occasionally hantavirus pulmonary syndrome (14
) develops; this syndrome has a mortality rate of almost 40% and no prophylaxis, treatment, or cure (15
). Most of the 506 confirmed cases in the United States have been caused by Sin Nombre virus (SNV). Studies have found that low diversity ecosystems dominated by the rodent hosts for 3 distinct hantaviruses had high infection prevalence in the host (16
), suggesting a role for species diversity. Although the mechanism of disease dilution would differ in directly transmitted zoonoses (e.g., hantaviruses), as opposed to vector-borne diseases, a dilution effect could occur if 1) individuals of the host species remain as species diversity decreases, 2) the disease is spread within the host species through direct encounters (such as biting), and 3) presence of other species causes encounters among the host species to decrease.
Other ecological factors could affect the number of intraspecific deer mouse (Peromyscus maniculatus
) encounters, including increased density of deer mice and vegetative factors that lead to variation in population numbers (e.g., available cover and forage) (). Some studies have found high SNV prevalence in host populations when deer mice densities were high (18
). However, although the concept of density-dependent transmission is not unique to hantaviruses, its applicability to the deer mouse–SNV system has been elusive. SNV prevalence also has been shown to vary with habitat characteristics and quality (15
), although interpretation of this variation has been difficult because SNV prevalence varies as much within as among habitat types (20
Vegetative factors measured within each site and their transformations, Portland, Oregon, USA, October 2002−September 2005
In this study we examined small mammal populations in 5 forested sites over a 3-year period, October 2002 through September 2005. We monitored mammal species diversity, deer mouse densities, and SNV infection prevalence in the mammals to test the hypotheses that 1) areas of higher mammal species diversity would exhibit lower prevalence of SNV infection in host populations, 2) areas of higher host density would contain higher infection prevalence of SNV in the host populations, and 3) vegetative factors could be related to prevalence of SNV infection among deer mice.