The subject of infectious disease became both fascinating and uncomfortably relevant with the global breakout of Covid-19 in early 2020. Are bats to blame, hunting and selling of wild game or seafood markets? It turns out that the destruction of nature is the root problem, according to the UN environment chief and lead scientists for the Intergovernmental Panel on Biodiversity and Ecosystem Services (IPBES). “Covid-19 is nature sending us a message,” writes the UN environment chief and colleague [Dasgupta & Anderson 2020]. They continue:
In fact, it reads like an SOS signal for the human enterprise, bringing into sharp focus the need to live within the planet’s means. The environmental, health and economic consequences of failing to do so are disastrous [Dasgupta & Anderson 2020].
“Covid-19 is nature sending us a message. In fact, it reads like an SOS signal for the human enterprise, bringing into sharp focus the need to live within the planet’s means. The environmental, health and economic consequences of failing to do so are disastrous.” – Sir Partha Dasgupta & Ingar Anderson
An April 2020 IPBES article [Settele 2020] echoes this alert:
As with the climate and biodiversity crises, recent pandemics are a direct consequence of human activity – particularly our global financial and economic systems, based on a limited paradigm that prizes economic growth at any cost.
… Our actions have significantly impacted more than three quarters of the Earth’s land surface, destroyed more than 85% of wetlands and dedicated more than a third of all land and almost 75% of available freshwater to crops and livestock production [Settele 2020].
“With more than 70% of all emerging diseases affecting people having originated in wildlife and domesticated animals,” the IPBES team explains, “activities that bring increasing numbers of people into direct contact and often conflict with the animals that carry these pathogens” lead to pandemics [Settele 2020].
A study [Rulli 2017] linking forest fragmentation with outbreaks of Ebola virus disease in West and Central Africa bears out this assessment. The authors stress that infectious disease emergence is among the many dangers stemming from ecosystem destruction.
The impact of forest loss on ecosystems and the services they provide is often evaluated in terms of habitat destruction, losses of biodiversity, carbon stock and emissions, land degradation, or altered climate and hydrologic conditions. This study, however, highlights that deforestation and forest fragmentation potentially have another important class of externalities associated with global health and zoonotic disease outbreaks [Rulli 2017: 5].
Using satellite data on forest cover change from 2000 to 2014, these researchers found that all 11 sites of the first human Ebola infections since 2004 occurred in close proximity (within 25 km) to areas with higher rates of forest fragmentation than the regional average. Similarly, the closer one approached to the centers of first infection, the greater the fragmentation.
What is forest fragmentation? It is the cutting of forest into isolated patches and irregular shapes, resulting in greater lengths of edge between forested and non-forested areas. The increased length of forest perimeter in turn increases contact between humans and the wildlife that are potential disease agents, which would not otherwise be crossing our paths.
In addition to increasing human-wildlife contact, forest fragmentation favors some species while harming or obliterating others, throwing the whole system out of balance. Various studies have shown that the animals that thrive in degraded ecosystems are the same ones that constitute reservoirs of diseases communicable to humans. For example, in the case of West and Central Africa, the species suspected in the emergence of Ebola in humans include gorillas, chimpanzees, duikers (similar to an antelope) and a handful of bat species, all of which have been observed to increase in density following forest disturbance.
In addition to increasing human-wildlife contact, forest fragmentation favors some species while harming or obliterating others, throwing the whole system out of balance.
Thus, it could be argued that while disturbance by deforestation destroys the habitat of specialist species, generalists – possibly including reservoirs of some zoonotic pathogens – thrive, thereby further enhancing the risk of infection in human populations close to the forest margins [Rulli 2017: 5].
A similar observation was made in North America. The white-footed mouse, an extremely “competent” host for Lyme Disease – meaning highly capable of harboring and transmitting the Lyme bacteria – does well in degraded forests, while many less competent hosts require more diverse, intact forests to thrive. Opossums, for instance, do poorly in impoverished ecosystems and also do not transmit the Lyme bacterium as readily as mice do. Furthermore, opossums kill ticks attempting to feed on them, making them a poorer host for the tick vector as well.
There may be a direct link between a species’ susceptibility to habitat degradation and its quality as a disease host. Among vertebrates,
resilience in the face of disturbances that cause biodiversity loss, such as habitat destruction and fragmentation, is facilitated by life history features such as high reproductive output and intrinsic rates of increase. Vertebrates with these features tend to invest minimally in some aspects of adaptive immunity; we hypothesize that this may make them more competent hosts for pathogens and vectors [Keesing 2010: 650].
The loss of less-competent disease host species, or of predators, for example, that would otherwise control a competent host population, thus allowing the latter to flourish, can create an “amplification effect.” The resulting higher concentration of competent hosts increases the likelihood of vector contact with infected hosts, thus increases disease transmission.
The amplification effect was observed also in the case of West Nile Virus (WNV) in North America in 2003-2004 [Ostfeld 2009]. Counties with higher passerine (perching) bird diversity were found to have lower human incidence of WNV disease, presumably due to lower concentrations of the bird species that were the primary disease reservoirs. With higher bird diversity, mosquito vectors were less likely to get infected due to a greater prevalence of uninfected birds upon which to feed.
With higher bird diversity, mosquito vectors were less likely to get infected due to a greater prevalence of uninfected birds upon which to feed.
Given multiple studies of particular disease systems like the ones described above indicating that biodiversity inhibits the spread of disease, another group of scientists [Civitello 2015] wanted to know how broadly and generally the amplification effect applies. Were these disease systems special cases, or do they suggest an inherent relationship between biodiversity and disease? Inverse of the amplification effect, “the dilution effect hypothesis suggests that diverse ecological communities limit disease spread via several mechanisms. Therefore, biodiversity losses could worsen epidemics that harm humans and wildlife” [Civitello 2015: 8667], the authors state to contextualize their research. They analyzed 202 studies of biodiversity and parasite abundance, and found “overwhelming evidence of dilution, which is independent of host density, study design, and type and specialization of parasites” [Civitello 2015: 8667]. From these results, it can be inferred that biodiversity generally limits infectious disease.
This message has not gone unheard by some in the public health field. An article [Granter 2016] published in the American Society of Clinical Pathology argues for health practitioners to become aware of the human health implications of environmental destruction, stating that:
Knowledge and prowess with infectious diseases for diagnosticians must be incorporated back into training with a reimagined lens crafted from the information we have gained by studying our environment, its destruction, and the ultimate resulting human infections [Granter 2016: 645].
A research team that included ecologists and a Center for Disease Control staff member [Kilpatrick 2017] analyzed the inclusion of biodiversity conservation among key public health tools. Without further research, the authors remain hesitant to recommend conservation generally as a public health tool (except insofar as exposure to nature boosts human wellbeing). However, they suggest that targeted interventions, such as reintroducing top predators to control host populations, installing bat or owl boxes to increase predation of mosquitos (vectors) or rodents (hosts) could be feasible public health interventions against infectious disease.
In their IPBES letter, Settele and colleagues  recommend the adoption of a “One Health” approach to public health. This concept recognizes the fundamental interdependence of humans, animals, plants and our shared environment, and stresses the importance to human health of the overall health of nature. Some assessments paint that interdependence in even starker terms: “Zoonoses [human diseases of animal origin] reveal that environmental stewardship is not simply related to public health; in many cases, they are the same,” writes science journalist Ferris Jabr .
In their IPBES letter, Settele and colleagues  recommend the adoption of a “One Health” approach to public health. This concept recognizes the fundamental interdependence of humans, animals, plants and our shared environment, and stresses the importance to human health of the overall health of nature.
Indeed, humans are not the only species to experience disease epidemics. Bovine tuberculosis, honeybee varroasis, rabbit hemorrhagic disease virus, herpes virus in pilchard fish, West Nile virus in birds, and amphibians worldwide ravaged by a fungal disease are a few examples of how other species suffer. The underlying factors causing livestock, wildlife and human epidemics are anthropogenic environmental change driven by globalization of agriculture, commerce and human travel, all of which spread disease. Habitat destruction and toxic pollution are additional factors [Daszek 2001].
Compendium readers will be aware that biodiverse, intact ecosystems provide multiple vital functions. Healthy ecosystems absorb stormwater, forestall drought, generate rain, cool the air and land, purify air and groundwater, and pollinate crops, for example, not to mention contributing to human psychological wellbeing by providing recreational opportunities and beauty. What pandemics like Covid19 have now made us aware of is that biodiversity also plays a key role in limiting the emergence and spread of infectious disease.
Biodiversity loss and pandemics article summaries
Anthropogenic environmental change and the emergence of infectious diseases in wildlife, Daszak, Cunningham & Hyatt 2001
Humans are not the only species to suffer global pandemics. Planetwide, fungal disease ravages amphibians, just as honeybees are ravaged by varroasis. A herpes virus caused mass mortality of pilchard fish off the coast of Australia and New Zealand in 1995, and seals from Antarctica to the Caspian Sea have contracted canine distemper viruses, for which domestic dogs are also hosts.
The authors point to multiple anthropogenic environmental changes as the underlying causes of disease emergence among wildlife, livestock and humans.
Emerging infectious diseases (EIDs) are deﬁned as diseases that have recently increased in incidence or geographic range, recently moved into new host populations, recently been discovered or are caused by newly-evolved pathogens [Daszak 2001: 103].
Two major known causes of disease emergence in wildlife are (1) “spillover” of livestock disease into wild populations; and (2) pathogen pollution, which stems from the global transport of domestic and wild animals, and contaminated products and materials. In addition, habitat destruction and fragmentation, and toxic pollution, are likely to contribute to disease emergence, although these factors hadn’t been as well studied (at least at the time of the writing in 2001).
The authors conclude with the following observation:
We have described a group of wildlife diseases that can be classiﬁed as emerging in the same way as human EIDs. These represent a link in the chain of emergence of human and domestic animal diseases, with pathogens, habitats and environmental changes shared between these populations. Parallels between causes of emergence across these groups of diseases demonstrates an important concept: that human environmental change may be the most signiﬁcant driver of wildlife, domestic animal and human EIDs [Daszak 2001: 112].
Effects of species diversity on disease risk, Keesing, Holt & Ostfeld 2006
This review article describes the potential mechanisms by which biodiversity affects disease risk. The authors explore the mechanisms at play in simple systems with only host and pathogen, as well as in more complex systems that include a vector species and/or multiple hosts. The reduction of disease risk by increased diversity is called the “dilution effect.” The opposite, termed the “amplification effect,” is when disease risk increases. “Both models and literature reviews suggest that high host diversity is more likely to decrease than increase disease risk” [Keesing 2006: 485].
The mechanisms by which diversity affects disease risk are as follows:
Encounter reduction: An additional species (such as a predator) suppresses the movement of host species or vector species, thereby reducing contact between susceptible hosts and infected hosts or vectors. (Alternatively, if the presence of a different species causes host species to clump together more among their own kind, then transmission could increase in an encounter augmentation.)
Transmission reduction: An additional species in a system (such as a prey) reduces host stress, boosting immune system response and lowering pathogen load. An added species could also modify host behavior in a way that reduces the duration of their encounters and thus limits transmission.
Vector or susceptible host [population] regulation: The addition of any species that reduces birth rates or increases death rates, limiting overall population, among hosts susceptible to the pathogen or among pathogen vectors. Transmission rates may be reduced, for example, with the addition of host species predators or with the addition of species that attract vectors (ticks, for instance), but then groom themselves in a way that kills many vector individuals.
Infected host mortality: An added species outcompetes infected hosts for resources or targets infected hosts for predation.
Recovery augmentation: The addition of a prey species as an added resource for host species could, for example, increase full recovery rates of host species, creating a dilution effect, or, by contrast, increase the longevity of sick hosts in an amplification effect.
When there are many hosts for a particular pathogen, some species transmit the disease more readily than others. Often, the species that most effectively spread the disease (the most competent reservoirs) are present in species-poor, degraded ecosystems, meaning that any additional host species is likely to dilute the presences of the more contagious species.
One key question in multi-host disease systems is whether the most competent reservoir is present in species-poor communities. If so, species added to these communities have, by deﬁnition, lower (if any) reservoir competence and thus have the potential to decrease disease risk. If the most competent reservoir is not present in species-poor communities, by contrast, then an increase in diversity could include the addition of the most competent reservoir itself, which is likely to result in an ampliﬁcation of disease risk. Ostfeld & Keesing (2000b) considered evidence that the most competent reservoir for a variety of vector-borne zoonoses was typically present in species-poor communities [Keesing 2006: 495].
Biodiversity loss and the rise of zoonotic pathogens, Ostfeld 2009
West Nile Virus is an infectious disease that arrived in New York City in 1999, and subsequently spread across the country to the west coast. It is transmitted to humans from passerine (perching) birds via mosquito vectors. This study tested the dilution effect hypothesis, which posits that greater diversity (of birds in this case) reduces the concentration of species that are the primary disease reservoirs (American robin, American crow, blue jay, western scrub jay, common grackle, house ﬁnch, and house sparrow), thus reducing vector contact with infected individuals, and ultimately transmission to humans. The study analyzed the incidence of human infection during 2003-2004, and found that biodiversity was indeed associated with reduced WNV infection rates among humans.
For all 3 years, the county-level human incidence of WNV disease was strongly, and signiﬁcantly, negatively correlated with bird diversity within that county [Ostfeld 2009: 41].
Similar results are reported for studies of the dilution effect of biodiversity on Lyme disease risk. Furthermore, having collected data on the competence of various mammalian hosts to infect ticks with Lyme disease, as well as each host species’ average tick burden, the authors state that “we can project the number of ticks that will feed on them and the proportion of those ticks that will become infected” [Ostfeld 2009: 42].
We conclude from these studies that high vertebrate diversity is negatively correlated with human risk of exposure to Lyme disease. Furthermore, knowledge of the species composition of these communities, beyond simple measures of species richness or evenness, strongly enhances our ability to predict risk [Ostfeld 2009: 42].
Evidence for a protective dilution effect of high diversity has been obtained for numerous infectious diseases of humans, wildlife, and plants. The weight of evidence suggests that protection against exposure to infectious diseases should be added to the list of utilitarian functions of biodiversity [Ostfeld 2009: 42].
“Evidence for a protective dilution effect of high diversity has been obtained for numerous infectious diseases of humans, wildlife, and plants. The weight of evidence suggests that protection against exposure to infectious diseases should be added to the list of utilitarian functions of biodiversity [Ostfeld 2009: 42].
Impacts of biodiversity on the emergence and transmission of infectious diseases, Keesing et al. 2010
This paper contextualizes reduced transmission of infectious disease as one of the many ecosystem services provided by biodiversity. Changes in biodiversity affect infectious disease transmission by changing the abundance of the host and/or vector; the loss of non-host species may increase the density of host species, increasing the encounter rates between pathogen and host.
Often, the species that remain when biodiversity is lost are those which are better pathogen hosts, while the lost species tend to be more resistant to infectious disease.
In several case studies, the species most likely to be lost from ecological communities as diversity declines are those most likely to reduce pathogen transmission [Keesing 2010: 648].
For example, the white-footed mouse, which are high-quality hosts both for the bacteria causing Lyme Disease and for the tick vectors, are abundant in both biodiverse systems and impoverished systems, while opossums, a poorer host for the Lyme bacterium that also kill/eat most ticks attempting to feed on them, do poorly in lower-biodiversity conditions.
Therefore, as biodiversity is lost, the host with a strong buffering effect – the opossum – disappears, while the host with a strong amplifying effect – the mouse – remains [Keesing 2010: 650].
There may be a causal link between a species’ susceptibility to biodiversity loss and its quality as a disease host. Among vertebrates,
resilience in the face of disturbances that cause biodiversity loss, such as habitat destruction and fragmentation, is facilitated by life history features such as high reproductive output and intrinsic rates of increase. Vertebrates with these features tend to invest minimally in some aspects of adaptive immunity; we hypothesize that this may make them more competent hosts for pathogens and vectors [Keesing 2010: 650].
Biodiversity also affects the emergence of infectious disease, such as the evolution of a new strain of pathogen in the same host (due to antibiotic resistance, for example), and the spillover to a new host species. Pathogen establishment in humans from other animal hosts is related to mammal species richness (a larger source pool), and land-use change (such as deforestation), which increases contact between humans and pathogen hosts. The pathogen then becomes an epidemic due to the new host species’ density (domesticated animals and humans).
The authors recommend preserving biodiversity by protecting natural habitat, while also preserving microbial diversity within organisms by limiting the use of antimicrobial agents. A diverse microbiome within an organism serves as a buffer against pathogens.
Biodiversity inhibits parasites: Broad evidence for the dilution effect, Civitello et al. 2015
Human activities are dramatically reducing biodiversity, and the frequency and severity of infectious disease outbreaks in human, wildlife, and domesticated species are increasing. These concurrent patterns have prompted suggestions that biodiversity and the spread of diseases may be causally linked. For example, the dilution effect hypothesis proposes that diverse host communities inhibit the abundance of parasites through several mechanisms, such as regulating populations of susceptible hosts or interfering with the transmission process. Thus, diverse communities may inhibit the proliferation of parasites, thereby promoting the stability of ecological communities and ecosystem services (e.g., nutrient cycling, carbon sequestration, and natural product production) [Civitello 2015: 8667].
This meta-analysis concludes that as a general rule across ecosystems, biodiversity inhibits parasitism. Previous studies had focused on particular host-parasite systems, and found that greater host diversity dilutes, or limits, the spread of disease. “Consequently, anthropogenic declines in biodiversity could increase human and wildlife diseases and decrease crop and forest production” [Civitello 2015: 8667].
Where the Wild Things Aren’t: Loss of Biodiversity, Emerging Infectious Diseases, and Implications for Diagnosticians, Granter 2016
This status-quo-challenging editorial is written for the American Society of Clinical Pathology, a group seemingly unrelated to the Bio4Climate community. The authors suggest that medical training in pathology over-emphasizes oncology at the expense of an adequate coverage of infectious disease, even though “between 1940 and 2004, a total of 335 human infectious diseases ‘emerged,’ and 60% of these were zoonotic” [Granter 2016: 645]. Having explained biodiversity loss as a factor driving disease rates, the authors make a plea for diagnosticians to become aware of the human health implications of environmental destruction.
Knowledge and prowess with infectious diseases for diagnosticians must be incorporated back into training with a reimagined lens crafted from the information we have gained by studying our environment, its destruction, and the ultimate resulting human infections. As loss of habitat, habitat fragmentation, and consequent biodiversity loss continue unabated, tools and skills will need to be in the hands of all diagnosticians if we hope to minimize the effect of these infections as they continually emerge [Granter 2016: 645].
This paper provides a particularly clear explanation of how biodiversity loss increases human infection risk.
The relationship between loss of biodiversity and human disease was first illustrated by Lyme disease. Its cause, the Borrelia burgdorferi bacterium, has the opportunity to encounter numerous vertebrate hosts – in one study estimated to be at least 125 species – in a diverse and healthy ecosystem. The potential hosts vary tremendously in their ability to harbor and transmit the bacteria, that is, their “reservoir competence.” Studies estimate the white-footed mouse infects more than 90% of ticks that complete their blood meal. While a few other hosts, such as eastern chipmunks and short-tailed shrews, are moderately competent, most tick hosts are marginally competent or dead-end hosts that are highly unlikely to transmit the infection. Since the white-footed mouse tends to thrive in impoverished ecosystems lacking biodiversity, infected ticks and, consequently, risk of human infection show a strong negative relationship with biodiversity. Because a diverse ecosystem with a range of vertebrate hosts – including many incompetent and dead-end hosts – “dilutes” the representation of the white-footed mouse and reduces human infection risk, this phenomenon has been termed the dilution effect [Granter 2016: 644].
“Because a diverse ecosystem with a range of vertebrate hosts – including many incompetent and dead-end hosts – “dilutes” the representation of the white-footed mouse and reduces human infection risk, this phenomenon has been termed the dilution effect” [Granter 2016: 644].
Conservation of biodiversity as a strategy for improving human health and wellbeing, Kilpatrick et al. 2017
This article very pragmatically addresses the question of whether biodiversity conservation could be an effective public health tool against infectious disease emergence and transmission.
Determining whether biodiversity conservation is an effective public health strategy requires answering four questions: (1) Is there a general, causal relationship between host biodiversity and disease risk? (2) If the link is causal and negative for most pathogens, does the increased diversity of pathogens with more diverse host communities result in net total increase or decrease in infectious disease burden? (3) Is the net benefit of biodiversity conservation greater than the net benefit of diversity-degrading processes (agricultural land-use change and wild animal harvesting)? (4) Are conservation interventions feasible and cost-effective compared to standard public health approaches (vaccines and treatments)?
Regarding the first question, experimental and observational research shows that increased biodiversity is associated with reduced disease burden.
Overall, the available data suggests that there is some correlational support in many zoonotic systems for a dilution effect, and that some species or species groups are more important than others in transmission [Kilpatrick 2017: 4].
The dilution effect hypothesis originated to explain the Lyme disease system. Greater numbers of hosts that are less “competent” (at spreading Lyme disease) – opossums, birds, raccoons and skunks – dilutes the transmission of Lyme bacteria to larval ticks by more competent hosts – white-footed mice, eastern chipmunks and shrews. Changes in community diversity affect, for example, host-vector encounter rates and host and vector abundances.
much more research is needed to show that observed correlations are causal and to identify the mechanisms by which diversity is influencing disease risk [Kilpatrick 2017: 4].
The possibility of confounding factors in observational field studies is high because the same disturbances that change host diversity alters other aspects of transmission as well. For example, an ecosystem disturbance may, in addition to decreasing host diversity, also increase vector abundance, making it difficult to discern the proximate cause of increased disease rates. The authors note that the dilution effect may well cause decreased disease rates – more research is needed to determine this. But they caution that if the dilution effect turns out not to be the direct cause of decreased disease rates in any given pathogen system, then interventions to increase host diversity could be in vain with respect to that desired outcome.
Examples of potential conservation interventions to improve public health include preserving or restoring forest land, reintroducing top predators to control host populations, installing bat or owl boxes to increase predation of mosquitos (vectors) or rodents (hosts). Our still limited understanding of the mechanisms driving disease incidence patterns, however, make it difficult to predict outcomes for broad-scale land-use interventions, according to the authors. They argue instead that more targeted interventions aiming to reduce populations of key hosts in transmission may be more feasible public health tools than general land preservation. Even this, however, requires “deep understanding of both disease and population ecology.”
Further research to address this knowledge gap may be worth the investment, both for human wellbeing and for the planet. Exposure to nature has been shown to improve human mental and physical health and wellbeing, the authors note, regardless of biodiversity’s potential to reduce infectious disease. Furthermore,
If diverse communities can be shown to provide net benefits to human wellbeing, this could provide a powerful motivation for preserving Earth’s remaining biodiversity [Kilpatrick 2017: 7].
The nexus between forest fragmentation in Africa and Ebola virus disease outbreaks, Rulli et al. 2017
Ebola virus disease outbreaks in West and Central Africa have been linked to spillover from potential disease reservoirs such as bats, apes, and duikers (an antelope-like animal). Spillover has been thought to be related to population density, vegetation cover, and human activities such as hunting, poaching, and bushmeat consumption. In this study, forest data from satellites coupled with disease outbreak records identify a nexus between forest fragmentation and Ebola.
The researchers identified 11 sites of the first human infection of Ebola from a wild species having occurred since 2004. Changes in forest cover between the year 2000 (baseline year) and the years of first infection for each of these outbreaks were determined using high-resolution satellite data on tree cover. All 11 centers of infection were found to be located in forested areas where the rate of forest fragmentation was greater than the regional average. Similarly, forest fragmentation decreased with increasing distance from the centers of infection.
All 11 centers of infection were found to be located in forested areas where the rate of forest fragmentation was greater than the regional average.
The centers of first infection … tend to occur in areas where on the outbreak year the average degree of forest fragmentation (e.g., within a 25 km, 50 km or 100 km distance from the infection center) was significantly higher than in the rest of the region [Rulli 2017: 2].
Furthermore, eight of the 11 centers of infection were located in fragmentation “hotspots,” meaning within a cluster of highly fragmented forest areas.
Bats are the commonly accepted host to filoviruses such as Ebola and tend to increase in population in fragmented habitats. The geographic distribution of potential bat hosts was consistent with the distribution of the zoonotic niche of Ebola. A decline in the population of insectivorous bats and an increase in the frugivorous (fruit-eating) bat species as a result of forest fragmentation was observed. Reshaping forest boundaries, habitat disruption, and biodiversity loss may enhance the likelihood of zoonotic infection by increasing the abundance of a particular species and thus the prevalence of that species’ pathogens.
The fact that spillover tends to occur in hotspots of forest fragmentation rather than in clearcut areas suggests that chances of human interactions with host wildlife are higher in areas where human encroachment leaves forest fragments that provide habitat for reservoir species [Rulli 2017: 5].
Pressure on land and its products is increasingly pushing people into forested areas. Given the danger of zoonotic disease outbreak, any evaluation of the costs, risk, and benefits of forest loss and fragmentation should include global health considerations.
Habitat fragmentation, biodiversity loss and the risk of novel infectious disease emergence, Wilkinson 2018
Habitat loss reduces biodiversity, which leads to infectious disease emergence. The way a habitat is fragmented (how many patches it is divided into, how those patches are shaped, and what the distance is between them) further affects the extent of disease emergence. Both the number of divisions of habitat into smaller patches and the irregularity of patch shapes tend to increase habitat perimeter, which in turn increases contact between disease agents and humans.
The hazard is greatest in places with greater pre-existing biodiversity, where there is a greater diversity of microbial pathogens and associated hosts. There is a double risk of developing wilderness areas in these places because there are more pathogens to begin with, and the resulting biodiversity loss tends to amplify disease transmission.
Human encroachment into species-rich habitats may simultaneously decrease biodiversity and increase exposure of people to novel microbes [Wilkinson 2018: 1].
Integration of wildlife and environmental health into a One Health approach, Sleeman et al. 2019
This article introduces the concept of One Health, a public health framework adopted by the Centers for Disease Control in 2009, which recognizes the interdependence of humans, animals and our shared environment. The concept has gained traction as a way to address health problems arising from global environmental change.
Climate change, loss of biodiversity, habitat fragmentation and pollution, and subsequent degradation of natural environments threaten the range of ecosystem services that support all life on this planet [Sleeman 2019: 91].
It was the challenge of responding to these complex [environmental] problems that led to the emergence of the concept of One Health, which is defined by the Centers for Disease Control and Prevention (CDC) as the collaborative effort of multiple disciplines and sectors – working locally, nationally, regionally and globally – with the goal of achieving optimal health outcomes, recognizing the interconnection among people, animals, plants and our shared environment. This definition acknowledges that human, domestic animal and wildlife health are interconnected within the context of ecosystem/environmental health and provides a useful conceptual framework for the development of solutions to global health and environmental challenges. Given this interconnection, it follows that actions aimed primarily at improving the health of one part of the human-animal-environmental triad may have unanticipated consequences for the system as a whole if the harms they may cause to the other components are not considered. However, previous authors have noted that, despite the acknowledged interdependencies, few public or livestock health interventions include a consideration of biodiversity conservation or ecosystem/environmental health. Instead, health-promoting interventions focus largely on single-sector outcomes and, thus, may miss the opportunity to concurrently optimize outcomes in the other two sectors [Sleeman 2019: 92].
The authors suggest that despite its potential, the One Health approach does not as yet fully integrate wildlife and environmental health, instead favoring human health. Yet failure to optimize the health of all three realms can lead to unexpected and outcomes, ironically increasing risk to humans in some cases. Therefore, the authors propose the clarification of One Health values and goals, and integration of a systems approach and a harm reduction perspective into the One Health framework.
Systems biology provides methods to understand how interactions among [interrelated and interdependent] parts [livestock, humans and wildlife, for example] give rise to the function and behavior of that system [Sleeman 2019: 96].
A harm reduction perspective recognizes that solutions to complex problems require a broad societal response and that elimination of risk is not feasible for most issues. Consequently, this perspective promotes collaborative, multisectoral approaches whereby reducing harm, despite uncertainty regarding the outcome, is valued over inaction spurred by a desire for a perfect solution [Sleeman 2019: 94].
Emerging human infectious diseases and the links to global food production, Rohr et al. 2019
Increasing agricultural production to feed >11 billion people by 2100 raises several challenges for effectively managing infectious disease. Of many factors examined in this article linking agricultural expansion to infectious disease, one is conversion of natural habitat to cropland or rangeland. Land conversion increases contact between wild animals, livestock and humans.
As natural ecosystems are converted to crop land or range land, interactions among humans, and domesticated and wild animals, could increase. … These interactions are crucial because 77% of livestock pathogens are capable of infecting multiple host species, including wildlife and humans, and based on published estimates from the 2000s, over half of all recognized human pathogens are currently or originally zoonotic, as are 60–76% of recent emerging infectious disease events [Rohr 2019: 451].
“As natural ecosystems are converted to crop land or range land, interactions among humans, and domesticated and wild animals, could increase” [Rohr 2019: 451].
Land conversion pushes humans and livestock up against wilderness areas, increasing contact between species with previously little to no contact. The jumping of a pathogen to a new host species is called “spillover.”
Spillover appears to be a function of the frequency, duration and intimacy of interactions between a reservoir and novel host population. For example, influenza is believed to have jumped from horses to humans soon after domesticating horses and then made additional jumps to humans from other domesticated animals, such as poultry and swine [Rohr 2019: 451].
Furthermore, agricultural intensification tends to involve greater concentrations of a single variety of a single species, increasing the risk that any new disease will spread quickly in the population.
A central tenet of epidemiology is that the incidence of many infectious diseases should increase proportionally with host density because of increased contact rates and thus transmission among hosts. Hence, increasing human and livestock densities could cause increases in infectious diseases unless investments in disease prevention are sufficient to prevent these increases [Rohr 2019: 451].
Industrial-scale confined livestock production is
vulnerable to devastating losses of animals to disease. For instance, in just the last 25 years, an influenza A virus (H5N1) and a foot-and-mouth outbreak led to the destruction of more than 1.2 million chickens and 6 million livestock in China and Great Britain, respectively, and a ‘mad cow disease’ epizootic led to the slaughter of 11 million cattle worldwide [Rohr 2019: 449].
Increased agricultural production tends to be accompanied by new irrigation infrastructure and increased pesticide, fertilizer and antibiotic use, all of which increase infectious disease risk. Dams (often created for irrigation schemes) increase risk of mosquito-borne disease. Antibiotic overuse for livestock fosters resistance among pathogens that can also infect humans. Greater pesticide use leads to resistance among disease vectors such as mosquitoes to insecticides, while also weakening immune systems among exposed humans and wildlife hosts, increasing infection rates/severity. Nutrient enrichment caused by fertilizer can also contribute to the spread of infectious disease, for example, through mosquitos or snail vectors.
Finally, the urbanization and globalization associated with agricultural intensification/expansion elongates food supply chains, which increases movement of people and goods over borders, spreading food-born illness, flu and other infections.
These analyses revealed that agricultural drivers were associated with 25% of all diseases and nearly 50% of zoonotic diseases that emerged in humans since 1940. These values are even higher if we include the use of antimicrobial agents as an agricultural driver of human disease emergence, given that agricultural uses of antibiotics outpace medical uses in the developed world nearly nine to one [Rohr 2019: 451].
The authors recommend numerous measures for improving agricultural production while limiting infectious disease, including reducing antibiotic use for livestock, conserving biodiversity, improving and diversifying livestock and crop genetic material, investing in urban agriculture, social investments, and inter-disciplinary research and collaboration.
Civitello, D., et al., 2015, Biodiversity inhibits parasites: broad evidence for the dilution effect, PNAS 112(28), https://www.pnas.org/content/112/28/8667.short.
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 Zoonotic diseases are those which are transmissible from animals to humans.
 Specialist species have specific, limited requirements for food and habitat, while generalists are more adaptable and can make do on a variety of food resources and environmental conditions.
 Vectors are organisms that can transmit a disease from an animal to a human or between humans.
 A host is an organism that can be infected by a given disease; from a virus’ perspective, a host organism is a suitable habitat.