The Ecology of Pathogen Spillover and Disease Emergence at the Human-Wildlife-Environment Interface

Alexander, Kathleen A.; Carlson, Colin J.; Lewis, Bryan; Getz, Wayne M.; Marathe, Madhav V.; Eubank, Stephen; Sanderson, Claire; Blackburn, Jason K.

doi:10.1007/978-3-319-92373-4_8

Cited by 57 publications

(57 citation statements)

References 86 publications

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“…S. scabiei infestation in multiple hosts including humans, companion animals, farm animals, lab animals, and wild animals throughout the globe points toward pathogen dispersal and spillover [47,48]. Bidirectional interactions among human, animals, pathogen, and environment might be the underlying reason behind its multi-host adaptation [49]. As morphological and serological tests are not much successful at variety level identification, molecular markers have emerged as alternative differential diagnostic tools.…”

Section: Discussionmentioning

confidence: 99%

Host-Parasite Interaction in Sarcoptes scabiei Infestation in Porcine Model with a Preliminary Note on Its Genetic Lineage from India

Sawhney

Mondal

et al. 2020

Animals

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The burrowing mite Sarcoptes scabiei causes scabies in humans or mange in animals. It infests a wide range of mammalian species including livestock, companion animals, wild animals, and humans. Differential diagnosis of Sarcoptes varieties is key for epidemiological studies and for formulation of an eradication program. Host-parasite interaction at the systemic level is very important to understand the pathogenicity of the mite. This communication deals with the preliminary report on the genetic characterization of S. scabiei from India. Moreover, the effect of S. scabiei infestation on host physiology with special emphasis on serum biochemical parameters, lipid profile, oxidant/antioxidant balance, stress parameters, and immune responses were evaluated in a porcine model. Cytochrome C oxidase 1 and voltage-sensitive sodium channel based phylogenetic study could distinguish human and animals isolates but could not distinguish host or geographical specific isolates belonging to animal origin. An absence of host-specific cluster among animal isolates argues against the hypothesis of delineating S. scabiei as per host origin. Elevated levels of markers of liver function such as albumin, AST, ALT, ALP, and LDH in infested animals indicated impaired liver function in infested animals. S. scabiei infestation induced atherogenic dyslipidemia indicated by elevated levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides, and a decreased level of high-density lipoprotein cholesterol. Oxidative stress in infested animals was indicated by a high level of nitric oxide and serum MDA as oxidative stress markers and low antioxidant capacity. S. scabiei triggered stress response and elevated levels of serum cortisol and heat shock proteins were recorded in infested animals. S. scabiei infestation increased the serum concentration of immunoglobulins and was associated with up-regulation of IL-2, IFN-γ, IL-1β, and IL-4 indicating both Th1 and Th2 response. The results of the study will be helpful for a better understanding of host-parasite interaction at the systemic level in crusted scabies in pigs.

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Section: Discussionmentioning

confidence: 99%

Host-Parasite Interaction in Sarcoptes scabiei Infestation in Porcine Model with a Preliminary Note on Its Genetic Lineage from India

Sawhney

Mondal

et al. 2020

Animals

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“…In the process, many animals will bring their parasites and pathogens into new environments 4,11 , creating new evolutionary opportunities for host jumps 8 . Most conceptual frameworks for cross-species transmission revolve around how these host jumps facilitate the spillover of new zoonotic pathogens into humans 12,13,14 , but viral evolution is an undirected process 15 , in which humans are only one of over 5,000 mammal species with over 12 million possible pairwise combinations 16 . Despite their indisputable significance, zoonotic emergence events are just the tip of the iceberg; almost all cross-species transmission events will occur among wild mammals, largely undetected and mostly inconsequential for public health.…”

Section: Main Textmentioning

confidence: 99%

Climate change will drive novel cross-species viral transmission

Carlson

Albery

Merow

et al. 2020

Preprint

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14Between 10,000 and 600,000 species of mammal virus are estimated to have the 15 potential to spread in human populations, but the vast majority are currently cir-16 culating in wildlife, largely undescribed and undetected by disease outbreak surveil-17 lance 1,2,3 . In addition, changing climate and land use drive geographic range shifts 18 in wildlife, producing novel species assemblages and opportunities for viral sharing 19 between previously isolated species 4,5 . In some cases, this will inevitably facilitate 20 spillover into humans 6,7 -a possible mechanistic link between global environmental 21 change and emerging zoonotic disease 8 . Here, we map potential hotspots of viral 22 sharing, using a phylogeographic model of the mammal-virus network, and projec-23 tions of geographic range shifts for 3,870 mammal species under climate change and 24 land use scenarios for the year 2070. Shifting mammal species are predicted to ag-25 gregate at high elevations, in biodiversity hotspots, and in areas of high human pop-26 ulation density in Asia and Africa, sharing novel viruses between 3,000 and 13,000 27 times. Counter to expectations, holding warming under 2°C within the century 28 does not reduce new viral sharing, due to greater range expansions-highlighting 29 the need to invest in surveillance even in a low-warming future. Most projected vi-30 ral sharing is driven by diverse hyperreservoirs (rodents and bats) and large-bodied 31 predators (carnivores). Because of their unique dispersal capacity, bats account for 32 the majority of novel viral sharing, and are likely to share viruses along evolutionary 33 pathways that could facilitate future emergence in humans. Our findings highlight 34 the urgent need to pair viral surveillance and discovery efforts with biodiversity 35 surveys tracking range shifts, especially in tropical countries that harbor the most 36 emerging zoonoses. 37 2 Main Text 38In the face of rapid environmental change, survival for many species depends on moving 39 to track shifting climates. Even in a best case scenario, many species are projected 40 to shift a hundred kilometers or more in the next century 9,10 . In the process, many 41 animals will bring their parasites and pathogens into new environments 4,11 , creating new 42 evolutionary opportunities for host jumps 8 . Most conceptual frameworks for cross-species 43 transmission revolve around how these host jumps facilitate the spillover of new zoonotic 44 pathogens into humans 12,13,14 , but viral evolution is an undirected process 15 , in which 45 humans are only one of over 5,000 mammal species with over 12 million possible pairwise 46 combinations 16 . Despite their indisputable significance, zoonotic emergence events are 47 just the tip of the iceberg; almost all cross-species transmission events will occur among 48 wild mammals, largely undetected and mostly inconsequential for public health. 49Of the millions of possible pairwise viral exchanges, the vast majority are biologically 50 implausible, as host specie...

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“…Growing global human population and population shift due to urbanization have increased exposure of domestic and wild animals and humans. Consequently, the evolving human–animal–environment interactions have significantly increased chances of potential spillover of viruses from domestic and or wild animals to humans [ 155 ]. Emerging infections caused by Ebola, Nipah, Hendra, influenza, and coronaviruses in the highly populated regions of Asia and Africa have been evident in the last two decades [ 156 , 157 ].…”

Section: Discussionmentioning

confidence: 99%

Sialic Acid Receptors: The Key to Solving the Enigma of Zoonotic Virus Spillover

Kuchipudi

Nelli

Gontu

et al. 2021

Viruses

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Emerging viral diseases are a major threat to global health, and nearly two-thirds of emerging human infectious diseases are zoonotic. Most of the human epidemics and pandemics were caused by the spillover of viruses from wild mammals. Viruses that infect humans and a wide range of animals have historically caused devastating epidemics and pandemics. An in-depth understanding of the mechanisms of viral emergence and zoonotic spillover is still lacking. Receptors are major determinants of host susceptibility to viruses. Animal species sharing host cell receptors that support the binding of multiple viruses can play a key role in virus spillover and the emergence of novel viruses and their variants. Sialic acids (SAs), which are linked to glycoproteins and ganglioside serve as receptors for several human and animal viruses. In particular, influenza and coronaviruses, which represent two of the most important zoonotic threats, use SAs as cellular entry receptors. This is a comprehensive review of our current knowledge of SA receptor distribution among animal species and the range of viruses that use SAs as receptors. SA receptor tropism and the predicted natural susceptibility to viruses can inform targeted surveillance of domestic and wild animals to prevent the future emergence of zoonotic viruses.

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The Ecology of Pathogen Spillover and Disease Emergence at the Human-Wildlife-Environment Interface

Cited by 57 publications

References 86 publications

Host-Parasite Interaction in Sarcoptes scabiei Infestation in Porcine Model with a Preliminary Note on Its Genetic Lineage from India

Host-Parasite Interaction in Sarcoptes scabiei Infestation in Porcine Model with a Preliminary Note on Its Genetic Lineage from India

Climate change will drive novel cross-species viral transmission

Sialic Acid Receptors: The Key to Solving the Enigma of Zoonotic Virus Spillover

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