scholarly journals Host traits and environment interact to drive host-pathogen coexistence following pathogen invasion

Author(s):  
Alexander Grimaudo ◽  
Joseph Hoyt ◽  
Steffany Yamada ◽  
Carl Herzog ◽  
Alyssa Bennett ◽  
...  

Emerging infectious diseases have resulted in severe population declines across diverse taxa. In some instances, despite attributes associated with high extinction risk, disease emergence and host declines are followed by host stabilization for reasons that are frequently unclear. While host, pathogen, and the environment are recognized as important factors that interact to determine host-pathogen coexistence, they are often considered independently. Here, we use a translocation experiment to disentangle the role of host traits and environmental conditions in driving the persistence of remnant populations a decade after they declined 70-99% and subsequently stabilized with disease. While survival was significantly higher than during the initial epidemic within all sites, protection from severe disease only existed within a narrow environmental space, suggesting host traits conducive to surviving disease are highly environmentally dependent. Ultimately, population persistence following pathogen invasion is the product of host-pathogen interactions that vary across a patchwork of environments.

2018 ◽  
Vol 285 (1892) ◽  
pp. 20181582 ◽  
Author(s):  
Calum X. Cunningham ◽  
Christopher N. Johnson ◽  
Leon A. Barmuta ◽  
Tracey Hollings ◽  
Eric J. Woehler ◽  
...  

Top carnivores have suffered widespread global declines, with well-documented effects on mesopredators and herbivores. We know less about how carnivores affect ecosystems through scavenging. Tasmania's top carnivore, the Tasmanian devil (Sarcophilus harrisii) , has suffered severe disease-induced population declines, providing a natural experiment on the role of scavenging in structuring communities. Using remote cameras and experimentally placed carcasses, we show that mesopredators consume more carrion in areas where devils have declined. Carcass consumption by the two native mesopredators was best predicted by competition for carrion, whereas consumption by the invasive mesopredator, the feral cat ( Felis catus ), was better predicted by the landscape-level abundance of devils, suggesting a relaxed landscape of fear where devils are suppressed. Reduced discovery of carcasses by devils was balanced by the increased discovery by mesopredators. Nonetheless, carcasses persisted approximately 2.6-fold longer where devils have declined, highlighting their importance for rapid carrion removal. The major beneficiary of increased carrion availability was the forest raven ( Corvus tasmanicus ). Population trends of ravens increased 2.2-fold from 1998 to 2017, the period of devil decline, but this increase occurred Tasmania-wide, making the cause unclear. This case study provides a little-studied potential mechanism for mesopredator release, with broad relevance to the vast areas of the world that have suffered carnivore declines.


2017 ◽  
Author(s):  
Tim C.D. Lucas ◽  
Hilde M. Wilkinson-Herbots ◽  
Kate E. Jones

AbstractZoonotic diseases are an increasingly important source of human infectious diseases, and host pathogen richness of reservoir host species is a critical driver of spill-over risk. Population-level traits of hosts such as population size, host density and geographic range size have all been shown to be important determinants of host pathogen richness. However, empirically identifying the independent influences of these traits has proven difficult as many of these traits directly depend on each other. Here we develop a mechanistic, metapopulation, susceptible-infected-recovered model to identify the independent influences of these population-level traits on the ability of a newly evolved pathogen to invade and persist in host populations in the presence of an endemic pathogen. We use bats as a case study as they are highly social and an important source of zoonotic disease. We show that larger populations and group sizes had a greater influence on the chances of pathogen invasion and persistence than increased host density or the number of groups. As anthropogenic change affects these traits to different extents, this increased understanding of how traits independently determine pathogen richness will aid in predicting future zoonotic spill-over risk.


2018 ◽  
Author(s):  
Konstans Wells ◽  
Rodrigo K. Hamede ◽  
Menna E. Jones ◽  
Paul A. Hohenlohe ◽  
Andrew Storfer ◽  
...  

AbstractEmerging infectious diseases increasingly threaten wildlife populations. Most studies focus on managing short-term epidemic properties, such as controlling early outbreaks. Predicting long-term endemic characteristics with limited retrospective data is more challenging. We used individual-based modelling informed by individual variation in pathogen load and transmissibility to predict long-term impacts of a lethal, transmissible cancer on Tasmanian devil (Sarcophilus harrisii) populations. For this, we employed Approximate Bayesian Computation to identify model scenarios that best matched known epidemiological and demographic system properties derived from ten years of data after disease emergence, enabling us to forecast future system dynamics. We show that the dramatic devil population declines observed thus far are likely attributable to transient dynamics. Only 21% of matching scenarios led to devil extinction within 100 years following devil facial tumour disease (DFTD) introduction, whereas DFTD faded out in 57% of simulations. In the remaining 22% of simulations, disease and host coexisted for at least 100 years, usually with long-period oscillations. Our findings show that pathogen extirpation or host-pathogen coexistence are much more likely than the DFTD-induced devil extinction, with crucial management ramifications. Accounting for individual-level disease progression and the long-term outcome of devil-DFTD interactions at the population-level, our findings suggest that immediate management interventions are unlikely to be necessary to ensure the persistence of Tasmanian devil populations. This is because strong population declines of devils after disease emergence do not necessarily translate into long-term population declines at equilibria. Our modelling approach is widely applicable to other host-pathogen systems to predict disease impact beyond transient dynamics.


2006 ◽  
Vol 4 (14) ◽  
pp. 479-489 ◽  
Author(s):  
David Fouchet ◽  
Stéphane Marchandeau ◽  
Nargès Bahi-Jaber ◽  
Dominique Pontier

Population fragmentation is a major problem for the conservation of mammalian species. Since the spread of an infectious disease is related to the intensity of contacts between individuals, fragmentation destabilizes the way the parasites circulate in their host population. Recently, Zinkernagel has proposed that a reduction in the frequency of infections by a parasite could lead to the emergence of severe forms of the disease, previously avoided because the disease was contracted early in life and attenuated by maternal antibodies. However, it is still unclear whether this change in disease expression increases the global mortality it induces because the disease becomes more severe and also less frequent. Here, we use a mathematical model to link population fragmentation with the hypothesis of Zinkernagel. Firstly, we show that there is a change in the severity of the disease during the fragmentation process, especially at a local scale, suggesting that host population fragmentation could be a widespread mechanism of disease emergence. Secondly, we show that the emergence of the severe form of the disease can lead to a significant increase in its induced mortality. Finally, we determine the types of interactions for which the fragmentation of the host population could be the most dangerous.


2016 ◽  
Vol 56 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Ali Safaie Farahani ◽  
Mohsen Taghavi

Abstract The natural resistance against the majority of potential pathogens that exist in most plant species is known as non-host resistance. Several reports suggest the role of antioxidant enzymes in non-host resistance. We assayed the expression or activity of four scavenging enzymes during non-host pathogen-plant interaction (Xanthomonas hortorum pv. pelargonii/mung bean) and host pathogen-plant interaction (Xanthomonas axonopodis pv. phaseoli/mung bean). The expression of superoxide dismutase (SOD) and ascorbate peroxidase (APX) and the enzyme activity of catalase (CAT) and peroxidase (POX) were investigated. The activities of CAT and POX were higher during non-host pathogen invasion vs. host pathogen attack. The expression of SOD and APX were also different between compatible and incompatible interactions. The expression of SOD and APX were higher in the incompatible compared to the compatible interaction. Additionally, induction of the antioxidant enzymes in response to non-host pathogen was earlier than induction in response to host pathogen. Such information is important for plant breeders, and useful when looking for alternative control strategies as well.


2012 ◽  
Vol 367 (1596) ◽  
pp. 1688-1707 ◽  
Author(s):  
Andrew R. Blaustein ◽  
Stephanie S. Gervasi ◽  
Pieter T. J. Johnson ◽  
Jason T. Hoverman ◽  
Lisa K. Belden ◽  
...  

Infectious diseases are intimately associated with the dynamics of biodiversity. However, the role that infectious disease plays within ecological communities is complex. The complex effects of infectious disease at the scale of communities and ecosystems are driven by the interaction between host and pathogen. Whether or not a given host–pathogen interaction results in progression from infection to disease is largely dependent on the physiological characteristics of the host within the context of the external environment. Here, we highlight the importance of understanding the outcome of infection and disease in the context of host ecophysiology using amphibians as a model system. Amphibians are ideal for such a discussion because many of their populations are experiencing declines and extinctions, with disease as an important factor implicated in many declines and extinctions. Exposure to pathogens and the host's responses to infection can be influenced by many factors related to physiology such as host life history, immunology, endocrinology, resource acquisition, behaviour and changing climates. In our review, we discuss the relationship between disease and biodiversity. We highlight the dynamics of three amphibian host–pathogen systems that induce different effects on hosts and life stages and illustrate the complexity of amphibian–host–parasite systems. We then review links between environmental stress, endocrine–immune interactions, disease and climate change.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alberto Polimeni ◽  
Isabella Leo ◽  
Carmen Spaccarotella ◽  
Annalisa Mongiardo ◽  
Sabato Sorrentino ◽  
...  

AbstractCoronavirus disease 2019 (COVID-19) is a highly contagious disease that appeared in China in December 2019 and spread rapidly around the world. Several patients with severe COVID-19 infection can develop a coagulopathy according to the ISTH criteria for disseminated intravascular coagulopathy (DIC) with fulminant activation of coagulation, resulting in widespread microvascular thrombosis and consumption of coagulation factors. We conducted a meta-analysis in order to explore differences in coagulopathy indices in patients with severe and non-severe COVID-19. An electronic search was performed within PubMed, Google Scholar and Scopus electronic databases between December 2019 (first confirmed Covid-19 case) up to April 6th, 2020. The primary endpoint was the difference of D-dimer values between Non-Severe vs Severe disease and Survivors vs Non-Survivors. Furthermore, results on additional coagulation parameters (platelet count, prothrombin time, activated partial thromboplastin time) were also analyzed. The primary analysis showed that mean d-dimer was significantly lower in COVID-19 patients with non-severe disease than in those with severe (SMD − 2.15 [− 2.73 to − 1.56], I2 98%, P < 0.0001). Similarly, we found a lower mean d-dimer in Survivors compared to Non-Survivors (SMD − 2.91 [− 3.87 to − 1.96], I2 98%, P < 0.0001). Additional analysis of platelet count showed higher levels of mean PLT in Non-Severe patients than those observed in the Severe group (SMD 0.77 [0.32 to 1.22], I2 96%, P < 0.001). Of note, a similar result was observed even when Survivors were compared to Non-Survivors (SMD 1.84 [1.16 to 2.53], I2 97%, P < 0.0001). Interestingly, shorter mean PT was found in both Non-Severe (SMD − 1.34 [− 2.06 to − 0.62], I2 98%, P < 0.0002) and Survivors groups (SMD − 1.61 [− 2.69 to − 0.54], I2 98%, P < 0.003) compared to Severe and Non-Survivor patients. In conclusion, the results of the present meta-analysis demonstrate that Severe COVID-19 infection is associated with higher D-dimer values, lower platelet count and prolonged PT. This data suggests a possible role of disseminated intravascular coagulation in the pathogenesis of COVID-19 disease complications.


2021 ◽  
pp. 1-9
Author(s):  
Hamood N. Al Kindi ◽  
Ayman M. Ibrahim ◽  
Mohamed Roshdy ◽  
Besra S. Abdelghany ◽  
Dina Yehia ◽  
...  

Abstract Background: Rhabdomyoma is the most common cardiac tumour in children. It is usually associated with tuberous sclerosis complex caused by mutations in TSC-1 or TSC-2 genes. This tumour typically regresses by unknown mechanisms; however, it may cause inflow or outflow obstruction that necessitates urgent surgery. Here we investigate the clinical features and the genetic analysis of patients with tuberous sclerosis complex presenting with large rhabdomyoma tumours. We also investigate the potential role of autophagy and apoptosis in the pathogenesis of this tumour. Methods: All the patients with cardiac rhabdomyoma referred to Aswan Heart Centre from 2010 to 2018 were included in this study. Sanger sequencing was performed for coding exons and the flanking intronic regions of TSC1 and TSC2 genes. Histopathological evaluation, immunohistochemistry, and western blotting were performed with P62, LC3b, caspase3, and caspase7, to evaluate autophagic and apoptotic signaling. Results: Five patients were included and had the clinical features of tuberous sclerosis complex. Three patients, who were having obstructive tumours, were found to have pathogenic mutations in TSC-2. The expression of two autophagic markers, P62 and LC3b, and two apoptotic markers, caspase3 and caspase7, were increased in the tumour cells compared to normal surrounding myocardial tissue. Conclusion: All the patients with rhabdomyoma were diagnosed to have tuberous sclerosis complex. The patients who had pathogenic mutations in the TSC-2 gene had a severe disease form necessitating urgent intervention. We also demonstrate the potential role of autophagy and apoptosis as a possible mechanism for tumourigenesis and regression. Future studies will help in designing personalised treatment for cardiac rhabdomyoma.


Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 905
Author(s):  
Estela Ruiz-Baca ◽  
Armando Pérez-Torres ◽  
Yolanda Romo-Lozano ◽  
Daniel Cervantes-García ◽  
Carlos A. Alba-Fierro ◽  
...  

The role of immune cells associated with sporotrichosis caused by Sporothrix schenckii is not yet fully clarified. Macrophages through pattern recognition receptors (PRRs) can recognize pathogen-associated molecular patterns (PAMPs) of Sporothrix, engulf it, activate respiratory burst, and secrete pro-inflammatory or anti-inflammatory biological mediators to control infection. It is important to consider that the characteristics associated with S. schenckii and/or the host may influence macrophage polarization (M1/M2), cell recruitment, and the type of immune response (1, 2, and 17). Currently, with the use of new monocyte-macrophage cell lines, it is possible to evaluate different host–pathogen interaction processes, which allows for the proposal of new mechanisms in human sporotrichosis. Therefore, in order to contribute to the understanding of these host–pathogen interactions, the aim of this review is to summarize and discuss the immune responses induced by macrophage-S. schenckii interactions, as well as the PRRs and PAMPs involved during the recognition of S. schenckii that favor the immune evasion by the fungus.


Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 210
Author(s):  
Johana Hrnková ◽  
Irena Schneiderová ◽  
Marina Golovchenko ◽  
Libor Grubhoffer ◽  
Natalie Rudenko ◽  
...  

Ticks are ubiquitous ectoparasites, feeding on representatives of all classes of terrestrial vertebrates and transmitting numerous pathogens of high human and veterinary medical importance. Exotic animals kept in zoological gardens, ranches, wildlife parks or farms may play an important role in the ecology of ticks and tick-borne pathogens (TBPs), as they may serve as hosts for local tick species. Moreover, they can develop diseases of varying severity after being infected by TBPs, and theoretically, can thus serve as reservoirs, thereby further propagating TBPs in local ecosystems. The definite role of these animals in the tick–host-pathogen network remains poorly investigated. This review provides a summary of the information currently available regarding ticks and TBPs in connection to captive local and exotic wildlife, with an emphasis on zoo-housed species.


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