Disease tolerance alters host competence in a wild songbird

2021 ◽  
Vol 17 (10) ◽  
Author(s):  
Rachel M. Ruden ◽  
James S. Adelman

Individuals can express a range of disease phenotypes during infection, with important implications for epidemics. Tolerance, in particular, is a host response that minimizes the per-pathogen fitness costs of infection. Because tolerant hosts show milder clinical signs and higher survival, despite similar pathogen burdens, their potential for prolonged pathogen shedding may facilitate the spread of pathogens. To test this, we simulated outbreaks of mycoplasmal conjunctivitis in house finches, asking how the speed of transmission varied with tissue-specific and behavioural components of tolerance, milder conjunctivitis and anorexia for a given pathogen load, respectively. Because tissue-specific tolerance hinders pathogen deposition onto bird feeders, important transmission hubs, we predicted it would slow transmission. Because behavioural tolerance should increase interactions with bird feeders, we predicted it would speed transmission. Our findings supported these predictions, suggesting that variation in tolerance could help identify individuals most likely to transmit pathogens.

2018 ◽  
Vol 11 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Emily R. Vana ◽  
Elizabeth R. Wrobel ◽  
Travis E. Wilcoxen

Congregation of individuals at high densities is known to increase disease transmission and bird-feeding activities are specifically aimed at attracting many birds to a single location. We surveyed nine potential host species for evidence of infection by each Mycoplasma gallisepticum (MG) and Avipoxvirus, or avian pox. We also examined differences in pathogen exposure at sites with bird feeders and sites without bird feeders. Finally, we compared prevalence of birds with antibodies against MG and avian pox to those that showed physical signs of infection. To test for pathogen exposure, we used indirect enzyme-linked immunosorbent assays. We found species-specific disease dynamics, as House Finches Haemorhous mexicanus had a significantly greater likelihood of having antibodies against MG than any other species. Birds at sites with feeders were more likely to have antibodies against MG. Birds at sites with feeders were no more likely to have antibodies against avian pox, but seroprevalence of avian pox did differ significantly among species. Overall, our findings suggest differential exposure and immune responses to each pathogen among species and that feeders increase the exposure of individuals to MG but not to avian pox, offering valuable new insights into the role of bird feeding activities in disease transmission among birds.


2018 ◽  
Vol 373 (1745) ◽  
pp. 20170090 ◽  
Author(s):  
Sahnzi C. Moyers ◽  
James S. Adelman ◽  
Damien R. Farine ◽  
Courtney A. Thomason ◽  
Dana M. Hawley

Anthropogenic food provisioning of wildlife can alter the frequency of contacts among hosts and between hosts and environmental sources of pathogens. Despite the popularity of garden bird feeding, few studies have addressed how feeders influence host contact rates and disease dynamics. We experimentally manipulated feeder density in replicate aviaries containing captive, pathogen-naive, groups of house finches ( Haemorhous mexicanus ) and continuously tracked behaviours at feeders using radio-frequency identification devices. We then inoculated one bird per group with Mycoplasma gallisepticum (Mg), a common bacterial pathogen for which feeders are fomites of transmission, and assessed effects of feeder density on house finch behaviour and pathogen transmission. We found that pathogen transmission was significantly higher in groups with the highest density of bird feeders, despite a significantly lower rate of intraspecific aggressive interactions relative to the low feeder density groups. Conversely, among naive group members that never showed signs of disease, we saw significantly higher concentrations of Mg-specific antibodies in low feeder density groups, suggesting that birds in low feeder density treatments had exposure to subclinical doses of Mg. We discuss ways in which the density of garden bird feeders could play an important role in mediating the intensity of Mg epidemics. This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife'.


1993 ◽  
Vol 177 (4) ◽  
pp. 1153-1164 ◽  
Author(s):  
A Bonomo ◽  
P Matzinger

Most current models of T cell development include a positive selection step in the thymus that occurs when T cells interact with thymic epithelium and a negative selection step after encounters with bone marrow-derived cells. We show here that developing T cells are tolerized when they recognize antigens expressed by thymic epithelium, that the tolerance is tissue specific, and that it can occur by deletion of the reactive T cells.


2013 ◽  
Vol 3 (2) ◽  
pp. 20120055 ◽  
Author(s):  
Robert Hoehndorf ◽  
Paul N. Schofield ◽  
Georgios V. Gkoutos

PhenomeNet is an approach for integrating phenotypes across species and identifying candidate genes for genetic diseases based on the similarity between a disease and animal model phenotypes. In contrast to ‘guilt-by-association’ approaches, PhenomeNet relies exclusively on the comparison of phenotypes to suggest candidate genes, and can, therefore, be applied to study the molecular basis of rare and orphan diseases for which the molecular basis is unknown. In addition to disease phenotypes from the Online Mendelian Inheritance in Man (OMIM) database, we have now integrated the clinical signs from Orphanet into PhenomeNet. We demonstrate that our approach can efficiently identify known candidate genes for genetic diseases in Orphanet and OMIM. Furthermore, we find evidence that mutations in the HIP1 gene might cause Bassoe syndrome, a rare disorder with unknown genetic aetiology. Our results demonstrate that integration and computational analysis of human disease and animal model phenotypes using PhenomeNet has the potential to reveal novel insights into the pathobiology underlying genetic diseases.


2019 ◽  
Vol 37 (1) ◽  
pp. 405-437 ◽  
Author(s):  
Rui Martins ◽  
Ana Rita Carlos ◽  
Faouzi Braza ◽  
Jessica A. Thompson ◽  
Patricia Bastos-Amador ◽  
...  

Pathogenic organisms exert a negative impact on host health, revealed by the clinical signs of infectious diseases. Immunity limits the severity of infectious diseases through resistance mechanisms that sense and target pathogens for containment, killing, or expulsion. These resistance mechanisms are viewed as the prevailing function of immunity. Under pathophysiologic conditions, however, immunity arises in response to infections that carry health and fitness costs to the host. Therefore, additional defense mechanisms are required to limit these costs, before immunity becomes operational as well as thereafter to avoid immunopathology. These are tissue damage control mechanisms that adjust the metabolic output of host tissues to different forms of stress and damage associated with infection. Disease tolerance is the term used to define this defense strategy, which does not exert a direct impact on pathogens but is essential to limit the health and fitness costs of infection. Under this argument, we propose that disease tolerance is an inherent component of immunity.


1996 ◽  
Vol 26 (8) ◽  
pp. 1807-1815 ◽  
Author(s):  
Yves Modigliani ◽  
Antonio Coutinho ◽  
Pablo Pereira ◽  
Nicole Le Douarin ◽  
Véronique Thomas-Vaslin ◽  
...  

2004 ◽  
Vol 82 (5) ◽  
pp. 755-763 ◽  
Author(s):  
Sonia Altizer ◽  
Andrew K Davis ◽  
Katherine C Cook ◽  
John J Cherry

House finches (Carpodacus mexicanus (Muller, 1776)) in eastern North America have been affected by annual epidemics of an eye disease caused by the bacterium Mycoplasma gallisepticum since 1994. To identify factors associated with seasonal changes in prevalence and variation in host susceptibility, we monitored mycoplasmal conjunctivitis among wild house finches in a region of high prevalence in southeastern North America. We captured 888 birds between August 2001 and December 2003 and observed seasonal outbreaks characterized by rapid increases in prevalence from August to October each year. During periods of high prevalence, infection probability was significantly higher among juveniles than adults, and the severity of conjunctivitis among juvenile females was greater than for any other host category. We found no evidence linking moulting status to elevated infection risk among adult birds. Finally, house finches with conjunctivitis were in poorer condition than birds with no clinical signs of infection, particularly among those with severe infections. Results from this study are consistent with recent reports of seasonal and regional variation in mycoplasmal conjunctivitis and suggest that annual changes in host reproduction, behaviour, and age structure might be important determinants of the timing and magnitude of local epidemics.


2021 ◽  
Author(s):  
Matteo D'Antonio ◽  
Timothy D. Arthur ◽  
Jennifer P. Nguyen ◽  
Hiroko Matsui ◽  
Agnieszka D'Antonio-Chronowska ◽  
...  

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we applied colocalization to compare summary statistics for 16 GWASs from the COVID-19 Host Genetics Initiative to investigate similarities and differences in their genetic signals. We identified 9 loci associated with susceptibility (one with two independent GWAS signals; one with an ethnicity-specific signal), 14 associated with severity (one with two independent GWAS signals; two with ethnicity-specific signals) and one harboring two discrepant GWAS signals (one for susceptibility; one for severity). Utilizing colocalization we also identified 45 GTEx tissues that had eQTL(s) for 18 genes strongly associated with GWAS signals in eleven loci (1-4 genes per locus). Some of these genes showed tissue-specific altered expression and others showed altered expression in up to 41 different tissue types. Our study provides insights into the complex molecular mechanisms underlying inherited predispositions to COVID-19-disease phenotypes.


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