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Effects of co-infections on the emergence of an avian disease Mycoplasma gallisepticum

Periodic Reporting for period 2 - ECODIS (Effects of co-infections on the emergence of an avian disease Mycoplasma gallisepticum)

Periodo di rendicontazione: 2020-06-16 al 2021-06-15

Coinfection is the simultaneous infection of a host by multiple pathogen species and is commonplace in vertebrate hosts. As pathogen species can (in)directly interact within the host, coinfections are considered to be of particular importance in the ecology of wildlife diseases. In general, pathogens do not exert their effects in isolation; they act in conjunction with other parasites infecting the host. The subject of coinfection is increasingly recognized as a complex process that breaks down the one-pathogen/one-disease paradigm, altering pathologic and immunologic effects in the host, the severity and duration of disease, and ultimately transmission in ways that are different, and often greater, than would be expected from single infections. In this project, I test the hypothesis that directly-transmitted Mycoplasma (MG) will transmit more efficiently when interacting with common songbird copathogens (Plasmodium relictum (PR), a mosquito-transmitted protozoan, and Borrelia burgdorferi s.s. (BB), a tick-borne bacterium), with coinfections exacerbating MG disease and transmission. Furthermore, I anticipate characterizing aspects of MG adaptation to the coinfected ‘host environment’.
The current COVID-19-crisis is providing ample evidence for pathogen evolution at rapid rates, fitness advantages allowing.
The objectives of this project - of which hypotheses have been tested within wild bird species - therefore are of high socio-economic value: understanding underlying processes of co-pathogen interactions on transmission dynamics is key to predict fitness landscapes favouring the one strain over the other, and therefore the population dynamics of both pathogen and host.
Hosts are typically co-infected by multiple parasite species whose interactions might be synergetic or antagonistic, producing unpredictable physiological and pathological impacts on the host. This study shows the interaction between Plasmodium spp. and Leucocytozoon spp. in birds experimentally infected or not infected with Mycoplasma gallisepticum. In 1994, the bacterium Mycoplasma gallisepticum (M. gallisepticum) jumped from poultry to wild birds in which it caused a major epidemic in North America. Birds infected with M. gallisepticum show conjunctivitis as well as increased levels of corticosterone. Malaria and other haemosporidia are widespread in birds, and chronic infections become apparent with the detectable presence of the parasite in peripheral blood in response to elevated levels of natural or experimental corticosterone levels. Knowing the immunosuppressive effect of corticosterone on the avian immune system, we tested the hypothesis that chronic infections of Plasmodium spp. and Leucocytozoon spp. in house finches would respond to experimental inoculation with M. gallisepticum as corticosterone levels are known to increase following inoculation. Plasmodium spp. infection intensity increased within days of M. gallisepticum inoculation as shown both by the appearance of infected erythrocytes and by the increase in the number and the intensity of positive PCR-tests. Leucocytozoon spp. infection intensity increased when Plasmodium spp. infection intensity increased, but not in response to M. gallisepticum inoculation. Leucocytozoon spp. and Plasmodium spp. seemed to compete in the host as shown by a negative correlation between the changes in their PCR-score when both pathogens were present in the same individual. Host responses to co-infection with multiple pathogens measured by the hematocrit and white blood cells count depended on the haemosporidian community composition. Host investment in the leukocyte response was higher in the single-haemosporidia infected groups when birds were infected with M. gallisepticum. A trade-off was observed between the immune control of the chronic infection (Plasmodium spp./Leucocytozoon spp.) and the immune response to the novel bacterial infection (M. gallisepticum).
Hosts are typically co-parasitized by multiple species. Parasites can benefit or suffer from the presence of other parasites, which can reduce or increase the overall virulence due to competition or facilitation. Outcomes of new multi-parasite systems are seldom predictable. In 1994 the bacterium Mycoplasma gallisepticum jumped from poultry to songbirds in which it caused an epidemic throughout North America. Songbirds are often parasitized by hard ticks, that can act as reservoirs for tick-borne diseases. We tested the hypothesis that Mycoplasma infection in house finches influences North America’s most important tick vector Ixodes scapularis, by affecting the tick’s feeding success, detachment behaviour and survival to the next stage. Ticks detached during the day irrespective of the bird’s disease status and time since infestation. Birds incrementally invested in anti-tick resistance mechanisms over the course of the experiment; this investment was made earlier in the Mycoplasma-infected birds. At higher tick densities, the feeding success in birds with more severe conjunctivitis was lower than in the control birds. Throughout the experiment we found positive density dependent effects on the tick’s feeding success. More diseased hosts suffered more from the tick infestations, as shown by reduced haematocrits. Three Mycoplasma-infected birds died during the weeks following the experiment, although all birds were kept in optimal housing conditions. Mycoplasma made the bird a less accessible and valuable host for ticks, which is an example of ecological interference. Therefore, Mycoplasma has the potential to ultimately reduce transmission outcomes of tick-borne pathogens via songbird hosts.

No specific project website has been developed.
A Generalized Framework will be built, in which different co-pathogen systems can be included. This will enable us to predict risk areas with highes R0-values.The continuous interactions with researchers of Uhasselt will further help me in becoming a disease ecologist and modeller. Societal impact is high, e.g. covid-19 crisis is the result of spill-over, which is one of the main topics of my project. Furthermore, population heterogeneities - including co-pathogen infections - determine the outcomes in a suite of ways: (1) transmission propability; (2) (a)symptotic infections; (3) mortality; (4) fertility and birth rates.
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