Haemosporidians are well-known and extensively studied parasites as Plasmodium gives rise to malaria in humans and animals, remaining one of the most common diseases in warm climate countries
. Investigating interactions between hosts and their parasites as well as the factors governing host susceptibility is key for understanding the epidemiology of the disease and host-parasite coevolution.
The importance of avian haemosporidian parasites (Plasmodium sp., Haemoproteus sp. and Leucocytozoon sp.) as a model system for studying host-parasite evolution and the consequences on ecology and conservation has been increasing over recent decades
. A number of studies have shown the costs on life-history traits associated with haemosporidian infection. Avian haemosporidian parasites can affect host body condition
, reproductive success
[4–6] and survival
[7–10], with extreme cases resulting in the extinction of the avian host
[11–13]. Consequently, these parasites can exert strong selective forces on their hosts.
As avian heamosporidians are ubiquitous
, birds are exposed to a variety of haemosporidian parasites
[8, 14–21] and the distribution of these blood parasites within and between host populations has the potential to reveal different evolutionary dynamics of host-parasite interactions
. Therefore, knowledge of the persistence of parasite communities and their composition across temporal scales is a prerequisite for investigating and determining these host-parasite interactions.
Many studies have investigated haemosporidian community composition across space and time at the population level
[22–25] and found that most parasite communities remained stable (but see
), even for up to 17 years
. However, few studies have investigated haemosporidian communities at the individual level. When studying communities at the population level only, changes happening at the individual level might be overlooked, especially if these changes have fast turn-over. Therefore, while parasite communities at the population level appear stable, at the individual level hosts might be experiencing rapid changes in parasite onslaught. At the individual level Hasselquist et al found that the likelihood of retaining the same infection status (infected vs. uninfected) for Haemoproteus payevskyi was higher than the probability of experiencing a change in status. Knowles et al showed that 26% of Plasmodium infection in individual blue tits (Cyanistes caeruleus) from the UK could be lost over time, Piersma and van der Velde
 found that 23% of house martins (Delichon urbicum) in the Netherlands showed no haemosporidian infection status changes over time and Latta and Ricklefs
 found high individual turn-over in haemosporidian infections between years in various host species on the island of Hispaniola.
While a number of factors can influence the persistence and abundance of a parasite in a host (e.g. host health or immunocompetence
[29, 30] and environmental condition
), the presence of multiple parasites within a host, i.e. co-infection, can critically impact infection dynamics and virulence. Co-infections with different haemosporidian genera can result in within-host competition leading to increased virulence
. On this topic, studies of mixed infections in birds have yielded diverse results. Palinauskas et al reported increased virulence in experimentally co-infected individuals although this effect was host-species specific. Conversely, Marzal et al showed that co-infection results in increased mortality but higher reproductive success in house martins, presumably as a result of increased investment in reproduction. Finally, Davidar and Morton
 revealed that although single infections of Haemoproteus prognei and filarial nematodes are relatively harmless in purple martins (Progne subis), a co-infection of these two parasites almost exclusively result in death of the host.
This study reports data from wild, free-living great tits (Parus major), sampled across a three-year period and addresses the following questions: 1) how persistent are the three haemosporidian genera (Plasmodium, Haemoproteus and Leucocytozoon)? 2) Are there lineage-specific (a lineage being defined as a Cyt b haplotype) differences in parasitaemia? and 3) what is the frequency of co-infections and do co-infections between Leucocytozoon and Plasmodium appear to impact Plasmodium parasitaemia and host body condition? Taken together, these data will enable a better understanding of the dynamics of parasite infection.