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Swifts (Apodidae) are an unusual group of birds that spend most of their lives in flight, landing only when breeding. Although this aerial lifestyle greatly reduces their likelihood of being bitten by vectors and infected by vector-born parasites, swifts can still be heavily infested during breeding by nest-based vectors such as louse flies (Hippoboscidae). Here, we investigated host, vector, and vector-borne parasite relationships in the three most widespread swift species in the Western Palearctic (WP): common swifts ( Apus apus ), pallid swifts ( A. pallidus ), and alpine swifts ( Tachymarptis melba ), their nest-based louse flies ( Crataerina pallida and C. melbae ) and avian haemosporidians (genera Haemoproteus , Plasmodium , and Leucocytozoon ). Studies of haemosporidian infections in Apodidae remain limited, with clear evidence of infection found to date in just four Neotropical and one Australasian species. The possible role of louse flies in transmitting haemosporidian infections has never been tested in swifts. We assessed the occurrence of haemosporidian infection by PCR screenings of DNA from blood samples from 34 common swifts and 44 pallid swifts from Italy, and 45 alpine swifts from Switzerland. We also screened 20 ectoparasitic louse flies present on 20 birds and identified them by both morphological features and cytochrome oxidase subunit 1 (COI) barcodes. Our results provide no evidence of haemosporidian infection in the 123 swifts tested or in the two louse fly species we identified. Our findings are consistent with available knowledge showing no haemosporidian occurrence in WP swift species and that the most likely infection route for these highly aerial species (via louse fly ectoparasites during nesting) is unlikely.

Changes to the structure and function of neural networks are thought to underlie the evolutionary adaptation of animal behaviours. Among the many developmental phenomena that generate change programmed cell death (PCD) appears to play a key role. We show that cell death occurs continuously throughout insect neurogenesis and happens soon after neurons are born. Mimicking an evolutionary role for increasing cell numbers, we artificially block PCD in the medial neuroblast lineage in Drosophila melanogaster , which results in the production of ‘undead’ neurons with complex arborisations and distinct neurotransmitter identities. Activation of these ‘undead’ neurons and recordings of neural activity in behaving animals demonstrate that they are functional. Focusing on two dipterans which have lost flight during evolution we reveal that reductions in populations of flight interneurons are likely caused by increased cell death during development. Our findings suggest that the evolutionary modulation of death-based patterning could generate novel network configurations. Just like a sculptor chips away at a block of granite to make a statue, the nervous system reaches its mature state by eliminating neurons during development through a process known as programmed cell death. In vertebrates, this mechanism often involves newly born neurons shrivelling away and dying if they fail to connect with others during development. Most studies in insects have focused on the death of neurons that occurs at metamorphosis, during the transition between larva to adult, when cells which are no longer needed in the new life stage are eliminated. Pop et al. harnessed a newly designed genetic probe to point out that, in fruit flies, programmed cell death of neurons at metamorphosis is not the main mechanism through which cells die. Rather, the majority of cell death takes place as soon as neurons are born throughout all larval stages, when most of the adult nervous system is built. To gain further insight into the role of this ‘early’ cell death, the neurons were stopped from dying, showing that these cells were able to reach maturity and function. Together, these results suggest that early cell death may be a mechanism fine-tuned by evolution to shape the many and varied nervous systems of insects. To explore this, Pop et al. looked for hints of early cell death in relatives of fruit flies that are unable to fly: the swift lousefly and the bee lousefly. This analysis showed that early cell death is likely to occur in these two insects, but it follows different patterns than in the fruit fly, potentially targeting the neurons that would have controlled flight in these flies’ ancestors. Brains are the product of evolution: learning how neurons change their connections and adapt could help us understand how the brain works in health and disease. This knowledge may also be relevant to work on artificial intelligence, a discipline that often bases the building blocks and connections in artificial ‘brains’ on how neurons communicate with one another.

Background As living vectors, arthropods play a crucial role in the transmission of viruses, bacteria and parasites. Previous research on virus transmission has focussed mainly on the roles of mosquitoes and ticks, while the potential importance of other blood-sucking arthropods such as louse flies (Hippoboscidae) has been somewhat neglected. The aim of this study was to detect viruses in avian louse flies from Germany to assess whether they could be used as sentinel organisms for monitoring arboviruses with zoonotic potential. Methods We collected 1000 louse flies of the species Crataerina hirundinis, C. pallida, Ornithomya avicularia, O. biloba, O. fringillina, O. chloropus, Ornithophila metallica and Pseudolynchia canariensis in Germany and screened the samples via RT-PCR for West Nile virus (WNV), Usutu virus (USUV) and Sindbis virus (SINV), which are arboviruses with avian hosts as reservoirs. Results While WNV was not detected, we found one louse fly positive for USUV and one for SINV RNA, both of which belonged to the species O. avicularia ( n  = 279). Therefore, the detection rates for both USUV and SINV were 0.1% (95% CI 0.0–0.3%) in the total sample and 0.36% (95% CI 0.00–1.09%) in O. avicularia . For the sample that tested positive for SINV, the PCR results were confirmed by sequencing a 288-bp segment that encoded part of the virus’s structural polyprotein. Conclusions This is the first time that USUV RNA and SINV RNA have been detected in louse flies. In addition, it is the first detection of human pathogenic viruses in the louse fly species O. avicularia . The results of this study indicate that louse flies should not be neglected as possible sentinels of viral pathogens with zoonotic potential in the sense of the One Health concept. Graphical abstract

AbstractIn 2017–2020, six species of louse flies of the subfamily Ornithomyinae and two species of the subfamily Lipopteninae were collected in two localities in the Lazovsky State Nature Reserve, Primorskii Territory, Russia. They were taken from 646 birds representing 62 species out of the 3833 birds of the 103 species examined. All the birds were ringed and released into the wild. Ornithoctona momiyamai (Kishida, 1932) and Ornithomya avicularia (Llinnaeus, 1758) were the most abundant louse fry species. Ornithomya fringillina (Curtis, 1856), O. comosa (Austen, 1930), Ornithoctona unicolor Speiser, 1900 and Crataerina hirundinis (Curtis, 1856) were less numerous. A few specimens of mammophilous louse flies Lipoptena cervi (Linnaeus, 1758) and L. fortisetosa (Maa, 1965) were found on birds. A comparative analysis of the louse fly faunas of the Lazovsky State Nature Reserve, Muraviovskii Park (Amurskaya Province, Russia), Hokkaido (Japan) and South Korea was carried out.

AbstractLouse flies (Diptera, Hippoboscidae) were collected off 38 species of birds from 16 genera of 14 families and 5 orders. Birds were captured in large funnel traps and mist nets on the Courish Spit (Kaliningrad Province, Russia). Five species of ornithophilic louse flies were found: Ornithomya avicularia (Linnaeus, 1758), O. chloropus (Bergroth, 1901), O. fringillina (Curtis, 1856), O. comosa (Austen, 1930), and Crataerina hirundinis (Linnaeus, 1758); besides, the mammalophilic species Lipoptena fortisetosa (Maa, 1965) was recorded on a non-specific bird host. The association of louse flies with their hosts, infestation parameters, collection data, and general geographic distribution of the recorded louse fly species are considered. The overall infestation of birds with louse flies was low. The louse fly fauna of Kaliningrad Province is compared with the faunas of the adjacent territories.

Numerous host qualities can modulate parasite fitness, and among these, host nutritive resources and immunity are of prime importance. Indeed, parasite fitness increases with the amount of nutritive resources extracted from the host body and decreases with host immune response. To maximize fitness, parasites have therefore to balance these two host components. Yet, because host nutritive resources and immunity both increase with host body condition, it is unclear whether parasites perform better on hosts in prime, intermediate, or poor condition. We investigated blood meal size and survival of the ectoparasitic louse flyCrataerina melbaein relation to body condition and cutaneous immune response of their Alpine swift (Apus melba) nestling hosts. Louse flies took a smaller blood meal and lived a shorter period of time when feeding on nestlings that were experimentally food deprived or had their cutaneous immune response boosted with methionine. Consistent with these results, louse fly survival was the highest when feeding on nonexperimental nestlings in intermediate body condition. Our findings emphasize that although hosts in poor condition had a reduced immunocompetence, parasites may have avoided them because individuals in poor condition did not provide adequate resources. These findings highlight the fact that giving host immunocompetence primary consideration can result in a biased appraisal of host‐parasite interactions.

1. Parasitism is a non-negligible cost of reproduction in wild organisms, and hosts are selected to partition resources optimally between current and future reproduction. While parents can compensate for the cost of parasitism by increasing their current reproductive investment, such change in resource allocation is expected to carry-over costs on future reproduction. 2. Life history theory predicts that because long-lived organisms have a high residual reproductive value, they should be more reluctant to increase parental effort in response to parasites. Also, when rearing successive infested broods, the cost of parasitism can cumulate over the years and hence be exacerbated by past infestations. 3. We tested these two predictions in the alpine swift Apus melba, a long-lived colonial bird that is infested intensely by the nest-based blood sucking louse-fly Crataerina melbae. For this purpose, we manipulated ectoparasite load over 3 consecutive years and measured reproductive parameters in successive breeding attempts of adults assigned randomly to 'parasitized' and 'deparasitized' treatments. 4. In current reproduction, fathers of experimentally parasitized broods produced a similar number of offspring as fathers from the deparasitized treatment, but the rearing period was prolonged by 4 days. Fathers that were assigned to the parasitized treatment in year x produced significantly fewer fledglings the following year x + 1 than those of the deparasitized treatment. The number of young produced by fathers in year x + 1 was correlated negatively with the number of days they cared for their brood in the previous year x. We also found a significant interaction between treatments performed over 2 successive years, with fathers of parasitized broods suffering a larger fitness loss if in the past they had already cared for a parasitized brood rather than for a deparasitized one. Similar effects of parasitism, although partly non-significant (0.05 < P-values > 0.10), were found in mothers. 5. Altogether, our results show that parasites can modify resource allocation between current and future reproduction in long-lived hosts, and that the cost of parasitism can cumulate over the years. It emphasizes the fact that effects of parasites can depend on past infestations and become apparent in future reproduction only.

1. Development plasticity is a common evolutionary and phenotypic response to poor growth condition, in particular in organisms with determinate growth such as most birds and mammals. Because various body structures can contribute differently to overall fitness, natural selection will adjust the degree of plasticity of each structure to its proportionate contribution to fitness at a given life stage. 2. Two non-mutually exclusive mechanisms can account for plasticity in the growth of offspring to compensate for the effect of parasites. First, if parasite infestation levels fluctuate over the nestling period, parasitized young may show reduced growth until peak parasite infestation, and accelerated growth once the conditions improve (the accelerated growth hypothesis). Secondly, if the period of tissue maturation is not fixed in time, hosts may grow slower than parasite-free hosts but for a longer period of time (the delayed maturation hypothesis). 3. To test whether hosts compensate for the effects of parasites on their development, the load of the blood-sucking louse-fly Crataerina melbae Rondani in the nests of Alpine swifts, Apus melba Linnaeus, was increased or decreased experimentally. Parasite prevalence was 100% in both treatments, but intensity (no. of parasites per nestling) was significantly lower for deparasitized nestlings. In both treatments, parasite intensity increased up to halfway through the rearing period (i.e. 30 days of age) and decreased afterwards. 4. In line with the accelerated growth hypothesis, wings of parasitized nestlings grew at a lower rate than those of deparasitized ones before the peak of parasite infestation, but at a greater rate after the peak. Louse-flies had no significant effect on the growth of body mass. In agreement with the delayed-maturation hypothesis, wings of parasitized nestlings grew for 3 additional days and were of similar size at fledging as in deparasitized birds. 5. In summary, the present study shows in a wild bird population that nestling hosts can compensate for the effect of parasitism on their phenotype. It emphasizes the need to take the dynamics of parasite populations into account in studies of host-parasite relationships, and to investigate the effect of parasites on host development over the entire growing period rather than only at fledging, as employed traditionally.

1. Sex-biased mortality in adult vertebrates is often attributed to lower immunocompetence and higher parasite susceptibility of males. Although sex-specific mortality has also been reported during growth, the importance of sex-specific immunocompetence and parasite susceptibility in explaining male-biased mortality remains ambiguous in growing individuals because of potentially confounding sources of mortality such as sexual dimorphism. 2. Here, we investigated sex-specific susceptibility to the blood-sucking louse fly Crataerina melbae and sex differences in cell-mediated immunity in a bird species that is sexually monomorphic both in size and plumage coloration at the nestling stage, the Alpine Swift, Apus melba. 3. For this purpose, we manipulated ectoparasite loads by adding or removing flies to randomly chosen nests in two years, and injected nestlings with mitogenic phytohae-magglutinin (PHA) in another year. 4. There were no significant differences between male and female offspring in immune response towards PHA, parasite load, and parasite-induced decrease in growth rate. Secondary sex ratios were however biased toward males in parasitized broods, and this was explained by a greater mortality of females in parasitized than deparasitized broods. 5. Our findings are in contrast to the widely accepted hypothesis that males suffer a greater cost of parasitism. We discuss alternative hypotheses accounting for female-specific mortality.

Aggregation of Crataerina melbae flies on breeding adult alpine swifts (Apus melba) was low when compared with other host-parasite systems and varied with sampling date, year, and sex of the flies. Generalized linear models were performed to ascertain which factors, extrinsic and/or intrinsic to the host, explained variability in the number of louse flies present on a single host, i.e., abundance. Overall abundance was unrelated to any host characteristic but varied slightly among years. Abundance of female flies varied among years, but also with date of sampling, the number of females increasing as the breeding season advanced. In contrast, abundance of males decreased as the season progressed, independently of host characteristics. Despite these different patterns, the number of flies of each sex on a given host was strongly intercorrelated. These results suggest that mate attraction may explain aggregation patterns in this louse fly species. Overall sex ratio of louse flies did not differ from unity. However, the proportion of males decreased during the breeding season, as a consequence of the opposite sex-related seasonal patterns in parasite abundance. Sex-ratio variability was not related to host characteristics or to infrapopulation sizes.