The available evidence suggests wild birds play a limited role in human infectious diseases. Direct transmission of an infectious agent from wild birds to humans is rarely identified. Potential factors and mechanisms involved in the transmission of infectious agents from birds to humans need further elucidation.

: Bird migration has been assumed, mostly implicitly, to represent a distinct class of animal behavior, with deep and strong homologies in the various phenotypic expressions of migratory behavior between different taxa. Here the evidence for the existence of what could be called a “migratory syndrome,” a tightly integrated, old group of adaptive traits that enables birds to commit themselves to highly organized seasonal migrations, is assessed. A list of problems faced by migratory birds is listed first and the traits that migratory birds have evolved to deal with these problems are discussed. The usefulness of comparative approaches to investigate which traits are unique to migrants is then discussed. A provisional conclusion that, perhaps apart from a capacity for night‐time compass orientation, there is little evidence for deeply rooted coadapted trait complexes that could make up such a migratory syndrome, is suggested. Detailed analyses of the genetic and physiological architecture of potential adaptations to migration, combined with a comparative approach to further identify the phylogenetic levels at which different adaptive traits for migration have evolved, are recommended.

Managing oxidative stress is an important physiological function for all aerobic organisms, particularly during periods of prolonged high metabolic activity, such as long-distance migration across ecological barriers. However, no previous study has investigated the oxidative status of birds at different stages of migration and whether that oxidative status depends on the condition of the birds. In this study, we compared (1) energy stores and circulating oxidative status measures in (a) two species of Neotropical migrants with differing migration strategies that were sampled at an autumn stopover site before an ecological barrier; and (b) a species of trans-Saharan migrant sampled at a spring stopover site after crossing an ecological barrier; and (2) circulating oxidative measures and indicators of fat metabolism in a trans-Saharan migrant after stopovers of varying duration (0–8 nights), based on recapture records. We found fat stores to be positively correlated with circulating antioxidant capacity in Blackpoll Warblers and Red-eyed Vireos preparing for fall migration on Block Island, USA, but uncorrelated in Garden Warblers on the island of Ponza, Italy, after a spring crossing of the Sahara Desert and Mediterranean Sea. In all circumstances, fat stores were positively correlated with circulating lipid oxidation levels. Among Garden Warblers on the island of Ponza, fat anabolism increased with stopover duration while oxidative damage levels decreased. Our study provides evidence that birds build antioxidant capacity as they build fat stores at stopover sites before long flights, but does not support the idea that antioxidant stores remain elevated in birds with high fuel levels after an ecological barrier. Our results further suggest that lipid oxidation may be an inescapable hazard of using fats as the primary fuel for flight. Yet, we also show that birds on stopover are capable of recovering from the oxidative damage they have accrued during migration, as lipid oxidation levels decrease with time on stopover. Thus, the physiological strategy of migrating songbirds may be to build prophylactic antioxidant capacity in concert with fuel stores at stopover sites before a long-distance flight, and then repair oxidative damage while refueling at stopover sites after long-distance flight.

Samples of flight and leg muscle tissue were taken from migratory garden warblers at three different stages of migration: (1) pre-flight: when birds face an extended flight phase within the next few days, (2) post-flight: when they have just completed an extended flight phase, and (3) recovery: when they are at the end of a stop-over period following an extended flight phase. The changes in body mass are closely related to the changes in flight (P<0.001) and leg muscle mass (P<0.001), suggesting that the skeletal muscles are involved in the protein metabolism associated with migratory flight. From pre- to post-flight, the flight and the leg muscle masses decrease by about 22%, but are restored to about 12% above the pre-flight masses during the recovery period. Biochemical analyses show that following flight a selective reduction occurred in the myofibrillar (contractile) component of the flight muscle (P<0.01). As this selective reduction accounts only for a minor part of the muscle mass changes, sarcoplasmic (non-contractile) and myofibrillar proteins of both the flight and leg muscle act as a protein source during long-distance migration. As a loss of leg muscle mass is additionally observed besides the loss in flight muscle mass, mass change seems not to be strictly associated with the mechanical power output requirements during flight. Whereas the specific content of sarcoplasmic proteins in the flight muscle is nearly twice as high as that in the leg muscle (P<0.001), the specific content of myofibrillar proteins differs only slightly (P < 0.05), being comparably low in both muscles. The ratio of non-contractile to contractile proteins in the flight muscle is one of the highest observed in muscles of a vertebrate.