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This paper reviews information from ecological and physiological studies to assess how extrinsic factors can modulate intrinsic physiological processes. The annual cycle of birds is made up of a sequence of life-history stages: breeding, moult and migration. Each stage has evolved to occur at the optimum time and to last for the whole duration of time available. Some species have predictable breeding seasons, others are more flexible and some breed opportunistically in response to unpredictable food availability. Photoperiod is the principal environmental cue used to time each stage, allowing birds to adapt their physiology in advance of predictable environmental changes. Physiological (neuroendocrine and endocrine) plasticity allows non-photoperiodic cues to modulate timing to enable individuals to cope with, and benefit from, short-term environmental variability. Although the timing and duration of the period of full gonadal maturation is principally controlled by photoperiod, non-photoperiodic cues, such as temperature, rainfall or food availability, could potentially modulate the exact time of breeding either by fine-tuning the time of egg-laying within the period of full gonadal maturity or, more fundamentally, by modulating gonadal maturation and/or regression. The timing of gonadal regression affects the time of the start of moult, which in turn may affect the duration of the moult. There are many areas of uncertainty. Future integrated studies are required to assess the scope for flexibility in life-history strategies as this will have a critical bearing on whether birds can adapt sufficiently rapidly to anthropogenic environmental changes, in particular climate change.

Birds use photoperiod to control the time of breeding and moult. However, it is unclear whether responses are dependent on absolute photoperiod, the direction and rate of change in photoperiod, or if photoperiod entrains a circannual clock. If starlings (Sturnus vulgaris) are kept on a constant photoperiod of 12h light:12h darkness per day (12L:12D), then they can show repeated cycles of gonadal maturation, regression and moult, which is evidence for a circannual clock. In this study, starlings kept on constant 11.5L:12.5D for 4 years or 12.5L:11.5D for 3 years showed no circannual cycles in gonadal maturation or moult. So, if there is a circannual clock, it is overridden by a modest deviation in photoperiod from 12L:12D. The responses to 11.5L:12.5D and 12.5L:11.5D were very different, the former perceived as a short photoperiod (birds were photosensitive for most of the time) and the latter as a long photoperiod (birds remained permanently photorefractory). Starlings were then kept on a schedule which ranged from 11.5L:12.5D in mid-winter to 12.5L:11.5D in mid-summer (simulating the annual cycle at 9 degrees N) for 3 years. These birds entrained precisely to calendar time and changes in testicular size and moult were similar to those of birds under a simulated cycle at 52 degrees N. These data show that birds are very sensitive to changes in photoperiod but that they do not simply respond to absolute photoperiod nor can they rely on a circannual clock. Instead, birds appear to respond to the shape of the annual change in photoperiod. This proximate control could operate from near equatorial latitudes and would account for similar seasonal timing in individuals of a species over a wide range of latitudes.

We previously reported evidence of West Nile virus (WNV) circulation in UK birds, probably introduced by migratory birds from overseas. We now demonstrate WNV-specific seroconversion in sentinel chickens raised on an English farm. Maternal neutralizing antibodies to WNV in hatchlings declined within three weeks. During the following months, healthy chickens developed WNV neutralizing antibodies that were confirmed by immunoblotting and indirect immunofluorescence tests using WNV antigens. The proportion of seropositive chickens was higher for WNV than for Usutu virus or Sindbis virus. Attempts to isolate infectious virus or to detect viral RNA in the sera, failed.

Exposure to organophosphate (OP) pesticides can occur in free-living mammals in treated areas. Risk to nontarget animals from OPs usually is assessed with acute exposure data, but exposure of wild animals is likely to be intermittent and chronic. We compared the effects of single or repeated (hourly and daily) exposure to dimethoate on acetylcholinesterase (AChE) activity in laboratory mice to assess the suitability of standard laboratory tests for assessing risk. Mice were exposed either to a single dose (10 or 30 mg/kg) or to short-term repeated (three hourly doses of 10 mg/kg) intraperitoneal doses of dimethoate, and brain and serum AChE activity were measured. No significant difference was found in the degree of inhibition of AChE activity following acute and short-term repeated exposure. In a second experiment, mice were given three daily doses of 10 or 20 mg/kg of dimethoate, and both AChE activity and hepatic cytochrome P450 enzyme activity were measured. Daily exposure resulted in a dose-dependent decline in brain and serum AChE activity, and inhibition increased progressively with successively repeated exposures. However, this effect was relatively small compared to the effect of dose. Cytochrome P450 enzyme activity (CYP2B) was inhibited in the dimethoate-dosed mice. Our results indicate that acute dose-response toxicity studies are suitable models for predicting the likely occurrence of adverse effects from either short- or longer-term exposure of wild mammals to anticholinesterase compounds. Likely differences in exposure pattern between the laboratory and the natural environment are unlikely to bias the predictive power of these studies significantly.