Effect of lipopolysaccharide on sickness behaviour in hens kept in cage and free range environments.

The aim of this study was to assess whether environmental enrichment and environmental conditions can influence the expression of sickness behaviour. The behaviour in response to injection of lipopolysaccharide or saline was examined in a total of 96 62-weeks old hatchmate hens kept in a free range or cage environment. There were eight experimental treatments, each with 12 birds. Half the birds were sourced from a commercial cage layer unit (C/-) and half from a commercial free range unit (FR/-). After intraperitoneal injection with either lipopolysaccharide or saline (as a control), the hens were placed in either a cage (-/C) or free range (-/FR) environment. Lipopolysaccharide caused greater suppression of activity in free range (FR/FR) than in caged hens, including less walking (53% reduction), roosting (-86%) and preening (-60%) (p<0.05). Those responses were not observed in caged birds released into free range, nor in free range birds introduced to cages, suggesting that both the presence of and the familiarity with an environment affected sickness behaviour patterns. Increased sleeping was the most consistent response (+147%; p<0.001), and it was least influenced by environment. It was concluded that free range layer hens can express a greater range of sickness behaviours than caged hens, and this may make it more difficult to recognise disease expression in the caged environment.

Development of antidotes for sodium monofluoroacetate (1080).

Baits containing sodium monofluoroacetate (1080) are commonly used in New Zealand during feral pest control operations. However, each year, a number of domestic dogs are unintentionally killed during these control operations, and a suitable antidote to 1080 intoxication is required. The primary toxic mechanism of 1080 is well known. However, as with other pathologies where energy deprivation is the main effect of intoxication, the cascade of effects that arises from this primary mechanism is complex. At present, putative antidotes for 1080 are generally unable to address the primary mechanism of intoxication but such agents may be able to control the cascade of secondary effects, which can result during intoxication. Part of the reason for this is that targeting the cascade can provide a longer window of time for antidote success. We have undertaken studies that identified some of the central nervous system (CNS) and systemic pathophysiological cascades caused by 1080 intoxication. Using this information we designed antidotes, on the basis of preventing different steps in this cascade. In the chicken model targeting systemic changes, in particular reducing effects of nitric oxide derivatives generated in cardiac muscle, proved successful in reducing fatality associated with 1080. In rats and sheep, targeting the CNS with a number of compounds including: glutamate; calcium and dopamine antagonists; gamma amino butyric acid agonists, and astressin-like compounds reduced fatalaties. However, to be successful in the rat and sheep model a given antidote needed to move quickly from systemic circulation across the blood brain barrier and into the CNS. The work also suggests ways in which specific biomarkers of 1080 exposure may be developed with respect to different species.

Dissociation constants of carboxymethyloxysuccinic acid.

The dissociation constants of carboxymethyloxysuccinic acid (CMOS) have been measured at 25 degrees and an ionic strength of 0.1M in sodium perchlorate. The values found were: pK(1) = 2.52, pK(2) = 3.77 and pK(3) = 5.00. CMOS is thus seen to be rather stronger than its isomer citric acid.