Alistair Dawson

Detection of seroconversion to West Nile virus, Usutu virus and Sindbis virus in UK sentinel chickens.

SummaryWe 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.

USE AND VALIDATION OF A MOLT SCORE INDEX CORRECTED FOR PRIMARY-FEATHER MASS

Abstract In European Starlings (Sturnus vulgaris), mass of new primary feathers increases linearly with time for most of the duration of molt (Dawson 2003). Here, we had two aims: (1) to confirm that mass of new primary feathers increases linearly in other species, and (2) to use that linear increase as the basis of a system to score the progress of molt. Increase in length of primary feathers during molt was recorded for captive Eurasian Magpies (Pica pica), Carrion Crows (Corvus corone), European Greenfinches (Carduelis chloris), and Eurasian Bullfinches (Pyrrhula pyrrhula). Wing shape differs among those species. Feather lengths during molt were converted into mass by using information on final feather length and mass and the distribution of mass from tip to base of feather. Rate of increase in total mass of new primary feathers was largely linear in all four species. A molt scoring method is described in which individual feather scores are weighted to account for the contribution of each particular primary feathers mass toward total primary-feather mass. When the method was tested on eight captive starlings, the increase in mass-corrected molt score was almost linear, unlike the increase shown by the standard scoring system, which exaggerated molt rate during the early part of molt and underestimated it later. In the four species studied here, mass-corrected molt score likewise closely tracked the actual increase in mass, unlike the standard molt score. Because it is based on feather mass, the method presented here is of greater physiological and energetic relevance than the standard method. Because the mass-corrected score increases more linearly with time, it has the additional advantage of enabling less complicated, and potentially more accurate, estimations of molt start dates and molt durations.

Enhancement of malathion toxicity to the hybrid red-legged partridge following exposure to prochloraz

Abstract The agricultural fungicide, prochloraz, which inhibits ergosterol biosynthesis in fungi, was shown to be a potent inducer of liver enzymes in the hybrid red-legged partridge. Pretreatment with a single oral dose of 180 mg/kg resulted in a dramatic potentiation of the toxicity of the organophosphorous insecticide malathion: three out of four prochloraz-pretreated birds died within 10 min from acute poisoning (82–100% inhibition of brain cholinesterase activity) following intraperitoneal administration of 3.3 or 16.7 mg/kg malathion, whereas no significant inhibition of serum cholinesterase activity was seen in control birds 1 hr after administration of the insecticide. Prochloraz pretreatment also resulted in a significant increase in susceptibility to low oral doses of malathion. In vitro metabolism of [ 14 C]malathion by microsomes from control birds resulted largely in the formation of the malathion monoacid, whereas the anticholinesterase, malaoxon, was the main metabolite generated by microsomes from prochloraz-pretreated birds. The dramatic amplification of malathion toxicity following induction with prochloraz is attributed to an increased activation of malathion to its active metabolite malaoxon by one or more induced monooxygenase forms; inhibition of “B”-esterase activity by malaoxon may contribute to this amplification of toxicity.