Composition, color, and texture of Thai indigenous and broiler chicken muscles

Chemical compositions and physical properties of mixed-sex Thai indigenous (Gallus domesticus) and broiler (commercial breed, CP707) chicken biceps femoris and pectoralis muscles were determined. Indigenous chicken muscles contained higher protein contents but lower fat and ash contents compared to broiler muscles (P < 0.001). The amino acid profile of the indigenous chicken muscles was similar to that of the broiler muscles except they were slightly richer in glutamic acid (P < 0.05). The indigenous chicken muscles contained more saturated and less polyunsaturated fatty acids than the broiler muscles. There were no differences in the monounsaturated fatty acid contents between the breeds. The total collagen contents of indigenous pectoralis and biceps femoris muscles were 5.09 and 12.85 mg/g, respectively, which were higher than those found in broiler pectoralis (3.86 mg/g) and biceps femoris muscles (8.70 mg/g) (P < 0.001). Soluble collagen contents were lower for indigenous pectoralis and biceps femoris muscles, 22.16 vs. 31.38% and 26.06 vs. 33.87%, respectively. The CIE system values of lightness (L*), redness (a*), and yellowness (b*) of indigenous chicken muscles were higher than those of broiler muscles. The shear values of indigenous chicken muscles either raw or cooked were higher than those of broiler muscles (P < 0.05). After cooking, the shear values decreased for broiler biceps femoris and pectoralis muscles (P < 0.05), whereas no change was observed for indigenous chicken biceps femoris muscle (P > 0.05). Shear values increased for indigenous chicken pectoralis muscle (P < 0.05).

Microstructure and thermal characteristics of Thai indigenous and broiler chicken muscles

The microstructure and thermal characteristics of Thai indigenous (Gallus domesticus) and broiler chicken (commercial line CP707) biceps femoris and pectoralis muscles were determined. Perimysium thicknesses were 14.2 mum for biceps femoris muscle and 7.10 mum for pectoralis muscle of indigenous chicken muscles, thicker than those of broiler muscles, which were 9.93 mum for biceps femoris muscle and 3.87 mum for pectoralis muscle (P < 0.05). Five endothermic peaks with peak transition temperatures (T-p) of 54.9, 61.7, 65.4, 70.6, and 76.1degreesC were obtained for broiler pectoralis muscle, whereas only 3 endothermic peaks (T-P of 56.6, 62.6, and 74.9degreesC were obtained for broiler biceps femoris muscle. Thai indigenous biceps femoris and pectoralis muscles had endothermic peaks with T-P ranges of 53.5 to 54.8, 60.7 to 61.9, and 75.9 to 76.9degreesC. The fiber diameters of Thai indigenous chicken muscles were greater (P < 0.05) than those of the broiler, 31.7 vs. 20.4 mum for biceps femoris muscle and 28.9 vs. 26.6 pm for pectoralis muscle, respectively. After cooking at 80degreesC for 10 min, the fiber diameter of indigenous chicken muscles significantly decreased while those of the broiler significantly increased. The mean of sarcomere lengths of the raw muscles ranged from 1.56 to 1.64 mun and decreased to 0.92 to 1.32 mum (P < 0.001) for broiler muscles and 1.22 to 1.35 mum (P < 0.001) for indigenous chicken muscles after cooking. The perimysium and endomysium of broiler muscles melted after cooking at 80degreesC, however, only slight disintegration was observed in these tissues in the indigenous chicken muscles.

A standardised BCR resistance test for all anticoagulant rodenticides

This paper presents a reappraisal of the blood clotting response (BCR) tests for anticoagulant rodenticides, and proposes a standardised methodology for identifying and quantifying physiological resistance in populations of rodent species. The standardisation is based on the International Normalised Ratio, which is standardised against a WHO international reference preparation of thromboplastin, and allows comparison of data obtained using different thromboplastin reagents. ne methodology is statistically sound, being based on the 50% response, and has been validated against the Norway rat (Rattus norvegicus) and the house mouse (Mus domesticus). Susceptibility baseline data are presented for warfarin, diphacinone, chlorophacinone and coumatetralyl against the Norway rat, and for bromadiolone, difenacoum, difethialone, flocoumafen and brodifacoum against the Norway rat and the house mouse. A 'test dose' of twice the ED50 can be used for initial identification of resistance, and will provide a similar level of information to previously published methods. Higher multiples of the ED50 can be used to assess the resistance factor, and to predict the likely impact on field control.

Preliminary study of the genetics of resistance in the house mouse

A wild house mouse (Mus domesticus) population originally trapped near Reading, Berkshire, United Kingdom, and maintained as a colony in the laboratory, was subjected to the discriminating feeding period of the warfarin resistance test, as used by Wallace and MacSwiney (1976) and derived from the work of Rowe and Redfern (1964). Eighty percent of this heterogeneous population survived the resistance-test. A similar proportion of the population was found to survive the normally lethal dose of bromadiolone administered by oral gavage. The majority of this population of mice were classified as "warfarin-resistant" and "bromadiolone-resistant." The dose of 10mg.kg-1 of bromadiolone administered by oral gavage appeared to give good discrimination between susceptible and resistant individuals. The results of breeding tests indicate a single dominant gene that confers both "warfarin-resistance" and "bromadiolone-resistance", with complete expression of the resistance genotype in both males and females. Individual mice were classified as to genotype by back-crossing to a homozygous-susceptible strain, and resistance-testing the F1 generation. Separate strains of homozygous-resistant and homozygous-susceptible house mice are now being established.

The current status of anticoagulant resistance in rats and mice in the UK

Introduction: Resistance to anticoagulants in Norway rats (Rattus norvegicus) and house mice (Mus domesticus) has been studied in the UK since the early 1960s. In no other country in the world is our understanding of resistance phenomena so extensive and profound. Almost every aspect of resistance in the key rodent target species has been examined in laboratory and field trials and results obtained by independent researchers have been published. It is the principal purpose of this document to present a short synopsis of this information. More recently, however, the development of genetical techniques has provided a definitive means of detection of resistant genotypes among pest rodent populations. Preliminary information from a number of such surveys will also be presented. Resistance in Norway rats: A total of nine different anticoagulant resistance mutations (single nucleotide polymorphisms or SNPs) are found among Norway rats in the UK. In no other country worldwide are present so many different forms of Norway rat resistance. Among these nine SNPs, five are known to confer on rats that carry them a significant degree of resistance to anticoagulant rodenticides. These mutations are: L128Q, Y139S, L120Q, Y139C and Y139F. The latter three mutations confer, to varying degrees, practical resistance to bromadiolone and difenacoum, the two second-generation anticoagulants in predominant use in the UK. It is the recommendation of RRAG that bromadiolone and difenacoum should not be used against rats carrying the L120Q, Y139C and Y139F mutations because this will promote the spread of resistance and jeopardise the long-term efficacy of anticoagulants. Brodifacoum, flocoumafen and difethialone are effective against these three genotypes but cannot presently be used because of the regulatory restriction that they can only be applied against rats that are living and feeding predominantly indoors. Our understanding of the geographical distribution of Norway rat resistance in incomplete but is rapidly increasing. In particular, the mapping of the focus of L120Q Norway rat resistance in central-southern England by DNA sequencing is well advanced. We now know that rats carrying this resistance mutation are present across a large part of the counties of Hampshire, Berkshire and Wiltshire, and the resistance spreads into Avon, Oxfordshire and Surrey. It is also found, perhaps as outlier foci, in south-west Scotland and East Sussex. L120Q is currently the most severe form of anticoagulant resistance found in Norway rats and is prevalent over a considerable part of central-southern England. A second form of advanced Norway rat resistance is conferred by the Y139C mutation. This is noteworthy because it occurs in at least four different foci that are widely geographically dispersed, namely in Dumfries and Galloway, Gloucestershire, Yorkshire and Norfolk. Once again, bromadiolone and difenacoum are not recommended for use against rats carrying this genotype and a concern of RRAG is that continued applications of resisted active substances may result in Y139C becoming more or less ubiquitous across much of the UK. Another type of advanced resistance, the Y139F mutation, is present in Kent and Sussex. This means that Norway rats, carrying some degree of resistance to bromadiolone and difenacoum, are now found from the south coast of Kent, west into the city of Bristol, to Yorkshire in the north-east and to the south-west of Scotland. This difficult situation can only deteriorate further where these three genotypes exist and resisted anticoagulants are predominantly used against them. Resistance in house mice: House mouse is not so well understood but the presence in the UK of two resistant genotypes, L128S and Y139C, is confirmed. House mice are naturally tolerant to anticoagulants and such is the nature of this tolerance, and the presence of genetical resistance, that house mice resistant to the first-generation anticoagulants are considered to be widespread in the UK. Consequently, baits containing warfarin, sodium warfarin, chlorophacinone and coumatetralyl are not approved for use against mice. This regulatory position is endorsed by RRAG. Baits containing brodifacoum, flocoumafen and difethialone are effective against house mice and may be applied in practice because house mouse infestations are predominantly indoors. There are some reports of resistance among mice in some areas to the second-generation anticoagulant bromadiolone, while difenacoum remains largely efficacious. Alternatives to anticoagulants: The use of habitat manipulation, that is the removal of harbourage, denial of the availability of food and the prevention of ingress to structures, is an essential component of sustainable rodent pest management. All are of importance in the management of resistant rodents and have the advantage of not selecting for resistant genotypes. The use of these techniques may be particularly valuable in preventing the build-up of rat infestations. However, none can be used to remove any sizeable extant rat infestation and for practical reasons their use against house mice is problematic. Few alternative chemical interventions are available in the European Union because of the removal from the market of zinc phosphide, calciferol and bromethalin. Our virtual complete reliance on the use of anticoagulants for the chemical control of rodents in the UK, and more widely in the EU, calls for improved schemes for resistance management. Of course, these might involve the use of alternatives to anticoagulant rodenticides. Also important is an increasing knowledge of the distribution of resistance mutations in rats and mice and the use of only fully effective anticoagulants against them.