Effects ofEimeria acervulinainfection severity on growth performance, apparent ileal amino acid digestibility, and plasma concentrations of amino acids, carotenoids, and α1-acid glycoprotein in broilers

This study tested the hypothesis that a host mucogenic response to an intestinal coccidial infection promotes the onset of necrotic enteritis (NE). A chick NE model was used in which birds were inoculated with Eimeria acervulina and E. maxima and subsequently with Clostridium perfringens (EAM/CP). A second group of EAM/CP-infected birds was treated with the ionophore narasin (NAR/EAM/CP). These groups were compared to birds that were either non-infected (NIF), or infected only with E. acervulina and E. maxima (EAM), or C. perfringens (CP). The impact of intestinal coccidial infection and anti-coccidial treatment on host immune responses and microbial community structure were evaluated with histochemical-, cultivation- and molecular-based techniques. Barrier function was compromised in EAM/CP-infected birds as indicated by elevated CFUs for anaerobic bacteria and C. perfringens in the spleen when compared to NIF controls at day 20, with a subsequent increase in intestinal NE lesions and mortality at day 22. These results correlate positively with a host inflammatory response as evidenced by increased ileal interleukin (IL)-4, IL-10 and IFN-gamma RNA expression. Concurrent increases in chicken intestinal mucin RNA expression, and goblet cell number and theca size indicate that EAM/CP induced an intestinal mucogenic response. Correspondingly, the growth of mucolytic bacteria and C. perfringens as well as alpha toxin production was greatest in EAM/CP-infected birds. The ionophore narasin, which directly eliminates coccidia, reduced goblet cell theca size, IL-10 and IFN-gamma expression, the growth of mucolytic bacteria including C. perfringens, coccidial and NE lesions and mortality in birds that were co-infected with coccidia and C. perfringens. Collectively the data support the hypothesis that coccidial infection induces a host mucogenic response providing a growth advantage to C. perfringens, the causative agent of NE.

Classically, polyamines is a family of molecules (i.e. putrescine, spermine, spermidine) derived from ornithine according to a decarboxylation/condensative process. More recently, it has been demonstrated that arginine can be metabolised according to the same pathway leading to agmatine formation. Polyamines are essential for the growth, the maintenance and the function of normal cells. The complexity of their metabolism and the fact that polyamines homeostasis is tightly regulated support the idea that polyamines are essential to cell survival. Multiple abnormalities in the control of polyamines metabolism might be implicated in several pathological processes. This paper summarises the knowledge about polyamines metabolism and point out the importance of these molecules as a target for the development of therapeutic tools and nutritional strategy.

A compartmentalised model is presented for the estimation of the monetary losses suffered by the world's poultry industry resulting from coccidiosis of chickens and costs of its control. The model is designed so that the major elements of loss may be separately quantified for any chicken-producing entity, e.g., a farm, a poultry company, a country, etc. Examples are presented and the sources, reliability and geographical relevance of the data used for each parameter are provided. Loss elements for specific geographical areas should be recalculated at appropriate intervals to take into account local and international fluctuations in costs of chicks feed, labour, financial inflation and world currency exchange rates. Equations are given for relationships among numbers of chickens, liveweights, weights of carcasses, feed consumptions, feed conversion ratio (FCR), prices of feeds, prices of anticoccidial therapeutic and prophylactic drugs, values of chickens, chicken rearing costs; and effects of coccidiosis on mortality, weight gain and FCR. Using these equations, it is theoretically possible for an international team of representatives, each using reliable local data, to calculate simultaneously each relevant loss element for their respective countries. Addition of these elements could give, for the first time, an accurate global estimate of the losses due to chicken coccidiosis. The total cost of coccidiosis in chickens in the United Kingdom in 1995 is estimated to have been at least GB pound silver 38 588 795, of which 98.1% involved broilers (80.6% due to effects on mortality, weight gain and feed conversion, and 17.5% due to the cost of chemoprophylaxis and therapy). The costs of poor performance due to coccidiosis and its chemical control totalled 4.54% of the gross revenue from UK sales of live broilers. This model includes a new method for comparing the profitabilities of different treatments in commercial trials. providing actual costs rather than the arbitrary numerical scores of other methods. Although originally designed for the study of coccidiosis, the model is equally applicable to any disease. It should be of value to agricultural economists, the animal feed and poultry industries, animal health companies, and to research scientists (particularly for preparing grant applications).