(a) Describe nutritional characteristics of feed ingredients which are generally incorporated in formulation of poultry feed. (20…

(a) Nutritional characteristics of common poultry feed ingredients

Energy sources. Maize is the main cereal: high in metabolisable energy (about 3,300–3,400 kcal/kg), low in protein (8–9%) and deficient in lysine, tryptophan and methionine; yellow maize supplies xanthophylls for yolk and skin colour. Sorghum and pearl millet (bajra) give slightly less energy and are fed with care because of tannins in sorghum; broken rice and wheat are alternatives. Fats and oils (soy, sunflower, palm) raise energy density and help absorption of fat-soluble vitamins. Rice polish and de-oiled rice bran give energy and B vitamins but become rancid, and high-fibre bran is limited.

Protein sources. Soybean meal (44–48% protein) has the best amino-acid balance, rich in lysine but relatively low in methionine, and raw soybean contains trypsin inhibitors, which heat processing destroys (checked by the urease test). Groundnut cake is good in protein but low in lysine and methionine and risks aflatoxin; sunflower cake is high in fibre; mustard or rapeseed cake contains glucosinolates and erucic acid, and cottonseed cake contains gossypol, so their levels are limited. Fish meal (55–65% protein) is rich in lysine, methionine, calcium and phosphorus, with a risk of high salt and fishy taint. Meat and bone meal adds protein, calcium and phosphorus.

Supplements. Synthetic DL-methionine and L-lysine correct limiting amino acids; limestone and dicalcium phosphate supply calcium and phosphorus (laying hens need high calcium for shell); salt gives sodium; and vitamin-mineral premixes (manganese to prevent perosis, zinc for feathering, selenium with vitamin E against exudative diathesis, and vitamin E alone for nutritional encephalomalacia), plus additives such as enzymes, coccidiostats and toxin binders.

(b) Haemorrhagic disorders and congenital thrombocytopenia in dogs

Haemorrhagic disorders: (1) vascular defects (vasculitis, Ehlers-Danlos syndrome); (2) platelet disorders, thrombocytopenia (immune-mediated, infectious such as ehrlichiosis, marrow suppression, congenital) and thrombopathies (Glanzmann's thrombasthenia); (3) coagulation-factor deficiencies, haemophilia A (factor VIII) and B (factor IX), von Willebrand disease, vitamin K deficiency (warfarin or dicoumarol poisoning, sweet clover poisoning) and liver disease; and (4) disseminated intravascular coagulation.

Congenital (inherited) thrombocytopenia in dogs is best known as macrothrombocytopenia in Cavalier King Charles Spaniels, caused by a β1-tubulin (TUBB1) mutation that impairs platelet production and gives a low count (often 20–100 × 10³/μL) of abnormally large platelets, and in Norfolk and Cairn Terriers. Most affected dogs have little or no bleeding because platelet mass is near normal, but they show epistaxis or petechiae after trauma or surgery. Diagnosis rests on repeated counts with blood smear and exclusion of immune-mediated thrombocytopenia, tick fever and marrow disease. Care is supportive: avoid antiplatelet drugs, and give platelet-rich transfusion for severe bleeding. Dogs with inherited defects should not be bred.

(c) Idealised population and the chromosomal theory of sex determination

Idealised population. Used in population genetics (Wright and Falconer) as a reference: a closed population of constant finite size N, with equal numbers of males and females where relevant, random mating including selfing in the simple model, non-overlapping generations, and no selection, mutation, migration or differential fertility. Changes in allele frequency then arise only from sampling (genetic drift), and the rate of inbreeding is ΔF = 1/(2N). Real populations are compared with it through the effective population size.

Chromosomal theory. Henking (1891) noted the X body, McClung (1902) proposed an accessory chromosome determining sex, and Stevens and Wilson (1905) showed the XX-XY mechanism. Types: XX–XY in mammals and Drosophila (males heterogametic; in mammals the SRY gene on Y triggers the testis); XX–XO in grasshoppers and some insects; ZZ–ZW in birds, moths and some reptiles (females heterogametic); and haplodiploidy in bees and ants. In mammals, the sex of the offspring depends on the sperm. Bridges' genic-balance and environmental mechanisms add to the picture.