Investigating Hatchery Practice - Effects of Nutrition

In the tenth article in this series, Dr Steve Tullett, consultant for Aviagen specialising in incubation and fertility, outlines the effects of nutrition on infertility, embryo mortality and hatchability. The article forms part of a recently published Ross Tech publication, Investigating Hatchery Practice.
calendar icon 23 February 2010
clock icon 5 minute read

The effects of vitamin and mineral deficiencies on embryo mortality and malformations are well documented. General knowledge of breeder ration supplementation requirements is good and severe vitamin and mineral deficiencies are relatively unusual nowadays because vitamin and mineral premixes are generally reliable if sourced from suppliers that are ISO-, HACCP- and GMP-accredited. However, occasional problems arise and the main findings from nutritional research and field observations are noted below.

Infertility may be associated with a deficiency of vitamin A, vitamin E or selenium, particularly in the male rations.

Early embryo deaths may be associated with a deficiency of vitamin A (failure to develop circulatory system), vitamin E (circulatory failure), biotin, niacin, pantothenic acid, copper, selenium or thiamin. Excess boron or molybdenum could increase the proportion of early deaths.

Mid-term embryo deaths have been associated with a deficiency of vitamin B12, riboflavin, phosphorus and zinc.

Mid to late deaths have been associated with a deficiency of vitamin B12, niacin, pyridoxine, pantothenic acid and riboflavin

Late embryo deaths have been associated with deficiencies of vitamin B12, vitamin D, vitamin E, vitamin K, pantothenic acid, riboflavin, folic acid, biotin, calcium, manganese, magnesium, phosphorus, zinc, iodine and thiamin. Excess selenium could increase the proportion of late deaths.

Excess iodine and vitamin D can cause high embryo losses.

Achieving the optimal level of selenium supplementation can be difficult because there are variable levels of selenium in the soil (and thus plant feeding stuffs) depending on geographic region. In some cases, the use of organic selenium has resulted in improved fertility and hatchability.

In case of prolonged vitamin B12 or niacin deficiencies, embryo mortality may change from early to late stage in incubation, and from late to early embryo deaths in case of prolonged riboflavin deficiency. Niacin can be formed from tryptophan, so a deficiency is usually the result of an antagonism with other dietary components. A deficiency of linoleic acid can affect embryos at all stages.

The supplementation requirements for egg production and hatchability differ. Egg production can be affected by deficiencies of energy, essential amino acids, vitamin A, pyridoxine (B6), B12, magnesium, manganese, sodium, iodine and zinc, whilst deficiencies of vitamin D, calcium, phosphorus or zinc may exert an effect on hatchability through effects on shell quality.

An excess of crude protein may reduce fertility and a low energy to protein ratio in breeder rations can reduce hatchability.

Contamination of breeder diets with ionophore anticoccidials (from the feed mill) or certain mycotoxins (from raw materials) can also lead to a reduction in hatchability.

Some specific malformations in late embryos have been associated with deficiencies in:

  • Vitamin B12 (short beak, poor muscle development in legs, perosis, early chick mortality).
  • Vitamin D (stunting, soft bones, shortened upper beak)
  • Vitamin E (haemorrhage in chicks after hatch)
  • Vitamin K (high level of late deads, ectopic viscera and haemorrhage in the late deads)
  • Biotin (shortened twisted legs, feet and wings, crooked beak (parrot beak))
  • Folic acid (bent legs, webbing between toes, parrot beak)
  • Niacin (face abnormalities, missing beak)
  • Pantothenic acid (subcutaneous haemorrhaging, abnormal feathering)
  • Riboflavin (dwarfing, curled toes, oedema, clubbed down)
  • Iodine (incomplete closure of the navel, prolonged incubation period).
  • Iron (anaemia, pale-coloured circulatory system)
  • Manganese (short leg bones, slipped tendons, parrot beak, deaths 18-21 days, globular head, short wings, protruding abdomen, oedema)
  • Zinc (spinal, limb and head abnormalities, small eyes).

Excesses of boron, e.g. from insecticides used to treat litter, have resulted in face abnormalities and excess selenium can lead to late deaths, crooked toes, shortened wings and a short or missing beak.

Loss of vitamin activity can occur if the vitamin premix is stored inappropriately.

Heat treatment of feed during conditioning and pelleting can result in the degradation of some vitamins. Vitamin recovery studies should be conducted at the feed mill in order to determine the level of degradation that occurs during heat treatment. This will enable supplementation levels to be adjusted to ensure that the final feed contains the desired vitamin levels.

Developmental abnormalities tend to be immediately obvious and memorable and it is usually important not to over-emphasise their relevance. It must be borne in mind that malformations of the embryo can be caused not only by nutrition but also by adverse incubation conditions, e.g. high temperature. Thus, if a trait is seen at high incidence (i.e. most or all of the late dead embryos) on two or three consecutive trays, this could indicate positional effects arising from uneven incubation conditions in the setter.

Further Reading

- You can see other articles in this series Investigating Hatchery Practice by clicking here.

February 2010
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