(a) “Silent heat is not a disease, but a failure of management.” Critically evaluate this statement in the context of dairy…

(a) "Silent heat is not a disease, but a failure of management" in dairy animals (15 marks)

Silent heat (sub-oestrus) is a cycle in which the ovary functions normally and ovulation occurs, but the behavioural signs of oestrus are weak or absent. The statement is partly right, and partly not.

Support for the statement:

• Most silent heat is a failure of heat detection, not of the animal: oestrus is short (cows about 12 to 18 hours, with more standing heat at night), so infrequent observation, absent records, slippery floors, tie stalls and understaffing miss it.
• Management causes: negative energy balance and low body condition, and deficiencies of phosphorus, copper, zinc and vitamin A, which reduce oestradiol; lameness; and heat stress in summer, which shortens and weakens oestrus, especially in buffaloes and high-yielding cows.
• It is solved by management: observing three times a day for 20 to 30 minutes, using tail paint, heat-mount detectors, pedometers or activity monitors, teaser bulls, milk progesterone tests, and by timed AI protocols.

Against the statement:

• Some silent heat is physiological: the first postpartum ovulation is normally silent, since oestrus needs priming by progesterone, and buffaloes and heifers show weak signs by nature, with low oestradiol.
• Endocrine and pathological causes (ovarian cysts, low oestradiol, and uterine disease) can also suppress signs.

Verdict: silent heat is a phenomenon of physiology, but its cost is mainly a management failure, because it becomes an economic loss only when unrecorded and undetected. Better detection and nutrition, cooling and synchronisation (PGF₂α, Ovsynch) largely remove the loss.

(b) Role of early embryonic mortality in repeat breeding, and factors affecting it (15 marks)

A repeat breeder is a cow or buffalo with regular cycles and a normal genital tract, that fails to conceive after three or more services. In most of these, fertilisation occurs (about 90%), but the embryo dies before or during maternal recognition of pregnancy (about day 16 to 17 in the cow, by interferon-tau) and before about day 42. Early embryonic mortality (EEM) is thus the main cause of pregnancy failure in repeat breeders, and up to 30 to 40% of embryos are lost. The animal returns to oestrus at a normal or slightly lengthened interval, so the loss is not detected, and it appears to be a failed insemination.

Factors:

• Genetic and chromosomal abnormalities of the embryo, and ageing gametes (mistimed insemination).
• Poor semen quality, and errors in AI technique.
• Uterine environment: subclinical endometritis, and inadequate uterine secretions.
• Hormonal: inadequate progesterone (luteal deficiency), delayed LH surge.
• Nutrition: negative energy balance, excess degradable protein (high urea in blood and uterus), deficiencies of selenium, vitamin E, vitamin A and minerals.
• Heat stress, and high milk yield.
• Infections: Campylobacter, Trichomonas, BVD virus, Brucella, Leptospira and others.
• Immunological and management stress.

(c) Effect of high temperature and humidity on spermatogenesis, libido and semen quality (10 marks)

The testes work best about 2 to 6 °C below body temperature, maintained by the scrotum, the pampiniform plexus and sweating. High ambient temperature with high humidity (a high temperature-humidity index) reduces evaporative cooling, so testicular temperature rises.

• Spermatogenesis: heat damages the developing spermatocytes and spermatids, and the seminiferous epithelium, so sperm production falls and testes shrink. The effect appears with a lag of about two to eight weeks, and recovery takes about two to three months (the cycle is about two months).
• Libido: heat stress lowers testosterone and LH, and feed intake, so sexual desire and mounting fall.
• Semen quality: lower volume and concentration, decreased motility and viability, more abnormal sperm (head and tail defects, proximal droplets, coiled tails), acrosome and DNA damage, mainly by oxidative stress, and poorer freezability and fertility.

Bos indicus and buffalo bulls are less affected than Bos taurus. Shade, sprinklers, fans, antioxidants (vitamin E, selenium, zinc) and collection during cool hours reduce the effects.

(d) Why chickens excrete nitrogenous waste mainly as uric acid (10 marks)

Chickens are uricotelic: they excrete about 60 to 80% of their nitrogenous waste as uric acid, for several reasons.

• Egg development: the embryo develops in a closed, shelled egg (cleidoic egg) with a limited water supply. Ammonia is highly toxic and needs a lot of water for dilution, and urea is very soluble and would accumulate in the fluids of the egg and disturb osmotic balance. Uric acid is almost insoluble in water and precipitates as crystals in the allantois, so it is harmless and takes almost no space.
• Water conservation: adult birds conserve water, since uric acid leaves as a semi-solid white paste with little water, and birds have no urinary bladder, which also saves weight for flight.
• Nitrogen efficiency: one uric acid molecule (C₅H₄N₄O₃) carries four nitrogen atoms, twice the two in urea.

Biochemistry: the avian liver lacks a functional urea cycle (for example carbamoyl phosphate synthetase I), and instead forms purines de novo from glycine, glutamine, aspartate, formate and CO₂ to inosine monophosphate. This is degraded to hypoxanthine, xanthine and uric acid by xanthine dehydrogenase. Uric acid is secreted into the renal tubules by active transport, and is passed to the cloaca. Synthesis costs more energy than urea, a price paid for saving water.