BRAHMAN NEWS SEPTEMBER 2012 Issue #176
BY ALEX ASHWOOD
Reproduction efficiency of bulls is a key driver of herd productivity and the economic viability of the beef enterprise. It is unfortunate that some stud bulls are sold to the meatworks because of reproductive failure.
“Sub fertile bulls are as big a problem as infertile bulls”
Hopefully, problem bulls are identified early to avoid lost production through reduced numbers of replacement stock, female wastage and low calving and weaning rates.
Reproduction dysfunction involves inadequate structural and functional development, injuries and diseases that compromise the maintenance and activity of the sexual organs. Other contributing factors include poor herd and feed management and various structural faults that impair sexual behaviour.
“Fertility assurances by seedstock providers need to be fair dinkum”
This article presents the key factors that lead to bull reproductive failure and support the information provided in recently published reproduction articles in ABBA Journals.
SPERMATOGENESIS
With correctly structured scrotums and testes climatic conditions have limited effect on semen quality and characteristics. However any condition and structural abnormality that reduces thermal cooling of the testes markedly reduces the quantity and quality of semen (eg overfed bulls and thermal stress).
“Defective structures contribute to fertilisation losses”
Testicular abnormalities that affect spermatogenesis (formation and maturation of sperm) include cryptorchidism and hypoplasia. Factors that lead to the degeneration of the testes also reduce the quality of semen.
CRYPTORCHIDISM
Failure of the testes to descend into the scrotum may be unilateral or bilateral but more frequently is the former. The cause for failure of the testes to descend is not fully understood. Bulls with the unilateral condition can reproduce but should not be retained for breeding purposes. Bulls with the bilateral condition produce testosterone but are generally sterile.
HYPOPLASIA
Underdeveloped testes are small but generally have normal consistency. Testicular hypoplasia (underdevelopment) results in reduced sperm production and less capacity to service suitable numbers of females. Due to the genetic nature of the condition and unsuitable servicing capacity, bulls with underdeveloped testes should not be kept for breeding purposes.
TESTICULAR DEGENERATION
Soft and too firm testes and abnormal changes to the size and consistency of the testes are signs of testicular degeneration.
“Seasonal semen morphological tests are a useful tool to determine degeneration”
Signs of degeneration are usually characterised by sperm ejaculates having an increased abnormal sperm count, poor sperm mobility and abnormal semen morphology.
Degeneration can be caused by temperature elevation (internal and/or external), pathogenic invasions and the presence of tumours. Common signs of testes degeneration include inflammation of the testes (orchitis) and/or the epididymus (epididymitis).
Tumours are more frequently found in bulls over 7 years of age. Bulls with tumours in the testes have a higher proportion of inferior sperm with lower fertilising capacity.
Temperature elevation of the testes due to disease, high fat levels in the scrotum and testes too close to the body cause poor thermal regulation (ie cooling and sweating) which leads to degeneration of the semen. Excessively pendulous scrotums and testicles are prone to damage due to injuries.
AGING
Breeding soundness rises in the post pubertal period then declines with age but there are quite large individual differences due to genetics and herd management factors. Semen characteristics and fertilizing capacity also show a gradual decline with age. As bulls get older mutations can affect the space and function of sperm reducing conception rates. Also, as testosterone levels decline with age, sperm counts start to decline reducing the service capacity of bulls.
MALFUNCTIONS
Inflammation of the epididymis and testes, vas deferens and vesicular glands can lead to lowered semen quality and reduced fertility. Infection and/or physical injury often accounts for the inflammation of these structures.
Overfeeding and lack of use of bulls can lead to the increased occurrence of abnormal semen indicating that these factors can lead to retrogressive changes in sperm during storage in the epididymus.
Underfeeding and overuse of bulls decreases seminal plasma, fructose, citric acid and probably other compounds essential for high quality seminal fluid.
ABNORMAL SEMEN
Under normal circumstances, the quality of semen is reasonably consistent. However, extreme stress (adverse management, hostile environments, poor transport) can impact on bull fertility.
Sperm is continuously produced and takes 6-8 weeks from the start of production to storage in the epididymis prior to ejaculation. Abnormal semen samples can reflect less than satisfactory conditions (heat, disease, stress) during spermatogenesis (semen production).
Semen evaluation is an indicator of reproduction efficiency. However, crushside semen assessments do not guarantee reproductive soundness of the bull since there are several factors that affect full reproductive failure.
Failure of some young bulls to ejaculate at crushside semen assessments is not evidence that the bull will not perform naturally. Similarly, low quality artificially collected semen from young bulls is not absolute proof that the young bull cannot produce suitable semen. In both instances, the young bulls should receive further assessment at a later date.
“Post mating assessments are a reliable indicator of breeding soundness”
SPERM ABNORMALITIES
Morphologic (structural) abnormalities are classified as primary if they are assumed to have happened during spermatogenesis and secondary if the mal formation has taken place in the male ducts.
“All semen has a percentage of abnormal sperm”
Morphological assessment requires that a semen sample (in a special diluent) is forwarded to accredited morphologists. Abnormalities fall into several categories and some morphological defects are more serious than others (eg separation of the head from the tail is a serious defect in infertile bulls). Generally, if not more than 15 percent of the semen is abnormal and particularly if no serious abnormalities predominate, fertilising capacity is not seriously compromised.
“Morphological abnormalities cannot be characterised in the field”
Recent studies have examined the nucleus within the sperm head and found that infertile bulls frequently have less DNA (deoxyribose nucleic acid) compared to normal bulls.
Unfortunately whilst DNA determination could be a useful tool in assessing bull fertility problems, difficulties in its measurement limit its field application.
COPULATION FAILURE
Sexual behaviour is dependent upon stimuli transmitted through the neural centres of the lumbar portion of the spinal cord. Copulation failure (inadequate erection and ejaculation) can be caused by anatomic defects of the sexual organs, by pain which prevents mounting or intromission, behavioural disturbances and structural unsoundness (eg straight hind legs).
PENILE AND SHEATH DEFECTS
Certain congenital defects can lead to reduced reproduction performance. Penile tumours and abrasions can limit copulation due to pain.
Small testes are often accompanied by an underdeveloped penis. Additionally, a bulls penis may be bent or spiral shaped which prevents vaginal penetration.
Much has been written about the need to avoid pendulous sheaths, however additional structural problems that should receive similar attention include poorly structured and badly attached sheaths and particularly sheaths that have heavy navel folds.
BEHAVIOURAL DISTURBANCES
Intimidation of males by other males is a phenomenon associated with multisire breeding. In addition to these behavioural problems some bulls have intromission without ejaculation. Failure to ejaculate sometimes happens with bulls even when demonstrating high levels of libido and accompanied by vigorous mounting, thrust and penetration of the vagina. Bulls experiencing pain at mounting and intromission may defer sexual activity for several months.
In hot climates obese bulls in addition to having low quality semen are less likely to show interest and service less females than bulls of a normal weight. Obese bulls are also more prone to leg and foot injuries which reduces sexual activity. Arthritis (often the result of heavy grain feeding) affecting the rear legs and spinal column is a secondary cause for failure to copulate.
FERTILISATION FAILURE
Whilst the greatest proportion of embryonic and foetal losses are attributed to the dam, some fertilisation and embryonic failures are attributed to the bull (eg reproductive diseases). It is also possible that fertilisation losses can occur due to sperm antibodies.
Aged semen within the epididymis is also detrimental to fertilisation. Genetic factors can also be involved, eg lethal genes carried by the sperm are a probable cause of fertilisation failure or embryonic loss.
Further ABBA reading : Selection – Bull Reproductive Soundness, Sept 2009; Selection – Structure and Lameness, Mar 2011; Selection – Functional Efficiency, Jun 2011; Reproduction – Herd Health, Sept 2011; Reproduction – Anatomy and Endocrinology, Dec 2011; Reproduction – Fertility and Infertility, Jun 2012
SUMMARY TABLE – PRINCIPAL ANATOMIC OR PHYSIOLOGICAL DEFECTS THAT IMPAIR REPRODUCTION PERFORMANCE
| DEFECT | CAUSE(S) | INCIDENCE |
| Cryptochidism (unilateral or bilateral; failure of testes to descend into scrotum) | Genetic; endocrine dysfunction; adhesion of testes | Congenital |
| Testicular hypoplasia (undersized testes; lack of resilience; decreased activity of the germinal epithelium) | Genetic | Puberty |
| Testicular atrophy (degeneration of former functional germinal epithelium) | Possibly genetic; infection; tumours | 7 years or later |
| Uneven testes size | Probably genetic and environmental | Congenital or later |
| Penile fracture | Forceful copulation with rupture and haemorrhage | Injury |
| Umbilical folds | Genetic may deflect penis | Congenital but can be accentuated with injury and infections of the umbilical cord |
| Prolapse of prepuce (lining of sheath hangs downward externally) | Genetic may also accompany penile rupture due to injury | Congenital or follows injury |
| Phimosis (insufficient penile penetration) | Genetic; retractor muscle does not relax resulting in failure of sigmoid flexture to straighten at erectionLesions and fibrous thickening of prepuce restricting full movement | Puberty Injury or infection |
| Corkscrew or spiral penis | Unknown; prevents intromission | Congenital |
| Penile tumours | Unknown | Anytime |
