Infertility

Male infertility in farm animals refers to the reduced or absent ability of a male animal to successfully produce offspring when provided adequate opportunities to breed fertile females. This condition encompasses a broad spectrum of underlying problems ranging from physical abnormalities and hormonal imbalances to infectious diseases and management-related factors. Infertility may present as complete sterility, where the male is entirely incapable of producing offspring, or as subfertility, where reproductive efficiency is reduced but some breeding success remains possible. The distinction between these presentations influences treatment decisions and prognosis for affected animals.

The prevalence of male infertility in livestock populations is substantial and represents a significant economic concern for producers. Studies examining bulls presented for breeding soundness evaluation report that ten to twenty percent fail to meet satisfactory standards, with higher rates observed in certain populations and age groups. Similar or higher failure rates are documented in rams and boars undergoing reproductive evaluation. Many cases of male infertility remain undiagnosed in commercial operations that do not routinely evaluate breeding males, resulting in reduced pregnancy rates, extended breeding seasons, and increased costs that are attributed to other factors. Subclinical male fertility problems contribute to production losses that may go unrecognized without systematic evaluation.

The economic impact of male infertility extends throughout livestock production systems and affects profitability at multiple levels. A single infertile or subfertile male used in natural service can fail to settle numerous females during a breeding season, resulting in open females, delayed calving or lambing dates, and reduced crop uniformity. In operations using artificial insemination, semen from subfertile males can affect conception rates across thousands of inseminations. The cost of infertility includes reduced weaning weights from later-born offspring, increased female replacement costs for animals culled due to breeding failure, extended feeding periods, and lost genetic progress when valuable males cannot contribute to the breeding program. Secondary costs include additional labor for pregnancy diagnosis, management of non-pregnant animals, and adjustment of production plans.

Early detection through systematic breeding soundness evaluation and appropriate diagnostic follow-up offer the best opportunity to identify and manage male infertility before significant production losses occur. Breeding soundness examination protocols evaluating physical structure, reproductive organs, libido, and semen quality provide a standardized approach to identifying potentially infertile males. Understanding that male infertility can result from numerous underlying causes enables appropriate diagnostic workup and targeted treatment when possible. Working closely with veterinarians to establish evaluation protocols, identify problems early, and make informed management decisions protects reproductive efficiency and overall operation profitability.

The causes of male infertility in farm animals are diverse and can be categorized into physical, functional, infectious, and management-related factors. Physical abnormalities affecting the reproductive tract directly impair the ability to produce or deliver viable sperm. Testicular hypoplasia results in inadequate sperm production due to underdevelopment of testicular tissue. Cryptorchidism, where one or both testicles fail to descend into the scrotum, causes infertility through thermal damage to sperm-producing cells. Penile abnormalities including persistent frenulum, penile deviations, and penile fibrosis prevent successful intromission and semen deposition. Preputial injuries and adhesions physically obstruct breeding capability. Congenital absence or segmental aplasia of reproductive tract structures eliminates the pathway for sperm transport.

Hormonal and functional causes of infertility interfere with normal reproductive processes without necessarily causing visible anatomical changes. Hypothalamic-pituitary-gonadal axis dysfunction results in inadequate gonadotropin stimulation of the testicles, causing reduced testosterone and sperm production. Thyroid dysfunction can impair reproductive function indirectly through metabolic effects. Age-related decline in both hormonal function and spermatogenesis reduces fertility in older males. Libido problems prevent breeding attempts despite normal physical capability and semen quality. Delayed puberty extends the period before males become reproductively functional. Seasonal infertility in species with photoperiod-responsive reproduction limits breeding to specific times of year.

Infectious causes of male infertility include both reproductive tract infections and systemic diseases with reproductive consequences. Epididymitis causes obstruction of sperm transport and reduced semen quality. Orchitis results in direct testicular damage and impaired spermatogenesis. Vesicular gland infection, particularly with Brucella species in cattle, affects semen quality and poses zoonotic risk. Campylobacteriosis causes reproductive tract infection affecting fertility. Viral diseases including bovine viral diarrhea and bluetongue can cause transient or permanent testicular damage. Systemic febrile illness from any cause impairs spermatogenesis for extended periods due to the thermal sensitivity of developing sperm cells.

Environmental and management factors significantly influence male fertility in farm animals. Heat stress damages developing sperm and reduces semen quality, with effects persisting for weeks after the stress event due to the duration of spermatogenesis. Nutritional imbalances, both deficiencies and excesses, impair reproductive function and semen quality. Inadequate protein intake reduces sperm production, while excessive energy causing obesity impairs fertility through hormonal disruption and physical limitations. Trace mineral deficiencies, particularly zinc, selenium, and manganese, affect sperm production and function. Toxin exposure from plants, chemicals, or contaminated feed can cause temporary or permanent reproductive damage. Poor housing conditions, transportation stress, and social stress affect fertility through hormonal pathways.

The pathophysiology of male infertility ultimately involves disruption of spermatogenesis, sperm transport, or breeding behavior, alone or in combination. Normal fertility requires functional testicles producing adequate quantities of normal sperm, patent reproductive tract structures allowing sperm transport and maturation, accessory glands providing normal seminal fluid components, penile function permitting erection and intromission, adequate libido driving breeding behavior, and physical capability to mount and breed. Impairment at any step in this complex system can cause reduced fertility or complete infertility. Many affected animals have multiple concurrent problems contributing to their reproductive failure. Understanding the specific mechanisms involved in each case guides diagnostic evaluation and treatment decisions.

Early warning signs of male infertility often appear during natural breeding behavior before fertility problems are formally identified. Reduced libido manifests as decreased interest in estrous females, reluctance to mount, or failure to complete breeding attempts. Males may approach females but show limited or no mounting attempts despite appropriate female behavior. Prolonged mounting time with repeated failed intromission attempts suggests physical problems preventing normal breeding. Unusually rapid service completion or dismounting may indicate pain or abnormal sensation. Changes in competitive behavior between males, with previously dominant individuals showing reduced aggression or breeding activity, can indicate developing problems.

Physical examination findings in infertile males vary depending on the underlying cause but certain patterns are commonly observed. Abnormal testicular size, whether hypoplastic underdevelopment or asymmetric enlargement from inflammation or tumors, indicates potential problems. Altered testicular consistency, with soft or excessively firm testicles, suggests abnormal testicular function. Epididymal abnormalities including enlargement, induration, or nodularity reflect transport system problems. Scrotal abnormalities including excessive thickness, adhesions, or abnormal positioning affect thermoregulation and indicate pathology. Penile abnormalities detected during examination or observed during breeding attempts directly impact breeding capability. Preputial problems including prolapse, lacerations, and abscesses physically prevent normal breeding function.

Behavioral symptoms of infertility extend beyond libido changes to include abnormal breeding behaviors. Failure to achieve full erection despite adequate sexual stimulation prevents successful breeding. Improper mounting position, mounting from the side rather than the rear, indicates behavioral or physical problems. Failure to thrust or abnormal thrust patterns suggest pain, physical restriction, or neurological problems. Rapid dismounting before ejaculation or absence of the characteristic pause indicating ejaculation reflects incomplete mating. Aggression toward females during breeding attempts may indicate pain or frustration. Complete absence of interest in breeding despite adequate stimulation occurs in severe libido disorders.

Semen quality abnormalities detected during breeding soundness examination provide objective evidence of infertility. Low sperm concentration indicates impaired spermatogenesis. Poor sperm motility, with reduced percentage of progressively motile cells, suggests epididymal dysfunction, accessory gland problems, or collection/handling issues. Elevated morphological abnormalities including head defects, midpiece abnormalities, and tail defects reflect spermatogenic disturbances. Presence of blood in semen indicates reproductive tract injury or inflammation. White blood cells in semen suggest infection. Abnormal seminal fluid consistency, color, or volume may reflect accessory gland pathology.

Symptom progression in male infertility follows patterns related to underlying cause. Acute causes such as systemic illness or heat stress produce sudden fertility decline with potential for recovery over time. Chronic progressive causes including degenerative conditions and some infections cause gradual fertility decline without recovery. Age-related fertility decline typically shows slow progressive changes over months to years. Seasonal patterns occur in species with photoperiod-responsive reproduction. Intermittent or cyclic problems may reflect management factors, nutritional changes, or environmental conditions. Documentation of symptom timeline and pattern helps identify likely causes and predict prognosis.

Emergency symptoms requiring immediate veterinary intervention include signs of severe reproductive tract injury or systemic illness affecting breeding males. Acute painful swelling of the scrotum suggests testicular torsion, acute orchitis, or trauma requiring emergency evaluation. Penile injury with hemorrhage, prolapse, or inability to retract requires immediate attention to prevent permanent damage. Signs of severe systemic illness including high fever, depression, and anorexia in a breeding male warrant urgent evaluation due to potential effects on long-term fertility. Paraphimosis, where the penis cannot be retracted, constitutes an emergency requiring prompt intervention to prevent tissue death.

Clinical examination through standardized breeding soundness evaluation provides the foundation for diagnosing male infertility in farm animals. The evaluation begins with assessment of general health, body condition, and locomotor soundness that could affect breeding capability. External reproductive organ examination evaluates scrotal contents including testicular size, consistency, and symmetry, epididymal palpation, and spermatic cord evaluation. Internal examination in appropriate species evaluates accessory sex glands through rectal palpation. Physical measurement of scrotal circumference provides objective data correlated with sperm production potential. Documentation of physical examination findings using standardized scoring systems enables comparison and tracking over time.

Semen evaluation constitutes an essential component of breeding soundness assessment and infertility diagnosis. Collection is performed using electroejaculation or artificial vagina depending on species, circumstances, and equipment availability. Immediate assessment of volume, color, and consistency provides initial quality indicators. Microscopic evaluation determines sperm concentration, progressive motility percentage, and morphological characteristics. Normal values vary by species, season, and collection method, requiring interpretation based on appropriate standards. Serial evaluations may be necessary to distinguish temporary from persistent abnormalities, particularly following known insults such as illness or heat stress. Ancillary testing including biochemical analysis of seminal plasma may provide additional diagnostic information.

Advanced diagnostic testing addresses specific suspected causes of infertility identified through history and examination. Hormonal evaluation including testosterone, luteinizing hormone, and follicle-stimulating hormone assesses hypothalamic-pituitary-gonadal axis function. Infectious disease testing targets organisms known to cause reproductive tract infection in the relevant species. Ultrasonographic examination of reproductive organs identifies structural abnormalities not detectable on palpation. Testicular biopsy provides histological assessment of spermatogenic activity when indicated. Genetic testing may identify inherited conditions causing infertility in species where such tests are available. Thermographic imaging can detect abnormal testicular temperature patterns suggesting vascular or thermoregulatory problems.

Differential diagnosis of male infertility must consider the broad range of potential causes and systematically evaluate each possibility. Physical examination findings direct attention toward structural versus functional causes. Semen analysis patterns help distinguish spermatogenic failure from transport problems or accessory gland dysfunction. History of previous fertility, recent illness, or environmental changes suggests acquired versus congenital problems. Age at onset differentiates developmental conditions from degenerative or acquired diseases. Unilateral versus bilateral involvement affects both diagnosis and prognosis. The diagnostic workup should proceed from least invasive and most informative tests toward more specialized procedures as needed. Complete evaluation may require multiple examinations over time to capture transient abnormalities and assess recovery potential.

Emergency treatment of male infertility relates primarily to acute conditions that threaten permanent reproductive damage if not promptly addressed. Testicular torsion requires emergency surgical exploration and correction or removal to prevent ischemic testicular death. Penile injury with prolapse demands immediate reduction, cleaning, and protection to prevent tissue desiccation and fibrosis. Severe paraphimosis requires emergency intervention including cold therapy, osmotic agents, and mechanical reduction with potential surgical intervention. Acute orchitis warrants aggressive antimicrobial and anti-inflammatory therapy to limit testicular damage. Traumatic injuries to reproductive structures require assessment, stabilization, and appropriate surgical repair. These emergency presentations should not be delayed for routine scheduling.

Medical management of male infertility targets treatable underlying causes when identified. Antimicrobial therapy addresses reproductive tract infections based on culture and sensitivity results when bacterial causes are confirmed. Anti-inflammatory treatment reduces tissue damage during inflammatory conditions and may preserve function during recovery. Hormonal supplementation, including gonadotropin-releasing hormone agonists or testosterone, may benefit selected cases of hormonal insufficiency, though response is variable. Nutritional correction of identified deficiencies supports reproductive recovery. Treatment of concurrent systemic illness removes factors impairing fertility. Stress reduction through environmental and management modifications addresses stress-related infertility. Medical treatment success varies substantially based on underlying cause, severity, and chronicity.

Surgical intervention offers definitive treatment for selected structural causes of infertility. Persistent frenulum can be surgically corrected with good prognosis for fertility restoration. Preputial adhesions may be amenable to surgical correction depending on severity and location. Penile fibropapilloma removal restores function when these growths obstruct breeding. Unilateral castration for animals with single affected testicle may permit breeding using the remaining gonad. Scrotal ablation addresses chronic scrotal conditions while preserving testicular function in some cases. Surgical success depends on the specific condition, its severity, and timing of intervention. Not all structural abnormalities are surgically correctable, and some carry guarded prognosis even with intervention.

Supportive care during treatment and recovery maximizes the chance of fertility restoration. Sexual rest during acute conditions prevents further injury and reduces stress on healing tissues. Optimal nutrition supports tissue repair and spermatogenic recovery. Environmental temperature management protects thermally sensitive spermatogenesis during recovery. Stress reduction through appropriate housing and handling facilitates healing. Protection from injury during recovery prevents setbacks. Monitoring for treatment response and complications enables adjustment of management as needed.

Herd-level management of infertility focuses on prevention and early detection rather than treatment of individual affected animals. Implementing routine breeding soundness evaluation identifies problems before breeding season begins. Multi-sire breeding groups provide insurance against individual male failure. Appropriate male-to-female ratios prevent overuse of individual males. Pregnancy diagnosis identifies fertility problems early in the breeding season, allowing intervention. Record keeping tracks individual male performance to identify developing problems. These management practices reduce the impact of male infertility on overall reproductive efficiency.

Treatment decision-making must incorporate economic analysis alongside clinical considerations. The cost of diagnostic workup and treatment must be weighed against the animal's breeding value and replacement cost. Prognosis for fertility recovery determines the likelihood of return on treatment investment. Time required for recovery affects the animal's availability for breeding and may require interim management solutions. In many commercial operations, culling subfertile males and replacing them with proven animals may be more economically rational than pursuing extensive treatment. Valuable genetic animals or those with particular sentimental value may justify greater investment in diagnosis and treatment. These decisions should be made in consultation with veterinarians who can provide realistic prognosis information.

Recovery timeline following treatment for male infertility depends primarily on the underlying cause and the degree of tissue damage present at treatment initiation. Acute conditions treated before permanent damage occurs may show clinical improvement within days to weeks. However, fertility recovery always requires time proportional to the spermatogenic cycle, which is approximately sixty days in bulls, forty-nine days in rams, and similar periods in other species. This means that even complete resolution of an underlying cause requires two to three months before improved semen quality is observed. Chronic conditions with established tissue damage may show limited or no recovery regardless of treatment, reflecting permanent reproductive damage.

Post-treatment care and monitoring are essential for evaluating recovery success and guiding management decisions. Serial breeding soundness examinations at appropriate intervals, typically thirty to sixty days apart, assess progressive improvement in physical findings and semen quality. Comparison of sequential semen analyses documents the trajectory of recovery and helps predict final outcome. Physical examination monitors resolution of palpable abnormalities in reproductive organs. Behavioral observation assesses return of normal libido and breeding capability. Documentation of recovery progress supports decisions about return to breeding service and provides prognostic information for similar cases.

Prognostic factors influencing fertility recovery include age, underlying cause, severity of damage, and treatment response. Young animals generally show better recovery potential due to greater regenerative capacity. Conditions affecting sperm transport or accessory glands may allow better recovery than those causing testicular damage. Unilateral conditions permit continued fertility through the unaffected side, while bilateral involvement carries graver prognosis. Early detection and treatment before extensive permanent damage improves outcomes. Response to initial treatment provides important prognostic information, with animals showing early improvement having better long-term prognosis. Complete elimination of infectious causes is necessary for lasting recovery.

Return to breeding service requires confirmation of adequate fertility and physical capability. Breeding soundness examination should demonstrate acceptable semen quality meeting established minimum standards for the species. Physical examination should confirm absence of conditions that would impair natural breeding. A test breeding period with limited numbers of females enables assessment of actual fertility before full breeding use. Gradual increase in workload allows assessment of physical capability to sustain breeding activity. Continued monitoring during the breeding season enables early detection of any fertility decline. Animals that fail to demonstrate adequate recovery after appropriate treatment and time should be removed from breeding service to prevent ongoing production losses.

Prevention of male infertility begins with selection of genetically sound breeding stock from sources with documented reproductive performance. Purchasing breeding males only from reputable breeders with transparent records reduces the risk of acquiring animals with heritable fertility problems. Verification of fertility through breeding soundness examination before purchase confirms reproductive potential. Parentage records documenting the fertility of sires and dams provide additional assurance. Avoiding inbred animals reduces the expression of recessive genetic defects affecting fertility. Selection programs that include reproductive performance in breeding objectives promote genetic improvement in fertility over generations.

Biosecurity measures prevent introduction of infectious causes of infertility into breeding populations. Quarantine of newly acquired animals allows testing and observation before integration with established breeding groups. Testing for specific reproductive pathogens including Campylobacter, Trichomoniasis in cattle, and Brucella in applicable species should precede breeding use. Avoiding shared use of breeding males between operations prevents disease transmission. Equipment sanitation and personnel hygiene when handling breeding males or semen reduces mechanical transmission. Isolation of animals with signs of reproductive tract infection prevents spread within the herd.

Nutritional management supporting optimal reproductive function represents a key prevention strategy. Balanced rations meeting species-specific requirements for protein, energy, and micronutrients provide the foundation for reproductive health. Particular attention to zinc, selenium, and vitamin E supports spermatogenesis and sperm function. Avoiding nutritional extremes, both deficiency and excess, maintains optimal body condition for breeding. Pre-breeding conditioning programs bring males to appropriate condition before the breeding season. Adequate nutrition during the breeding period sustains performance throughout extended breeding activity.

Management practices that reduce stress and optimize environmental conditions protect male fertility. Heat stress prevention through shade, cooling, and breeding season timing protects thermosensitive spermatogenesis. Appropriate male housing prevents injury from aggressive interactions while avoiding isolation stress. Gradual conditioning for breeding through increasing exercise and social exposure prepares males for breeding season demands. Appropriate male-to-female ratios prevent overuse and associated physical stress. Veterinary health programs address concurrent illness that could impair fertility. Staff training on proper handling and management of breeding males prevents injuries and reduces stress.

Routine breeding soundness evaluation provides the cornerstone of infertility prevention by identifying problems before breeding season begins. Annual examination of all breeding males establishes baseline reproductive status and identifies developing problems. Pre-purchase examination prevents acquisition of infertile or subfertile animals. Examination following illness, injury, or other insults documents fertility status before breeding use. Standardized evaluation protocols ensure consistent assessment across animals and over time. Recording and tracking of examination results enables identification of trends and early intervention. This systematic approach prevents production losses by ensuring only reproductively sound males enter breeding service.

Daily management and monitoring of breeding males should incorporate attention to behavioral and physical indicators of reproductive health. Observation of libido and breeding behavior provides early warning of developing problems. Monitoring feed intake, body condition, and activity level supports general health assessment. Regular inspection of external reproductive organs identifies injuries, swelling, or other abnormalities. Recording of breeding observations including service frequency and success creates baseline data for detecting changes. Attention to social dynamics in multi-male groups identifies individuals being excluded from breeding or subjected to excessive aggression.

Housing and environmental management significantly impact male fertility and should optimize conditions for reproductive health. Adequate space in male housing reduces stress and aggressive injuries. Appropriate flooring prevents leg and foot problems that impair breeding capability. Environmental temperature management protects spermatogenesis from heat and cold stress. Shade provision during hot periods and shelter during cold extremes maintains thermal comfort. Clean, dry bedding reduces disease exposure and maintains health. Visual barriers and spatial separation reduce social stress in group housing. Individual housing during recovery from illness or injury facilitates monitoring and prevents further damage.

Herd health programs should integrate reproductive management with overall health protocols. Annual breeding soundness examination of all males intended for breeding establishes their reproductive status. Vaccination programs protect against diseases that can impair fertility. Parasite control prevents condition loss and associated reproductive effects. Foot care maintains locomotor soundness necessary for breeding activity. Health monitoring identifies illness early, enabling treatment before significant fertility impact. Integration of reproductive health monitoring with regular veterinary visits ensures comprehensive coverage. Documentation of health events affecting breeding males enables correlation with fertility outcomes.

Record keeping and monitoring systems support reproductive management and enable data-driven decisions. Individual identification of breeding males enables tracking of health and performance. Breeding soundness examination records document reproductive status over time. Breeding records tracking which males bred which females enable performance assessment. Pregnancy diagnosis results correlated with breeding dates identify fertility problems. Treatment records document interventions and outcomes. Culling records tracking reasons for removal provide population-level fertility information. Analysis of accumulated data identifies patterns and guides management improvements.

Economic considerations shape breeding male management programs and influence resource allocation. The breeding male represents a significant investment with substantial impact on herd genetics and production. Cost-benefit analysis of health management, examination, and treatment programs guides resource allocation. Insurance options for valuable breeding males provide financial protection against loss. Replacement costs for breeding males factor into treatment versus culling decisions. Return on investment from breeding soundness examination programs typically justifies their cost through prevention of larger losses. Consultation with veterinarians and production advisors helps optimize investment in breeding male management for maximum return.

Certain breeds and breed types demonstrate varying susceptibility to specific causes of male infertility based on genetic background and selection history. Breeds with high levels of inbreeding may show elevated rates of genetic defects affecting fertility. Rapid selection for production traits without attention to reproductive performance may inadvertently reduce fertility in some lines. Breeds with characteristic scrotal or penile conformation may face elevated risk of specific structural problems. Show-oriented selection emphasizing appearance over function can affect reproductive capability in some breeds. Conversely, breeds subjected to rigorous breeding soundness evaluation over generations typically show improved fertility.

Production type considerations influence infertility risk through differing management systems and selection pressures. Intensively selected commercial lines may prioritize production over reproduction, potentially affecting fertility. Extensively managed populations may accumulate fertility problems due to less rigorous selection. Dairy breeds selected primarily for milk production show higher rates of some reproductive problems compared to beef breeds. Seasonal breeding species face particular challenges related to photoperiod and breeding season timing. Terminal sire breeds used only for crossing may receive less attention to long-term fertility. Artificial insemination programs typically apply stringent fertility requirements that improve genetic merit for reproduction in contributing males.

Genetic selection and testing offer tools for improving fertility within breeds and populations. Estimated breeding values for fertility-related traits, where available, should be incorporated into selection decisions. Scrotal circumference measurement provides a heritable indicator of sperm production potential. Selection against specific defects reduces their frequency over generations. Progeny testing through evaluation of offspring fertility provides information about breeding value. Genomic testing may identify genetic markers associated with fertility traits in breeds where such tools have been developed. Breed associations and genetic improvement organizations coordinate industry-wide efforts to improve reproductive performance. Collaboration between producers, veterinarians, and geneticists optimizes genetic progress for male fertility.

Several conditions commonly co-occur with male infertility or contribute to its development. Cryptorchidism directly causes infertility through testicular damage from elevated body temperature. Epididymitis impairs sperm maturation and transport, causing reduced fertility or sterility. Orchitis damages sperm-producing tissue and may result in permanent testicular atrophy. Vesicular adenitis affects semen quality through abnormal accessory gland secretions. Penile abnormalities including deviations, persistent frenulum, and injuries prevent normal breeding. Locomotor problems affecting the ability to mount and breed result in functional infertility despite normal reproductive organs. Systemic illnesses causing fever impair spermatogenesis through thermal effects.

Conditions with similar presentations require differentiation during diagnostic evaluation of infertility. Low female fertility may be misattributed to the male in single-sire breeding programs. Female reproductive diseases including metritis, pyometra, and ovarian abnormalities cause conception failure independent of male fertility. Infectious causes of early embryonic death produce apparent infertility despite successful fertilization. Behavioral problems in females may prevent successful breeding despite normal male function. Management factors including timing of breeding relative to ovulation affect conception independent of male fertility. Nutritional problems in females impair reproduction separately from male factors. Complete fertility investigation should evaluate both male and female factors when conception rates are unsatisfactory.

Complications and consequences of male infertility extend beyond the affected individual to impact herd productivity. Reduced pregnancy rates result in extended breeding seasons and increased open females. Non-uniform calf or lamb crops from extended breeding create management challenges. Economic losses accumulate from reduced weaning weights, increased replacement costs, and culling of open females. Genetic progress slows when valuable males cannot contribute offspring. Stress on producers from fertility failures affects decision-making and operation sustainability. Early identification and appropriate management of male infertility through systematic breeding soundness evaluation prevents many of these consequences.