Myths in small animal reproduction (Proceedings)

Generally, coping with disorders in small animal reproduction, is a rewarding subspecialty in veterinary medicine. Clients owning pets with urogenital problems are usually very motivated to achieve resolution. Although demanding of the clinician's time and expertise, the breeder client tends to be very loyal and compliant. A good reproductive practice generates its own referrals, and usually is quite busy. Obstetrics and pediatrics are undeniably rewarding parts of the specialty for veterinarians and their staff. Reproductive practice incorporates the interesting fields of physiology, endocrinology, embryology, genetics, metabolism, nutrition, pediatric and maternal critical care, anesthesia, pharmacology and anatomy. The field is uniquely both medical and surgical.

Frustrations do exist in the small animal reproductive practice, not just limited to the demanding breeder client. Technology in the small animal field has not kept pace with that in the equine or bovine fields, and even less so with the human obstetrics, gynecology and urology. The primary reason is a lack of funding supporting the development of technical expertise in a field where anticipated financial returns are poor. The Westminster Best in Show stud dog will never match the financial expectations of the Triple Crown winner or the syndicated bull. The value of pet dogs and cats is more personal, but even the most motivated dog or cat owner cannot generally afford to back the development of a technique for intra cytoplasmic insemination, cryopreservation of ova, or embryo transplant in their pet. Technology developed for equine and bovine patients is usually not applicable nor effective in the canine or feline. Canine and feline neonatology and pediatrics are exacerbated by small patient size. The natural fecundity of dogs and cats and the consequent pet overpopulation problem (and the recent successful dog cloning) raise further ethical concerns in the field. Clinicians should guide their clients through the myriad of genetic screenings advised for the particular breed, as well as discuss responsible puppy placement and early neutering. Some dogs and cats simply should not be bred (aggressive or defective individuals), a recommendation all veterinarians should feel comfortable making.

Unsolved and controversial clinical problems are not uncommon to the reproductive practitioner. Progress in understanding the etiology, pathophysiology and proper therapeutics of such problems has also been hampered by anecdotal information abounding amongst the breeder clientele and often amongst veterinarians as well. The internet frequently becomes an annoyance, used by clients to challenge a clinician's decisions. University residencies and post doctorate programs limited to and promoting advances in small animal theriogenology are uncommon. Collaboration amongst small animal reproductive specialists is developing but remains limited. Discussion of some of the frustrating clinical problems familiar to the small animal reproductive practice follows.

MYTH: Puppy Vaginitis is always a Disease that Needs Treatment

Chief complaint

An apparently healthy female puppy is presented with mucoid vulvar discharge, usually white to yellow, and sometimes copious. The discharge can be accompanied by mild perivulvar dermatitis. The puppy is not typically attentive to the discharge, and there is not any associated change in urinary behavior (dysuria or pollakiuria). Clients often have a difficult time deciding if a puppy has normal urinary behavior or not. The age of onset ranges from 6 weeks to puberty, the duration days to months, and the disorder often intermittent.

Diagnostics

Cytologic examination of the discharge finds suppurative inflammation. Vaginal cultures (aerobic) generally fail to grow anything but normal flora in small mixed numbers. Similar organisms could be cultured from an asymptomatic littermate. A urinalysis, acquired by cystocentesis, is characteristically normal (a decreased urine specific gravity is typical for young dogs lacking adult concentrating abilities), and urine culture, if performed, negative. The clinician needs to perform enough diagnostics to rule out more significant causes of vulvar discharge and feel comfortable with the diagnosis of benign puppy vaginitis.

Etiology

The specific etiology of puppy vaginitis is unknown. An imbalance of juvenile vaginal glandular epithelium is postulated. The condition is reported in the literature to resolve both with puberty and with ovariohysterectomy, two very different events endocrinologically, therefore neither likely to truly cause resolution. Puppy vaginitis diminishes with maturity. The term "puppy vaginitis" is a misnomer, as it is asymptomatic and not indicative of inflammation. Important rule-outs (some of which are associated with inflammation) include urinary tract infection, urinary incontinence with associated mucosal scalding, the onset of the initial estrous cycle, vaginal foreign bodies (i.e. foxtails) and urogenital anatomic anomalies (ectopia, disorders of sexual differentiation, significant strictures).

Therapeutics

Cleansing the perivulvar area with a gentle solution (non alcoholic otic preparations or "baby wipes") and benign neglect and tincture of time are advised.

MYTH: Chronic Vaginitis is a Consequence of Puppy Vaginitis

Chief complaint

Variable vulvar discharge, which is mucoid to hemorrhagic or purulent, accompanied by signs of discomfort (licking, scooting, pollakiuria). Perivulvar and vulvar dermatitis are also frequently present. The condition is invariably seen in ovariectomized bitches, of any age, and at variable times from the spay procedure. The history usually includes multiple therapeutic efforts without resolution, although transient improvement can occur. The duration is generally chronic, from weeks to months and sometimes lasting years.

Diagnostics

A minimum data base: CBC and serum chemistries, including a urinalysis (preferably acquired by cystocentesis) and culture or culture "if" is advised. A careful vaginal examination, under adequate sedation or anesthesia, with endoscopic equipment allowing evaluation of the entire vaginal vault should be performed. This usually means a rigid cystourethroscope with saline infusion is a necessity. Otoscopes and vaginal speculums do not permit adequate evaluation of the entire vaginal vault. Pediatric proctoscopes lack the sensitive optics of cystourethroscopes. Radiography (vaginogram /urethrogram /cystogram /IVP) and ultrasound of the entire genitourinary tract can be helpful in localizing the problem and eliminating differentials. Vaginal cytology, aerobic and mycoplasma guarded vaginal cultures, and pinch biopsy of affected vaginal mucosa may be helpful in better defining the problem. Identification of any contributory anatomic abnormalities is important (significant strictures, mass lesions, redundant dorsal vulvar folds, anomalous ureteral anatomy. It is helpful to evaluate the bitch in a normal standing position to accurately assess external anatomy (redundant folds?), followed by another examination after she has urinated, and again after recumbency (urine pooling and scalding?). The presence of urine pooling in the vaginal vault, noted only when the bitch is under anesthesia, can be misleading; the presence of redundant vulvar folds difficult to ascertain when the bitch is positioned for vaginoscopy.

Etiology

The etiology of chronic vaginitis is usually multifactorial and the primary cause often masked and exacerbated by previous therapies, including long term antimicrobial use, self mutilation and topical irrigations. Vaginal mucosal biopsy frequently shows non specific lymphoplasmacytic inflammation, but sometimes suppurative (neutrophilic) or eosinophilic inflammation is predominant. Vaginal cultures can show overgrowth of an atypical bacterial species (pure gram negative cultures, resistant organisms, pseudomonas spp.) or pure culture of mycoplasma spp. if antibiotics have been used extensively. Occasionally a yeast overgrowth is identified. Primary bacterial vaginitis is rare. The most common documented etiologies of chronic vaginitis at the VMTH include:

1. Extensive perivulvar dermatitis associated with redundant dorsal and lateral vulvar folds

2. Granulomatous uterine stump

3. Vaginal foreign bodies (foxtails, bone fragments)

4. Chronic urinary tract infection with urethritis/vestibulitis/vulvitis

5. Cystic, urethral, vaginal or vestibular neoplasia

Vaginal strictures are commonly identified but unusually causal in this author's opinion. Most cases are idiopathic.

Therapeutics

General guidelines apply to most cases: the discontinuation of topical irrigations, prevention of self mutilation with Elizabethan collars and initiation of antimicrobial therapy only when indicated by proper interpretation of culture and sensitivity testing should be undertaken. Antimicrobial therapy should be limited to those cases where pathogens have been identified as displacing normal flora. Analgesia and anti inflammatory therapies are indicated in many cases. A short anti-inflammatory course of corticosteroids can be useful in diminishing vaginal inflammation, but the subsequent propensity for urinary tract infection must be kept in mind, and problems with long term use limits usefulness. Non steroidal anti-inflammatories are therefore superior. Narcotics may be necessary for adequate analgesia (Tramadol).

If a specific cause is identified resolution is more straightforward. Surgical correction with careful post operative control of self mutilation is indicated if anatomic abnormalities (redundant dorsal vulvar fold, significant vaginal stricture, granulomatous uterine stump) have contributed to or caused the condition. Obviously the identification and removal of foreign bodies should cure chronic vaginitis. Appropriate management of chronic urinary tract infection if identified should resolve associated vaginitis. Therapy of urogenital neoplasia can include surgery and or chemotherapy.

If the condition is idiopathic (no anatomic, foreign body, infectious, granulomatous or neoplastic cause can be discerned) oral estrogen replacement therapy is often helpful in establishing normal mucosal integrity and eventual normalization of the vaginal vault. The condition is likely similar to post menopausal vaginitis in women secondary to low estrogen levels. Women improve with vaginal estrogen application, difficult in the dog. Oral diethylstilbestrol (compounded) ("DES") is therefore advised, the dose is empiric and usually the same as used for urinary incontinence due to sphincter incompetence. Several weeks of therapy with DES may be required before improvement is recognized. Side effects are uncommon: mild over dosage results in signs of proestrus (attraction to male dogs, vulvar swelling), myelosuppression is highly unlikely if dosage is conservative (I.E. 60 lb dog would receive 1 mg once or twice weekly).

MYTH: Thyroid Supplementation Improves Fertility

Chief complaint

A euthyroid dog or bitch is presented for supplementation to enhance fertility. Hypothyroidism is perceived by the dog fancy to be a common disorder of great concern. Hypothyroidism is blamed for sub-optimal hair coats, tendencies to gain weight, reproductive problems and lackluster athletic performances. Hypothyroidism is perceived by the veterinary community as a frustrating disorder to correctly diagnose, or, more commonly not diagnose. Many dogs presented to reproductive clinicians are already on thyroid supplementation, generally sodium levothyroxine, less commonly sodium liothyronine or a combination product. Some of these dogs have historical laboratory and clinical data supporting the diagnosis of hypothyroidism, but many may not. Most commonly, the diagnosis of hypothyroidism was made based on a single total T4, usually part of a comprehensive general chemistry profile, and often performed when the dog was ill or on confounding medication. Some dogs have been placed on thyroid supplementation by referring veterinarians based on perceived clinical signs, without clinical documentation of hypothyroidism. Some dogs have had numerous thyroid tests performed, all with normal results, but were then placed on supplementation anyway as a therapeutic trial. Mention of breed specific normals higher than established normal levels at commercial laboratories has been made as a rationale for therapy despite euthyroid test results. Some clients have given their dogs thyroid supplementation at their breeder's insistence. Most clients perceive thyroid supplementation as harmless at worst, and are unaware of and unhappy to learn about resultant iatrogenic hypothyroidism. Most are reluctant to wean their dog off thyroid supplementation to permit meaningful testing. Veterinarians are understandably reluctant to discontinue thyroxine supplementation in bitches presented for infertility, even if there was no compelling evidence the individual was hypothyroid. Evaluation of these dogs requires time and multiple tests as the thyroid axis is re established. Dosages of sodium levothyroxine are frequently lower than recommended (22 µg/kg body weight q12h), but post pill tests are normal. Annual re-evaluation of post pill thyroid levels is usually uncommon.

Diagnostics

Any T4 result should be interpreted in light of the dog's clinical signs, CBC and chemistry results and additional thyroid testing if indicated. Currently, diagnostic laboratories tend to utilize chemiluminescence methodology for T4 testing, which has an excellent correlation with radioimmunoassay, the gold standard.

Adequate and complete laboratory evaluation of the thyroid status of the dog can be accomplished using 1 or more of the following tests. The total T4 concentration, if normal and over 2.0 µg/dl rules out hypothyroidism in >95% of dogs. It is thought to be the best screening test, except in the presence of antithyroid antibodies or significant non-thyroidal illness. Antithyroid antibodies artificially elevate T4 values in a radioimmunoassay. Significant non-thyroidal illness can lower measured T4 levels in euthyroid dogs (euthyroid sick). If T4 levels are low or high, a free T4 by equilibrium dialysis (FT4ED) is useful. The FT4ED has a diagnostic sensitivity of 98%, specificity of 93%, and accuracy of 95%. Adding the endogenous canine TSH test (cTSH) can improve specificity to 98%. Thyroglobulin autoantibodies (TGAA) aid in the diagnosis of immune mediated thyroiditis.

Etiology

Hypothyroidism in the dog is usually secondary to immune mediated thyroiditis. Veterinarians have tended to prescribe thyroid supplementation as a panacea for reproductive failure where no other etiology is defined.

What is believed (on the internet and in non reviewed publications)? Information concerning the effects of hypothyroidism on canine reproduction is largely anecdotal. Hypothyroidism has been popularly associated with several reproductive problems; in the male: infertility, poor libido, testicular atrophy and azoospermia; in the female: infertility, persistent anestrus, irregular estrous cycles, abortion, galactorrhea and high neonatal mortality. Hypothyroidism is not always accompanied by reproductive disorders, normal pregnancy and whelping has occurred in bitches with documented, untreated hypothyroidism. No studies exist showing that fertility in healthy, normal dogs has been enhanced by thyroxine supplementation.

What is actually known (documented by peer reviewed research and publications)? Thyroid hormones are reported to support ovarian granulosa cell function and placental trophoblast function. Thyroid hormones have also been reported to support testicular growth, gametogenesis, and Leydig cell development. Reports of diminished libido, diminished spermatogenesis, and abnormal sperm morphology and motility as a consequence of hypothyroidism have been negated by a controlled study. Libido, total sperm count, and scrotal width have been shown not to be affected by hypothyroidism induced by I 131. Hypothyroidism can cause prolongation of the interestrous interval, a reversible condition. In one study of 35 bitches diagnosed as hypothyroid based on TRH stimulation testing or thyroid scintigraphy, reproductive failure was reportedly reversed with thyroxin supplementation.

Some details of reproductive implications of hypothyroidism in human medicine are of interest. In humans, subclinical hypothyroidism has been associated with reduced fertility and a twice-normal rate of spontaneous abortion. Interestingly, the conception rate is not reportedly affected, yet this is the concern of most breeders. Women with multiple recurrent spontaneous abortions are more commonly hypothyroid. Thyroid antibodies are not thought to have an adverse effect on pregnancy; rather, a general tendency toward the development of autoimmunity exists. The most common complication of autoimmune thyroiditis associated with pregnancy in women is progressive postpartum thyroiditis, resulting in overt hypothyroidism four or more years later.

Hypothalamic anterior pituitary function has been reported to be abnormal in hypothyroid children. Although in most children thyroid hormone deficiency leads to delayed sexual development, occasional children manifest precocious sexual maturation. Increased levels of circulating gonadotropins have been measured in both male and female children with such manifestations. In females, serum prolactin levels also tend to be increased, and galactorrhea may occur if serum estrogen levels are high enough to permit breast development and lactogenesis. The mechanism of the precocious gonadotropin and prolactin hypersecretion is not clear. Delayed sexual development due to abnormalities of hypothalamic-pituitary function secondary to hypothyroidism are reportedly more common in adolescent children. Puberty often is delayed or incomplete. Additionally, the menstrual cycle may be irregular and nonovulatory for longer than normal. Because hypothyroidism is considered to have genetic implications, clinicians should be very secure in their diagnosis with breeding animals.

Therapeutics

Treat only documented hypothyroid cases (22 µg/kg L-thyroxine po bid brand name).

MYTH: Vaginal Cultures Should be a Part of the Prebreeding Examination and Protect the Stud Dog against Disease

Chief complaint

Veterinary clinicians are commonly asked to perform pre-breeding cultures of the vaginal tract of healthy, apparently fertile bitches as a prerequisite to acceptance for natural cover by a stud dog owner. Breeders may request antibiotics for treatment of apparently infertile bitches during estrus and pregnancy. Douching of the vaginal tract with antibiotics or antiseptics is not an uncommon procedure advocated by some as a method of controlling vaginitis. Subfertile stud dogs are often treated with a course of antibiotics in an attempt to improve reproductive performance. Semen cultures are requested by breeders in some of these cases. Natural breedings are refused by some stud dog owners, for fear of contagious disease promoting infertility. Artificial insemination is promoted as a method of avoiding such problems. The presence of certain maligned microbes in vaginal or semen cultures causes great alarm amongst breeders.

Veterinary clinicians accustomed to a rational approach to microbiology and therapeutics become uncomfortable with these demands and practices. Breeder clients can be demanding and may take their business elsewhere if not accommodated. Familiarity with the current literature concerning reproductive microbiology coupled with the ability (and time) to relay such information to breeders is the key to achieving an ethical and effective practice.

Etiology

Both the male and female reproductive tracts harbor normal flora whose function is to prevent colonization and invasion of such tissues by more harmful pathogens. Negative vaginal or urethral cultures are therefore not normal. Male and female dogs have been documented to exchange normal flora during copulation with no impact on fertility or fecundity. Because semen acquired by ejaculation travels through the urethra, semen cultures commonly reflect normal urethral and preputial flora. Cultures following prostatic massage and urethral catheterization are similarly contaminated by normal urethral flora. Ultrasound guided transabdominal intraprostatic sampling may be more accurate. Urine acquired by cystocentesis can reflect prostatic microbiology when cultured. Ultrasound guided testicular or epididymal aspirates can similarly provide more reliable results. These methods are more invasive and expensive, making the rationale for reproductive cultures a valid concern. Quantitative coincident urethral and semen cultures can be informative but are expensive. Culture of aseptically acquired testicular biopsies can be accurate, but is invasive and raises concerns about the blood testes barrier.

The uterus has been shown to harbor transient vaginal flora during estrus, when the cervix is open. Such organisms are cleared by intrauterine factors during other parts of the reproductive cycle. Sampling of the uterus via a vaginal, transcervical approach can reflect or transplant normal vaginal flora. Sampling of the cranial vagina in hopes of identifying true intrauterine organisms obviously carries the potential of misinterpretation. Trans cervical sampling can reduce the chance of vaginal contamination with proper technique. Culture of aseptically acquired uterine biopsy is accurate, but invasive.

The male and female reproductive tracts are commonly inhabited by a mixed flora, with both gram negative and positive organisms present in low numbers, as well as mycoplasma species. Pure cultures of an organism excluding other flora may be abnormal. Prior antibiotic therapy and topical antiseptic use can alter normal flora.

Therapy

Once true clinical suspicion of a microbiologic factor contributing to infertility has been established (ruling out husbandry and breeding management problems, using optimal ovulation timing and a proven fertile mate, documenting failure to conceive vs fetal loss, etc.) then rationale evaluation of the uterine, testicular or prostatic flora is indicated. Client education and Brucella canis screening remain the most important reproductive microbiology tools.

MYTH: Primary Hypoluteoidism is a Documented Cause of Pregnancy Failure in the Dog

Chief complaint

Healthy bitches sometimes exhibit a failure to carry litters to term with no infectious or septic cause of the premature delivery apparent. Premature canine and feline neonates have a very poor prognosis for survival, especially if less than 62 days gestation.

Etiology

Commonly, measured progesterone levels at the time of premature delivery are low, suggesting hypoluteoidism. Actual hypoluteoidism has not yet been documented in the bitch as a primary cause for late term abortion. Progesterone levels decline as a consequence of local prostaglandin release, which occurs as a consequence of myometrial activity.

Diagnostics

Late gestational hemorrhagic vulvar discharge can occur, followed by the appearance of uteroverdin, and eventually the delivery of neonates if intervention does not occur. Premature labor can be documented in the bitch by performing uterine monitoring during the last two to four weeks of gestation, using a commercially available uterine monitor (Veterinary Perinatal Services, Inc.). Monitoring can be performed by clients in the home setting or acutely in the clinic. No more than 1 or 2 contractions should occur during a one hour monitoring session before first stage labor is appropriate (56-58 days from the diestral shift or 64-66 days from the LH surge or initial rise in progesterone). Monitoring should take place twice daily during the last 10-14 days of gestation in suspect cases, earlier if clinical signs suggest a problem or ultrasound identifies non viable fetuses. Previous examination of the aborted fetuses and bitch should have ruled out any infectious (i.e. brucellosis) or septic (i.e. metritis) causes for early delivery, the aborted fetuses should have been normal other than immature with atelectasis.

Therapeutics

The administration of exogenous progestational compounds can prolong gestation in the normal bitch, but may not alleviate premature myometrial activity. Their administration can cause abnormal differentiation of fetal gonads and inhibit development of normal lactation. The administration of terbutaline, by the subcutaneous or oral route, titrated to effect, can inhibit premature uterine activity. Terbutaline is a tocolytic agent, a beta adrenergic receptor agonist. The initial dose is 0.03 mg/kg q 8h. The administration should be discontinued 48 hours prior to the calculated delivery date, to permit normal labor and delivery to occur. Exogenous progesterone can be added if myometrial contractility cannot be controlled with tocolytics. Two forms are available: progesterone in oil, given at 2 mg/kg IM q 72h (cross reacts in assays) or altrenogest (Regu-Mate) a synthetic given at 0.088 mg/kg q 24h (does not cross react in assays). Both must be withdrawn 2-3 days prior to the predicted whelp date to permit labor to begin.

MYTH: Failure to Lactate Means Get Out the Bottles

Chief complaint

Post partum otherwise healthy bitch with inadequate lactation to meet neonatal demand. Normal gestational length and husbandry is typical.

Diagnostics

Determination that adequate lactation is evident should be performed prior to elective C section, this helps confirm that the gestation is at term. If an emergency section is required, regardless of the status of lactation, intervention can be indicated (see below). Bitches with inadequate lactation at term should be thoroughly evaluated for metabolic or inflammatory disorders (metritis, eclampsia, mastitis), as well as nutritional and hydration status and treated appropriately. Occult illness may require evaluation of the hemogram, serum chemistries and vaginal discharge, as well as ultrasound evaluation of the uterus. The normal presence of colostrum (typically not copious) should not be confused with agalactia. The level of neonatal contentment and weight gain indicates adequate lactation.

Etiology

Lactation results from proper integration of mammary parenchymal and glandular development during gestation, and is under the control of pituitary and ovarian hormones (prolactin and estrogen). Milk let down is promoted by oxytocin release, a reflex triggered by nursing, therefore neonates must spend adequate time suckling. Disruption of the pituitary-ovarian-mammary gland axis can result in idiopathic agalactia. Agalactia can be associated with premature delivery of neonates, and is suspected (by breeders) to be a potential complication of ovariohysterectomy performed at the time of a C section. Because estrogen promotes lactogenesis, the adequacy of mammary development should be assessed prior to removal of the ovaries at C section. Bitches with adequate lactogenesis at term should not be negatively impacted by ovariohysterectomy; estrogen production by the post partum ovaries is probably negligible. A genetic component may be present with this disorder (Bull Mastiffs).

Therapeutics

Lactation can be promoted in many cases if treated promptly. The administration of mini dose oxytocin (0.5-2.0 units per dose), subcutaneously, every 2 hours should be initiated. The nurslings should be removed from the dam prior to each injection, and replaced 30 minutes later. The neonates should be supplemented adequately to insure survival, but not excessively, such that they will suckle vigorously. Gentle hand stripping of the mammary glands should take place if suckling is not vigorous. Concurrent administration of metoclopramide, subcutaneously (0.1-0.2 mg/kg) every 6-8 hours promotes prolactin release. The administration of ace promazine at mild tranquilization dosages may also facilitate milk let down. Therapy should continue until lactation is adequate, usually 12-24 hours later. Failure to establish lactation with consequential failure to provide colostrum to neonates should be addressed by giving immune serum to the neonates, 100 ml/kg; this can be given orally if within the first 24-36 hours or subcutaneously thereafter to establish normal serum immunoglobulin levels.

MYTH: A Positive Semen Culture Implicates Infection as the Cause

Chief complaint

An apparently healthy, young, formerly fertile stud dog with normal libido begins to produce small litters or frequently fails to cover bitches.

Diagnostics

Ideally, the breeding behavior of the dog should be witnessed, to rule out problems with husbandry. Failure to achieve a normal copulatory lock, due to poor breeding habits (most commonly a dog that attempts to turn before complete engorgement of the bulbis has occurred) can cause poor breeding success. If breeding behavior is normal, a complete physical examination, CBC, serum chemistries, Brucella screening, urinalysis with culture (sample acquired by cystocentesis), semen evaluation with appropriate consideration of microbiology (see above) and ultrasound evaluation of the reproductive organs should be performed to rule out infectious, septic and metabolic causes of acquired subfertility. Assessment of the thyroid status alleviates client concerns (Total T4, fT4ed, TGAA and cTSH). Semen cytology typically finds oligospermia, asthenospermia and sperm morphologic abnormalities. Epithelial cells, lymphocytes and monocytes are increased in the ejaculate. Sperm to sperm agglutination may be evident. Multiple semen evaluations over a 90-120 day period should be performed to be valid. Complete azoospermia should prompt evaluation of semen alkaline phosphatase levels (an epididymal marker) to assess libido and rule out bilateral obstructive disorders (if > 5000 a testicular sample was obtained). Testicular biopsy can be performed to characterize adequacy and completeness of spermatogenesis and the intact presence of spermatogenic apparatus. Culture of the biopsy specimen can be helpful if semen and urethral cultures have been difficult to interpret or not performed due to expense. If neutering is elected, the complete testicles should be submitted for histopathologic evaluation.

Etiology

Generally, no infectious, endocrinologic or metabolic cause for the acquired subfertility can be identified. Testicular biopsy can identify lymphoplasmacytic inflammation if performed early in the course of disease. The measurement of or assessment for anti-sperm antibodies would be of interest but are not readily commercially available. The cause of this inflammation is unknown, prior traumatic or infectious etiologies are generally not identified. Some break in the blood testes barrier is suspected, which may be present without trauma. Biopsy late in the course of the disorder shows no evidence of inflammation, instead diminished spermatogenesis and atrophy is evident. A familial tendency is suspected in some breeds (Bull Mastiff, Bernese Mountain Dog).

Interestingly, testicular biopsy has been shown not to increase the incidence of anti sperm antibodies.

Therapeutics

The diagnosis of premature testicular degeneration warrants a poor prognosis for return to normal fertility. Assisted reproductive techniques, such as intrauterine insemination, optimal ovulation timing, and semen banking can improve pregnancy rates somewhat for a limited period of time. The use of immunosuppressive agents is contraindicated due to their effect on spermatogenesis. The heritability of the disorder should be discussed with a client before proceeding with heroics.

Hind Quarter Elevation Following Artificial Insemination Optimizes Conception

Most textbooks and lay publications still recommend elevating the hind quarters of the bitch for up to 20 minutes after vaginal artificial insemination in order to optimize fertility. Presumably this procedure helps the semen drain into the uterus. A study done in 1998 at Louisiana State University showed that elevating the hind quarters is not needed to obtain good fertility or fecundity. Bitches were bred by artificial insemination every other day during cytologic estrus by proven males. A total of 11 bitches were elevated for 10 minutes, 22 elevated for 1 minute and 10 bitches (bred during 12 estrous cycles) were not elevated at all. Pregnancy rates for the groups were 82% for the 10 minute group, 91% for the 1 minute group and 100% for the zero holding time group. Fecundity for the groups averaged 7.5 for the 10 minute group, 7.3 for the 1 minute group and 6.9 for the zero holding time group. In conclusion, pregnancy rate and litter size are unaffected by reducing the hindquarter elevation time from 10 minutes to zero minutes. Canine vaginal AI can be simplified while maintaining satisfactory reproductive performance.

Natural Breeding Gives Better Conception than Artificial Insemination

It is common to hear lay people state that natural breeding gives better conception than artificial insemination. Oddly enough there is only one study that directly compares artificial insemination and natural breeding when the same females were bred by the same males. Breeding artificially with fresh good quality semen (vaginally) gives fertility and fecundity at least equal to that of natural breeding when using fertile males and females. Semen processing (chilled extended and frozen) diminishes fertility and fecundity. Frozen semen achieves better conception rates when deposited into the uterine lumen, either surgically or via trans cervical insemination.

Bitches Should Have a Non Bred Cycle (Skip) Between Pregnancies

Breeders' codes of ethics commonly advocate breeding on only every other cycle, skipping at least one breeding cycle between each pregnancy. There are no refereed papers that address this. In the author's opinion this is not necessary, and may be detrimental to conception. The reason bitches come into estrus every six months is to become pregnant and have puppies every six months. If a bitch has a pyometra, it is always recommended that the bitch be bred on the subsequent estrous cycle to reduce the chance that recurrence of the pyometra will occur. It seems that pregnancy may actually have a protective effect against pyometra. Pregnancy must be considered the normal condition and not an abnormal condition. Open cycles during which a bitch is not bred simply increase the amount of progesterone exposure to the uterus, increasing the likelihood of cystic endometrial hyperplasia, pyometra and infertility. Optimal perinatal husbandry maintaining bitches in good condition and planned consecutive breedings will maximize fertility and fecundity.