The Ohio State University

In the last five to ten years, there has been a great increase in awareness of inherited canine diseases. This increase of interest in inherited disease has led to a desire to try to selectively remove these diseases from specific breeds. This is typically a four step process including: determining how the trait is inherited, collecting DNA samples from dogs that are definitively affected and definitively unaffected, developing a DNA marker that will identify affected dogs with certainty, and an educated plan to breed unaffected individuals. Today's discussion will center on understanding the pattern of inheritance.

Pedigree analysis

In the standard scientific pedigree, female animals are represented as circles; males are represented as squares. Affected animals are represented as solid shapes, usually in black.

Patterns of inheritance

Every individual has two copies of a gene; they inherit one from each parent. Another way of thinking of this is that each parent gives only one copy of his or her gene, two genes to each puppy. The parent does not give the same copy of each gene to each puppy in the litter. They are assigned randomly, thus only some puppies in each litter may become affected. Sometimes only one copy of the gene will carry the disease (i.e., maybe only one parent was affected), sometimes both copies of the gene will carry it.

The five most common patterns of inheritance include autosoma.I dominant, autosomal recessive, X-linked (dominant and recessive) and mitochondria).

Autosomal Dominant

Autosomal dominant is a very common form of inheritance. This form of inheritance is characterized by the appearance of the disease in multiple generations, equal occurrence of the disease in both sexes, and father to son transmission. The offspring of affected individuals have a 50 percent chance of expressing the disease. With this form of inheritance, only one copy of the "affected" gene is needed to display the trait. There are no silent carriers of the disease if it is inherited as autosomal dominant.

Autosomal recessive

If an autosomal recessive pattern is noted, two copies of the gene must be present to demonstrate the disease. Therefore both parents have to contribute at least one affected gene. If they only have one copy of the affected gene, the parent may be a silent carrier. If the parent has two copies of the trait, they wilt demonstrate the trait. Silent earners exist. Since two copies of the affected gene are needed to have the disease characteristics expressed, it often takes inbreeding (linebreeding) to demonstrate the trait. Equal involvement of both sexes is noted and, typically, one fourth of the offspring should be affected. Skipped generations are common.

X-linked

In this pattern of inheritance, the disease gene is carried on the X chromosome. Female dogs have two copies of the X chromosome and male dogs have one X and one Y chromosome. In X-linked inheritance, the disease can only be passed from mother to son, or mother to daughters. Fathers cannot pass the disease to their sons.

Mitochondria inheritance

This is the rarest form of inheritance. Mitochondria) inheritance only occurs from mother to offspring. Fathers can not pass on the disease.

The first step in controlling inherited disease is understanding how it is inherited. This requires careful pedigree evaluation and honest documentation of the disease status of each animal.

Selected Dermatologic Issues in Golden Retrievers, Standard Poodles, Bichon Frise, Collies and
Shetland Sheepdogs

Dr. Gwendolen Lorch
The Ohio State University

A number of dermatological conditions can be shown to have a heritable basis on the strength of the analysis of test breeding programs and in heritance studies. Many of the more common dermatoses such as atopy (inhalant allergies), generalized demodicosis (red mange) or sebaceous adenitis, for example, can be shown to exhibit breed or familial predisposition that suggest, in part, a heritable factor. Some heritable dermatoses are refractory to treatment; however, in some disorders such as familial dermatomyositis or sebaceous adenitis some of the more severe signs may be ameliorated by treatment.

Atopic dermatitis (AD), also referred to as atopy, is a common inflammatory dermatosis caused by aeroallergens (dust mites, pollens, animal dander, molds, etc.) and affects an estimated 10-15 percent of the canine population. AD is characterized by chronicity, itching, recurrent ear infections, typical lesion distribution and a family history of the disease. Numerous breeds have been reported to be at increased risk for developing AD; including the Golden Retriever and the Bichon Frise.

Sebaceous adenitis is a disease that is characterized by an inflammatory attack on the sebaceous gland of the hair follicle. The cause is unknown but the disease is most frequently diagnosed in Standard Poodles. Recently, there has been a major effort on the part of breeders and veterinarians to better understand and decrease the prevalence of Standard Poodle sebaceous adenitis. The disease has marked variability in its clinical severity but the most typical presentation is dry, scaly skin with patchy zones of hair loss involving the top of the head and body, neck and ear flaps.

Familial dermatomyositis is a disease of rough Collies and Shetland Sheepdogs. The cause is unknown but may result from immune complex deposition, which may be induced by drugs, infections, toxins or inheritable factors. Clinical signs are usually visible by 1 year of age and may affect pups as young as seven weeks. Typically, this is crusting ulcerative dermatitis. The most commonly affected areas are the face, tips of ears, tip of the tail and lower limbs. The severity of the disease is variable. Severe cases usually have muscle damage that cause the dog to have difficulty eating, drinking, swallowing or walking. A rare dog has skin lesions only in adulthood. These cases could represent an adult-onset variant of the disease or possibly represent dogs that had mild unrecognized disease as puppies.

Familial Renal Disease In The Dog
Stephen P. DiBartola, DVM

Familial Renal Diseases

Most familial renal diseases result in chronic renal failure at a young age (less than five years) but some are characterized by renal tubular problems (e.g., Fanconi syndrome in the Basenji) or presence of blood in the urine (e.g. renal telangiectasia in Pembroke Welsh Corgi dogs). A familial disease is one that occurs in related animals with a higher frequency than would be expected by chance. Congenital diseases are present at birth and may be genetically determined or result from exposure to adverse environmental factors during development. In many familial renal diseases of dogs, the kidneys are thought to be normal at birth but undergo structural and functional deterioration early in life. Some familial renal diseases of dogs probably are examples of renal dysplasia. The term renal dysplasia refers to disorganized development of renal parenchyma due to abnormal differentiation, and is characterized by the presence of structures in the kidney inappropriate for the stage of development of the animal.

Breeds Affected

Many familial renal diseases are variable in severity and rate of progression among individual animals. Most of these diseases are progressive and ultimately fatal, and therapy usually is limited to conservative medical management of chronic renal failure. The mode of inheritance and specific pathogenesis for many of these diseases are unknown.

Familil renal disease has been reported in many breeds of dog (e.g. Norwegian Elkhound, Lhasa Apso, Shih Tzu, Cocker' Spaniel, Soft-Coated Wheaten Terrier, and many other breeds) and may occur sporadically in mixed breed animals. Familial renal disease should be considered whenever chronic renal failure occurs in immature or young adult dogs.

In most of these diseases there is no clear sex predilection. In Samoyeds, however, hereditary glomerulopathy arises from an X-linked dominant trait. The age of onset of familial renal disease usually is 6 months to 5 years, with many animals presented before 2 years of age.

The most common historical findings in dogs with chronic renal failure due to familial renal disease are loss of appetite, lethargy, stunted growth or weight loss, increased urinations, increased water consumption, and vomiting.

Dogs with chronic renal failure due to familial renal disease may be thin and dehydrated. On oral examination, pallor of the mucous membranes, foul odor, and urernic ulceration may be noted. The kidneys usually are small and irregular. Signs of fibrous osteodystrophy such as "rubber jaw" or pathologic fractures usually are detected in young growing dogs with renal failure. Signs of renal osteodystrophy rarely are apparent in older dogs with renal failure.

The most common laboratory findings in dogs with familial renal disease resulting in chronic renal failure are azotemia, hyperphosphatemia, isosthenuria, and non-regenerative anemia. Serum calcium concentrations in dogs may be normal, decreased, or increased. Hypercalcemia may be more common in young dogs with renal failure than in older ones. Compensated metabolic acidosis also may be observed. The presence of hyperaholesterolemia and proteinuria should lead the veterinarian to suspect primary glomerular disease. Proteinuria is variable and dependent upon the extent glomerular involvement in Chinese Shar-Pei dogs with familial amyloidosis. Glucosuria is found in Norwegian Elkhounds and Basenjis with primary renal tubular disorders.

Inherited Epilepsy in the Dog

Michael Podell MSc, DVM, Diplomate ACVIM (Neurology)

Definition and Tyres of Seizures

Seizures are the most common neurologic disorder in dogs. A wide range of causes can induce a seizure in dogs. An epileptic seizure is defined as the clinical manifestation of excessive and/or hypersynchronous abnormal brain activity. Thus, an epileptic seizure has a specific neural origin, which is not true of all seizures. Absolute confirmation that a seizure is epileptic may be difficult, because it requires simultaneous identification of behavioral and brain recording (electroencephalography) changes. As a result, historical information is often used in human and veterinary medicine to diagnose an epileptic seizure. If an underlying cause for the seizure cannot be identified, the epileptic seizures are defined as primary (PES: hereditary or idiopathic). If the epileptic seizures are the result of changes in brain structure (e.g. tumor, infection), then they are defined as secondary (SES). If the epileptic seizures are a reaction of the normal brain to transient metabolic abnormalities or physiologic stresses, then they are defined as reactive (RES). If a patient has a chronic brain disorder characterized by recurrent epileptic seizures (PES or SES), then that patient has epilepsy. A patient with recurring RES is not defined as having epilepsy because a chronic brain disorder does not underlie the seizure activity.

Primary epilepsy is a diagnosis of exclusion. That is, all other potential causes for the seizures must be ruled-out before the diagnosis can be made. It is believed that these animals suffer from changes in brain chemistry, resulting in excessive brain excitation or decreased brain inhibition. Furthermore, dogs with any cause for seizures may appear normal at the time of examination by the veterinarian. Therefore, the ability to differentiate the probability of a dog having either PES, SES, or RES based on physical characteristics and history is helpful in deciding which dogs need more extensive testing, and which breeds may be studies for possible inherited epilepsy.

Research Summary

On initial evaluation for seizure disorders at non-referral veterinary practices, 50 previously healthy dogs were enrolled in a study at The Ohio State University to determine the probability of identifying a specific cause for the seizures. Treatment was not administered prior to entry of dogs in the study. A diagnosis of PES was more probable when the dog was between one and five years of age at the first seizure, when the dog was a large breed (greater than 15 kg), or when the interval between the first and second seizure was long (greater than four weeks). Labrador and Golden Retrievers were the most represented purebred dogs in the PES group. A diagnosis of SES was more probable when the dog was less than one or greater than seven years old at the first seizure, or when the first seizure was a partial seizure. A diagnosis of RES was more probable only when the interval between the first and second seizure was brief (less than four weeks). Additional studies have shown that low amounts of the inhibitory neurotransmitter GABA and high amounts of the excitatory neurotransmitter glutamate were found in the cerebrospinal fluid (CSF) of primary epileptic dogs. Moreover, primary epileptic dogs with an initial lower CSF GABA level prior to Phenobarbital therapy did not respond as well as dogs with a higher CSF GAGA level. These studies demonstrate that select population characteristics are associated with canine primary epilepsy, and that there may be an influence of altered inhibitory neurotransmission on epileptic susceptibility. Current studies are underway to determine if there is an inherited genetic basis for these changes.

Congenital Canine Liver Problems

Dr. Susan E. Johnson
The Ohio State University

I. Where is the liver and what does it do?

The liver is the largest solid organ in the body. It is located in the abdominal cavity. The liver is responsible for many metabolic functions. For example, it removes toxins from the blood, excretes the yellow pigment bilirubin into the bile and feces, maintains the blood sugar in the normal range during fasting, and it breaks down drugs and removes them from the body. The liver has a large functional reserve capacity which means that signs of liver disease often are not recognized until the disease is advanced.

II. What are the signs of liver disease?

Dogs with liver disease show signs such as lack of appetite, weight loss, vomiting, diarrhea, drinking a lot of water and urinating large volumes, abdominal distention due to fluid accumulation (ascites), yellow discoloration of the skin and mucous membranes (icterus), and neurologic signs such as abnormal behavior, dementia, circling, pacing, head pressing, and seizures (hepatic encephalopathy).

III. What types of disease can occur in the liver?

The liver can be affected by poisons and drugs, infections, inflammation (hepatitis), gallstones (rare), obstruction of the bile ducts, liver cancer, and cirrhosis. A congenital malformation of vessels to the liver is a common problem (congenital portosystemic shunt). The cause of persistent inflammation in the liver (chronic hepatitis) is often not determined but one important cause is copper accumulation in the liver which is toxic. Viral infections are not an important cause of liver disease in dogs as they are in humans.

IV. Which liver diseases are congenital?

Copper-associated liver disease in Bedlington Terriers (and other breeds?)

Diagnosis requires a liver biopsy. Treatment includes a low copper diet and drugs to bind the copper and help the body get rid of it (penicillamine, zinc). Lifelong treatment is required.

Congenital portosystemic shunt (many breeds)

Diagnosis requires demonstration of the abnormal blood vessel going around the liver, usually by radiographs and a dye injection into the portal blood vessels. Treatment of choice is surgery to tie off the abnormal vessel or to place a metal band around it so it is eventually occluded.

HIP DYSPLASIA - A CAUSE FOR CONCERN

Jonathan Dyce, MA, VetMB, DSAO, MRCVS
The Ohio State University

• Look at his x-ray. He has severe hip dysplasia and needs two hip replacements.

• I did not realize you could diagnose hip dysplasia before two years old.

• My Lab cannot have hip arthritis. He is only 8 months old.

• I cannot believe I spent $800 on a Retriever with hip dysplasia. I want to put the breeder out of business. (Quotes from clients visiting the OSU orthopedic service.)

There are many misconceptions regarding hip dysplasia (IM). In this seminar common questions regarding the prevention, diagnosis, and management of HD will be addressed.

The disease

HD is defined as a developmental abnormality of the hip joint. Dogs which will develop HD are structurally and functionally normal at birth. The subsequent development of hip laxity is the cause of HD. There is a strong genetic basis to the disease which is seen particularly in large and giant breed dogs. Hip dysplasia has a polygenic mode of inheritance. It follows that the incidence of HD should be reduced by appropriate management of the breeding stock. Regrettably, the incidence of HD in some breeds is actually increasing. The expression of the disease is modified by environmental factors such as exercise and diet, e.g. overfeeding to produce rapid growth, and calcium over-supplementation. Abnormal loading of the articular (joint) cartilage in the loose hip initiates degenerative changes within the joint (osteoarthritis). The primary importance of HD and osteoarthritis is that they can cause pain.

Diagnosis

Difficulty in rising and going up steps, a reluctance to play, and bunny hopping are common complaints. Physical examination can reveal hind limb lameness, pain on hip manipulation, hip instability, and loss of muscle bulk. Radiography is used to confirm the diagnosis. The application of OFA versus Penn hip radiography will be explained.

Treatment

The majority of dogs with HD will never require medical or surgical treatment. It is imperative that we treat the dog and not the radiograph.

For those dogs with clinical signs, medical management involves diet to maintain lean body condition, low impact exercise, and symptomatic use of non-steroidal anti-inflammatory agents, or disease modifying osteoarthritic agents.

Surgical options target two distinct types of patient.

1. The immature dog with no significant osteoarthritis and a well-preserved acetabulum (socket). Corrective

osteotomies including triple pelvic osteomtomy (TPO) may be appropriate. Note that there is a limited

time window for the performance of such techniques.

2. The mature (greater than ten months) dog which may have severe osteoarthritis. The salvage options of

femoral head ostectomy (FHO) or total hip replacement (THR) may be considered.

The rationale for these surgical options will be described and the probable outcome following surgery discussed.

IS THERE A BREED PREDISPOSITION TO THE COMMON CANINE CANCERS:
LYMPHOMA, MALIGNANT HISTIOCYTOSIS, MAST CELL TUMOR?

Karma D. Valerius, DVM, MS,
Diplomate ACVIM (Oncology)

Introduction

Today dogs live longer due to the advent of excellent preventative programs to control infectious diseases that were previously fatal. Nowadays, it is common to have pets that live to be over ten years old. As pets get older the incidence of neoplasia increases. Veterinary medicine has also become more sophisticated and we have better diagnostic equipment that helps us detect cancer. Recent studies have shown cancer is the most common cause of death in dogs. A recent study done at the University of Pennsylvania Veterinary Hospital during a ten-year period from 1986 to 1996 showed that the death rate from cancer of Golden Retrievers was 64 percent, for German Shepherds was 42 percent, and for Labrador Retrievers was 41 percent. We know that a specific cancer may be more commonly seen in certain breeds, however we do not know whether a specific cancer in dogs is hereditary.

Lymphoma

Lymphoma (malignant lymphoma, lymphosarcoma) is defined as cancer of the lymphocytes. A lymphocyte is a type of white blood cell that is part of the immune system. Lymphocytes originate from solid organs, such as lymph nodes, liver, and spleen.

There is a distinct breed predisposition to lymphoma in dogs and certain breeds appear to be over represented: Boxer, Golden Retriever, Cocker Spaniel, Basset Hound, Rottweiler, Bullmastiff, St. Bernard, Scottish Terrier, Airedale Terrier, and English Bulldog. In a group of 59 Bullmastiffs, rune dogs developed lymphoma over a three-year period and cases seemed to follow a familial distribution.

Most dogs with lymphoma present with no clinical signs, and enlarged lymph nodes are detected on physical examination. Lymphoma is a fatal cancer and without treatment most dogs will live only one to two months. Fortunately, lymphoma is one of the most responsive cancers and most animals' quality of life improves tremendously once treatment is initiated. Treatment options vary from steroids to chemotherapy with life expectancies of one to two years with chemotherapy.

Malignant Histiocytosis

Malignant histiocytosis is a rapidly progressive, fatal cancer that affects cells in many organs, such as liver, lung, lymph nodes, skin, and bone marrow. It primarily affects young to middle-aged large breed dogs. We tend to see it more commonly in Flat Coated Retrievers, Bernese Mountain Dogs, Rottweilers and Labrador and Golden Retrievers. Survival of dogs with malignant histiocytosis is short and chemotherapy seems to prolong survival for only a few months.

The Flat Coated Retriever has been anecdotally noted to have an unusually high incidence of cancer. An epidemiological survey of the Flat Coated Retriever population in the United States showed that cancer was overwhelming cause of death in the Flat Coated Retriever breed, accounting for 63 percent of the deaths. Moreover, the incidence rate of cancer in this breed is five times the incidence rate in the general canine population.

Mast Cell Tumor

Mast cells are located in the skin and subcutaneous tissues, where they play an integral role in allergic reactions and inflammatory processes. Mast cells can degranulate and release histamine causing itching, redness, swelling, and ulcers in the stomach. In dogs, mast cell tumors are most commonly found in the skin of the trunk and hindquarters and sometimes in the skin of the extremities. In most dogs, tumors are solitary, but in ten percent of the dogs, the tumors are multiple. Tumors usually occur in older dogs (nine years) with no sex predilection. Boxers, Boston Terriers, Chinese Shar-Peis, Bullmastiffs, and Labrador Retrievers are at high risk for developing mast cell tumors. The behavior of mast cell tumors depends on the histologic grade. Dogs with well-differentiated tumors can be cured with surgery. Dogs with poorly differentiated tumors have a poor prognosis and die from metastasis within six months. Most dogs present with moderately differentiated mast cell tumors, which can be cured with surgery if there is no evidence of metastasis to lymph nodes, liver, spleen, and bone marrow. Boxers and Boston Terries usually present with well-differentiated tumors, whereas Chinese Shar-Peis usually present with poorly differentiated tumors.

Selected Retinal Diseases of Purebred Dogs

Michelle Willis, DVM, DACVO

Breed Certification eye examinations (CERF - Canine Eye Registration Foundation) are an important consideration for any animal in your breeding program. The exams are meant to help you make sound breeding decisions, and to catalogue the lesions identified in order to continue to learn more about the incidence and prevalence of these diseases in the canine population.

The identification of retinal disease requires an examination of the back (posterior) part of the eye - this is performed with indirect ophthalmoscopy. As there is a great degree of normal variation in the appearance of the canine retina (breed and individual), experience is required to make a judgement as to whether the dog is normal or affected by a potentially heritable disease.

Most of the inherited eye diseases in dogs have a recessive pattern of inheritance. This means that an affected puppy was given an abnormal "gene" from each parent - this would infer that each parent would at least be a carrier of the trait, it is not phenotypically (we can see the lesion in them) affected. The genetics of some traits are much more complicated, which of course makes breeding decisions more complicated!

Two common and very important retinal diseases will be discussed, Retinal Dysplasia and Progressive Retinal Atrophy (PRA):

Retinal Dysplasia - This is a congenital maldevelopment of the retina, and has three basic forms:

Retinal Folds

- Linear, triangular or curvilinear foci of retinal folding that may be single or multiple in number

- Unless numerous folds exist in a large area of retina, usually of no functional significance for the dog

Geographic Dysplasia

- An irregular, often "horseshoe"-shaped region of maldevelopment

- May include retinal elevation in the center of the lesion, which usually does not progress

- May be associated with visual impairment

Retinal Detachment/Non-attachment

- Either of the above forms of dysplasia, associated with separation of the retina

- May also see vitreal dysplasia in affected dogs

- Can be associated with vision impairment or complete blindness

- Secondary problems of intra-ocular bleeding and cataracts formation add to ocular morbidity

*** The genetic relationship between the three forms of retinal dysplasia is not known for all breeds

Progressive Retinal Atrophy- A degenerative disease of the visual cells in the retina, which will progress to complete blindness

- The age of onset may vary among affected breeds

- Often manifests in the early stages with "night blindness" or difficulty seeing in dim-light situations

- Presumed in most breeds to follow a recessive pattern of inheritance although this has not been proven in

many breeds

- Because of the significance of this disease, parents of affected animals should be presumed to be carriers,

and siblings of affected dogs should not be used for breeding

- Because PRA may not show up on an eye exam until the dog is several years of age, annual exams of all

actively breeding animals and foundation dogs are recommended

SELECTED CONGENITAL HEART DISEASES IN THE DOG

Linda B. Lehmkuhl, DVM, MS, Diplomate, ACVIM
The Ohio State University

Congenital cardiac defects are relatively rare, but their importance is evidenced by the new owners who have been informed their apparently healthy puppy has a fatal heart malformation or the breeders who learn their prized stud dog is a carrier of subvalvular aortic stenosis and should not be bred. In most instances, congenital cardiac defects are first recognized in asymptomatic puppies during the immunization series following auscultation of a murmur. This creates an initial dilemma, however, since normal puppies can exhibit innocent cardiac murmurs. The typical innocent murmur is soft, short, heard best on the dog's left side, and often varies with heart rate and changing body position. These murmurs, which are often musical in quality, should resolve by the time the animal reaches sixteen weeks of age. These murmurs do not have any clinical or breeding implications (as long as they are truly resolved in the individual in question).

A tentative diagnosis for a dog with congenital heart disease can usually be attained by a noninvasive evaluation including the breed, history, physical examination, thoracic radiography, and electrocardiography. Breed is especially important because a genetic basis is suspected for most of the cardiac defects (Table 1). Definitive diagnosis of CI3D often requires referral for Doppler echocardiography. The most common defects, listed in decreasing order of frequency according to a recent clinical survey conducted by Dr. Buchanan, are: patent ductus arteriosus, subvalvular aortic stenosis, pulinoruc stenosis, ventricular septal defect, tetralogy of Fallot, and tricuspid and mitral valve dysplasia. This short proceeding will focus on the two most common defects.

Patent Ductus Arteriosus (PDA)

In the fetus, the ductus bypasses the non ventilated fetal lung by shunting blood from the pulmonary artery to the aorta. At birth, this communication should close. PDA is an inherited defect transmitted as a polygenic threshold trait. Breeds at greater risk for development of PDA include the Chihuahua, Collie, Maltese, Poodle, Pomeranian, English Springer Spaniel, Keeshond, Bichon Frise. Cavalier King Charles Spaniel, German Shepherd Dog, and Shetland Sheepdog. Affected dogs should not be bred.

Pups may be clinically healthy or may demonstrate signs of left-sided congestive heart failure including cough, shortness of breath, or tiring. Physical examination alone is usually diagnostic. More than half of dogs diagnosed with PDA will be dead within one year of diagnosis without surgical treatment of the condition. Surgical ligation of the PDA is recommended in essentially all cases of left-to-right shunting PDA diagnosed in dogs. The optimal time for surgery has not been determined but surgery should be done early, usually between eight and sixteen weeks of age, or sooner if impending cardiac failure is suspected. Prognosis with surgery is excellent.

Subvalvular Aortic Stenosis (SAS)

In dogs with SAS, there is added tissue between the main pumping chamber of the heart (left ventricle) and the body. This abnormal tissue is located below the aortic valve (hence "subaortic") and creates an obstruction ("stenosis" is the scientific term) that the heart has to overcome to pump blood to the body. Dogs affected with SAS are usually large breed dogs including Newfoundlands, Golden Retrievers, Rottweilers, and Boxers. Breeding studies in Newfoundland dogs have confirmed that SAS is inherited, and the mode of transmission is most compatible with a defect in a single gene with minor modifying genes or environmental variables resulting in complex inheritance patterns.

Severe SAS is characterized by progressive exercise intolerance, fainting, cough, or sudden death; whereas, clinical signs are usually absent in dogs with mild to moderate subaortic obstructions. Mildly affected dogs represent a diagnostic dilemma for both veterinarians and breeders. Physical examination of these dogs is characterized by a soft murmur. Distinguishing murmurs caused by mild SAS from "functional" murmurs is difficult. A normal two-dimensional echocardiogram (ultrasound) study, without Doppler, is not sufficiently sensitive to exclude a diagnosis of mild SAS.

Dogs with mild to moderate SAS should not be used for breeding and should receive prophylaxis of heart valve infections in appropriate circumstances, but are otherwise treated normally. Therapeutic options are frustratingly limited for moderate to severe SAS. Surgery, balloon catheter dilation, and chronic oral therapy with a beta-blocker have been used with some successes.

Table 1 BREED PREDISPOSTIONS TO COMMON CONGENITAL HEART DISEASE
MALFORMATION Patent ductus arteriosus (PDA)	BREED Maltese, Pomeranian, Shetland Sheepdog, English Springer Spaniel, Keeshond, Bichon Frise, Toy and Miniature Poodles, Yorkshire Terrier, Collie
Subaortic stenosis (SAS)	Newfoundland, Golden Retriever, Rottweiler, Boxer, Samoyed, German Shepherd Dog, Great Dane
Pulmonic stenosis (PS)	English Bulldog, Mastiff, Samoyed, Miniature Schnauzer, West Highland White Terrier, Cocker Spaniel, Boykin Spaniels
Mitral valve dysplasia	Bull Terrier, Great Dane
Tetralogy of Fallot	Keeshond, English Bulldog
Tricuspid valve dysplasia	Labrador Retriever, German Shepherd Dog, Boxer
Ventricular septal defects (VSD)	English Bulldogs

Nutritional Issues and Answers

Sarah K. Abood, DVM, PhD

The field of nutrition is filled with myth-information that often persists despite few if any scientific facts to support a given myth (even in the face of data that clearly disputes a myth). Nutrition myths are interesting to consider from two aspects. First, they are often centered on some small bit of truth. Over the years of translation and retelling, however, the truth begins to take on characteristics of myth and any truth is distorted and replaced by misinformation. Second, many nutrition myths focus on the erroneous belief that pets have a physiologic need for certain ingredients in their diets. In fact, dogs have requirements for nutrients, not individual ingredients. The important factor in the nutritional well being of a pet is whether the diet contains the correct nutrients in the right amounts in a form the dog can digest and utilize. It is not dependent on which exact ingredients are used to supply those nutrients. This presentation will briefly review the validity of some common nutrition myths, as well as address the people, dietary and animal factors involved when advising new owners on what and how to feed their dog.

Myth #1: Excessive protein causes over-development of puppies

Known Facts: Dr. Hazewinkle (Utrecht University, The Netherlands) has shown that high protein intakes in growing Great Dane pups does not cause disturbances in bone development. Low protein diets, however, were of concern in that they did not support adequate growth as evidenced by low serum albumin levels and low body weight. Scientific work conducted at the Purina Pet Care Center has shown that excessive calories may cause obesity and increase the risk of orthopedic problems in Labrador Retriever dogs.

Best Nutritional Advice: Feed a well-balanced product in amounts to support proper growth but to avoid obesity. Maintain a good body condition (feed the animal and not the food bowl!).

Myth #2: Puppies (and lactating bitches) need calcium supplements

Known Facts: Adding extra nutrients does not automatically assure a healthier bitch and litter, nor does it improve the growth of puppies, and may in fact result in problems. Dr. Hazewinkle found that 1.1 percent calcium (dry matter basis) was adequate for fast growing Great Dane pups and that 3.3 percent calcium was excessive and resulted in severe skeletal abnormalities. The AAFCO nutrient minimum for reproduction and growth is 1.0 percent calcium and the maximum is 2.5 percent calcium. Still unknown is the precise upper level of calcium at which significant problems in skeletal development may occur.

Best Nutritional Advice: Feed a nutritionally complete and balanced pet food. Do not supplement the diet except on the advice of a veterinarian who is treating a specific problem in a dog.

Myth #3: Beet pulp or soy causes bloat (and both are poor nutrient sources)

Known Facts: Beet pulp is a by-product of the beet industry. It has no known nutrient value but does serve to absorb water within the intestinal tract. The potential benefit of beet pulp is that it may help to absorb water from digests and therefore help to maintain firmer stools. Soy, in its many forms, does provide usable nutrients in a diet such as protein, essential fatty acids and fiber. Based upon epidemiological studies, bloat in dogs is thought to be associated with 1) the dog? Anatomy-length and depth of chest and abdominal cavities and 2) management of the dogs feeding, watering and exercise regimens. Specific type of diet or particular ingredients has not been found to cause bloat.

Best Nutritional Advice: Dogs that are prone to bloat should be managed to minimize risk for bloat:

1. feed two or three smaller meals throughout the day

2. don't allow dog to gulp water immediately after exercise or eating (small amounts)

don't run/exercise dog immediately after a meal

Myth #4: Excessive protein can cause kidney problems

Known facts: Research in dogs has not proven that this myth is true. Research has shown that for those dogs with significant kidney disease already present, reducing the level of dietary phosphorus may help prevent further kidney damage.

Best Nutritional Advice: Healthy dogs (regardless of age) should be fed a complete and balanced dog food that has been tested according to AAFCO feeding trails and has a claim for the appropriate lifestage. Dogs that have been diagnosed with kidney disease may benefit from a product that is restricted in phosphorus and those animals with actual clinical signs of uremia may benefit from a product with reduced amounts of protein.

Myth #5: Supplements are beneficial to dogs

Known Facts: Most commercial products that are marketed as complete and balanced provide more than enough vitamins and minerals for young growing puppies and adult dogs. Supplements on the market today do not meet the AAFCO guidelines for vitamin or mineral requirements and could upset the balance of vitamins/minerals already in the dog's current diet.

Best Nutritional Advice: Feed a complete and balanced product that has been tested according to AAFCO feeding trials and has a claim for the appropriate lifestage.

Myth #6: Dogs are carnivores and therefore must eat meat.

Known facts: The gastrointestinal physiology of dogs is fully capable of digesting and absorbing plant protein sources as well as meat protein sources. Both plant and animal protein sources provide amino acids which are the substances dogs require to build protein. There is nothing in the scientific literature to suggest that dogs consuming meat products only will achieve greater health benefits than dogs consuming commercial dry or canned foods. Feral dogs and wolves also eat plants, berries, insects, fish, etc. When these dogs kill and eat other wild animals (caribou, deer, elk, mouse), they rip into and eat the guts first. The intestinal tract of these ruminants is full of partially digested grasses, leaves, and plants... so the feral dog is an herbivore also!

Best Nutritional Advice: Feed a complete and balanced product tested according to AAFCO feeding trials.

Myth #7: Corn or wheat is a poor source of nutrients

Known Facts: Corn contains approximately 8 percent protein, 4.5 percent fat, 1.9 percent linoleic acids, and B-vitamins. Wheat contains approx. 12.5 percent protein, 1.5 percent fat, 0.9 percent linoleic acid and B-vitamins. Dogs can digest these ingredients readily and nutrients are available.

Best Nutritional Advice: Choose a product based on its ability to deliver 100 percent complete and balanced nutrition. Individual ingredients are not important. It's the overall content and balance of nutrients which make a product a good choice to feed your dog.

Myth #8: All supermarket dog foods are junk food

Known Facts: Foods should be evaluated based upon their ability to adequately nourish animals, not where they are sold. Criteria to evaluate dog foods include: reputation of the manufacturer, nutritional adequacy statement on the package (feeding tests versus nutrient profile), and the 1-800 number or address of the manufacturer.

Best Nutritional Advice: Choose a pet food designed for the proper lifestage, one that has undergone animal feeding studies and is produced by a manufacturer for extensive testing in various breeds.

Reproductive Problems in the Bitch

Theriogenology Area

Walter R. Threlfall, DVM, PhD, ACT

Ovary
I. Developmental

Hermaphroditism
Pseudohermaphroditism
Hypoplasia
Aplasia
Diagnosis
Appearance
Karyotype
Treatment

Castration (?)

2. Cystic Ovaries

Diagnosis
Persistent estrus with corresponding vaginal cytology
Differentiate from granulosa cell tumor
Proestrus (normal)
3-17 days (average 9 days)
Hemorrhagic discharge
Turgis vulvar swelling
Estrus (normal)
3-17 days (average 9 days)
Straw-colored or red tinged
Flaccid vulvar swelling
Total of proestrus + estrus = 21 days or less (normal)
Treatment
500 to 1000 1U HCG
50 ug GnRH

3. Pseudocyesis

False pregnancy
    Abdominal enlargement
    Increased appetite
    Mammary development
    Behavioral change (nest building)
        Adoption of inanimate objects
Cause
    Unknown
Treatment
    None - depends on tolerance of owners
    Mibolerone (cheque drops) 18 ug/lb OID orally for S to IO days
        Excellent
Testosterone

Second Choice
0.5 to 1.0 mg/lb daily for 7 to 10 days or repositoI form

4. Neoplasms

Low incidence - less than one percent of all canine tumors
Signs

Dependent on type
Granulosa cell tumor
Most frequent
Can produce estrogen, progesterone or both

Uterus

1. Pyometra

Etiology - Progesterone

Estrogen priming increases incidence
Endogenous
Cystic ovaries also can simulate etiology
Exogenous
Mismating treatments with estrogens simulate estrogen then progesterone

Development

Cystic endometrial hyperplasia occurs first

Signs

Will discuss only reproductive aspects
Increased uterine size with or without discharge

Treatment

Life - spay
Reproduction

Prostaglandin Fz alpha (not approved)
Cervix (?)
250 ug/kg/day SQ (20 cc volume) for 1 to 5 days
Side effects
Salivation, vomiting, frequent urination, diarrhea, hyperpnea, ataxia
Maximal for 30 minutes following treatment
LD50 5 mg/kg

2. Metritis

Infection (or inflammation) of uterus

Occurs postpartum, post-breeding

Acute (postpartum - within 3-4 days)

Depression, discharge, fever

Diagnosis

Enlarged uterus

Vaginal cytology

Treatment

Systemic antibiotics

PGFz alpha (2"d or 3rd day of treatment)

Infuse uterus (2°d or 3rd day of treatment)

Fluids

Ovariohysterectomy

3. Brucellosis

Brucella Canis

Human significance

Ampicillin treatment

Excellent prognosis

Transmission

Ingestion

Abortion

Vaginal discharge

Milk

Venereal

Congenital

Infected by time of birth

Bacteremia may last 2 years

Reproductive problems

None

Male

Orchitis

Epididymitis

Scrotal irritation

Testicular atrophy

Female

Abortion

Infertility

Persistent vaginal discharge

Diagnosis

Serology

Culture (difficult)

Blood

Lymph nodes

Bone Marrow

Negative serology has occurred with organism cultured

Treatment

Euthanasia - my recommendation

Neuter

Tetracycline 60 mg/kg divided TID for four weeks, off four weeks, repeat for four weeks

Minocycline (Lederle)

50 mg/kg divided BID orally for two weeks plus streptomycin 20 mg/kg divided

BID IM for seven days

Elimination of organism from prostate extremely difficult (if possible)

4. Neoplasms

Less than 0.5 percent of canine tumors

Diagnosis

At time of Ovariohysterectomy or necropsy

Treatment

Ovariohysterectomy

5. Uterine subinvolution

Delayed involution of postpartum uterus

Signs

Persistent hemorrhagic

Vulvar discharge

May persist for 8 to 10 weeks

Vaginal cytology

RBC's (numerous)

Uterus - segmented enlargement of uterus

Treatment

Ovariohysterectomy

Spontaneous recovery

PGFZ alpha

250 ug/kg/day SQ

Ergonovine

May be of value

6. Mismating

History

If occurred within hours previous to examination - do vaginal smear, look for sperm

Treatment

Ovariohysterectomy after estrus

Permit pregnancy if occurs

Medical treatment

DES -1 mg/30 lbs QII3 orally for seven days (start at time of breeding)

ECP - I do not recommend Safety? Aplastic anemia, thrombocytopenia, leukopenia - may be permanent

PGFz, alpha - not good repeated doses

Vagina and Vulva

1. Congenital

Hymen

Hypoplasia

Signs - penetration impossible

Dystocia

Diagnosis

Vaginal

Treatment

Dilation or incision

2. Vaginitis

Pre-puberal

Prior to first estrus

Discharge only sign

Adult

Increased licking

Pain on urination

Diagnosis

Culture anterior vagina

Cytology of vaginal smear

BSE

Treatment

Pre-puberal

No treatment

Specific antibiotic for 2 to 4 weeks

Low dose DES - tablets 1 mg/day (over 20 lbs) for 7 days

Adult

Specific antibiotic for 2 to 4 weeks orally

Local antibiotics

Vaginal douche

MAXIMIZING CONCEPTION RATES USING FRESH COOLED OR
FROZEN CANINE SEMEN

Robert V. Hutchison, DVM
Animal Clinic Northview, Inc.

Since the American Kennel Club's recognition of litters conceived from frozen semen in 1981 and the subsequent acceptance of fresh chilled semen, practitioners are being asked more frequently to assist clients with maximizing conception rates using these breeding techniques. The gratification one feels when successful is one of the great rewards in veterinary medicine. The basis of fresh chilling and freezing semen is energy conservation within the sperm cell so that the semen can be shipped or used at a later date. The drawback to these methods is that even though some energy is conserved, enough energy is used to shorten the sperm cell's life.

Fresh semen is thought to live four to six days in utero. The freshly ejaculated sperm life allows for successful breeding when the bitch exhibits standing and acceptance of the male, even though in many cases the timing is 4 to 6 days before the prime fertilization period of the mature ova.

FRESH CHILLED SEMEN

Fresh chilled semen uses energy as it is cooled to 40°F (4°C) and eventually re-warmed to body temperature. The life in utero of a spermatozoon having experienced the chilling and subsequent warming process is 24 to 72 hours, necessitating a more precise manner of ovulation timing and breeding. When sperm is frozen for future use, it is eventually stored at -322°F. (-180°C). This extreme temperature preserves a sperm cell indefinitely but not without stress and energy output. The thawed spermatozoa has a maximum life span of twelve to 24 hours after insemination into the bitch. The ultra-short life span makes success with frozen semen only possible with precise mapping of the bitch's estrous cycle with definitive detection of the LH release and the subsequent time of ovulation. When a veterinarian receives a fresh chilled sample, the package should be opened immediately. Attention should be paid to the "impression of coolness". The ice packs should be at least cold, if not still frozen. The package containing the semen should be removed from the packaging material (usually newsprint). The tube should contain the extended semen in a liquid state. Unfortunately, occasional mishandling by the shipping company or by the shipper placing the semen package in a non-pressurized compartment of the airplane will cause the sample to arrive frozen. The freezing kills the sperm cell and renders the sample useless.

One drop of the sample should be placed on a warmed microscope slide. The rest of the sample should be refrigerated. Allowing the chilled sample to warm to room temperature only allows the sperm cells to speed up, using precious energy and shortening their life span.

As the drop warms on the slide, the accompanying paperwork with the semen collector's evaluation of the semen quality, time of collection and post-collection motility should be studied. The semen drop is then analyzed and compared to the collector's evaluation.

In many cases, the semen will appear to be non-motile. However, as the semen drop warms gradually side to side motility becomes noted. The continued warming eventually shows the cells to have achieved a normal forward progression. If no motility is noted after fifteen minutes, the sample is most likely non-viable. If this occurs the collector of the semen should be contacted to determine, if possible, the cause of the semen's demise. In other cases where only partial semen recovery is noted, the inseminator must use judgment based on the connection of the semen, estimated total spermatozoa numbers and the percent recovered. It may also be necessary to alter the insemination method to that of an intra-uterine deposition of the fresh chilled sperm to further remove sperm cell stress and to aid its arrival at the fallopian tubes.

It is recommended that the refrigerated fresh chilled sample not be warmed to room temperature or body temperature before insemination. Having the sample in the uterus as it warms makes maximum use of the conserved energy. All fresh chilled semen samples are handled in a similar manner. However, many different commercial companies sell packaging kits and extenders. One should always read their instructions for any specific handling recommendations.

FROZEN SEMEN

Frozen semen does require even more precise handling than fresh cooled semen. Frozen semen will usually be shipped in a dewer with nitrogen vapor keeping the sample frozen rather than with actual liquid nitrogen in the container.

When the shipper arrives, the tank will be in a protective shell. The shell should be opened and the plug pulled (not twisted) from the nitrogen tank. Visible vapor should be seen assuring the recipient that the tank is charged properly and that the sample is still frozen. If vapor is noted the plug should be replaced until the time of insemination. If no vapor is seen, an attempt should be made to ascertain that the sample is still in a proper frozen state. This can be accomplished by grasping the cane that holds the semen and raising it to the mouth of the dewer. If the sample is thawed, the semen will not be viable and a replacement sample should be obtained if possible.

If the sample is frozen, the person that shipped the sample should immediately be contacted to discuss the tank status and determine if some liquid nitrogen should be added to the dewer to assure that the sample will remain frozen until time for the insemination.

Canine semen is frozen in two different forms, I) pellets and 2) straws. Both are extremely successful in achieving conception; however, it is essential that the doctor doing the insemination follows the thawing instructions precisely. Most thawing techniques require that the person using the semen has a form of warm water bath available. A form describing the semen's quality, both pre and post thaw should have accompanied the shipment. These values can be used to judge the quality of the thaw before insemination. Each individual that freezes canine semen has a specific manner of handling and thawing their product. There is no room for error.

TIMING OF INSEMINATION

Historically, methods of timing the estrous-cycle of the bitch such as color of discharge, swelling of the vulva and flagging of the tail allowed breeders to get bitches bred, but using these signs, in many cases, created more confusion than answers. Vaginal cytology, a rough gauge of estrogen level, has been used by veterinarians and breeders to "pinpoint" the time of ovulation. Vaginal smearing at best gives a retrospective view of the cycle with diestrus, day one, occurring six days post-ovulation. However, vaginal smearing does not allow prospective timing other than giving information as to when other testing needs to begin. Vaginal cytology is not useful by itself in timing fresh cooled or frozen semen. The same can be said of vagino-scopy, a visual method of evaluating vaginal fold swelling and crennulation that equivocates with estrogen rise and fall.

The serial testing of serum samples from the bitch for either progesterone testing or luteinizing hormone (LH) testing will give the veterinarian a prospective view of the ovulation, ova maturation and the prime fertile period for using the fresh cooled or frozen semen.

PROGESTERONE

The release of progesterone from the ovary and its subsequent rise to an average of two to three ngm corresponds with luteinizing hormone release from the pituitary gland and signifies the start of the ovulatory process. The rise of progesterone is greater than five ngms (five to eight ngm) indicates that ovulation has occurred. Once the ovulation day has been confirmed, fresh cooled semen inseminations in two to three days or frozen semen insemination in three to four days can be planned. Progesterone not being specific, can be tested far by many methods. Numerous elisa kits for in office use are currently available. Progesterone, can also be evaluated by radio-immune assay (RU) by many human and veterinary laboratories.

Progesterone rises and continues to stay elevated for approximately two months in the hitch, whether she is pregnant or non-pregnant. The bitch needs to be tested every 48 hours to anticipate the prime breeding time.

When using the progesterone elisa kits, negative features include that hemolyzed blood samples will give lower than normal results. If the elisa kits are not handled properly or warmed to room temperature, an artificially high result will be recorded. Ideal testing for progesterone level would include screening with the elisa kits, but obtaining RIA progesterone numbers, to define the exact day of ovulation and the corresponding breeding time.

Cortisol release needs to be a concern when doing progesterone testing as stressed bitches may have a delayed period between a rise of two to three ngm/rnl and the time that the progesterone rises greater than five ngmlml. Some bitches under stress have been shown not to ovulate even after a rise of progesterone above two ngm. It is essential if using progesterone testing to corm that the bitch has risen above five ngm/ml and has indeed ovulated.

LUTEINIZING HORMONE

Luteinizing hormone (LIT/ is a species specific hormone arising from the pituitary gland. The release of the hormone spikes over a twelve to 24 hour period. The release of the LH triggers ovulation in 48 hours, allowing for a final meiotic division of the ova and shedding of the polar body (approximately another 48 hours) before the ova can be fertilized. An accurate evaluation of the LH spike can give the veterinarian and breeder four to five days anticipation of the prime insemination dates and reasonable confidence as to the maximum chance of conception.

Unfortunately LH assays are not easily available for canines at the time of this writing. As LH is species specific human laboratories cannot run this assay. An immuno-chromatinographic testing kit is currently available for in office use. The test, status LH (International Canine Genetics, Inc., Malvern, PA 19355 USA), uses a wicking paper with a reaction test zone and is run with 4 drops of serum.

The test develops a distinct colored line (red) when the serum LH rises above one ngm/ml. When the line appears one would anticipate prime breeding time to be in four to five days with fresh cooled semen and five to six days with frozen semen (the variation based on anticipated sperm life in utero).

Negatives to the LH test are that daily samples must be drawn (even greater than 24 hours between tests may miss the LH rise). The cost of daily testing, owner compliance and veterinarian availability far testing every day have created some problems for this testing method. Serum samples that are hemolyzed or lipemic also affect the testing results. LH testing is especially useful in bitches previously tested by progesterone assay that did not conceive or that showed irregular progesterone levels.

ARTIFICAL INSEMINATION

Artificial insemination has been a commonly used procedure in small animal reproduction. However, the advent and common usage of canine frozen and fresh cooled extended semen has refocused clinicians' attention to more precise methods of semen delivery to the bitch's reproductive system the shortness of spermatozoa life. Loss of sperm cell energy in fresh cooled extended semen and frozen semen has necessitated the development of new methods of semen delivery in the bitch. Frozen semen especially benefits from techniques by passing the cervix and the cervical mucous and being deposited directly into the uterine lumen.

Two techniques of artificial insemination are routinely performed and are amenable to the veterinary practitioner dealing with canine reproduction. The two techniques to be described are vaginal insemination and the surgical intra uterine deposition of semen.

VAGINAL INSEMINATION

When proper timing of the estrous cycle is performed on the bitch and proper semen handling and delivery is accomplished, conception rates should rival those of natural breeding. Delivery technique problems such as improper placement of the insemination rod, improper semen placement or semen damage due to mishandling have convinced many dog breeders and veterinarians that artificial inseminations are only used as a last ditch desperate measure.

PROCEDURE

The estrous cycle for the bitch should be monitored using serum progesterone assaying or some other reliable manner to ascertain that ovulation has occurred. Semen motility is evaluated as previously described.

The bitch is positioned with her rear elevated either manually or on a breeding ramp. Care should be taken to avoid pressure on the bitch's abdomen. The semen is drawn from the collection tube through an insemination rod of proper length to reach the cervical OS. It is important that the semen be deposited at the entrance to the cervix so that the semen can be drawn into the uterus. With gloved hands the veterinarian gently inserts the insemination rod through the lips of the vulva at an upward 45 degree angle. The rod is gently passed over the pubis and along the dorsal median fold until it is parallel with the lumbar spine and localized in the area of the cervix. If resistance is encountered the rod should be gently twisted or withdrawn a short distance then re-advanced.

When the insemination rod is property positioned the semen should be gently inseminated. The syringe is then removed from the rod. It is not necessary to push large amounts of air into the rod nor normal to get semen backflow if the rod is properly positioned and the bitch is in the estrus stage of estrous. Excess air "bubbling" through the semen is detrimental to the fragile plasma membrane of the head of the spermatozoa.

The bitch is then "feathered" digitally for one minute. The rear of the bitch is maintained in an elevated position for six minutes to allow gravitational feeding of semen to the anterior vagina. The bitch owner is instructed to confine the bitch or restrict her activity for one to two hours post-insemination.

SURGICAL INTRA-UTERINE DEPOSITION OF SEMEN

A technique for surgical insemination in the bitch was first described in 1974. The infra-uterine deposition was initially used to increase poor conception rates in the use of canine frozen semen. Since that time, surgical deposition of semen into the uterus has become a routine technique used in numerous situations encountered in canine reproductive medicine.

A) Frozen Semen - Due to the lack of spermatozoa energy buffer chemical makeup, or cervical resistance the conception rates from cryo-preserved canine semen have been historically low when used with a vaginal insemination. Surgical deposition into the uterine lumen has resulted in conception rates equal to those from natural breeding.

B) Fresh Cooled Extended Semen - Shipment of semen rather than shipping bitches has become common place due to shipment time, and spermatozoa energy depletion. Numerous clients have chosen surgical semen insemination for their bitches in hopes of increasing conception rates.

C) Bitches with Suspected Uterine or Ovarian Disease - The ability to access uterine and ovarian health at breeding time is advantageous to clinicians presented with bitches with histories of reproductive failure or problems.

D) Giant and Toy Breeds - Individuals on the extreme ends of size have historically been recognized for conception difficulties. The ability to overcome anatomical barriers and inseminate directly into the uterus has increased litter numbers and relieved client frustration.

E) Males with Lowered or Compromised Spermatozoa Numbers - Little work has been done in the canine to definitively define minimum semen parameter necessary for conception by directly depositing the semen into the uterus and bypassing the cervix and vaginal vault. Conception can possibly be achieved with lesser sperm numbers and lesser overall semen quality.

TECHNIQUE

A pre-surgical evaluation is performed on the bitch. Anesthetic induction consists of coning smaller individuals with gas anesthesia (i.e. isoflurane). Larger bitches may require an injection of a standard short acting anesthetic (i.e. propofol) to achieve relaxation for intubation and maintenance with gas anesthesia.

The bitch is prepared in the same manner as a bitch undergoing an ovariohysterectomy. The ventral abdomen is clipped and the bitch is placed in the surgical theater in dorsal recumbency. Prepping of the surgical site is done in a routine manner. The abdomen is draped in preparation for the surgery.

A four to six centimeter incision is made midway between the pubis and the umbilicus. The incision is made in the skin subcutaneous fax through the linea alba. The uterus is identified and elevated to the surface through the incision. The uterus is draped with a saline moistened laparotomy pad as the semen is prepared for the injection procedure.

A volume of semen varying between .5 ml and four ml is prepared for insemination. If the volume is greater than four ml, the semen should be centrifuged for five minutes. The supernatant is decanted and disposed. The semen pellet is gently re-suspended with the remaining supernate or with a semen extender. The semen to be injected is gently drawn into a six-ml syringe through an insemination rod. The rod is removed and a 22 gauge, '/a inch needle is attached to the syringe.

The surgeon inserts the needle into the lumen of the uterine body at a 45-degree angle with the bevel of the needle up.. The semen is slowly injected into the uterus. The semen should flow easily with obvious distention of the uterine horns. If the injection cannot be achieved or is difficult, the needle should be repositioned. A saline moistened gauze is held over the injection site after the needle is withdrawn. After one minute, the gauze is removed and the uterus is replaced into the abdomen. Closure of the fascia, muscle, subcutaneous tissue and skin is routine.

The bitch's rear is elevated as she recovers from the anesthesia. The infra-uterine pressure during the surgical deposition of the semen may cause mild backflow through the cervix into the vaginal cavity, this appears to be of no concern. if the surgeon has doubt as to the semen being placed in the uterine lumen, a post-operative vaginal smear will confirm spermatozoa, if the technique has been performed properly.