Review theASCA general guidlines to breeding for more information, as well as a chart, developed to help you determine if your dog is breeding quality.

Collie Eye Anomaly (CEA) is a disease that is present at birth and does not get worse through the years of the dog's life. It ranges form inadequate development of the choroid (choroidal hypoplasia) to defects of the choroid, retina, or optic nerve (Coloboma), and complete retinal detachment. All of these parts of the eye are located in the back of the eye and aid the dog in seeing. Vision is normal except when there is retinal hemorrhage or detachment or a very large Coloboma. It is strongly recommended that puppies get tested for this at 6-7 weeks of age. Positive diagnosis can only be made by a Veterinarian Ophthalmologist. The following information on CEA was obtained from CA Sharp.

• CEA is caused by a recessive gene.
  
   
• Both sire and dam must carry the defective gene to produce an affected pup.
  
   
• Production of a confirmed CEA puppy proves both sire and dam are carriers.
  
   
• If a CEA puppy is produced, one grandparent on each side is a carrier. There is no way to tell which, unless they have also produced CEA puppies
  
   
• Statistically, only 25% of the puppies from the breeding of two carriers will be affected
  
   
• Carrier animals show no symptoms and there is no medical test to detect carriers.
  
   
• There is no known relation between CEA and coat or eye colors.
  
   
• CEA has been identified in other breeds, including Collies, Shetland Sheepdogs and Border Collies, all of which probably share some common ancestry with Australian Shepherds
  
   
• There is no complete listing of carrier animals, however a reference file of proven and suspected carriers is maintained with CA Sharp. Additional data is always welcome.

   

It is very important that any dog with this disease NOT be bred.

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The lens is a unique living ocular tissue that is usually clear or transparent and is referred to as 'the crystalline lens' by doctors. The normal lens focuses light on the light-sensitive nervous tissue located in the back of the eye, which is known as the retina. A cataract is an opacity (or cloudy change) of the lens that scatters light and looks gray or white. The word cataract literally means, "to break down." The word applies to waterfalls and rapids as well as to the lens. Cataractous changes of the lens may appear as small insignificant dots, microscopic blisters, a cracked-glass appearance, a diffuse haze, a "pearl-like" sheen, white streaks or a completely white lens. The cataract usually starts as small dots or microscopic blisters and progresses to involve larger areas of the lens. The rate of progression is difficult to predict and may be very slow or quite rapid. At times the cataract appears to worsen overnight. Cataracts may develop in one or in both eyes. If a large portion of the lens becomes white, it prevents formed images from reaching the retina and blurred vision results. When a light is shined into the eye of a patient with a complete cataract, the patient only sees a white light and no images can be seen. In Australian Shepherds, hereditary cataracts are always bi-lateral (in both eyes). This is the most common eye disease in Australian Shepherds.

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The iris is the color potion of the front of the eye. It works with the pupil to allow light in or out of the eye. Coloboma means a thinning or hole. So Iris Coloboma is a thinning or hole in the Iris. This is not a disease that hinders in the ability to see. In some dogs you can see the thinning without magnifying equipment. Dogs that have this should not be bred, for the larger the hole the more light enters the eye. This causes the dog to squint. It is not advisable for a dog on cattle to have to squint because of the sun! It is unknown how this disease is passed on to the offspring.

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Distichiasis is the condition of eyelashes coming out of an abnormal position such as the glands that are located along the eyelid edge. The eyelids are normal, just the eyelashes grow inward. This could cause scratching and scaring of the Cornea.

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During the embryological development of the eye, the iris initially forms as a solid sheet of mesodermal tissue. This is called the pupillary membrane. Later on, some of this mesodermal tissue dissipates, and this results in the formation of the pupil. Sometimes, after birth, a few of these fine strands of pupillary membrane remain. It is not unusual to see such pupillary membrane remnants in 6-to-8 week old puppies, however, if they persist beyond this age they are then are described as persistent pupillary membranes (PPM) and are considered to be defect. The most common manifestation of Persistent Pupillary Membrane is a fine strand of pigmented tissue which arises from the iris collarette and attaches to another spot on the iris. Sometimes the strand will cross the opening of the pupil. In more serious cases, the PPM arises from the iris and attaches either the lens - where it may produce a cataract, or to the inner surface of the cornea - resulting in corneal damage, scarring or persistent corneal edema. In the latter cases, impairment of vision may occur. When looking at the eyes in serve cases, it looks as a spider web in inside the eye.

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This is in associated with homozygous merles. With the problems associated with the homozygous merles several eye problems can develop these include but are not limited to: Micropthalmia (abnormally small eyes) Coloboma, Cathartics, subluxated pupils, and PPMS.

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Progressive retinal degeneration (PRD) is also known as progressive retinal atrophy (PRA) and refers to retinal diseases that cause blindness. Some breeds have blindness by abnormal development of the retina and this is called dysplasia. Other breeds have a slowly progressive degeneration or death of the retinal tissue and this is degeneration. These two types of diseases affect many breeds. In general these diseases are thought to be inherited but inherited differently in each breed. In all animals with PRD the outcome, age of the patient and what the veterinary ophthalmologist sees are the basis for the classification of exactly what type of condition the patient has. Different breeds of dogs have variations in the age the problem starts and speed with which the blindness develops. As the name PRD implies, a slow death of retinal tissue occurs. It is a slowly progressive disease and the earliest signs may be overlooked. As stated above, these diseases are known to be passed from parents to offspring even though the parents may have normal eyes. Therefore, identification of breeding animals with PRD is essential to prevent spread of this condition.

To better understand PRD, a basic understanding of the function of the retina is needed. The retina is a highly complicated tissue located in the back of the eye. Light strikes the retina and starts a series of chemical reactions that causes a nerve impulse. The impulse passes through the layers of the retina to the optic nerve and from there to the brain where vision takes place. In the retina, cells called rods are involved with black and white or night vision and cells called cones are involved with color or day vision. Progressive retinal degeneration may effect the rods alone, the cones alone or both the rods and cones together.

Progressive retinal degeneration is not a painful condition so your pet will not have a reddened eye or have increased blinking or squinting. For this reason most owners will not notice the early stages of the condition. Some owners will notice an abnormal shine coming from their pet's eyes. This abnormal shine is because the pupils are dilated and don't respond as quickly to light as pupils of normal dogs. The earliest signs of PRD include night vision difficulties that in most cases will progress to day blindness. Owners will often remember that their pets seemed disoriented when going out to the yard at night and they had to leave a light on for them. Night blindness may be manifested by a pet that is afraid to go into a dark room. Occasionally these pets will get lost in their own home after the lights have been turned off.

The veterinary ophthalmologist examines the retina with an instrument called an indirect ophthalmoscope. Changes in the retinal blood vessel pattern, the optic nerve head, and the reflective substance within the dog's eye called the tapetum can be seen which are classic for PRD. However in some breeds PRD characteristics have little or no early changes. The eyes of these dogs may appear normal until they are in the later stages of the disease. Progressive retinal degeneration will progress at different rates in different breeds. This variation causes difficulty in determining just how long any particular dog will continue seeing.

PRA has been reported in Aussies, but only rarely. It is a recessive, though there are several genetically distinct forms. Which of these, if any, occur in Aussies is unknown. Since the disease is progressive, it may require multiple exams before diagnosis can be confirmed. All of the cases of Aussie PRA have been in active working dogs. Because of this, it is possible that dogs so diagnosed may have one of two similar trauma-induced (and therefore not genetic) conditions, Acquired Focal/Multi Focal Retinopathy or Acquired Sector Retinopathy. If an Aussie which is regularly engaged in heavy physical activity that can include blows to the head, such as working stock, is diagnosed with PRA, the owner should arrange for a second opinion from a certified veterinary ophthalmologist who is familiar not only with PRA but with the acquired retinopathies.

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The term hip dysplasia means poor development of the formation of the hip joint and describes a developmental disease in young dogs of many different breeds. Unsound hip joints are a common problem in the larger breeds, and hip dysplasia can be a serious problem in any dog, especially if that is to be trained for a demanding activity. Hip dysplasia is an inherited defect with a polygenic ("many genes") mode of inheritance. The degree of hereditability is moderate in nature, meaning that the formation of the hip joints can also be modified by environmental factors such as over nutrition, excessively rapid growth, and certain traumas during the growth period of the skeleton. As with any quantitative trait hip joint conformation can range from good to bad with all shades in between. Signs of hip dysplasia cannot be detected in the new born puppy, but usually appear in the rapid growth period between four and nine months of age. Signs of the disease can vary widely from slight irregularities of gait to crippling lameness. Improvement or even apparent disappearance of lameness can occur as the dog matures, as a result of the joint stabilizing, inflammation subsiding, and musculature strengthening. However, the dysplastic dog will usually develop arthritis later in life. The only accurate means of determining the condition of the hip joints is by proper radiographic (X-ray) examination. Sedation or a short-acting anesthetic may be needed to restrain the dog so that a diagnostic film can be made, as positioning is of great importance. Signs of hip dysplasia found on X-ray include shallow sockets, irregular shape of femoral heads, looseness of the joint and degenerative joint disease or osteo-arthritis. Hip dysplasia may be diagnosed by X-ray between six months and a year of age, but this is not entirely reliable, and dogs intended for breeding should be X-rayed when fully mature in order to select for sound hips. Two years of age is considered to be the minimum age for accurate radiographic determination of desirable conformation. X-rays should be sent to the Orthopedic Foundation for Animals (OFA) in Columbia, Missouri (See Appendix H), for a diagnostic evaluation. The charge is $15 for a preliminary evaluation (,.or dogs X-rayed prior to two years of age), I and $20 for the assignment of a permanent OFA Registry number (for dogs two years of age or older). The dysplastic dog should not be used for breeding. During the acute phase of the disease, your veterinarian may suggest rest and supportive care. Moderate and regular exercise, control of weight and perhaps anti-inflammatory are helpful in the management of arthritis associated with hip dysplasia in the older dog. Many dogs with hip dysplasia will show no outward signs at all until perhaps 7 or 8 years of age when muscle tone decreases and arthritis and wear and tear on the joint become more noticeable. Australian Shepherds often seem to have high pain thresholds, and do not show signs of pain when other breeds might be very uncomfortable. An X-ray does not always show you how your dog feels, as many dysplastic Aussies are completely unaware that they have a problem.

Most recent statistics from OFA report an incidence of 6.5% of Aussies with HD from 9,712 evaluated. This sounds like a small percentage, but it is about 1 out of 15 which would be one in every two litters. This statistic comes from dogs owned by conscientious breeders and owners who use the OFA, and not the general population so this may be deceiving. To be a conscientious breeder, breed only OFA certified individuals and guarantee pups to be free from HD. Littermates and siblings are also important. An animal diagnosed as having HD should never be bred.

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A disease that can cause lameness in the joints of young dogs (usually from 6 to 12 months of age) is Osteochondritis Desicans (OCD). This is a degenerative disease of the joints, and is possibly associated with over-nutrition and too-fast growth of puppies. Treatment includes rest and/or surgery.

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The blood clotting process is extremely complex. If something goes wrong with the process, and a person or animal is unable to control the minor damage to blood vessels which occurs during the course of living, or even worse if they experience serious injury or surgery, the results can be extremely devastating. Von Willebrand's disease (vWD) is not common within our breed, but it does occur, and has proved fatal to more than one Aussie. It is inherited. In Dobermans 90% of dogs were carriers or affected with the disease at one time, by careful screening the occurrence has been reduced to less than 70%. Just one popular sire was found to be the source of the problem. Let's not let it happen to Aussies. In order for blood to clot it requires thirteen "factors" (handily numbered I to XIII) or proteins made in various parts of the body, calcium, platelets and von Willebrand's factor. Chemical signals initiate clotting and yet other factors oppose clotting, and encourage the clot to break up (hopefully) after it's served its intended function. Lack of one or more of the factors, a reduction in the number of platelets, or a loss of their cohesiveness, or an exuberance of action by the anticoagulants (or introduction of artificial anticoagulants - such as aspirin, warfarin or other rat poisons), can all lead to abnormal bleeding.

The three most common inherited conditions, in which deficiency of a single factor leads to impaired clotting or spontaneous bleeding, are hemophilia A (deficiency of factor VIII:C), hemophilia B or Christmas disease (deficiency of factor IX), and vWD (deficiency of von Willebrand's factor - vWF). While large hematomas may be seen more commonly with one of the hemophilias, vWD is more likely to produce chronic bleeding of mucous membranes (gums, gastrointestinal and urogenital tracts, nose bleeds) and skin, and may more closely resemble platelet deficiency. Both hemophilias are X-linked traits. Carrier dams will pass the condition to approximately 50% of their sons. Bitches are only affected if they received defective X genes from both parents. VWD is the most common of the three. In Aussies and most other dog breeds, the condition is inherited as an autosomal, incompletely dominant trait, with variable depth of penetrance, accounting for varying degrees of expression (type 1 vWD). A rare homozygous form is lethal, pups may be resorbed, born dead or die within a few days. VWD is exacerbated by concurrent hypothyroidism. Daily replacement thyroid medication may resolve clinical signs in mild to moderate cases. Abnormal platelet function and thrombocytopenia (low platelet count) may also accompany hypothyroidism, exacerbate the tendency to bleed and respond to thyroid replacement therapy. VWF is made by the cells lining the blood vessels. It forms a complex with the factor VIII:C. The complex acts as a precoagulant, speeding up clot formation. VWF is also necessary for normal adhesion of platelets to injured blood vessels, especially when blood flow is rapid or turbulent, and to attract further platelets to the growing clot.

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Hemophilia is a sex-linked genetic disease that results in deficient blood coagulation or clotting. The disease causes excessive bleeding which occurs spontaneously or upon slight injury. In normal blood coagulation, a complex interaction of plasma protein, called clottin factor, results in a gelatinous, fibrillar plug that seals leaks in damaged blood vessels; however, this is not the case for animals with hemophilia.

There are two types of hemophilia. Hemophilia A is the most common form of the disease. The animal lacks factor VIII of plasma proteins, retarding the clotting process. Hemophilia B, called Christmas disease, occurs when factor IX is lacking.  

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Aussies have a variety of problems related to the teeth and jaw structure. They are all probably polygenic and none are genetically related to the others‹in other words, there is no single ³bad bite² gene. The problems seen inn Aussies are as follows:

Undershot ­
the lower jaw extends beyond the upper, causing some degree of malocclusion (the teeth don¹t fit together properly.)

Overshot ­
the lower jaw does not reach proper length in proportion to the upper, again resulting in some degree of malocclusion. Both over and undershot jaws are relatively common.

Wry ­
One side of the jaw has grown longer than the other, causing it to ³bend² to one side resulting in alocclusion of the teeth in the front of the jaw. This is sometimes hard for people who haven¹t seen it to envision. Move your own jaw from side to side. Put it to one side and hold it there.. (Remember that a dog does not have lateral movement in its jaws as we do.) This is wry mouth. This one is very rare in Aussies (common in some terrier breeds) but there have been a few reports lately.

Missing/Extra Teeth ­
Dogs will lack one or more teeth, usually pre-molars. Sometimes there will be an extra pre-molar or molar.

Dropped Center Incisors ­
The two center lower incisors will be shorter than the others. Sometimes they will tip forward giving the illusion of a level or slightly undershot bite when viewed from the side.

It is not recommended to breed a dog with an over, under or wry mouth. The jaw is deformed and obviously the dog is carrying defective genes. Breeding a dog with these problems is a guarantee that you are giving a significant dose of those genes to its offspring. (Rather like breeding a dog you know is dysplastic.) If an unaffected dog produces multiple affected offspring, particularly from different and unrelated mates, you should withhold that dog from further breeding. Do not repeat breedings that produce these defects. The parents and siblings (full and half) should not be bred to near relatives and should only be bred to mates from families where the fault in question is not a problem.  

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General Information:
The developing fetus within the womb does not use its own lungs to mix blood and oxygen. Instead, it receives oxygen-rich blood from its mother through placental circulation. A blood vessel (the ductus arteriosus) in the unborn fetus bypasses the lungs to send blood to the rest of the body. Only a small amount of fetal blood flows through the lungs.

Normally, the ductus arteriosus closes within a few hours of birth. In some animals, the bypass does not close, and blood continues to bypass the lungs and not pick up oxygen. A human infant with patent ductus arteriosus is called a "blue baby."

This defect occurs more in Poodles, Collies, Pomeranians and Shetland Sheepdogs than in other breeds. Many affected pups die of heart failure within the first few weeks of life, but most pets that live to 8 weeks of age survive into adulthood. When the bypass is small, the dog may live a normal life without ever showing any ill effects. Patent ductus arteriosus also occurs in cats. Surgical closure is the only means of correcting patent ductus arteriosus. Medical therapy helps stabilize animals in heart failure only for short periods.  

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This condition is often referred to as a "liver shunt" but the current favored term appears to be portosystemic shunt. It has also been referred to by more exact terms, since there are specific types of shunts that vary slightly. The broad categories are extrahepatic and intrahepatic shunts, depending on whether or not the shunt occurs in the liver or outside of it. Specific types of shunts are patent ductus venosus, portal-azygous, portocaval (portal-abdominal vena cava), atresia (lack of development) of the portal vein and acquired shunts that occur due to changes in blood pressure or circulation.

Most shunts cause recognizable clinical signs by the time a dog is a young adult but occasionally, one is diagnosed at a later time in life. Since the severity of the condition can vary widely depending on how much blood flow is diverted past the liver, it is possible for a lot of variation in the clinical signs and time of onset of the signs to occur. Often, this condition is recognized after a puppy fails to grow, making an early diagnosis common.

Signs of portosystemic shunts include poor weight gain, sensitivity to sedatives (especially diazepam), depression, head pressing (pushing the head against a solid object), seizures, weakness, salivation, vomiting, poor appetite, increased drinking and urinating, balance problems and frequent urinary tract disease or early onset of bladder stones. If the signs of problems increase dramatically after eating this is a strong supportive sign of a portosystemic shunt.

It is frustrating, since there isn¹t one specific test for this condition. Although, there almost is one - special dyes are injected into the liver circulation, showing up on X-rays and can usually outline the problem pretty clearly. However, this is a pretty invasive test, making it a poor choice for "screening" purposes. There are a number of possible abnormalities that might point towards a portosystemic shunt on routine labwork, including low BUN (blood urea nitrogen), low albumin, mild anemia, increases in ALT (serum alanine aminotransferase) or ALKP (serum alkaline phosphatase). If these signs were present, it would be a good idea to test the serum bile acid levels prior to eating and after eating. If this test is supportive of poor liver function then it may be a good idea to consider ultrasonagraphy and dye contrast X-rays.

At the present time, Hepatic Porto-Systemic shunts are considered to be UNQUESTIONABLY genetic by some of the leading canine experts, but the mode has not been identified at the present time; research is being conducted at Michigan State University to identify this pattern.  

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Also known as idiopathic, genetic, inherited, or true epilepsy. There are no positive diagnostic findings that will substantiate the diagnosis. It is a case of ruling out every other possibility. The first seizure in a dog with primary epilepsy usually occurs between the ages of 6 months and 5 years. However, a diagnosis of primary epilepsy is not proof of a genetic defect; only careful breeding studies could prove that. The breed, the age, and the history may suggest a genetic basis for primary epilepsy if there is a familial history of seizures.

Secondary epilepsy refers to seizures for which a cause can be determined, and there are many. In dogs less than one year of age, the most commonly-found causes of seizures can be broken down into the following classes: degenerative (storage diseases); developmental (hydrocephalus); toxic (lead, arsenic, organophosphates, chlorinated hydrocarbons, strychnine, tetanus); infectious (distemper, encephalitis, and others); metabolic (such as transient hypoglycemia, enzyme deficiency, liver or kidney failure); nutritional (thiamine, parasitism); and traumatic (acute injury). In dogs 1-3 years of age, a genetic factor is most highly suspected. In dogs 4 years of age and older, seizures are commonly found in the metabolic (hypoglycemia, cardiovascular arrhythmia, hypocalcemia, cirrhosis) and neoplastic (brain tumor) classes.

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This is a generalized metabolic disease characterized by atrophy or malfunction of the thyroid gland. Clinical symptoms include obesity, lethargy, and/or coat problems. Affected animals may also have various reproductive problems, including irregular or absent estrus (heat cycle), and lack of fertility in both male and female.

Diagnosis of hypothyroidism is by laboratory tests measuring levels of T3 and T4 (produced by the thyroid gland) in the blood. Treatment consists of daily administration of L-thyroxin orally and, when successfully treated, the prognosis is excellent and the dogs life span is normal although the dog may require lifelong thyroid supplementation.

Aussies with Hypothyroidism should not be used for breeding.
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Discoid lupus is an immune mediated skin disease, it primarily affects the nose and face. The disease normally starts as loss of pigment around the nose. There may be scabby sores or just scaling of the nasal tissue. The surface of the nose may change from its typical cobblestoned appearance to a smooth surface. As this disease progresses it can cause deep sores on the borders of the nose where it meets normal skin and the sores start to progress up the bridge of the nose.

Some dogs seem to be really bothered by this condition and others show little reaction to the sores. Ultraviolet light seems to make the sores worse, so the disease may appear to be seasonal. It is more common in areas in which exposure to ultraviolet light is increased, such as high altitudes. If the depigmentation leads to sunburn, squamous cell carcinoma becomes more likely than in other dogs. Topical sunscreens can be very beneficial, although it is hard to get dogs to leave them on. Keeping the dog in during the peak sunlight hours is probably the most effective way to prevent excessive exposure to UV light.

Treatment depends on the severity of the disease. In many cases, topicaltreatment will be all that is necessary, using a orticosteroid ointment (Panalog, Synalar and others). It is usually necessary to use a fairly potent corticosteroid. Vitamin E supplementation is sometimes beneficial but can take several months to show much effect. Severe cases equire treatment with orticosteroids. It is possible that other immunosuppressive therapy such as gold salts or azathioprine (Immuran) could be beneficial but this is rarely necessary to consider. Because Lupus can be environmental, a dogs that produces it should not immediately be taken out of the gene pool. However, it is recommended not to breed dogs with the diease.  

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Canine demodecosis is an inflammatory parasitic disease of dogs, characterized by the presence of a high number of mites on the hair follicles, which often leads to a secondary bacterial infection. The mite, Demodex canis, is a part of the normal funna of canine skin and is normally preset in small numbers. The mite resides in the hair follicles and sebaceous gland of the skin. Pathologic changes develop for the mite infestation when numbers exceed that tolerated by the immune system.

There are two types of Demodex infestations: localized and generalized.

Localized cases occur in young dogs usually going though puberty. This can happen anywhere from 3-18 months old. It is a mild case, usually on the face. Patches of hair lost can also occur on the limbs or trunk of the body. Most cases (90%) resolve spontaneously with no treatment. This is not a genetic problem.

Generalized cases can occur in young or old dogs. It is a severe disease that causes hair loss all over the body. As hair follicles become distended with large numbers of mites, secondary bacterial infections are common, often with rupturing of the follicles. Dogs with generalized demodex must be dipped regularly to try and kill the excessive mites. In the worst cases, the dog would have to be euthanized. These dogs are thought to have a poor immune system that is unable to fight off the excessive mites. These dogs are NEVER to be breed.  

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Cryptorchidism is a condition affecting the dog in which one or both testicles do not fully descend into the scrotum. The condition may be presented in two forms:

1.) Unilateral cryptorchidism refers to the normal descent of a singular testis.

2.) Bilateral cryptorchidism results in the retention of both testes.

Due to the thermal suppression of spermatogenesis, bilateral cryptorchids are sterile while unilateral cryptorchids are usually fertile.

Cryptorchidism is estimated to exist in 6-8% of the canine population (Canine and Feline Endocrinology and Reproduction, Feldman and Nelson). It is a congenital anomaly which is described as a sex limited (occurs only in males) trait. Current research provides that it is probable that multiple genes are responsible for the condition of cryptorchidism. Dogs that are ryptorchid should be neutered and any sire or dam that reproduce it repeatedly should also be spayed or neutered.  

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