Episode 210: Using Screening Health Tests

Fran Smith, DVM, PhD, DACT discusses how to select breeding stock to help you improve your breeding outcomes.

Watch the video version of the presentation here.

Transcript

Nicole Engelman  00:04

Welcome to the Good Dog Pod. Join us every other Wednesday when we discuss all things dogs, from health and veterinary care to training and behavior science, as well as the ins and outs of Good Dog and how our platform can help you successfully run your breeding program. Follow us and join Good Dog’s mission to build a better world for our dogs and the people who love them. 

Welcome everyone officially to our Good Breeder webinar for this month, which is using screening health tests and conformation traits that impact your breeding program with one of our favorite guests, Dr. Fran Smith. Dr. Smith joins us today to share how to select breeding stock to help you avoid producing offspring with health and physical traits that impact both puppy health and marketability. So lots of things for us to dig into together today. Before we get to all that we want to, of course, thank Purina for helping us bring this webinar to you. We're really excited to dive into this topic today. We've heard from some members of our community that this was something that you're interested in learning a bit more about, and no better expert to join us here to cover it today than Dr. Smith. And as I always mentioned at the top of these webinars, we've hosted so many already this year. I know we're almost finished with April, but we've hosted at least two webinars a month in 2026 already, and we have years and years of webinar recordings as well that are all housed in the Good Breeder Center. So if this is your first time joining us, and you've never attended a Good Dog webinar before, we have recordings of every single webinar we've ever done to date, covering a wide variety of canine health topics. So we just want to remind everyone that that is always there if you're looking to poke around at things that we've covered in the past with different guests, because we've been doing this for a number of years now, and we've really built up such a treasure trove of content that I want to make sure everyone knows where that is, and I think those are all the housekeeping things. And in case there are people here that are new, I just want to share a little bit more about Good Dog for anyone who's unfamiliar with who we are: Good Dog is on a mission to build a better world for our dogs and the people who love them by advocating for dog breeders like yourselves, educating the public, and promoting canine health and responsible dog ownership. We are an online community created just for breeders like you to connect with quality Good Dog applicants from across the country and find forever homes for your puppies. We use technology to help breeders run all aspects of their program, so everything from getting your new litter of puppies listed, helping you market that litter, helping you get to know buyers through our platform, get payments securely, and all of those small things that kind of happen between puppies being born and going off to their new homes—Good Dog is really here to help support you in that and your buyers as well. And we also have a number of free educational resources, webinars, and events just like this. We have health related discounts too, to help your programs thrive in other ways beyond business management. So if you are not yet a member of our community, we would love to have you join us and learn more about our mission so you can do so at GoodDog.com/join. 

And last thing for me, before I pass things over to Dr. Smith, I just want to share a little bit more about her really incredible background in canine health, if this is your first time joining us for a presentation with Dr. Smith. Dr. Smith became a diplomat of the American College of Theriogenology in 1986. After a long career, Dr. Smith retired in 2023 from full time private practice as a small animal practitioner specializing in canine reproduction. She's one of few board certified theriogenologists in private practice. Her expertise in genetic counseling, chilled and frozen semen, and reproductive infertility of male and female canines is known throughout the United States. Dr. Smith maintains veterinary licenses in Minnesota, Mississippi, and Colorado, and she frequently speaks to breed groups, veterinary associations, and students and the general public—and the Good Dog community, I would add. She has been a guest with us for many, many webinars. We're so excited to have her back. So with that, I will pass things over to you, Dr. Smith, to kick off our presentation.

Dr. Francis Smith  04:19

Thank you very much, Nicole. I'm going to make one small change to what Nicole said about me. I just recently retired my Minnesota license because I knew I would never practice in Minnesota again. And all of those veterinary licenses are a significant expense. Anyway, so now it's just two states rather than three. So what we're going to talk about today is: I hope to teach you what you can do in examining your own dog and what tests to use to avoid producing puppies that A) are not healthy (that's the most important) but B) are likely to be rejected, either by brokers or buyers because of readily identifiable issues. 

So I am a DVM with a PhD. I'm a diplomat of the American College of theriogenology. Veterinarians have specialties, just like human doctors do. We have oncologists. We have kidney specialists. We have cardiologists. Theriogenology is the specialty that involves male and female reproductive behavior, and it is comparative, meaning it's all species. So I have worked on—not for pay—but I have donated my services to multiple zoos. I've worked on wolves, bears, gorillas, tapirs, tigers, a pygmy slow loris, and other exotic animals, and I believe I've been able to help the zoos and these animals out as well. That's a lot of fun, but it's always very, very challenging. So I am board certified, and as I say, theriogenology is comparative. But my practice in real life, earning an income, was small animals, dogs, cats—and actually, at the University of Minnesota, I taught goat reproduction. Breeder, owner, trainer, handler, and judge of Retriever breeds. I've had Labradors since 1970. I'm the president of the Labrador Retriever Club, Inc. I have been renominated. My three-year term is up in January of ’27 and I may or may not be re-elected. I'm the health chairperson for the Labrador Retriever Club, and I've been that since 1994. And I'm the president of the Orthopedic Foundation for Animals, the Canine Health Information Center, which is the world's largest animal health database. So screening health tests are used to minimize the incidence of known inherited disease. And just so you know, all breeds of dogs and individual dogs, and for that matter, each of us as mammals, carry some deleterious traits. The easy diseases to control are inherited in a simple recessive inheritance pattern. And I should also add “simple autosomal” meaning it does not involve sex chromosomes. So we're going to talk about these diseases first and then move to the more complicated ones, which afflict many dogs, many diseases, and are also breed traits that we select for. 

So a simple autosomal recessive—the simplest example is the PRCV form of Progressive Retinal Atrophy, which is seen in many breeds, including Poodles. Interestingly, the reason that we today have what was once called SURF, but now is called CAER (the Canine Animal Eye Registry) is due to the influence of a single Poodle breeder whose name was Dolly Trotner, and she was concerned because she had Poodles that lost their vision at a relatively young age, meaning seven years plus. In a simple autosomal recessive male and female dogs are equally affected, and any animal affected inherits two copies of the gene, one from each parent. I think it's important when we talk about genes and disease—this is not the place to play the blame game. This is an educational event and instructional image. You can decrease the numbers of animals that have problems, but it's no one's fault. No one set out to produce defective animals, nor do people set out to have children that inherit bad traits. Here's an example, another one, and actually through a very, very good case, juvenile hereditary cataracts are inherited in the Boston Terrier through an autosomal recessive pattern inheritance in the HS4F gene. What is particularly interesting about that to me: my granddaughter—I purchased a Boston Terrier for her—and these juvenile hereditary cataracts show up between 18, usually, and 24 months. And the breeder that I bought her from, at that point, this test was not available, and this young Boston developed cataracts under two years of age. And she was very important in my granddaughter's life and health, and as a result, she ended up having cataract surgery bilaterally before she was even four years of age. Now the good thing is, she did very, very well. My granddaughter was committed, because after care for cataracts is huge, but today you don't really have to have juvenile hereditary cataracts in Bostons at all, because we have a test for that gene. As we talked about, in order to have the cataracts actually affect the eye, she would have had to inherit one gene from each parent. Her name was Daisy. I don't remember her parents’ names. So Daisy got one copy of that gene from each parent. You can also get cataracts as a secondary complication seen with PRA, so those are not juvenile. Those are old age cataracts. 

So we talked about alleles, which are the genes that are affecting the occurrence of these diseases. A Normal allele—so we're going to call that a capital N for Normal. An animal with that has no disease risk. The genotypes, the combinations that you get when you breed animals, and N/N—it does not have that mutation we talked about. So that mutation cannot pass it on. And that becomes important when people talk to me about “But the grandmother was a carrier.” That doesn't matter if the dog involved is N/N. It’s Normal/Normal. It can't pass on the mutation because it does not have the gene for that. When you breed a Normal dog to a PRCD carrier, they look normal. They don't get cataracts, but they can pass the mutation to their offspring, and approximately 50% of their offspring will carry the gene for cataract. Now when we talk about percentage, you all need to know that those percentages and calculations are based on a litter size of 100. So we're not going to have litters of 100, so you could have a litter where none of the puppies develop cataracts, but yet one or more could be a carrier if one of the parents was a carrier. On the other hand, if you have PRCD, PRCD affected both genes, 100% of those dogs will develop the disease and pass the mutation to all offspring. So in the case of PRCD, which is a retinal disease that results in blindness, 100% of the puppies in that breeding at some point in their life (usually older age) will develop PRA and will become blind. The good thing—if there is anything good about PRA—is it does not hurt, unless they develop cataracts, then it's the cataract problem that is the issue. And additionally, dogs adapt very well to blindness.

Now, so you still want to do this kind of gene testing to make sure that you're not going to produce puppies that will go blind, or, in the case of Bostons, that will get cataracts at a young age. So again, with our breeding implications, clear versus clear. So they're normal to normal, there's no risk of affected puppies. Carrier to carrier: 25% of puppies would be affected, 50% are carriers, and there still will be 25% clear. The only way to know in the carrier breedings which puppies are clear versus not, is to do the genetic testing. And a clear versus a carrier: 50% chance of a carrier offspring, no affected puppies. And I'll use the color example in Labradors. If you have a black Labrador bred to a yellow Labrador, 100% of the puppies will carry the gene for yellow. But unless the black Labrador carries a gene for yellow, none of them will be yellow. So they will be carrying yellow. Examples of polygenetically inherited traits, which are the ones that we have to deal with on a more complicated basis are luxating patellas (which are also called slip stifles), improper bites, abnormal eyelids, hip dysplasia, and many other afflictions. Polygenetic inheritance is a type of inheritance in which a single trait—here we're going to say hip dysplasia—is controlled by multiple genes, each contributing in some kind of fashion that adds up to the phenotype, resulting in continuous variation. So I want to expand on that, because with being involved with the OFA, I will get people who will call me and say, “I bred two OFA goods. How is it possible that some of the puppies end up with hip dysplasia?” That is because there are multiple genes involved, and in that mixture, some could be dysplastic and some could be OFA excellent. But what is known with polygenetic inheritance is by breeding the best to the best, you tip the scale towards better and better. You're not going to totally eliminate hip dysplasia in dogs at this stage in our life, but you can certainly impact the incidence. Polygenetic traits typically follow a bell-shaped or normal distribution in populations. Most of the individuals will have intermediate, but there will be some extremes. If you were to look at the OFA database of the dogs that pass and realize the OFA database is biased towards normal because owners have the right not to submit the results of their testing, and many people elect not to. Now, I will tell you the best thing to do is submit all of your results, because that allows you to apply more selection pressure and will allow you to make progress towards better dogs more quickly. Polygenetic inheritance then explains the continuous variation of traits that are controlled by multiple genes with additive effects and environmental influences shaping the final phenotype. So I'm going to rely on Nicole to remind me to talk about the effective environment, particularly on hip dysplasia towards the end of this talk, where there really is some hard data that really gives us some information.

Conformation effects: Conformation is the shape or structure of something, especially in an animal. In dogs, we select the breed types, which is all about conformation. Conformation traits are such: erect ears, eye shape, width of nostril, length of tail, color, size, head shape, muzzling, bite, muzzle width, etc. When we select any of those traits, it's polygenetic. I'm sure you've all observed this within your litter of puppies. They don't all have exactly the same length tail, they don't all have exactly the same ear shape or set and then there's the whole additional pressure of conformation dog shows, which trends tend to vary a little bit, and we select for that as well. 

So let's first of all talk about mouth and the reason I say this, in my years as a practitioner, I would see a lot of puppies that were purchased from breeders other than the breeders that were in the circle, which I most operated. I showed dogs. So I would say, typically, members of a parent club. And so one of the most common things that I would see is abnormalities of the mouth or the bite. You should know that missing teeth have a polygenetic mode of inheritance. The Labrador Retriever standard says that missing teeth are a serious fault. Government pincher standard disqualifies dogs with a certain number of missing teeth. So these dogs that have missing teeth, if they are used in a breeding program, are more likely to produce missing teeth than a dog with full dentition, but all of their offspring aren't going to miss teeth. And hence, two dogs with normal dentition, still, in some categories and bloodlines can produce missing teeth. The typical bite for most breeds of dogs and all wild dogs, all of our wild canines—the wolf, the coyote, the fox—is a scissors bite, meaning the outer surface of the bottom teeth, which is called the jaw, the mandible, are in contact with the inner surface of the upper teeth, the maxilla. This mouth is the most efficient for catching, biting, chewing and consuming food. So if you think about it, rooted in development, it makes sense. In some breeds of dogs, a level bite is considered acceptable in their standard meaning the top and the bottom teeth meet straight on. The downside of that is that the mouth does wear on both the top and bottom teeth, but it is allowable and it is normal. So this happens to be one of my dogs, and this is a scissors bite seen from the side. As you can see, his big canine teeth interdigitate, and there's a groove there, which holds things, and his bottom teeth are just behind his upper teeth. That's a beautiful example of a scissors teeth. The canine teeth interdigitate, each of those incisors, and if you count those, those are the little teeth. A normal dog's mouth has six incisors—1,2, 3, 4, 5, 6, and then the two canines. Some breeds require an undershot jaw, where the lower jaw extends beyond the upper jaw, depending upon the degree, the tongue may hang from the mouth and the lower teeth may be visible. An undershot bite, even though the breeds allow for it, may contribute to health issues and dental disease. So does that mean if I saw a Pug or a Frenchie or a Boston, and the mouth was what we call a reverse scissor, which means the upper teeth were just behind the lower teeth—is that going to be problematic for the dog? Probably not, but I will show you some examples of mouths that are problematic. And me, as a veterinarian, seeing a puppy like this, would feel obligated to tell the client they could be facing some serious costs and issues with the mouth. 

Here's a cute little Frenchie—undershot, and this is the issue that I want to spend a lot of time on with you. It's called base narrow canines. Base narrow canines occur when the lower canine teeth erupt too vertically or are positioned too close together. It causes the lower teeth to hit the upper gums or hard palate instead of aligning properly. This condition is also called linguoverted canines. Puppies with base neuro canines may experience pain every time they close their mouth, which can affect eating, bite, and social interaction. 

On a different note—now I'm going to show you pictures of these with the amount of dental education that veterinary students get today. They're very aware of this condition, and they are aware of the issue that it can cause in puppies. So typically, a buyer of a puppy with that will get a lot of information on the costs and need of correcting that type of a bite issue. So this is a subtle example. This is the side of the mouth, and you can see that the canines, rather than meeting in that room, as they did on my black dog, that tooth is towards the middle of that dog's mouth, and there's a little hole. Now you can see that hole more clearly. And this dog's mouth is even worse in that his lower canine tooth is more towards the middle of his mouth. Additionally, this dog, if you look at the distance between the upper jaw and the lower jaw, there's a pretty good gap there. So this dog is significantly what we would call overshot. 

Parrot mouth is the most extreme version of base neural canines, in which the lower jaw (the mandible) is smaller than normal, particularly narrower with base neuro canines. Puppies with parrot mouths often require dental surgery to allow them to live comfortable lives, and thus veterinarians commonly will recommend being returned to the breeder for health reasons. So here's a real example of that. You can see how narrow that lower jaw is. You can barely see the bottom canine on that side. It's so far towards the middle of the mouth. Here's an example: the blue arrows point out the holes in the palette up there that those teeth are causing. And as you can imagine, that is very, very uncomfortable. I also want to point out to you, if you look at the ridges in this dog's mouth, the gray ridges, you will see that they line up very, very in a nice curve. They're very symmetrical. In this dog, you can see the huge hole where that canine was poking into the palate. But additionally, in the second row of ridges, you can see that there is not symmetry there, and the right hand side is slightly above the left. This is called a mismatched ridge. The ridges in the mouth develop towards the end of development in the fetus, and it is theorized that particularly in brachycephalics, dogs that have mismatched ridges are more likely to produce cleft palates in their offspring. 

Eye issues. Cherry eye is a prolapse of a third eyelid gland that produces tears. And the third eyelid is a thin membrane located in the inner corner of a dog's eye, and it contains a tear producing gland that is normally not visible. A prolapse of the gland can interfere with normal tear production and treatment of choice for cherry eye is surgical replacement of the gland. Cherry eye is heritable. It's polygenetic, so every puppy produced by a bitch or stud dog that has cherry eye is not going to have it. But in a perfect world, you would select your breeding stock for those dogs that do not have their cherry eye prolapse or pop. Cherry eye is common in many breeds of dogs, including Bulldogs, Frenchies, Pugs, Bostons, American and English Cockers. Believe it or not, I've seen it a fair amount with some Mastiffs and Great Danes. The old treatment for cherry eye was to surgically remove the gland, which certainly took care of the fact that you couldn't see this ugly red mass in the corner of the eye, but that did tend to decrease tear production, resulting in what we call KCS (Keratoconjunctivitis sicca) which requires lifelong treatment. So the treatment today—here's a really good example—is to make a little pocket in the tissue of that gland, pop it back in and close it so that gland is still in the dog's eye and can produce normal tears. 

Entropion is the condition where the eyelids roll inward, causing eyelashes and hairs to rub on the cornea. It causes pain, irritation, and potentially can affect vision. Severe, untreated entropion can result in blindness. Now we talked briefly previously about CAER (Canine Animal Eye Registry), which is housed at the OFA. Every year the ophthalmologist at their annual meeting, they have a huge health committee, and they tabulate all of the issues they have seen in dogs of each breed that year, and they decide which diseases primarily are vision threatening, and which ones, while a real issue (meaning they're not a normal eye), are tolerable in a breeding program. And diseases that fit that description are given in what is called the Blue Book, which comes from the ophthalmologist, a breeder option. Entropion is one of those diseases that is considered a breeder option, and it comes from loose skin on the head, droopier eyes, and hereditary or secondary. But it has a lot to do with eye shape. Primary entropy, and is usually genetic and seen in breed with specific face shape and skin folds. Secondary entropion—if a dog gets a weed seed in its eye and it's not taken care of, it can get a corneal ulcer, eye irritation, and can create enough inflammation that through contraction of the muscles of the eyelid, they can have what is called spastic entropion. The good thing about spastic entropion is once the irritant is removed, it resolves on its own. Here's an example of entropion, and the hallmark of this, this isn't a terrible one. We have lashes on the bottom hanging on the cornea. That dog's eye is always wet. And you may notice on your puppies or dogs that have entropion, that their faces are always kind of gooey and wet and they rub their eyes. There's another example. This is a Bulldog, and in this Bulldog, the outer portion of the eye, meaning the corner of the eye towards the ear, is pretty normal, but here we have what we call medial campus entropion, and the eyelid is rolling in from the nasal fold to about the middle of the eye. Now, actually, for a Bulldog, that's not the worst eye I've ever seen. So breeds at risk for entropion are Sharpays, Chows, Neapolitan Mastiffs, St. Bernards, and English Bulldogs. In really extreme cases of entropion, extensive, it's basically a facelift. Some of the Sharpay puppies that we used to see in the ’90s basically needed huge pieces of skin removed above their eye to open the lid up enough so that these puppies could really see. We don't see that as much anymore, thankfully. Other breeds that have entropion are Bloodhounds, Bull Mastiffs, Chessies, Goldens, Labs. Almost all of the brachycephalics have an increased risk. Treatment is surgical. So in addition to why do you not want that in your breeding program, you don't want your dogs to hurt. You don't want to produce puppies with that. And for the owners who get them and these puppies, surgical repair of these diseases is expensive, and you don't want a puppy to go untreated because the cost is so high that it is not a financial possibility for the owner. 

Hernias. A hernia occurs when there's a weak spot in the muscle or connective tissue, allowing an organ or tissue to push through. Umbilical hernias occur due a failure of complete closure of the linea alba, the midline, often at or very near the umbilicus. And I want to tell you a hernia does not occur because the bitch pulled on the umbilical cord too hard, because she stood up, the cord didn't break and she dragged the puppy around the whelping box. If the linea alba closes appropriately, you will not end up with a hernia. Mares often pull standing up, and that pull comes out with a thud, and believe me, there's a lot of pressure on the abdomen, like in horses, like in dogs, you don't end up with a hernia unless there's a defect in the linea alba. Hernias have a heritable basis and tend to increase in size in subsequent generations of breeding dogs. What that means is, years ago, I worked with a Shih Tzuh breeder who had definitely a hernia problem in her dogs, and she recognized that, but by selecting for other traits and ignoring the hernias, she reached a point after several generations where a percentage of her puppies were born with a hernia big enough that the intestines were outside the puppy, which is not compatible with life. So take hernias seriously. From a surgical standpoint, umbilical hernias are no big deal, and costs are not astronomical, but again, it is something you should strive to do, and you should be able to detect a hernia. You stand a puppy on its hind legs and it gets evolved near its belly button. That is a hernia. There is a hernia on an adult dog, and it's old and that if you felt that the object in the very middle is actually abdominal fat, which has gotten trapped there and now is stuck through the umbilical hernial ring. That's not going to hurt that dog, but that would be a good reason that that dog could be rehomed. 

This big bulge in the groin of this dog is what is called an inguinal hernia. These are really bad news, so we're going to talk a little bit about the inguinal ring. The inguinal ring is right where the hind leg joins the abdomen. It is the avenue in which the testicle comes out of the abdomen for the puppy, and down into the scrotum. And in females, nothing is supposed to come through there. But if a female has a big hernia, or she's pregnant or she's really active, her bladder or her pregnant uterus can fall through that hole. A herniated pregnant uterus is an emergency and can certainly result in the death of the female if they don't get emergency surgical care. So if you have animals with hernias, I encourage you to at least lift them up every day and check them carefully, visually. In the case of a male dog with an inguinal hernia, a piece of intestine may come through the ring or fat and end up in the scrotum. And you may think that this dog suddenly developed a giant testicle. It's not a testicle. So inguinal hernias are in the groin area, more common in female dogs. During pregnancy, the uterus may become trapped in the hernia, resulting in life threatening illness. I've also seen bladders entrapped in there. And in the male the intestine or fat may come through, resulting in a scrotal hernia. 

So we're going to spend the rest of the time talking about another polygenetic trait called patellar luxation. Again, patellar luxation is polygenetically inherited laxity of patellar ligaments causing luxation, meaning out of place, lameness, and later, degenerative joint disease. So I want each of you listening—I assume you're all sitting—flex and extend your knee and feel your patella, and the patella should ride in grooves at the end of your femur, which is the large bone in your upper leg. Okay? The reality is, there's nothing wrong with the patella that causes the patella to luxate. It's the way the rest of the hind leg is made. So if the patella is fine, it's the rest of the leg. So in the stifle anatomy, which we're going to talk about, we're going to talk about the femur, your upper leg bone, the tibia and fibula, which are the bones in the lower leg. The tibia is much bigger than the fibula. The patella—patella ligaments go up and down, and then within that stifle joint, we have lateral and medial collateral and cranial and caudal cruciate ligaments, all of which support that whole hinge device that makes the knee work. Patellar luxation involves complex inheritance from at least 15 different chromosomal regions. So you can see why it can happen and also why it's not an easy fix. There are two forms of patellar luxation: medial patellar luxation (the most common) and lateral patellar luxation (less common, usually in larger dogs). In the larger breeds of dogs, two breeds that have a fairly significant amount of patellar luxation are the flat coated Retriever and the Newfoundland. In Pomeranian dogs, the incidence of patellar luxation may be as high as 75% which is really frightening. What causes it? So here's where we're talking about the rest of the leg. Remember, it's not the kneecap. The pathology begins up by the hip. In normal dogs, the origin of the rectus femoris muscle is immediately adjacent to the hip. The quadriceps angle is formed between the axis of this muscle and the patellar tendon. Small increases in the Q angle cause medially directed vector forces pulling the patella medially. The opposite direction would be true for lateral patellar relaxation. So the earlier the luxation occurs in the dog (meaning the pull out of place), the more significant is the effect on function of the joint and how much arthritis that dog develops. Puppies with very severe patellar relaxation may require surgery early in life. Now, the trade off with that is they stand crouched. Their poor little kneecaps are way off in the middle, towards the center of their body, but their little bones, and because they're usually small breed dogs are like butter, and it's very hard to put pins or stabilize the knee, so oftentimes they have to deal with that until their bones become a little harder. Dogs that develop patellar luxation later in life may remain sound without intervention. 

So again, let's talk about that from the standpoint of the practitioner who gets a dog and it's eight months old, and it's been for a normal exam, and it's part of a physical. Typically, patellas are examined. If the dog has a grade one patellar luxation and it's not lame, it's likely to be fine for life. And I will say to the client, this dog has kneecaps that are not normal, but it is likely it will be fine for all of its life. However, there is a risk that at some point it will become lame due to its kneecaps and may need surgery. So not an alarmist, just an information. The OFA patella database is open to a dog of any breeder combination of at least 12 months of age. Very, very, very young puppies—everything on very young puppies is very loose. So I would be reluctant to say that many puppies have really bad patellas. Many of them are kind of loose at eight or nine weeks and tighten up and are normal. The examination for patella may be performed by any licensed veterinarian. This is a skill that is taught in veterinary school, even if people are not intending to do, meaning veterinarians, patellar exams on small animals. And it's performed on the standing dog, typically without sedation. I stand the dog so that it's relaxed on a table and it's not slipping. You simply pick the dogs up, which flexes the knee, and then bring it back down to standing on the surface, which is extension. Again, it needs to be on a non-slip surface. If a dog is profoundly nervous, the exam may be difficult because you could misinterpret what's going on. If the patella can be moved while the dog is standing, meaning without flexing or extending the leg, it has to be graded at least grade three. And there are four grades of patellar luxation that are applied to both medial and lateral patellar luxation. 

Grade one, when I bring that knee up and down, the patellar easily slides off to the inside when the leg is extended, but comes back to normal position when I let the dog put its leg down. The dog is typically not lame. Fortunately, a lot of the patellas that we see are grade one. Grade two, there's more frequent patella relaxation, which may become more or less permanent. The dogs learn how to deal with that, because when the patella isn't where it should be, the dog can't straighten its leg. So you may see dogs that go along and then all of a sudden hop and kick out their leg. What they're doing is they're jiggling their kneecap back to where it needs to go. The dog may or may not be lame. Many years ago, during the Westminster Dog Show, I watched the Terrier group, the dog who ultimately won the group, when I saw her on the table, and her handler put her on the table, you could see—although I'm sure the camera didn't intend to do this—her patella pop off to the inside. He set her down, she kicked out her leg and went off, and she did, in fact, win the group, so many dogs can adapt to that, but it's certainly not ideal. In grade three, the patella is permanently luxated; the tibia is bent and the tibial crest is deviated between 30 and 50 degrees from the cranial caudal plane. Flexion and extension of the joint causes abduction and adduction of the heart. So what do these dogs do with really, really bad patellas? They change some of the motion to their hock joint, and they do strange things at the hock. In grade four, the tibia is medially twisted, and the tibial crest may show further deviation, with the result that it's 50 to 90 degrees from a cranial cauda. The patella is permanently luxated. The leg is carried, meaning, if it's on one side, the dog doesn't use the leg, or if it's both, the dog stays crouched like it's trying to stand up and the leg is flexed. 

What are the risks by breed? In order to understand risk, one needs to understand incidence and odds ratio. So incidence is: how frequently do you see a disease in a population? And that is heavily influenced by areas of the country, the population of people owning the dogs, etc, etc. Odds ratio is: how likely are your new dog—we're going to call it a Smith dog—how more likely is the Smith dog to have a luxating patella than “the normal dog,” which is an odds ratio of one. Odds ratio is a statistic that quantifies the strength of the association between the breed of the dog and patella luxation. So one is normal. If you have a one, you are no more likely to luxate your patella than any dog of any breed. Incidence, again, is occurrence rate or frequency, and incidence even in the OFA database, is underestimated, because most people do not report abnormal results. Here we're going to talk about the docs and old OFA data, indicate 7.1% affected with patellar luxation. The newer data shows that we have 4,027 Dauchshunds in the database, with patellas at 96% normal. Now is that likely? Remember, many people don't register abnormal data. Why is that important? If you use the vertical pedigree feature on the OFA website, you can compare dogs to see how strong the strength of their orthopedic soundness is compared to another dog, and my example would be you have a Dachshund with normal patellas. You look at the vertical pedigree, his parents have normal patellas, and you go one more generation, all of which is easy to do, and his grandparents do. Then you compare another Dachshund, and he's normal, but his father is normal and his mother's patellas are not. Obviously the first dog, the more depth of normals that you have, the more likely that you are to have normal patellas in the offspring. In the Chihuahua, the old OFA data was 5.5% incidence. The current list is 4,817 with 94% normal, 6% not, but if you look at the odds ratio in the veterinary literature, you will see that if you are a Chihuahua, you have an eight time increased risk of having patella problems than a normal dog. So I want to show you this picture, because you can see the patellas, which look like those little almond shaped objects right at the end of the femurs, which are the big bones. The big bone right in the picture on the side that says R, which is right, the skinny little bone is the fibula, and the bigger bone there is the tibia. And you can see that there is some curve to that tibia. The more curve there is to that tibia., you increase that stress on all those angles that we talked about. So you want to try to have nice straight legs, which should be instinctively obvious. The Maltese—older data lists 5% affected, and now our data says 96% normal; odds ratios on two different sites lead about two times more increased risk to six and a half percent increased risk. Yorkshire Terriers: odds ratios for them is 7.8 or 8.3 but the health survey that was filled out in 2006, only 2.6% of the people who filled out that health survey said that their dogs had bad patellas. Probably is closer to this 23.8; it is much closer to the effect of not having very good patellas on a large population. The Poodle: Toy Poodles currently now say 97% are normal, but odds ratios are 9.7 so a Toy Poodle is almost 10% more likely to have trouble with its knees than just a dog. Mini is 4.1 and standard poodles 3.2. That is the end of my slides. Do we have time for questions?

Nicole Engelman  52:00

We do. I just had a note here to make sure I reminded you about talking about environment on the effects of hip dysplasia. 

Dr. Francis Smith  52:08

Thank you very much. Let’s do that first. So people say, or breeders will say, or a client will say to me, “I bought a puppy and now it has hip dysplasia, and the breeder is telling me this is all my fault because of the way I fed it or the way I allowed it to exercise.” Hip dysplasia has a very, very high genetic basis. It can be influenced by environment. There have been two very, very good studies. The first one was in German Shepherds, and it's a long time ago, and they had a colony of German Shepherds that genetically was very, very geared towards having terrible hips. So in this study, they knew the genetics already. They divided groups of puppies up, and they severely restricted calories. I don't mean they starved these puppies to death, but they kept them profoundly lean, and they restricted exercise. And they found that while those puppies still ended up with an increased risk of hip dysplasia, the severity of the hip dysplasia was decreased. So environment can make a genetically based disease worse or not as a parent. Now, in my own breeding program, and I get criticized for this, but it's my right to do so, and I'm happy to share it. I breed Labradors, and as you all know, Labradors like to get fat. I've been doing OFAs since the ’70s, and I overfeed my puppies, meaning I let Labrador puppies pretty much eat what they want, which is too much food, and I let them exercise to whatever level they want. I let them play with big dogs. I let them go up and down steps. Why do I do that? I don't want to mask something that has a genetic basis by controlling the environment. Now that being said, I don't intend for them to get hurt and I don't want them to have hip dysplasia, but if I were to restrict their calories severely and not allow them to exercise and play, I could potentially mask some degree of dysplasia. So I think that's an important thing to understand. I will also tell you that puppies on vinyl floors and slipping when they're four, five, and six months old, that's not going to make a dog dysplastic that wouldn't have been otherwise. So I think that's just important for all our breeders to know. Thank you, Nicole.

Nicole Engelman  55:04

Oh, of course. I'm glad you're able to cover that. Is it okay if we go over just a few questions?

Dr. Francis Smith  55:10

Absolutely, I have plenty of time.

Nicole Engelman  55:13

Okay, great. Thank you. I thought this was an interesting question, especially for breeders that are in, you know, the dog show world, or really, for any breeders: do you ever see breeders overlook any structural faults, often because the dog just looks pretty or everything looks okay?

Dr. Francis Smith  55:31

Absolutely, there is absolutely no question that that happens. I would say, relatively frequently. When it comes to a health issue, my recommendation is—particularly, we're talking here about keeping breeding stock—and I'm going to say if this puppy was ugly, rather than had the prettiest head you've ever seen on an English Cocker Spaniel puppy, knowing what you know about its genetics, would you keep it? And if the answer is no, don't keep it. Don't keep it, because it's just beautiful. Dogs have to function. So yes, that definitely happens.

Nicole Engelman  56:15

Great. And then this is a kind of a similar question for breeders who might be just a bit conflicted about how to balance structure and health testing with temperament, and where they should compromise if they have to?

Dr. Francis Smith  56:30

Well, that's a really difficult question. I do not believe you can ever compromise on temperament, because our dogs today live with us as family members, in many cases, bed mates. So you have to have dogs that are stable like people and can survive in our crowded, busy environments. Temperament, temperament, temperament, health, and last, but very important, I show dogs that I have champions. I want them to be beautiful, but I would rather have a fabulous temperament, genetically sound dog, than a spooky Labrador or a Labrador who doesn't get along with other dogs in a heartbeat. absolutely, I would say, never compromise on temperament. And the temperament of the mother is very reflected in the puppies, because puppies start hewing off their mother's behavior way earlier than we ever appreciated.

Nicole Engelman  57:44

Great. Thank you for answering that one, and I agree with that perspective as well. We had some questions come up about conditions that show up later in life, like degenerative myelopathy or late onset cardiac issues. How can breeders plan for things that they can't even see yet? If that's possible.

Dr. Francis Smith  58:03

That's a great question. So degenerative myelopathy is a very complicated disease, and typically the dogs that get DM are elderly, and I mean elderly. Now the other thing that is complicated about that: the genetic test for DM is based on risk assessment. It is not a single gene. So even though a dog has two copies of the gene for DM, it does not mean that that dog will develop paralysis, inability to use its rear end at any time in its life, and until very recently, the only definitive diagnosis of DM was an autopsy looking at the spinal cord. So while I encourage DM testing, I would not discard a dog that had everything else about it, that had two copies of the DM gene, because it's risk assessment. And the DM gene exists in almost all breeds of dogs, yet the clinical signs of DM really are only seen in a few. Now, PRA is a late onset disease. You could argue both sides of that coin in that if a dog has PRA and goes blind, it's usually eight plus, and it doesn't hurt, but our dogs live longer and longer now. So again, in a perfect world, you would not want to have a dog with two copies of the PRA gene. We also have enough dogs now that we don't need to use affected dogs with PRA in breeding programs in order to maintain genetic diversity.

Nicole Engelman  1:00:12

Great. Thank you for answering that one. I agree it was a great question. Lots to think about there. For our last two questions, they're both about luxating patellas, which I know we kind of close this presentation with. At what age can you reliably evaluate patellas? I've heard conflicting advice about waiting until 12 months versus doing it earlier.

Dr. Francis Smith  1:00:33

Twelve months. And the reason that I would leave it at 12 months is that's the accepted age at which you can continue patella sound, and those criteria are developed through the other veterinary specialties. In the case of patellas, it was designed or approved, recommended by the surgeons group. So prior to that, you could have a puppy that has sound patellas at six months that, at eight months, still has bilateral luxating patellas. But at a year, most of the small breeds, which is where patella luxation occurs, have done most of their growth, and that's the reason.

Nicole Engelman  1:01:15

Great. That actually brings me right into my last question. So luxating patella rates, of course, in smaller breeds/toy breeds, are really high. Is it realistic for breeders of these breeds to think about breeding it out, or is the goal just to reduce severity? Because I know those could be two very different things for breeders.

Dr. Francis Smith  1:01:34

In a perfect world, we'd like to breed it out, but unless we can actually identify each of the genes that cause them, it's unlikely that it'll happen in our lifetime. Again, I would minimize the risk. Certainly I would never—if I bred toy breeds—keep a stud dog that has luxating patella. Not that girls are less important, but males can produce so many more offspring than females; they have a bigger impact on whether it's your kennel or your breed. So certainly you want boys that have sound, sound, sound patellas and then keep girls from the best litters that you have. So say you had a litter of six, I'm going to say Lhasa puppies, and one of them had bad patellas at nine months, and you heard this somehow, and the other five were fine. A puppy from that litter is an ideal choice. The more depth of normal you can get, the better you're going to do, but we're not going to make it zero. And again, the good thing with patellas is most of the grade one dogs will never need an intervention.

Nicole Engelman  1:02:52

Great. Thank you for answering all of those. I think that was the last question we had, but we can't thank you enough for doing this for us again. This was so great. So thank you again. Dr. Smith.

Dr. Francis Smith  1:03:02

Thank you very much!

Nicole Engelman  1:03:03

Of course, and thank you so much to our community for joining us as well and asking such great questions. I will leave everyone with just a little sneak preview of what we have coming up in May. So our next webinar is a two part series with Dr. Adam Boyko, and Part One of the Coefficient of Inbreeding will be on Wednesday, May 13, at 1pm Eastern. So we will be getting invitations out for that. You can RSVP, all of those things, but we'll just leave everyone with that preview. Well, we will get the recording of this shared in our Friday newsletter as well, so everyone can re-watch this and yeah, thank you so much again for being here, and we'll see you at our next webinar. Bye, everyone. Thank you.

Dr. Francis Smith  1:03:43

Thank you.