canine health

"Do we really know if dog breeds used to be healthier than they are today?"

Even as I’m focusing my energy on creating my breeding project website, I still remain prone to writing lengthy comments in FB discussions about dog breeding. This is an adaptation and expansion of one of those comments. It’s obviously not an article with citations, but rather my thoughts on an interesting and frequently raised question. I thought I would share it for the sake of giving y'all some brain fodder to mull over and to provoke discussion. 

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A question that’s often raised in the discussion of genetic health in dogs is whether we definitively know that dogs today are more sickly than they once were. 

This question is actually a red herring in the wider discussion of breeding and genetic health. 

Since there’s no good data on the disease prevalence of the dog breeds of the past or measuring disease prevalence in breeds over a significant amount of time, it’s an unanswerable question. In many situations where this question is raised, the fact that we can’t definitively answer this question is actually the point of raising it. This is because it shifts the focus of the conversation to the presumed importance of monitoring disease prevalence in specific breeds instead of addressing the basic, undeniable fact that congenital disorders DO have a genetic basis and CAN be effectively prevented with proper breeding techniques. 

It also suggests the possibility that purebred dogs are “supposed” to suffer from a certain level of genetic disease. This is, of course, an unfounded belief as we know that breeds of other animals exist without the alarmingly high rate of disease found in purebred dogs. 

Further, it potentially suggests that the breeding techniques of yesteryear are something to be held up on a pedestal. The fact remains that the earliest dogs of our breeds may not have been more or less healthy because of the methods used by the breed founders but perhaps in spite of them. After all, the basic principles of dog breeding, such as the concept of blood purity and breeding only the best as a means of improving the breed, have remained largely unchanged in mainstream dog breeding culture to this day. Some of the specifics, like the implementation of genetic health and diversity testing, have changed, but the underlying principles are essentially the same as they were a century ago. 

The truth is that the lack of data on the health of the dogs in the past is irrelevant as even today, there’s not really reliable data on the prevalence of health problems within particular breeds. Most of what we know is self-reported data from breeders in breed health surveys (hardly complete, certainly not randomly selected samples, and arguably biased) and a couple of datasets collected by veterinary hospitals (which only record the number of reported cases of diseases and do not evaluate what percentage of dogs within a breed have those diseases). 

However, what we DO definitively know is that an increase in homozygosity, caused both by inbreeding and other factors like genetic drift, creates an increase of disease expression and a decrease of fertility, lifespan, and immune function. Most of the studies on this are done on livestock (Wright first formulated the COI in the early ‘20s based on livestock studies), but the principles are the same in dogs. There are a few studies in dogs which corroborate these findings, all of which are available on the ICB website. 

Ultimately, I think too many breeders get caught up in trying to assess disease prevalence rather than simply applying known principles of genetics to guide their breeding practices. Once a genetic disorder becomes a noticeable problem, the gene pool is already going to be full of carriers, making those disorders impossible to “breed out” without reducing genetic diversity so much that another disease becomes a problem. This is what happened with Basenjis when breeders were overzealous about eliminating carriers for PRA from the gene pool, inadvertently causing Fanconi Syndrome to become a fixed trait and requiring an outcross to COO dogs to save the breed. With immune diseases, the problem is even worse, as immune health is founded in the diversity of DLA haplotypes rather than the absence of specific deleterious alleles. Once you lose enough of that diversity to cause immune disease, there’s no way to get it back without opening up the gene pool and widely disseminating the genes of many crossbred dogs to even out allele frequencies. No matter how much data you have on disease prevalence, it’s irrelevant as it does not facilitate the improvement of breed health in and of itself and typically comes only once it’s too late to utilize any simple solutions for the problems that have appeared. 

Ideally, breeders SHOULD focus on crisis prevention and not damage control. Of course virtually no breeders do this and the way registries and clubs are currently run make it all but impossible for breeders to attempt it even if they wanted to. Closed studbooks, strict breed standards which often vary from country to country, and differing regulations on what can be registered as “purebred” are huge obstacles to restoring and protecting genetic diversity in dog breeds, which have effective population sizes so small that maintaining a closed gene pool forever is impossible. 

For some breeders, there will NEVER be enough research or data to justify crossbreeding for improved health. This is a huge problem in Italian Greyhounds, which suffer from more immune diseases than any other breed. IG breeders continue to chant, “We need more studies before we change our breeding practices,” while the small window of ability to save the breed continues to close. Empirically proven methods for reducing the incidence of genetic diseases in animals are already well-studied and widely applied in other animal breeds and species, but they are intentionally ignored by the breeder community who insist that somehow, a vast body of breed-specific research is necessary to make smart breeding decisions. The truth is that nobody actually wants to change their traditional mindset and practices regardless of what modern science indicates. They simply want to find data to justify their presuppositions about breeding, and they will wait until hell freezes over to get it. 

Lack of data is NOT the problem. Lack of scientific education, a refusal to apply all of what modern science has taught us about genetics rather than picking and choosing bits to support traditional practices, and an unrealistic determination to cling to outdated breeding principles as though they were quasi-religious truths transcending time and culture are the REAL roots of the problems our breeds face.

youtube

Bloating Akita caught on film. 

A must watch for dog owners. Know the signs; it could save your dog’s life.  

Canine Growth Plate Closures Diagram (Average Time in Months)

The various and assorted time the bones which form the joints of puppy’s limbs will stop growing, begin to fill in and finally mature. Science has provided us with the average times for growth plates to close.

Image source: Racine Hyatt, Racine’s Dogworks Allfit Puppies Facebook page (20 Sept. 2013). See her 27 Sept. 2013 post (and this one) for the physical effects of early neutering/spaying (ie. refer to the diagram “to see which growth plates have closed at the time of neuter and which will experience continued growth”).

Brief Musings on DLA Haplotype Diversity and Distribution

What a title, am I right? :P

I’m doing some research into canine immunogenetics right now, and re-read the chapter on immunogenetics in The Genetics of the Dog ed. Ostrander & Ruvinsky to brush up on some concepts. While I was reading through it again, some statistics on DLA haplotype diversity and distribution which I had forgotten about caught my eye. Here’s a quote from page 106 of The Genetics of the Dog:

There is clearly much diversity to be found in semi-tame and feral street dogs, as has already been demonstrated in Bali street dogs (Runstadler et al.,2006). […] These dog populations are more outbred than most domestic dog breeds, and this is demonstrated when we assess the number of different haplotypes found in each group (where n = 50-100 dogs) and compare the frequency of the most common haplotypes. The highest haplotype frequency is around 12%, and there are, on average, 15 haplotypes with frequencies of 2-10%, with a further 30 or more haplotypes at lower frequencies.

Since street dogs are subject to much stronger natural selection and virtually no artificial selection compared to purebred dogs, the make-up of their MHC provides insight into the level of genetic diversity required to create a the ideal, healthy, highly effective canine immune system. The key to making the immune system work is the presence of many varied DLA haplotypes with relatively even distribution throughout a population. The fact that genetic diversity in and of itself, rather than deleterious alleles, can make or break the immune system is part of what makes immunogenetics so fascinating to me.

Later in the same chapter, there’s a brief discussion of the high degree of genetic diversity found in Salukis which is also interesting. The Saluki has the most DLA haplotypes found in any breed. One study found 31 haplotypes, while the analysis referenced in The Genetics of the Dog found 28:

There was one major haplotype at a frequency of 37.9%, plus 12 haplotypes with frequencies of 2-10%, and a further 15 with frequencies of <2%. The majority of atypical haplotypes occur in at least two dogs, and often in 4-7 dogs.

The Saluki is a good example of the kind of genetic diversity that remains possible even when breeding for specific traits. The two are not inherently mutually exclusive.

In stark contrast to the healthy diversity of the street dog is the genetic homogeneity of the Italian Greyhound, which suffers from the highest number of immune-mediated diseases of any known breed as a result. According to the research done by UC Davis, the breed is split into two genetically distinct subpopulations of American and European dogs with slightly different DLA haplotypes and allele frequencies. Together, the two subpopulations have 18 DLA haplotypes, with 5 of these being unique to the US and 4 unique to Europe. 

Of the two groups, the American dogs are slightly more diverse and have somewhat more evenly distributed allele frequencies. Of their 14 DLA haplotypes, 2 have a frequency >20%, 2 have a frequency of 10-19%, 5 have a frequency of 2-9%, and 5 have a frequency of <2%. Their most common haplotype has a frequency of 21.5%, and the second most common a frequency of 20.1%. All of the 5 haplotypes that are unique to the US subpopulation are very rare, with a frequency of <2%.

The European IG population has 13 known DLA haplotypes with a notably uneven distribution. 2 of these have a frequency of >20%, 1 has a frequency of 10-19%, 4 have a frequency of 2-9%, and 6 have a frequency of <2%. Their most common haplotype has a frequency of 31.5%, and the second most common a frequency of 24%. All of the 4 haplotypes that are unique to the European subpopulation are exceedingly rare, with a frequency of <1%.

Altogether, there’s a vast divide between the high level of DLA diversity and fairly even distribution found in the street dog and Saluki, and the highly homogeneous, skewed statistics of the IG. Even with the two subpopulations combined, the IG doesn’t even come close to the benchmark of natural canine genetic diversity. The implications of this are the subject of the article I’m currently writing, which will focus on IG health problems and their possible solutions.

In the meantime, enjoy some more tasty statistics from The Genetics of the Dog on DLA haplotype distribution in dog breeds:

I’m making this PSA because my dog recently had infected anal glands and they caused him a lot of pain. Scooting can also be a symptom of other problems, like parasites, intestinal issues, or worse. So please don’t think lightly when your pup scoots. Take them to the vet to get them checked out. It’s better to be safe than regret not doing it sooner.

Canine Vaccinations

This is an excellent source of information regarding canine vaccines. 

So the core vaccines for dogs in the UK are given in the DHPPi shot. Here’s a general summary:

Canine Distemper: 

Spread by all bodily secretions, e.g. saliva. Dogs of all ages can be affected. Symptoms include fever, coughing, vomiting, diarrhoea and discharge from eyes and mouth. Mildly affected dogs will recover, but some will go on to have neurological problems in later life, for instance the degeneration of the nervous system as well as seizures. Nonlife-threatening symptoms include the thickening of the skin on the paws pads and the end of the nose.

There is no specific treatment; however intravenous fluids can be given to prevent dehydration and medication can help to control seizures. Quite often, in old age, the dogs are euthanised as their quality of life is low due to the deterioration of motor skills. 

Canine Infectious Hepatitis (aka canine adenovirus):

Spread by contact with the saliva, urine, faeces, blood or nasal discharge of infected dogs. The urine of an infected dog can be infectious for up to a year! The disease replicates in the tonsils after being contracted through the nose or mouth. It then goes on to infect the liver and kidneys. Symptoms include lethargy, coughing, fever, vomiting and diarrhoea, jaundice and abdominal pain. 

The symptoms are each specifically treated, there is no one treatment. 

Canine Parvovirus:

Caught by contact with faeces from infected dogs. Mainly seen in puppies between six weeks and six months of age. Common symptoms include severe vomiting and bloody diarrhoea causing dehydration. Puppies are left vulnerable to other infections due to a drop in white blood cells. Infected dog may be put on a drip and given antibiotics to prevent any secondary infections. In my experience the puppies are quarantined to prevent infection to other animals.

Canine Parainfluenza:

A highly contagious respiratory virus that infects the respiratory tract. Symptoms include loss of appetite, nasal discharge, coughing, lethargy and fever. Antibiotics can be used to treat the disease, but if the symptoms are mild it can be left to run its course, like a cold in humans. 

Leptospirosis:

This disease can be transmitted between humans and animals. The main source of infection is via infected urine, or by contaminated water, so dogs are at risk if they swim or drink from stagnant water or canals, especially in areas with high numbers of rodents.
Symptoms include fever, lethargy, increased thirst, vomiting, bloody diarrhoea and jaundice. Treatment involves antibiotics and intravenous fluids and supportive treatment. An infected animal’s urine is an infection risk to humans too. 

I was browsing through some of the comments on the ridiculous Say No to Mutt Breeders FB page, and while it’s easy to just laugh (or inwardly cringe) over how wrong some of them are, this thread caught my eye. I wanted to write a serious explanation about why the second commenter’s reasoning is incorrect because it’s a very common argument against crossbreeding that I hear all the time, but it has no foundation in science.

This will get very long since it involves explaining some of the basic principles of population genetics and how they apply to dog breeding and dog breed health. This post assumes you’re familiar with basic genetics terms and concepts. If you’re not, I’d highly recommend reading this basic introduction to genetics and this glossary of basic genetics terms which both use dog breeding examples. I’ll also link to additional articles and research studies throughout this piece for those who want to read more on the concepts addressed.

Without further ado, here is the long answer to this common question:

Is crossing two breeds more or less likely to produce health problems than breeding two purebreds?

Keep reading

Is Your Sighthound Fat?

Sighthounds are not built like non-sighthound dogs. Not many people are aware of what a fat sighthound looks like, since an ideal weight sighthound looks emaciated by normal dog standards! So here’s a quick visual guide.

(Image from: Sighthound Underground: Does this martingale make my dog’s butt look big?)

Although individual dogs are different and there is no one weight that is good for all dogs of a certain breed, here are a few things to look for in judging your sighthound’s weight:

On an ideal weight sighthound, you will be able to:

-See several of your dog’s ribs, and some of their spine.

-See the tips of the hips.

-See a well-defined tuck in the waist.

Here’s some examples of ideal vs. obese sighthounds:

Ideal Greyhound:

Obese Greyhound:

Ideal Greyhound:

Obese Greyhound:

(From: Greyhound Crossroads: How to know if your Greyhound is at the proper weight)

As with any other type of dog, obesity in sighthounds can lead to numerous health problems. Although uniformed people might accuse you of starving your pet (happens all the time to me), keeping your sighthound at a good weight is vital to her health and well-being! Pet obesity is a huge problem with over 50% of dogs in the US being obese as of 2012. Don’t unintentionally contribute to this statistic with your lovely lithe sighthounds.

In 2012 there was a fascinating study done in dogs with lameness from osteoarthritis. […] So, what did the study investigators find?  Well, they found that in almost 40 per cent of the cases, there was a placebo effect on the owner.  That is, when dogs were given a treatment that didn’t do anything (placebo), nearly 40% of the time, the owners thought that the treatment was effective.  And for veterinarians, it was worse, that is, when veterinarians examined dogs at the walk, or at the trot, or examined them for signs of pain to feeling (palpating) the joint, nearly 45% of the time, the veterinarians were sure that the dogs who received nothing were improved.  And, the effect got more pronounced with time.

What about the dogs?  Well, the dogs remain unchanged. […]

The changes were in the observers.  All of the “improvement” was in the eyes of the owners.  Or in the eyes of the veterinarians, (who, among other interests, had a stake in the success of the treatment).
— 

Dr. David Ramey, “If You See “Results,” What Else is There to Say?David Ramey, DVM (1 September 2015).

Here’s the thing: I’m not here to tell you that you’re doing anything wrong, I’m just trying to open your eyes to the possibility that what you’re doing may not be necessary.

The study mentioned in the quotation is:
MG Conzemius and  RB Evans. “Caregiver Placebo Effect for Dogs with Lameness from Osteoarthritis”. J Am Vet Med Assoc. 2012 (241.10): 1314-9.

Which dog breeds are the healthiest? It's a trick question!

This is a response to this prompt on the Canine Debate Forum: “What in your opinion is the most genetically healthy breed? The least healthy? What major health concerns does your breed of choice suffer from and how would you as a breeder go about fixing them?”

I got carried away and ended up writing a massive overview of why it’s difficult to classify which breeds are the most unhealthy and the reason why in the grand scheme of things it doesn’t really matter anyway due to the way genetics work. Since it got too long for me to post in good conscience on FB, I’m turning it into a blog post instead. Apparently I get too excited when writing on this topic! :P

The following overly long spiel is me trying to speak from an objective (scientific) rather than a subjective (anecdotal) standpoint like most of the responses on this thread, so it will get long and complicated and thick with genetics terms. :P

I think it’s misleading to label any breed “most/least genetically healthy.” A more accurate term would be “phenotypically diseased.” The former label wrongly suggests that some breeds simply have fewer “bad” genes than others, and so they are naturally more healthy. It also leads to the overly simplistic, scientifically inaccurate conclusion that in order to eliminate congenital disease from a breed, all you have to do is create a test for each disease and then breed away from disease-causing genes. Genetic health is much more complex than this, and not so easily measured.

Even when altering the label to “phenotypically diseased,” it’s a virtually impossible question to answer because it’s so nuanced. What makes a breed more or less healthy than others? Is it the overall number of known disorders in the breed? Is it the average prevalence of these disorders? Do we weigh different diseases differently since some are more lethal and untreatable than others (i.e. DCM is a much graver health concern than color dilution alopecia)? Does average lifespan and litter size figure into this equation somewhere? Are polygenic and monogenic disorders rated differently since the latter is easier to test for and avoid? Are the diseases with available genetic tests weighted differently than those without them since breeders can more accurately identify carriers? Should immune mediated disorders and diseases which become “fixed” be weighted more heavily since they’re impossible to “breed out” without crossbreeding? How do you rate diseases with high breed-specific prevalence but overall low heritability (eg hip dysplasia)?

If you want a truly objective answer to that question, you would have to create a complex rating system taking all these factors into account AND have access to data that doesn’t really exist. Most of what we know about breed health is due to self-reports by breeders to breed clubs and registries. These tend to have tiny sample sizes and sometimes people will deliberately falsify or exclude data to make themselves look better. Many breeders don’t complete these surveys at all so it gives only an incomplete picture of a breed as a whole. While these data certainly are better than nothing, their accuracy should not be taken for granted.

On the other hand, empirical studies on breed-wide prevalence of health problems are few, and a number also suffer from the problem of having a very limited sample size. Some studies have been indirectly biased by receiving funding from breed clubs which encourages research toward a specific goal (most often developing a genetic test for a given disease) rather than keeping an open mind about the best methods to tackle a breed health problem (such as avoiding certain phenotypes altogether), and this affects both the direction of the study and what conclusions the researchers draw from their data. The UC Davis Standard Poodle genetic diversity test is one notable example. The test created a means of measuring relatively tiny differences in genetic diversity between individuals, proposing this sort of testing as the solution to widespread disease, rather than going with the simplest solution that makes the most scientific sense: creating a well-designed crossbreeding program to restore diversity to the breed before it’s too late. In general, genetic diversity tests are an attempt to cater to the mainstream dog breeding community’s desire to “breed out” health problems while maintaining blood “purity,” even as this flies in the face of the ideal solutions as determined by applying basic population genetics. There’s profit to be made in placating the desires of a group by providing them the solutions they want, but not so much by proposing ideas which may be objectively more effective but go against the status quo.

Even more worrying is when researchers falsify data to support their presuppositions about breed health. One study of genetic diversity in Nova Scotia Duck Tolling Retrievers actually contained intentionally misleading, incomplete data. One of the researchers involved in the study, Clare Wade, is a Toller breeder and consequently has a strong (but unreported) conflict of interest, desiring to make her breed’s health appear better than it really was. Her study was almost certainly a response to another recently published study that reported levels of inbreeding to be dangerously high in Tollers and found that the gene pool was too shallow for long term survival of the breed. Clare Wade’s study claimed that the opposite was true and that Tollers were remarkably genetically diverse and healthy, basing her conclusions on incomplete, incorrectly compiled pedigree data. It wasn’t long after the study’s publication that other professionals publicly criticized her work as intentionally misleading. (Summary of this case of academic fraud here: http://www.border-wars.com/2011/10/academic-fraud-in-toller-research.html).

All this goes to say: if even professional scientists are willing to cast an unrealistically optimistic light on empirical data (or even falsify data entirely), it’s clear that data regarding breed health must be taken with a grain of salt whether it’s self-reported or the result of a research study. The overwhelming tendency is to under-report health problems, so it’s typically safe to assume that any breed’s health is less optimistic than may be presented or reported.

You also have to consider the fact that the more common breeds will be better studied than the less common breeds, which can easily give the misleading impression that one is very sick and the other is very healthy when in reality, the difference in reported health problems is merely a matter of insufficient data. According to one study (http://www.instituteofcaninebiology.org/blog/what-does-health-tested-really-mean) GSDs were found to have 77 genetic disorders; by contrast Japanese Spitzes are only reported to have 1. Does this mean that Japanese Spitzes are overall healthier than GSDs, with fewer genetic disorders? Possibly, but it’s also quite likely that a very popular breed like the GSD has a lot more data available for analysis and a lot more public interest in genetic health research which leads to a greater number of genetic diseases being identified and reported. There may well be dozens of unreported (or currently unidentified or latent) genetic disorders in Japanese Spitzes, but there’s no way to tell without reliable data.

Because of these factors, when comparing breed health problems, rather than lining breeds up along a spectrum of most to least healthy, I find it more helpful to split breed health problems into general categories like: “Will suddenly drop dead before age 10” (like the Doberman with high rates of DCM); “Will die young but with a longer, more drawn out death” (Flat-coated Retrievers with cancer, Cavaliers with congestive heart failure); “Will probably live a long time but will suffer from at least one health issue that has a moderate to strong negative effect on quality of life” (Italian Greyhounds, which often live to 15+ years but suffer from chronic allergies, epilepsy, hypothyroidism, and various immune disorders while their teeth rot out due to genetic factors); “Will have an overall poor quality of life directly due to their physiology” (many extreme brachycephalic breeds, and also Shar Peis with familial Shar Pei fever); “May not suffer from obvious serious health issues but won’t live beyond age 6” (Irish Wolfhounds, Great Danes); “Will likely suffer a chronic health problem that can be somewhat managed with medication” (Standard Poodles and Addison’s disease); “May have serious behavioral problems due to genetics that may or may not be effectively managed due to the owner’s circumstances and experience” (Rage Syndrome in English Springer Spaniels, OCD in Bull Terriers, extreme noise sensitivity in Border Collies); “High chance of being born with or having a propensity for developing a disability that will decrease quality of life unless effectively managed in the right environment” (Dalmatians and deafness, Australian Cattle Dogs and congenital blindness and deafness, Dachshunds and IVDD). I’m sure I could come up with more if I kept thinking about it.

Each of these categories will be more or less acceptable to different people, so classifying some as objectively worse than others is pointless. Some people may prefer having an especially short-lived dog over a longer-lived dog with a disability or chronic health issues, and vice versa. Every breed will fit into one or more of these categories which highlights the nature of a disease rather than focusing on poorly known prevalence estimates. This is important because while disease prevalence can and will fluctuate over time, few diseases will ever be truly eliminated from a breed via selective breeding. No breed should be considered inherently healthier as a rule, but at risk for varying diseases.

The fact is that every organism has numerous deleterious alleles, regardless of how phenotypically healthy they are. In humans, the average is 0.29 recessive lethal alleles and about 6 disease-causing alleles. Because of this, breed health is not so much related to “genetic health” (i.e. this breed has few or no disease-causing genes) so much as it’s related to how well a breed’s genetic diversity has been managed. Poor management can increase the risk for health problems at any time in any breed, as well as specific lines.

If you’ve got a breed with very low genetic diversity due to things like small founder size, popular sire syndrome, numerous bottlenecks etc. you will inevitably run into salient health problems more quickly. The least genetically diverse breed in existence, the Norwegian Lundehund, is fixed for a severe, fatal immune-mediated bowel disease that affects 40% of the population and the entire population carries the genes for the disease. Less extreme but still concerning examples are Italian Greyhounds, Bernese Mountain Dogs, Standard Poodles, and Nova Scotia Duck Tolling Retrievers. As genetic diversity decreases, the frequency and expression of diseases will increase, and dogs will also be affected in more subtle ways like slightly reduced lifespan, reduced fertility, smaller litters with less ability to thrive, slightly reduced immune function etc.

These negative effects are often subtle and not very salient when only judging health on an individual basis or via anecdotal horizontal analysis (casually comparing all dogs in the same generation) rather than empirical vertical analysis (systematically comparing all dogs over many generations). Because of this, a breed can slip into poorer health and lowered reproductive fitness gradually with no breeders noticing this steady loss of vitality and increase of disease until genetic diversity is too severely depleted to be restored within a closed studbook. The breed gets stuck in a bad situation that can only get worse unless drastic measures are taken in time. This is the main way most dog breeds have become unhealthy, despite the best efforts of responsible breeders and passionate fanciers.

Because genetic diversity always decreases in a closed system over time, it’s not uncommon to see newer breeds that appear to be very healthy currently. The Alaskan Klee Kai is generally regarded as having few health problems, and has only had a closed studbook for a couple decades. However, on a genetic level, UC Davis’ genetic research on the breed has only found 9 DLA haplotypes in the entire breed, which is less than half the known haplotypes of breeds with very low genetic diversity and a high amount of disease as a result (namely Standard Poodles and Italian Greyhounds). While the distribution of DLA haplotypes in Klee Kais is currently is not as uneven as in some other breeds like the IG, the inevitable loss of alleles over time due to selection and genetic drift essentially dooms them to become an unhealthy breed given enough time, unless they periodically accept new founders to reverse gene loss and impose strict guidelines limiting the number of litters per sire to balance allele frequencies.

The longer a breed remains in a closed system, the lower genetic diversity will inevitably become (https://drive.google.com/open?id=0B3ry0Kv4xqooRm5YX2NnOFUySTA2c3czVHhReG9QdXdFczlJ), and the more prone to health issues.

Just as low genetic diversity produces more health problems, higher genetic diversity avoids them. Therefore, as a general rule, any breed with greater, more evenly distributed genetic diversity will suffer from fewer expressed genetic diseases at a lower prevalence.

(As an aside, it’s important to note that genetic diversity must be fairly evenly distributed throughout a population in order to be beneficial, as disease expression boils down to allele frequencies. When a large number of alleles have a fairly similar level of distribution in a population, there’s a lower probability of two alleles “doubling up” in a homozygous state or of genes developing strong linkage disequilibrium which can be dangerous for additive disorders. For instance, IGs have a decent amount of genetic diversity breed-wide overall, but it is very poorly distributed due to heavy use of popular sires and the genetic isolation of IG populations in different countries due to differences in breed standards that discourage interbreeding. The majority of DLA haplotypes in the breed have a prevalence of <5%, and many are very rare with a prevalence of <1%. Of their 20 known DLA class 1 haplotypes, only 4 have a prevalence >19%. Their immune systems are compromised and very dysfunctional breed-wide as a result.)

Breeds with greater phenotypic diversity will typically tend toward greater genetic diversity, as long as these varying phenotypes are not segregated into isolated subpopulations (eg working vs show lines which don’t interbreed). Dogs bred for work tend to be slightly more genetically diverse than those bred solely for conformation (https://drive.google.com/open?id=0B3ry0Kv4xqooTlc2cVBRQWFKRDQ), likely because behavioral traits generally have a lower level of heritability than physical traits so this calls for different breeding strategies and generally allows for greater phenotypic variation.

Landraces will have fairly high levels of genetic diversity overall, as their phenotypes have a relatively wide range of geographic variations. Even with this variety, they still maintain a measurable amount of genetic homogeneity as a group which indicates common ancestry and warrants a shared classification into a spectrum of types within one landrace rather than distinct, separate breeds like those found in Western registries.

Regarding purebreds specifically, breeds like Salukis where COO dogs are still regularly imported and bred with registered dogs will have greater diversity as a breed as well, and Salukis have the most DLA haplotypes of any known breed as a result. Of course, breeders that reject COO dogs due to concerns of breed “purity” won’t benefit from this greater diversity. Without taking the genetic contributions of COO dogs into account, the gene pool of “pure” Western Salukis is rather small and inbred, and they are predisposed to hemangiosarcoma, DCM, and thyroid problems.

Ultimately, the greatest level of diversity in any type of dog is that of the humble, indigenous street dog. Wild animal populations tend toward heterozygosity under ideal conditions, and the only selecting factor for pariah dogs is their ability to survive and reproduce. Dogs that get sick easily from faulty immune systems will die. Dogs born with a serious hereditary illness will be naturally culled. Dogs that are born with deformities or any physical trait that reduces reproductive fitness will not pass their genes onto the next generation. Dogs that are infertile, bad mothers, or produce small litters, all of which are consequences of high levels of inbreeding, will have few offspring if any at all. On a genetic level, allele frequencies will be much more balanced as the sexes contribute fairly equally and popular sire syndrome can’t skew the distribution of genes so wildly as in domestic purebreds. The only significant factors preventing any two dogs from mating are geography and reproductive fitness; there are no distinctions between breeds resulting in genetically isolated populations that are arbitrarily distinguished like in purebreds.

However, there is a notable downside to this high level of genetic diversity: the lack of specific selection that many people desire in a dog, whether a working dog or a companion, which is necessary for a predictable appearance and temperament. With stronger, tighter artificial selection and greater predictability comes lower genetic diversity. This is inevitable due to the direct, inverse relationship between homozygosity and heterozygosity.

This is the deepest, most significant conflict of interest that’s at the heart of all dog breeding. Both breed health and breed predictability are highly desirable traits that breeders strive for. Achieving success in both goals is a complex task of striking a balance between breeding for enough homozygosity to produce a dog with a specific appearance and function while maintaining enough heterozygosity to prevent high levels of crippling disease.

There are means of achieving this, like choosing assortative mating over linebreeding; breeding dogs with faults that don’t impede health or function even though they may be considered “undesirable;” and the introduction of new blood via outcrossing or crossbreeding periodically.

However, some current breeding practices are simply unsustainable due to significantly favoring homogeneity over health: linebreeding heavily to develop a distinct look for your lines or attempt to “fix” a trait in as few generations as possible; maintaining a closed studbook merely over concerns of blood purity which have no scientific founding; utilizing popular sires to the point where a dog may father hundreds of puppies which will widely distribute both his desirable traits and any latent diseases throughout the breed; narrowing the allowed phenotypes of a breed due to politics rather than science, function, or basic logic (eg disqualifying colors and markings which are already present in a breed’s gene pool, and strict selection for minor aesthetic features like the presence of a ridge or a perfectly curled tail). Wide use of these methods has created the health problems found in most dog breeds today, and in breeds and lines where these techniques have been used especially often, it’s fair to expect their health to eventually deteriorate whether quickly or over the course of many generations.

The bottom line is that it’s impossible to single out specific breeds as objectively being the “most unhealthy” due to the complexity of categorizing and measuring the impact of genetic diseases with the current lack of quality data. Furthermore, no breed should truly be considered “genetically healthy,” though they may perhaps be phenotypically healthy; this incorrectly suggests that some breeds have few or no disease-causing alleles, and that achieving genetic health is a simple matter of identifying every faulty gene and eliminating it from the gene pool. The reality is that every breed has health issues, and every breed is capable of becoming highly diseased when their genetic diversity is poorly managed. Every single dog has numerous deleterious genes and must be considered a carrier for at least one disease even if they’re phenotypically healthy and are tested clear for the minuscule fraction of diseases with genetic tests. When genetic diversity is managed properly and an ideal balance is struck between selection for homozygosity to maintain type and function and allowing for enough phenotypic variation and providing a steady flow of new blood to maintain heterozygosity and reduce risk of congenital disease, THAT’S where you’ll find the healthiest breeds. Anything else is just splitting hairs.

Canine Vaccines: Which should your dog get and why

So after seeing several posts recently regarding infected or deceased dogs suffering from diseases which are preventable via vaccination, I decided to write a little piece on the most common vaccines for dogs in the US.

Note: This article regards vaccines which are regularly given in the US. Other countries may follow a very different vaccination schedule and the legal issues addressed in this article will not necessarily apply there.

Common Canine Vaccines:

1. Rabies:

What is it? Rabies is a deadly disease which affects the nervous system of animals and humans (CDC link). It is most commonly spread via saliva when an infected animals bites another animal. According to the CDC:

The early symptoms of rabies in people are similar to that of many other illnesses, including fever, headache, and general weakness or discomfort. As the disease progresses, more specific symptoms appear and may include insomnia, anxiety, confusion, slight or partial paralysis, excitation, hallucinations, agitation, hypersalivation (increase in saliva), difficulty swallowing, and hydrophobia (fear of water). Death usually occurs within days of the onset of these symptoms.

Why should my dog get vaccinated? In the US, it is a legal requirement for your dog to be vaccinated for rabies. Furthermore, if an unvaccinated dog bites someone, the dog must be euthanized and decapitated for rabies testing. Most vets will not service your dog unless it is vaccinated for rabies (unless it is coming in to get a rabies vaccine);  at my clinic, we can’t even perform nail trims on dogs without a current rabies vaccine. Even if you don’t want to vaccinate your dog for anything else, you must vaccinate your dog for rabies, or risk serious legal consequences.

2. DAPP (Distemper, Adenovirus, Parainfluenza, Parvovirus):

What is it? This vaccine comes in several forms: DAPP, DA2PP, DHPP, DHLPP, DA2PPC etc. A2 signifies that both Adenovirus type 1 and 2 are in the vaccine, H is sometimes used instead of A to show that the vaccine prevents hepatitis (vaccinating for Adenovirus type 1 prevents infectious canine hepatitis), L stands for Leptospirosis (which is also given as a separate vaccine, which will be addressed later), and C stands for Coronavirus.

Canine DistempterThis incurable viral disease is highly contagious and has a high mortality rate (50%); it is one of the leading causes of death by infectious disease in dogs. It infects the GI system and the nervous system, including the brain. It is spread through contact with bodily fluids and feces, in addition to aerosol transmission.

Adenovirus: Adenovirus type 1 causes respiratory and eye infections in dogs, in addition to causing deadly canine infectious hepatitis. It is spread through feces, urine, blood, saliva, and nasal discharge. Adenovirus type 2 can potentially cause canine cough (kennel cough).

Canine ParainfluenzaThis disease is highly infectious though typically not fatal, and causes respiratory infections in dogs, including canine cough. Infection spreads through contact with an infected dog or its excretions. Although in some cases, dogs can fight off the infection on their own, it can progress to pneumonia which is potentially fatal.

Canine ParvovirusThis is a highly infectious and virulent disease with an extremely high mortality rate (over 90%), and is one of the leading causes of death in dogs due to infectious disease. Puppies are at a higher risk of death to the disease, as they are more likely to suffer from secondary infection due to dehydration caused by vomiting and diarrhea resulting from the virus, if they do not die from dehydration outright. The virus is also very difficult to kill, and most household cleaners cannot eliminate it (bleach is required for sterilization). Areas exposed to the virus can remain vectors for infection for over a year afterward if not properly decontaminated. It is predominantly spread through contact with feces or areas which have been infected via feces.

Why should my dog get vaccinated? Distemper and parvovirus are both highly contagious and have a high mortality rate, especially in puppies. While every dog should ideally be vaccinated for DAPP, it is vital to do so with puppies as their chances of survival are very slim if infected with the virus. The medical treatment required in case of infection is intense and expensive. If your dog spends time with other dogs, they need to be vaccinated for DAPP. It is also a required vaccine for dogs in boarding, daycare, and grooming facilities.

3. Bordetella:

What is it? Bordetella is a genus of bacteria which are one of the components in a dog contracting canine cough (kennel cough). Canine cough is an infection of the upper respiratory system resulting in hacking coughs and nasal discharge. While spread via aerosol infection and highly contagious, it is generally not serious.

Why should my dog get it? Bordetella is more or less an optional vaccine, and whether your dog needs it depends on your lifestyle. If your dog is frequently around other dogs, you should consider it. Furthermore, most boarding, daycare, and grooming facilities require the vaccine, meaning if you ever use these services, your dog will need to have a bordetella vaccine. Unlike most vaccines, bordetella can be given orally (or intranasally), which minimizes the discomfort of the dog while receiving the vaccine.

4. Leptospirosis:

What is it? Leptospirosis is a zoonotic (i.e. can infect both humans and animals) disease caused by bacteria of the genus Leptospira. It can infect dogs and many other animals, including wildlife and livestock, as well as humans, and can be transmitted between species. The disease can be lethal, with a mortality rate between 10%-50% in both dogs and humans. It is spread primarily through urine and bodies of untreated fresh water such as lakes, rivers, and streams.

Why should my dog get it? Leptospirosis is a very serious disease, and since it can infect humans, all dogs diagnosed with leptospirosis must be placed under a strict quarantine during treatment. However, not all dogs are at risk for contracting the disease. If you frequently go hiking and/or swimming with your dog, it’s a good idea to get this vaccine as your dog may be exposed to infection. However, if your dog is mostly an inside dog and you live in an urban area, vaccination is probably not necessary. The leptospirosis vaccine is one of those which is more likely to cause an adverse reaction in dogs (an adverse reaction being swelling of the face and difficulty breathing/swallowing), so it’s a good idea to get this vaccine separately rather than in a combination vaccine like DHLPP to minimize the risk of complications.

6. Lyme Disease:

What is it? Lyme is a disease which can be contracted by both dogs and humans when bitten by a tick carrying the bacteria which cause the disease. It cannot be transmitted between infected persons or animals, however. Symptoms include lethargy and lameness (due to joint pain), depression and possible kidney problems if left untreated. There is no cure for Lyme, but dogs can be treated with antibiotics to minimize the symptoms of the disease.

Why should my dog get it? Lyme disease is very common in some parts of the States, and a dog can never be cured of the disease. If you take your dog hiking, or live in a rural area where your dog could be exposed to ticks even in your backyard, you should strongly consider getting him the Lyme vaccine.

This is not a comprehensive list of every vaccine available in the US, just the most commonly offered/required ones. I’m also not going to cover the pros and cons of vaccination, as that’s a whole separate, and very divisive, topic. Maybe another day, though!

anonymous asked:

what can i do for a dog that seems to be overheating???? it's really freakin hot where i am right now and my dog is being lethargic and panting heavily!!!!!!

If you can take your dog’s temperature, do so. Anything above 103 is abnormal. Start getting cool (not cold) water on your dog, you want to moisten places like the underside, the paws, and the head. If you have any fans, direct them at your dog and, if your dog has particularly thick fur, part the fur with your fingers so that the air is reaching skin. Make sure your dog has plenty of cold water to drink.

Read more here:

How to Prevent Overheating in Dogs

- Dark

If I ever came off that I was judgmental about what some people feed their dogs I want to apologize because it’s come to my attention that it’s possible I might have come off that way. As long as you feed the best you can afford without totally screwing yourself over (and please, please never feed Beneful) we have no problem.

Laura's List of Spay/Neuter Resources

My reflection on the currently available literature lead me to opt out of neutering Bosco- it’s my responsibility to manage Bosco’s life so that he doesn’t roam around the Alberta countryside impregnating hundreds of female dogs. However, I’m not advocating for strangers to cease neutering/spaying their dogs. What I am gently advocating is for folks to read the available literature and make an informed decision about when and/or if to spay/neuter their dog. Not just neuter/spay their three month old puppy because that’s just what has always been done.

Here’s a list of resources on spaying/neutering- many of them are light meta-analyses. I’m not pretending that this list is comprehensive and frankly, my citation style is atrociously lazy. At some point, I’ll cave to my inner science librarian and update the list using a proper citation style.

Keep reading