Programmi di allevamento
Breeding Programs
X-ray program: In order to receive reliable X-ray results for HD, ED and LÜW, all breeding candidates must present an X-ray evaluation by an appropriate specialist from the GRSK e.V. (Society for X-ray diagnostics of hereditary skeletal diseases in small animals - https://grsk.org/ ). We are pleased about the successful collaboration with Dr. med. vet. Kurt Witteborg, founding member of the GRSK, chief assessor and assessor of the FCI and special evaluator for collies, who has been preparing the expert evaluations for us, since our association's foundation.
HD (hip dysplasia): Hip dysplasia is a malformation of one or both hips. Fortunately, American Collies are not among the breeds with an increased risk for HD, almost all have HD A (free). To maintain this, only Collies, that have been radiologically examined as being HD A (free) or HD B (borderliner) are accepted for breeding. At least one mating partner must have achieved the result HD A.
ED (elbow dysplasia): ED summarizes several malformations oft he elbow. Here too, the American Collies are not among the breeds with an increased risk for ED; almost all have ED 0 (free). To maintain this, the ED x-rayed Collies, that have been radiologicaly examined as being ED 0 (free) and ED 1 (borderliner) are accepted for breeding. At least one mating partner oft he ED x-rayed Collies must have achieved the result ED 0. Collies that have already been x-rayed for HD an/or come from another club where ED testing was not yet mandatory at that time are exempt from the ED examination requirement. They do not need to be unnecessarily exposed tot he risk of anesthesia again, even if it is small, to have them x-rayed again. However, all new breeding candidates must also be x-rayes for ED and LÜW, together with the HD x-ray.
LÜW (lumbar transitional vertebra): LÜW refers to modifications in the area of the lumbar transitional vertebra. Primarily the focis is on data collection, in cooperation with the GRSK. But here too, the LÜW x-rayed Collies, that have been radiologicaly examined as being LÜW 0 (free) and LÜW 1 (borderliner) are accepted for breeding. At least one mating partner of the LÜW x-rayed Collies shall have achieved the result LÜW 0. Collies that have already been x-rayed for HD and/or come from another club where the LÜW examination was not yet mandatory at that time are exempt from the LÜW examination requirement. They do not need tob e unnecessarily exposed tot he risk of anesthesia again, even i fit is small, to have them x-rayed again. However, all new breeding candidates must also be examined for LÜW along with the HD and ED x-rays. A good HD X-ray is usually sufficient for this. If not, an additional image must be taken. It is best to point this out to the radiologist straight away.
Clinical eye examination: All breeding candidates must present test results from an Ophthalmologist (eye-specialist) of the DOK (https://www.dok-vet.de - Dortmund Circle of Ophthalmologists of/or the superior authority European ECVO or alternatively ACVO in America) for hereditary eye-diseases, such as RD, CEA, PRA and KAT. Only Collies that are free from inherited eye disease will receive a breeding license. Currently an exception still applies to Collies affected by CEA-CH (Chorioretinal hypoplasia) or MPP (PPM) (psb), if their vision is not impaired. The breeding partner should be free. In addition, all puppies born in our association also receive an examination by an ophthalmologist of the DOK (or ECVO/ACVO), before they are handed over, at an age of 6-7 weeks. Due to these strict requirements for the parents, in combination with the mandatory genetic tests for CEA & PRA, no puppy with visual impairments was born in our AC e.V., since the association’s founding.
MPP (Membrana Pupillaris Persistens): In the embryonic phase, the eye is covered with a fine membrane. This disappears when the eyes open. Sometimes, however, tiny remnants of tissue remain, called MPPs (or PPMs = Persistent Pupillary Membrane). They can also be completely reabsorbed later. They are found in many breeds. In Collies, if they are present at all, they are so small (usually just one or two tiny pieces, which are then also outside the lens) that there is no impairment of vision. They can then also be approved for breeding with the recommendation that they be mated with free dogs. In addition, all puppies are examined by a specialized ophthalmologist from the DOK (or ECVO/ACVO) before being handed over, we can say with certainty that no puppy with visual impairment has yet been born in our association AC e.V, from the founding on.
MDR1 (Multi-Drug-Resistance): This multiple drug intolerance (https://mdr1-defekt.transmit.de/ , https://www.colliehealth.org/collie-health-101/mdr1-mutation/ , https://prime.vetmed.wsu.edu/ ) is very common amongst many herding dogs and related breeds (as well as some cats), including the Collie. The so-called MDR1 transport system, which is also an important component of the blood-brain barrier, is affected. It normally ensures that undesirable substances, such as medication, are kept away from important organs (e.g. brain) and functions, such as the intestinal barrier, placental barrier, excretory processes (liver, kidney) and even the bone marrow and blood. Usually unaffected genes cover affected ones, as in most diseases listed below (autosomal recessive inheritance). It is different here, because the coverage is only achieved with incomplete penetrance, so that MDR1 carriers (MDR1 +/-) can also react somewhat more sensitively to some medicines and anesthetics, so that medication and dosage should be adjusted. The treating veterinarian should always be informed about the respective MDR1 status (https://mdr1-defekt.transmit.de/kritische-arzneistoffe-bei-mdr1-gendefekt ). It should also be noted that, regardless of the MDR1 defect, i.e. also in genetically free collies (as well as other dog and cat breeds), in rare cases there have been intolerances or even deaths within 5 days of administration of the anesthetic ketamine, apparently regardless of the dosage. That is why it makes sense to inform the veterinarian also about this. For all puppies born in the association, the MDR1 status must be certain before they are handed over. If the status of the parentage is not clear (as soon as one parent is a carrier, i.e. +/-), an appropriate MDR1 genetic test must always be carried out. The same applies to all breeding candidates. The worldwide proportion of MDR1 affected Collies in 2021 was a shockingly high 70% https://prime.vetmed.wsu.edu/2021/10/19/breeds-commonly-affected-by-mdr1-mutation/ , according to a study by Washington State University. Thanks to our strict breeding program, from the association founding on, not a single MDR1 affected puppy has been born in our club! Instead, we can proudly point to a proportion of 65% of MDR1 genetically free born puppies! The proportion of carriers has steadily decreased and will continue to do so. Because from the founding of the club, the rule applies that by every mating, at least one parent must be genetically free (MDR1 +/+). Every breeding candidate must be genetically tested for MDR1. In our association AC e.V. the birth of MDR1-affected puppies has been and will continue to be completely excluded!
DM (Degenerative myelopathy): DM is an incurable, neurodegenerative, painless disease of the nerve pathways with increasing paralysis, starting in the hindquarters, which then progresses to the forehand with increasing paralysis also in the muscles for voices, swallowing and breathing, while the dogs are full consciousness (https://www.uni-giessen.de/de/fbz/fb10/institute_klinikum/klinikum/kleintierklinik/Chirurgie/neurologie/Patienteninformation/d/degenerative-myelopathie). In the beginning, it is like other diseases and degenerative symptoms of the hindquarters that are accompanied by muscle loss. Sometimes they also run parallel, as DM usually only occurs with advancing age. A final diagnosis is currently only possible after death through a spinal cord incision. The disease is comparable to ALS (amyotrophic lateral sclerosis) in humans, as was the case with Stephen Hawking. Unfortunately, the exact genetic cause has not yet been identified with certainty. However, the risk gene SOD1 (superoxide dismutase 1) has been identified in affected people such as dogs if it is affected by certain mutations. They can cause incorrect protein structure (misfolding, e.g. due to too many disulfide bridges, resulting in aggregation and toxic inclusions in the mitochondria of neuronal cells: https://pmc.ncbi.nlm.nih.gov/articles/PMC9857031/ ), which not only leads to functional impairment, but also prevents the transmission of stimuli and causes the affected nerve cells to die. It seems to be similar with Alzheimer, Parkinson and Huntington. In ALS and DM, the connection between the brain and the transmitting nerves in the spinal cord is increasingly blocked, which results in their death (loss of motor neurons). Without nerve stimuli, the associated muscles are no longer active, stop functioning and become degraded, what is leading to increasing paralysis. In contrast to dogs, a whole series of mutations have now been identified in humans. In many dog breeds, including the Collie, the so-called Exon2 mutation in the SOD1 gene could be identified. It cannot be ruled out that there are others that can cause DM. Multiple mutations can also include carriers. The fact is, however, that in the study at the time, all dogs suffering from DM were also affected by the SOD1-Exon2 mutation. It should also not be forgotten that we are talking about a risk gene. Even in genetically affected dogs, it is said that (only) around 40% of dogs can develop DM. Fortunately, a genetic test has been developed, which we naturally use from the founding of the association, so that thanks to our strict breeding program, not a single DM (SOD1-Exon2) affected puppy was born and none suffers from DM to date. We have also been able to significantly reduce the number of carriers (and will continue to do so in the future), as the offspring statistic shows, with only 15% carriers and 85% genetically free dogs! We maintain that every breeding candidate must be tested for DM and that at least one parent in every mating must be genetically free (DM (SOD1-Exon2) +/+ or N/N). This means that in our association AC e.V the birth of DM (SOD1-Exon2)-affected puppies has been and will continue to be completely excluded!
CEA (Collie-Eye-Anomalie): CEA is a congenital, stagnant, genetic change in the fundus of the eye. Congenital means that it can be detected in puppies before they are handed over, if they are examined by an eye specialist from the DOK (or ECVO/ACVO) at 6-7 weeks, as has been required by our AC e.V. association since our founding. CEA is very common in herding dogs and related breeds, especially Collies. It is assumed that around 67% of all collies are affected by the mildest form (mild CEA or Chorioretinal Hypoplasia), which for most collies does not mean any impairment of vision, as there are either no or minimal changes to the retina. Usually there may be (but must not be) nothing more than small areas of the choroid and retina, which are not completely extensively or intensely pigmented. A phenomenon that can only be detected by an eye examination up to 8 weeks. After that, it is usually completely covered by pigments of the tapetum lucidum, which causes many animal eyes to light up brightly in the dark, when they are illuminated with light. It has a mirror-like reflective effect and thus helps to use even dim light to orientate oneself in the twilight. The Collies are then referred to as "go-normals" because no changes are visible. However, such dogs can still be identified using reliable, high-quality genetic tests (Laboklin), as they have the status CEA -/- or CEA/CEA (affected). Even though there are no visual impairments in this mild form, we have made it our mission, since the club was founded, to reduce the number of affected genes through breeding programs. Our offspring statistic shows that only just 8% of the Collies are affected (out of approx. 67% affected Collies worldwide), with a steadily decreasing trend. And on the other hand, almost 40% of the Collies are genetically free (by approx. 8% genetically free Collies worldwide), with a steadily increasing trend!
Colobomas, which are now only rarely seen, are currently (still) considered to be CEA. This is where congenital changes occur in the optic nerve head and the adjacent sclera, which are also visible at 6-7 weeks of age during an eye examination by a DOK specialist (ECVO/ACVO). If there is prior breeding selection, as in our club, in the worst case, usually very rarely only the mild form occurs, in which there are hardly any visible changes during the eye examination and no visual impairments. Without breeding selection outside of our club, unfortunately there are always cases with more severe tunnel and/or slit-like bulges in the optic nerve head. There you very rarely can also find the worst form, which is accompanied by severe changes in the blood vessels, which can lead to bleeding and retinal detachment, so that the dogs go blind. Through our breeding program we have been able to reduce the rate of puppies born with coloboma to under 0.25%, and in such a mild form that there are no visual impairments here either, as the specialized eye examination shows. In addition, not a single puppy has been born with a coloboma since about half of the time since the club was founded!
Our breeding program, which has been in place since the club was founded, consists of two important components. The first is the mandatory eye examination by a specialist from the DOK (ECVO/ACVO), not only for all puppies born in the club, but also for all breeding candidates. This allowed us to carry out a pre-selection for breeding from the very beginning by consistently excluding all breeding candidates before they were used for breeding as soon as they showed even the slightest changes to the optic nerve. This meant that colobomas did not even make it into the breeding pool. It is now assumed that there is a separate inheritance mechanism for colobomas. A Danish-Swedish study has already shown this in Tollers: https://onlinelibrary.wiley.com/doi/abs/10.1111/vop.12488?fbclid=IwAR0ah7pM11p-i60AgaIfHUHrBoje_HXSX2PP-vkB8_kOWaJwqI_6Cynrd-A. Supported by the Collie Health Foundation, coloboma studies are currently being conducted on collies with the aim of developing a test. The University of Pennsylvania has already found that there appears to be a region of the genome that is resistant to colobomas, which is in line with our successful pre-selection. We can look forward to the final results.
The second important component of our breeding program is a high-quality genetic test for CEA (Laboklin) in order to be able to reliably identify the dogs listed above with mild CEA, even if they are all free of visual impairments. From the very beginning, we spared no expense and effort and in the first few years we always sent all samples (CEA & PRA and later DMS) to the USA, which involved a lot of effort and time and was very expensive, as the newly developed tests were only available there at the time. Today, we are happy that our local partner laboratory Laboklin is also providing us with reliable results here. All breeding candidates had to be tested then, as they are now. From the beginning, it was clear that genetically affected dogs should not be mated with each other. They were only allowed to be bred if they were free of visual impairments. Through selective breeding, we were able to continually increase the gene pool of healthy genes (see above) to the point where we now go so far that in every mating, one partner should preferably be genetically free (CEA +/+ or N/N). And of course, every puppy, born in our association, obligatory has an eye examination by a specialist at the DOK (or ECVO/ACVO), so the exact clinical status of each puppy is also known before it is handed over.
PRA-rcd2 (Progressive Retinal Atrophy): PRA is a widespread, incurable, hereditary eye disease that affects great many breeds. It is comparable to retinitis pigmentosa (RP) in humans. PRA in dogs and some cats progresses much more quickly and becomes increasingly worse, always leading to blindness in both eyes. The cause is the death of the photoreceptors in the retina. There are breed-specific differences in the progression, depending on the particular mutation. Rarely, new mutations arise in individual breeds, which first have to be identified and for which a suitable test must then be found. In most cases, as in the Collie, the rod receptors, which are specialized for vision at dusk, are affected first, and only later the cone receptors, which are specialized for vision in daylight. The disease is usually characterized by the onset of night blindness, which occurs in the Collie as early as around 6 weeks of age. Later, vision also deteriorates in daylight (with the pupils dilating on both sides, also in bright light). In Collies, the disease progresses very quickly, so that they are usually completely blind by the age of one year. The cause here is the so-called rod-cone dysplasia type 2, abbreviated PRA-rcd2. From the founding of the association, we spared no expense and effort and in the first few years we always sent all samples (CEA & PRA and later DMS) to the USA, which was a lot of effort and time and at great expense, because the newly developed tests were only available there at the time. Today, we are happy that our local partner laboratory Laboklin is also providing us with reliable results here. Thanks to early breeding selection, we have a sufficiently large gene pool of healthy genes. This is why we were able to set up a rule from our founding on, that at least one parent in every mating must be genetically free (PRA-rcd2 +/+ bzw. N/N). The birth of PRA-rcd2 affected puppies has been and will continue to be completely excluded in our association AC e.V.!
GCS (Gray/Grey Collie Syndrome or Cyclic Neutropenia-CN): This is a rare genetic disease of blood cell formation in the bone marrow, which leads to a cyclical reduction, especially of neutrophil granulocytes, which are extremely important for the immune system. The latter are the main component of the cellular immune system. Their strong reduction every 11 (10-14) days means that affected dogs are very susceptible to infection. As long as puppies are still being suckled, the antibodies from the mother's milk still seem to have a supportive effect, and the environment is usually relatively germ-free. Until then, the most noticeable feature is the slightly lighter, usually grayish coat color (not caused by Merle), with a nose that does not completely turn black over the course of development, which also remains rosy at first and later grayish. In addition, the tan markings are missing. The greatest risk of symptoms developing is at 8-10 weeks. With few exceptions, a terrible ordeal then begins with infections that become increasingly severe and, sooner or later, life-threatening, initially often caused by the simplest pathogens, that have only little effect on healthy puppies and young dogs. The illnesses are often accompanied by recurring fever, diarrhea, sometimes vomiting, joint pain that soon develops into arthrosis, sometimes accompanied by misalignment. Respiratory infections that develop into serious, life-threatening pneumonia are also typical. The eyes, skin, mouth and teeths are also very susceptible to all kinds of pathogens. Since the entire blood formation is disrupted by the cyclical changes (hence also called cyclic hematopoiesis), anemia can easily develop, possibly accompanied by a blood clotting disorder and symptoms such as nosebleeds and omnipresent additional general weakness. The affected dogs usually die within the first three years of life. Reciprocal bone marrow transplants from sick dogs to healthy ones, which then became ill, and vice versa from healthy dogs to sick dogs that had a chance of recovery, have proven that the cause can clearly be found in the bone marrow. Unfortunately, there is no sufficient developed system for finding suitable bone marrow donors in dogs. There is a similar disease in humans, cyclic neutropenia (CyN). A mutation in exon 20 of the AP3B1 gene has now been identified (https://omia.org/OMIA000248/9615/ ). This primarily causes a deficiency in the enzyme elastase (including agglutination of the precursors that cannot be completed) and, as a result, a disruption in the movement and function of the granulocytes, up to the failure to trigger a final immune response to fight infections. The gene is also the cause of a form of coat dilution, that causes the eponymous gray coloring in affected animals. It can also vary to a beige-yellowish color, depending on the base color and as a new color variant after the rare coat change. The harsh structure is usually also missing. This mutation has now been found in distantly related breeds, and the search is still ongoing in other breeds. These matuations probably occurred very early in the evolutionary history of dogs. In all probability, both parents (carriers) already have limited granulocyte function. We are happy that a suitable genetic test has been developed. Everything suggests that our gene pool is also completely free of carriers and ideally stays that way. When our association was founded, we established the rule that at least one parent in every mating must be genetically free (GCS +/+ or N/N). In the meantime, every breeding candidate must be tested for GCS. This means that the birth of GCS-affected puppies has been and will continue to be completely prevented in our association AC e.V.!
DMS (Dermatomyositis): DMS (dermatomyositis): DMS is an autoimmune disease, similar to JDM (juvenile dermatomyositis) in humans. It occurs primarily in Shelties. There are rare cases in Collies and very rarely in other breeds. Crusted lesions evolve on protruding bones that are sparsely covered with muscles, such as in the face (nose, eyes, ears), but also on the tip of the tail and paws. The skin is sometimes flaky, reddens and the fur falls out. It is typical that the affected regions do not itch, especially in the early stages before a secondary infection appears. Wounds heal in mild cases, although most of the times areas remain changed for a long period of time, shaped by dark or stained pigmention and ongoing loss of hair. In severe cases, the muscles can also be affected, making walking (like muscle soreness in humans) and swallowing more difficult. The most common outbreak occurs in the first half of life. Apparently, a trigger is needed for this, which is associated with severe stress. Milder stress factors can later act as intensifying effects, such as hormonal changes (castration if necessary), over-vaccinations (or live vaccines), increased infection pressure and intolerances, and lots of sunlight. Preparations containing omega-3 and -6 fatty acids, vitamin E and Trental, and possibly antibiotics, seem to help. Inflammatory skin lesions can be treated with special germ-reducing foam solutions. In addition, a study is currently underway at the University of Georgia on the use of Janus kinase (JAK) inhibitors in DMS, which have also recently been successfully used in human medicine for JDM. The so-called JAK-STAT signaling pathway was recently shown to be the main driver of various autoimmune processes when they cause an excessive inflammatory reaction, such as the skin lesions in DMS. Oclacitinib (Apoquel® from Zoetis) currently appears to be the drug of choice in veterinary medicine, especially since it is already being used successfully for inflammatory skin reactions, even if the main purpose there is to reduce itching and allergies. But it also has an anti-inflammatory effect as an inhibitor of Janus kinase. We will see to what extend this treatment makes sense.
Similar to DM, the causative genes in DMS have not yet been fully identified, but in 2016 Leigh Anne Clark & Jacquelyn Evans et al. in the USA discovered three risk factors for DMS and developed a suitable genetic test, which we immediately made use of. In the meantime, we no longer need to send samples to the USA, as Laboklin has also been offering reliable test results since a few years. Two high-risk genes were identified, called "A" (PAN2) and "B" (MAP3K7CL). The genes are important in the area of inflammation regulation. DMS can therefore also be described as an inability to regulate inflammatory reactions correctly. Since the genes are always present in duplicate (alleles), they can be intercepted by free genes "a" and "b" ("Aa" or "Bb"), so that the risk of disease is reduced. In general, "B" is less common than "A" in Collies. Interestingly, merle genes are always linked to an "a". According to research results from 2016 (http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1006604 ), the risk assessment of the genetic test is enclosed: Basic risk (approx. 3%): aa bb, Low risk (approx. 4%): Aa bb & aa Bb & AaBb, Moderate risk (approx. 39%): AA bb & aa BB, High risk (approx. 90%): Aa BB & AA Bb, Very high risk (approx. 97%): AA BB. The risk test is not a means of detecting the disease; that can only be done via appropriate biopsies on the affected areas if it breaks out. It is purely a risk assessment. This also does not mean that every genetically affected dog automatically becomes ill; it simply has a low, moderate or high risk of the disease breaking out. Conversely, a dog with the lowest possible risk still has a residual risk of developing the disease, as there is no such thing as "no risk" according to the current state of science. When testing all of the breeding dogs in our club, it was fortunately found that there are no dogs with a high or very high risk. The majority were dogs with a low risk (4%), although there are hardly any B variants, and there were a few with only a basic risk (3%) and only a few with a moderate risk. This meant that we were in a good starting position to improve the trend even further through selective breeding. The percentage of dogs with the lowest possible risk was significantly increased and the percentage of dogs with a moderate risk was further reduced. We are currently working to eradicate the latter as well. Dogs with a moderate risk should only be mated with dogs with the lowest risk. According to the current state of knowledge, since the club was founded, no puppy has been born with DMS and it should stay that way. This means that every breeding candidate must be tested for DMS (Laboklin) and the matings must be chosen accordingly so that no puppies with a high or very high risk are born and the proportion of moderate cases continues to fall. In this way, the birth of puppies with an increased risk of contracting DMS has been and will continue to be completely ruled out in our association AC e.V.!
Further research is currently underway, particularly into the significance of the third risk factor, the risk gene "C", which relates to subvariants of the immune system, more specifically to the DLA-DRB1 system. Immune system variants can also promote an outbreak of human JDM. In dogs, it is about the MHC II class leukocyte antigens, more specifically the DLA genes, made up of the combination DLA-DRB1/-DQA1/-DQB1. They are expressed in numerical combinations depending on their genetic composition. Unfortunately, variations are very sparse among Collies. In the study, Collies almost without exceptions showed the combinations 002:01/009:01/001:01, rarely the combinations 015:01/009:01/001:01 and the very rarely combi 020:01/009:01/001:01 was added later. Therefore, there is a general breed-related tendency to DMS, at 3%. There is another extremely rare DLA variant, with the combination 006:01/050:11/007:01. Due to the small number, it is unfortunately not yet possible to say whether the risk is lower here. But even if it were, intensive breeding selection would hardly be feasible due to the rarity. Since the greatest variance occurs with DLA-DRB1, at our suggestion the research group switched to stating this value on the findings instead of the DQA1 value as before. Nowadays, to simplify things, it is common practice to designate the most common variant 002:01 with the risk gene "C" and all other variants, such as 015:01, 020:01 and 006:01 with a "c", although it is not really certain that the risk decreases; this remains to be observed. That is why we continue to state these in numbers. This also makes it easier for breeders to use specific variants in order to maintain the widest possible genetic range and to further support the health of the Collies born.
IPD (Inflammatory pulmonary disease): IPD is a recurrent inflammatory lung disease with a hereditary background. It usually breaks out in the breeder, a few days after birth. The dogs suffer from repeated foamy vomiting, nasal discharge, fever, shallow breathing, increased breathing noises and coughing. Medications such as antibiotics and secretolytics only help for a short time, after which there are rapid relapses. Many die very early. Thanks to a study supported by Laboklin with the University of Bern (https://www.mdpi.com/2073-4425/10/8/567/htm ), a mutation was found in the AKNA gene, which is responsible for regulating inflammatory processes. Fortunately, a genetic test was subsequently developed. So far, the rare disease has only been diagnosed in British Rough Collies, but it is known that diseases with comparable symptoms also exist in the wider dog gene pool. Because possible gene carriers cannot be traced back far enough, it cannot be ruled out that they can also be found in other Collies, especially since they go back to common ancestors. That is why we have changed the test recommendation into a test requirement. The whole thing is made easier by the fact that Laboklin has included the test in the Collie test package, so that many dogs are already tested anyway, and many others have had their dogs tested voluntarily. All of them have been genetically free so far, so we have a good starting point. For each mating, at least one parent must be genetically free (IPD +/+ or N/N). This means that the birth of IPD-affected puppies can be completely ruled out in the AC e.V. association!
MH (Maligne Hyperthermie): This rare genetic defect affects the calcium regulation of the striated muscles and, in contrast to the diseases mentioned above, is inherited autosomal dominantly. This means that genetically free genes of the breeding partner cannot mask those that are affected. The defect still occurs. It is found in many mammals, including humans. Triggers, rarely stress, but above all medications such as some inhalation anesthetics and certain muscle relaxants, can lead to massive muscle cramps and even to their damage(rhabdomyolysis). Added to this are cardiac arrhythmias (rapid heartbeat), lack of oxygen, excessive CO² and heat production (hyperthermia). Degradation products lead to, among other things, massive kidney problems, up to organ failure and death, if not treated immediately (Dantrolene). This test is voluntary, as no report has been found to date that Collies are actually affected. Since carriers are also affected, it is nevertheless strongly recommended that all Collies be tested for this so that none of them can be used for breeding and the birth of carriers and affected puppies is further avoided and only genetically free puppies (MH +/+ or N/N) are born.
. HUU (Hyperurikosurie / Hyperurikämie): This is a genetic disorder of urinary metabolism (purines), from birth on. In contrast to humans, the final product uric acid is further degrated to allantoin that is better water soluble by healthy dogs. This process is disrupted in dogs affected by HUU due to a mutation in the SLC2A9 gene (autosomal recessive). The uric acid content can arise up to double or even quadruple (hyperuricemia), which can lead to crystalline residues and even the formation of bladder stones (possibly requiring surgical removal). The test developed for the SLC mutation is voluntary, as the disease only occurs extremely rarely in Collies. Here too, ideally at least one breeding partner should be genetically free (HUU +/+ or N/N), so that the birth of affected puppies can then be completely ruled out in the AC e.V. association.
Collie Health Foundation (CHF): We always stay up to date and can react to new research results at short time and include them in our breeding program. This is because our association is a member of the CHF in the USA (https://www.colliehealth.org/ ). It is the world's largest organization for Collie health and supports numerous studies in this regard, which often result in important tests (see above) that help us prevent the birth of affected puppies. We are pleased about the intensive cooperation. We would particularly like to thank the long-serving President Robette Johns and Vice President Krista Hansen and many other current and former holders of important offices there, such as Mary E. Benedict, Judith A. Pitt, Lori M Montero and David Hansen, who have all visited our association in recent years and shared their specialist knowledge with us through many great seminars and discussions. Many of our members also support the CHF through private memberships and donations. And of course, we also work with other competent partners.
AVK (Ahnenverlustkoeffizient = ancestor loss coefficient): In order to preserve the genetic diversity of each individual dog to a high degree, the AVK of the puppies must not fall below 86% over 4 generations. This implies the prohibition of inbreeding or tight line breeding. Only with as many diverse genes as possible (heterozygosity) the individual of a breed can remain as healthy as possible in the long run.
IK (Inzuchtkoeffizient = inbreeding coefficient): The IK, in contrast to the AVK, also incorporates the closeness of relatives. Thus, double ancestors that are more distant (like great-great grandparents) have less severe influence than if e.g. the father would appear several times. It is recommended that the IK of puppies should not exceed approximately 6%. Furthermore, the circumstance of double ancestors should generally be avoided during the first three generations to preserve and promote the diversity and variety of genes.
Genetic diversity: The aim is to maintain the largest possible gene pool for the entire breed. The excessive use of an individual stud dog should be avoided (Popular Sire Syndrome) to preserve the genetic diversity of the breed. The more dogs are related to each other, the more the gene pool of a breed is reduced. Some diseases and other defects only develop at a higher age. Should affected dogs have produced abundant offspring, there is the danger that these defects have spread unintentionally and irreversibly. In all breeds, the gene pool drops from generation to generation, as with every dog that is not used for further breeding, its unique gene variants disappear forever. Of course, this does not mean that every dog should be bred. This should definitely be reserved for those who have sufficient knowledge and the opportunity and time. In addition, far too many puppies would be born for which there would be no suitable home. That would not be responsible breeding. With the American Collie, the aim was and still is to maintain the basic features of the original breed type, with all its advantages. The fact that it continues to be used for herding and dog sports has meant that the American Collie, unlike many of its relatives on the continent of origin and many other breeds, has not undergone extreme changes to its exterior, which always entails cuts in mobility, endurance, agility, expression, character, in other words the breed's fitness. Because one change always leads to a change in the whole. The original genes that support the breed's health, along with the genetic diversity, are also somewhat lost. The usual artificial shrinking of the gene pool by removing color variants that are free of health restrictions as well as the ban on mating of different hair variants (here Rough and Smooth) has also never happened with the American Collie. So, the fitness of our breed is still largely intact. This can be seen in the joy of life and movement, agility, enthusiasm, expression and often born large litters. But of course, we don’t become blinkered and are nevertheless concerned about the long-term preservation of the breed. In the background, we are already considering and developing measures to support heterozygosity (e.g. diversity check) and possible cross-breed outcross or backcross procedures.
American Lines: The aspired goal is to have at least 50% (good if more) of American bloodlines (Collies bred on the American continent over several generations in accordance to the breed type). More important for preserving the breed however is in the long run the conservation of the genetic diversity (of the individual) as well as a large gene pool (of the breed) and especially the exterior (according to the original American breed standard), besides character etc., with regard to the expected puppies.
Character: It is very important that character and temper are taken into consideration when choosing mating partners. It should especially be looked at how already existing offspring developed. Do I want to bring calm dogs into the world in the long term, or rather very active ones? Do I have enough interested parties for the latter who can do justice to such animals? Or would I rather aim for dogs with a medium temperament?
Exterior: The aim of breeding is always to breed a dog that comes as close as possible to the ideal image of the American Collie. To do this, you have to look at the potential of the available breeding partners and take a closer look at their ancestors. Good breeding judges, the breed manager and breed warden can certainly help. When choosing mating partners, it must be never forgotten that it is not a question of breeding the dog with the best health values, but rather the overall package must be right so that the Collie continues to look like an American Collie. That is the true art of breeding. Many characteristics, especially also of the unique Collie head, are inherited recessively, while deviations, such as too narrow muzzles and too wide heads, rounded on the sides with protruding bones, instead of flat, smooth sides (to form a beautiful wedge), tend to come through dominantly, by changing the position of the eyes ect. and being difficult to get back into shape. In all of this, the body structure must not be ignored. More details can be found here: https://www.amerikanische-collies-europa.de/index.php/en/american-collie/breed-standard. It is not without reason that the Collie is considered one of the most difficult breeds to breed, right down to its unique proud expression.
Color specifics: Color variations that can lead to health problems are not desired. This includes the Double Merle (genetically homozygous carriers of Merle (M/M), originating from the mating of two dogs carrying the Merle factor) are excluded from breeding according to current to the legal animal protection laws, even if there are variants that do pose any health risks is to be expected. A desired mating that might result in such puppies is also not allowed! Only one breeding partner may carry the Merle factor, as a heterozygous carrier of the Merle gene (m/M). In order to be able to reliably identify Hidden Merles (with a not (clearly) visible Merle, such as Sable Merles, Cryptic Merles and Minimal Merles) before mating, every breeding candidate must be genetically tested for Merle, so that the alleles are broken down (this was not the case with the old Merle tests). For all puppies that result from Merle matings, it is recommended that they are all tested for Merle alleles so that the exact status of each puppy is known. Buyers of dogs with a Merle factor must be informed that, in accordance with legal requirements, the dogs may not be mated with other Merles! It must also be pointed out that the Merle factor is not visible in many dogs, even across breeds, so that no "accidents" can occur to safely rule out the birth of Double Merles. To ensure that the eyes and inner ear always have enough pigment to be fully functional, Harlequins, Fawnequins and Minimal Merles (all m/Mh) must not be mated with Collies that have a White factor and/or a blaze that reaches up to the forehead. With all White variants, it is also important to ensure that the head remains completely colored (color head), as required by the breed standard. Excessively large blazes are therefore also undesirable. Ideally, dogs with very large blazes should only be bred with those without blazes. Also undesirable are deviating colors, such as the E-locus, because in the e/e expression the original basic color is completely overlaid with "yellow", pronounced as a Sable-like coloring with a lightened nose. Also undesirable is the Dilute factor, which in the d/d expression leads to an unnatural pale lightening (Maltese Blue/Gray) and possible health problems cannot safely be ruled out. (More information is available here, including very detailed information on Merle, here: https://www.amerikanische-collies-europa.de/index.php/en/american-collie/collie-colors ).
Mental maturity: Bitches must be at least 22 months of age for breeding, stud dogs must be at least 18 months of age.
Quality before quantity: Besides complying with above mentioned values that ensure and enhance the quality, it must also be considered that a dog should not be used for breeding excessively. For the stud dogs this was described under the point “Genetic diversity”. The breeding of bitches should be designed in such a way that there is at least a year between successful matings. A recovery year between litters is also aimed for, because our bitches are not breeding machines! Overwork also inevitably reduces the quality of the puppies and that must never happen! This is why a bitch is only allowed to have a maximum of four litters in her life. The first mating of a bitch should take place before her 5th birthday. After a second Caesarean section, the bitch must be taken out of breeding. Multiple litters should not be raised at the same time in one breeding facility. In general, no more than 3 litters per year should be raised per breeding facility. Kennels, run by the A.C. e.V. may only breed Collies under this association, otherwise any further breeding permit will expire. The breeding permit for bitches expires on their 7th birthday. However, a one-year extension can only be requested in particularly justified exceptional cases if a veterinary health certificate including a certificate of no objection for further breeding use is presented. The breeding commission makes the final decision by majority. The breeding permit for males expires on their 8th birthday. However, an extension can be requested, especially if their semen is particularly valuable. The breeding commission makes the final decision by majority.
Data collection: To be able to keep high-quality standards long-term and to optimize them further, it is essential that irregularities (anomalies, diseases, etc.) are reported to the stud book office, as is the death of all dogs registered in the stud book, including all born puppies. Depending on the cause, frequency, etc., appropriate follow-up steps can be taken to further optimize future breeding if required.