asal

my goodness, what a lesson on control, notice not one of them paid attention the to the dog challenging them... then when he said they could free hurtle across the fields.. like scattered rice....on call and it was if they were magnatised chips back to his bike. who feels a tad inadequate??????? although i have had one dog i think could outdo them, he was a poodle.. think it was the brains of the doggie rather than mine. he was a one of kind that Bel Ami Picolo.

that article written by Mrs Sharp was so right. she calls them "The Incorrigibles’ " ive thought of them as the "precious ones" they forget people in glass houses shouldnt throw stones. but "they" feel they are "precious" and special because they have cupboards full of trophies and ribbons and they are there fore above and better. but do not understand, when you spread ill will it blows across all in the end.

laws and rulings have even been passed on the assumption that reining in pedigree breeders is going to somehow eliminate the unwanted genes by eliminating for example parent to progeny or brother sister matings. and line breeding discouraged. dozens of other unwanted genes remain unknown in a large proportion of the population. and will turn up regardless of whether the parents are purebred or x bred yet only the purebreeder gets the blame if it occures in their litter. all the millions of wild animals descended from a few imports to a foreign country that are now in the millions and billions are ruthless culled in the wild. thats why u dont see the unlucky ones. does it make the wild unethical or guilty? when will the guilt mongering stop and encouragement and support to irricate what no person put there and all work together for the common good? then maybe less people will hide from admiting they discovered a problem. You are so right. until the guilt mongering stops and we all work together it just fractionises everyone and slows what we all really want to achieve

here is part of one i found "1. EXPLANATION Doramectin is a member of the avermectin class of compounds, which includes abamectin and ivermectin. It is a semisynthetic avermectin that has close structural similarity to abamectin and ivermectin. It is used as an endoparasitic agent in non-lactating cattle. Doramectin was previously evaluated by the Committee at its forty-fifth meeting (Annex 1, reference 119), when it established an ADI of 0–0.5 µg/kg bw on the basis of a NOEL of 0.1 mg/kg bw per day for mydriasis in a 3-month study in dogs treated by gavage and using a safety factor of 200. An additional safety factor of 2 was applied because doramectin was not tested in CF-1 mice, which is the test animal most sensitive to the neurotoxic effects of this family of drugs. In 1997, the Joint FAO/WHO Meeting on Pesticide Residues (JMPR) concluded that the sensitivity to avermectins of CF-1 mice was due to a genetic variation that causes reduced expression of P-glycoprotein in the blood–brain barrier (FAO/WHO, 1998). The JMPR further concluded that the results of studies with CF-1 mice were not appropriate for establishing ADIs for avermectins. P-glycoprotein was expressed in the brain and jejunum of all species studied. P-glycoprotein is a cell membrane protein that acts to remove a wide variety of lipophilic compounds from cells, including avermectins. In the capillary endothelium of the central nervous system, it serves as a functional component of the blood–brain barrier. In intestinal epithelium, P-glycoprotein can limit intestinal absorption of a range of compounds. The Committee at its fiftieth meeting (Annex 1, reference 134) accepted the conclusions of the JMPR and considered that it was no longer necessary to apply an additional safety factor of 2 for avermectins and milbemycins that had not been tested in CF-1 mice. Doramectin was re-evaluated by the Committee at its present meeting in order to determine whether removal of the additional safety factor of 2 was appropriate. On the basis of the Committee’s decision taken at its fiftieth meeting, the present Committee concluded that use of an additional safety factor of 2 in establishing the ADI for doramectin was no longer necessary. No new data were provided to the Committee. The literature was reviewed for published information on the toxicity of avermectins considered relevant to this evaluation. The Committee reviewed information on the mechanism of the toxicity of ivermectin in a subpopulation of collie dogs and observations of its toxicity in a subpopulation of Murray Grey cattle. The Committee also considered a published review of the relative sensitivities of mice, rats, rabbits, dogs and non-human primates to avermectins. The relative potencies of doramectin, ivermectin and abamectin were also considered. The Committee examined information about variants of the human gene that codes for P-glycoprotein and reviewed observations in humans. 2. BIOLOGICAL DATA 2.1 Toxicological studies 2.1.1 Genetic basis for sensitivity to the toxicity of avermectins (a) Collie dogs The genetic basis for the sensitivity of collies to avermectins was studied in 13 clinically normal collies, previously identified as being sensitive or insensitive to ivermectin. Seven animals were identified as sensitive after displaying typical clinical signs of neurotoxicity, including depression, ataxia, mydriasis, salivation or drooling, after receiving a single oral dose of 120 µg/kg bw. The objective of the study was to determine whether altered gene expression of P-glycoprotein or a polymorphism of the canine Mdr1 gene that codes for P-glycoprotein exists in avermectin-sensitive collies. The sensitivity of the CF-1 mouse strain to the neurotoxic effects of avermectin has been traced to a polymorphism of the murine Mdr 1 gene resulting in decreased expression of P-glycoprotein (Umbenhauer et al., 1997). The level of Mdr1 expression was similar in sensitive and insensitive collies, as determined by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) analysis. Sequence analysis of canine Mdr1 by RT-PCR was conducted on RNA isolated from blood leukocytes obtained from the sensitive and insensitive collies and also from other breeds (one beagle, two golden retrievers and one Staffordshire terrier cross-bred dog). Sequence analysis of clones from three ivermectin-sensitive collies revealed an identical four-base pair deletion in the first 10% of the transcript. This deletion causes a frame-shift mutation resulting in the production of a truncated, non-functional protein. The same four-nucleotide deletion was detected in all samples from ivermectin-sensitive collies, which were also homozygous for the deletion. Insensitive collies had a heterozygous genotype, with one mutant allele and one wild-type allele. Blood samples from all the other breeds showed homozygosity for the wild-type. The investigators concluded that their study provided evidence that the sensitivity of collies to ivermectin results from a frame-shift deletion of four base pairs in the canine Mdr1 gene (Mealey et al., 2001). (b) Observations in Murray Grey cattle Murray Grey cattle on one farm in the central tablelands of New South Wales, Australia, were reported to be sensitive to the toxicity of avermectin B1. The first cases were noted in October 1985, in 50 Murray Grey heifers aged 18–26 months treated with avermectin B1 at an estimated dose of 175–200 µg/kg bw by injection. Three of the heifers died within 2 days of treatment. Two weeks later, 144 Murray Grey cattle aged 4–18 months and weighing 200–450 kg were treated with avermectin B1 at an estimated dose of 120–200 µg/kg bw by injection. The numbers of males and females treated were not stated. Within 48 h of treatment, three steers weighing 400–450 kg developed severe neurological signs, and all three were slaughtered for necropsy. A fourth steer in this group showed mild neurological signs and was slaughtered 19 days after treatment. A field trial was conducted on this farm with 208 Murray Grey cattle, comprising 90 steers that had been treated with avermectin B1 1–2 months earlier and a second group of 118 cattle that had not been treated previously. The animals were weighed and treated with the recommended therapeutic dose (200 mg/kg bw) or injected with the vehicle only. One steer in the group that had not been treated previously developed neurological signs 42 h after treatment and was slaughtered for necropsy. Brain, spinal cord, liver, kidney, lung, heart, spleen, intestines, skeletal muscles, adrenals, lymph nodes and peripheral nerves from the four initial cases, the case found in the field trial and one normal treated animal were examined macroscopically and histologically. No pathological changes were found that would explain the severe neurological syndromes observed. The concentrations of avermectin B1 in plasma and/or serum, liver, brain and spinal cord from the five clinically affected animals and the normal animal were assayed by high-performance liquid chromatography with fluorescence detection. The average concentration of avermectin B1a was 56 µg/ml in brain tissue from affected animals and 4 µg/ml in brain tissue from the normal animal. Two additional field trials were undertaken with Murray Grey cattle in other areas of New South Wales and in Victoria. A total of 83 cattle were treated with at least twice the normal therapeutic dose of avermectin B1. No adverse reactions occurred. The authors stated that no other incidents of toxic effects of avermectins have been reported in Murray Grey cattle. They also noted that the farm on which the adverse reactions were seen had maintained a virtually closed herd for approximately 15 years (Seaman et al., 1987). 2.1.2 Relative sensitivities of mice, rats, rabbits, dogs and non-human primates to the toxicity of avermectins The relative sensitivities of the central nervous system in mice, rats, rabbits, dogs and non-human primates to avermectins have been reviewed (Lankas & Gordon, 1989). The studies conducted with ivermectin addressed acute toxicity in mice, rats, dogs and rhesus monkeys treated orally; short-term studies of toxicity in rats, dogs and rhesus monkeys; and studies of developmental and reproductive toxicity in mice, rats and rabbits. The studies with abamectin given by oral administration comprised long-term studies of toxicity and carcinogenicity in mice and rats, a 1-year study of toxicity in dogs and a study in rhesus monkeys given single doses. The authors concluded that clear species differences exist in the sensitivity of the central nervous system to the toxicity of avermectin, rodents being the most sensitive. A dose of 0.2 mg/kg bw in mice and slightly higher doses in rats resulted in clinical signs of central nervous system toxicity, comprising tremors and ataxia, while these doses caused no adverse effects in rabbits, dogs or rhesus monkeys. The authors described a study of acute toxicity in which groups of two male and two female rhesus monkeys were given abamectin or ivermectin at single oral doses of 0.2, 0.5, 1, 2, 8, 12 or 24 mg/kg bw. The time between administration of the next higher dose to the same group of monkeys was 2–3 weeks. The authors noted that the minimum single oral dose of ivermectin or abamectin that was toxic (2 mg/kg bw) was approximately 10-fold greater than the human clinical dose of ivermectin. Emesis was the only toxic effect observed in rhesus monkeys after an oral dose of ivermectin of 2 or 8 mg/kg bw; the clinical signs of toxicity observed after a dose of 24 mg/kg bw were emesis, mydriasis and sedation. The authors compared the effect at 8 mg/kg bw with effects seen in a child (age and sex not stated) after the apparently accidental ingestion of approximately 8 mg/kg bw. The toxic effects observed in the child were emesis, mydriasis and sedation. In view of the similarity of the toxic effects observed in rhesus monkeys and the child, the authors proposed that rhesus monkeys are an appropriate model for predicting the acute toxic effects of ivermectin in humans. The NOEL for acute effects after administration of abamectin or ivermectin to rhesus monkeys was 1 mg/kg bw. The review of the developmental and reproductive toxicity of ivermectin included the results of studies conducted in mice, rats and rabbits. The reported NOELs for maternal toxicity in mice, rats and rabbits were 0.1, 5 and 3 mg/kg bw per day, respectively. The reported NOELs for developmental toxicity in mice and rabbits were 0.2 and 1.5 mg/kg bw per day, respectively. A NOEL of 0.2 mg/kg bw per day was reported for neonatal and developmental toxicity in a multigeneration study in rats (Lankas & Gordon, 1989)." this is the link to the whole article http://www.inchem.org/documents/jecfa/jecmono/v49je02.htm#2.1.1.2

thats the point. how often are we told this only happens in purebreds because they are inbred? or the breeder is unethical, either way the result is the same finger pointing and guilt directed. yet the same occurs in the so called hybrid vigour filled x breds. nothing is that black and white yet so much has been slated against purebreds when this happens in their ranks. do you understand?

trouble is reporting stuff like that is more likely to get you accused of being paranoid and being a conspirity nutter. if you are thinking that...google Ivemectin n murry grey cattle...n collie dogs did some myself. very interesting the ones who react have a gene all right that doesnt cope. so is it the fault of the animals or people they carry a gene the new u beut wonder drug affects or the manufacturers for not designing one that doesnt kick into that gene? chicken before the egg really. one of the leaders in the field of designing worming drugs in the very early days it was mooted should we select for worm risistant animals? or drenches to protect all? they went the drench way and after decades of trying to outwit the constantly evolving worms to resistance to every one of them in an astonishing amount of time, he wondered if he and his collegues had made the wrong choice. his name is Hugh Gordon. or H Mc Al to many. http://en.wikipedia.org/wiki/Hugh_Gordon there have been some significant worm resistant strains of sheep that were not continued with unfortunately. so the choice was and still is out there. as well they discovered strains of nemanaphargic fungi (guessing at the spelling) that actively hunt and eat worm larve in the field. this is them http://notexactlyrocketscience.wordpress.com/2007/12/15/prehistoric-meat-eating-fungus-snared-microscopic-worms/ there are strains that exist that eat the larval stages of sheep and cattle worms and inoculated onto feed and fed to cattle and sheep, they kill and eat the worm larve passed in the manure. years later the paddocks when tested still had the fungai working, fasinating stuff. wonder if there are ones that hunt dog worm larve as well?

cannot name names for obvious reasons but quite a few vets have admitted to me they now no longer give the full dose. one was shocked to see a puppy he had just vaccinated colapse and die while he was still holding it. Never wants to experience that again. so is it faulty parents or fault in the makeup of the new vaccines??????????? incidently i have no idea why vets bother to have insurance or the drug companies. even when a known faulty batch kills for example 600 before its withdrawn the owners of the dead are never told, nor compensation ever a possibility. i know because one batch of kitten vaccine was contaminated and killed an entire litter of at the time extremely rare lilac himilayan kittens. we only discovered they were killed by the vaccine when a friend working at the company saw the recall notice and the death figures reported in by the vets and over 600 notifications of the dead were received at the office of the vaccine company before the recall went out.

From my own experience I dont entirely believe its the puppies parents at fault. none of this happend until the vaccine companies came up with a "better" vaccine. forget the year but its over 10 years ago now. I bred my first pups in 1979 and up until about 1983 or there abouts never lost a pup after vaccination. same family of dogs in some cases same parents. then the new u beaut more "effective" vaccine was released. that day I took 10 pups for their vaccinations. next morning all but 4 were dead. another two had their immune systems shut down over the next 2 weeks and they too died. that was three litters of pups the parents of two of the litters had previous litters vaccinated with the "old" vaccines with no reactions whatever. by the second lot of puppies to be vaccinated and equal death rate i realised this was the new reality to vaccination. and yes when I phone the company was told, "its only the small breeds dying" change to a bigger breed. and no they had no intention of researching a safer version. so? are our dogs really now carrying a "new" weakness gene. or like the murry grey cattle and collie dogs the victums of a new drug that was not tested for safety sufficiently. eg ivermectin. this culling of the innocents because a new improved product is killing a percentage of who they are supposed to be vaccinating would never be tolerated if the babies were human surely? at the time i raised the question on a forum and to my astonishment the replies came thick and fast. even adult dogs were dying after their booster shots. and its taken how long for it to be disclosed that the yearly shots are severe overvaccination but (maybe more likely didnt believe or want to), it was a guaranteed income. only in the very recent past has it been acknowledged that once they have had their initila shots yearlies are not needed. well thats for the survivors that is. many vets flatly refuse to give a reduce dose. i have found the only way to have the puppies survive in reduce the dose so i will not use a vet who will not consider a half dose. for goodness sake they give the same dose to a great dane weighing ten and more times that of a toy breed puppy. and yes it does work and no i havent lost any to disease despite protests that the vaccine is not guaranteed to work at less than the recommended dose. well given the choice that the full dose none of the dead puppies will ever catch any disease they are right on the ball there.

clicked on one of the links at the bottom of the Link in the previous post. very interesting reading Looking over the Fence Sometimes others face similar problems and express themselves in such a perfect manner, that it is well done to read their take and apply it to one's own situation. One such is the article "The biggest problem" by C.A. Sharp, a dog breeder who has faced many, repeated and enduring troubles while trying to instill some sense of responsible and genetically sound breeding in her favorite breed. What she writes here about the reactions of breeders so epitomizes common reactions among breeders of just about any type of animal, including the recent reactions of the Akhal Teke breeding community, that it can serve to explain what is happening exactly (when people deny genetical diseases), why they do it and how this ought to be understood. We can only underline ourselves what C.A. Sharp concludes with: we should openly talk about this, not deny it and find ways to deal with it. The Biggest Problem by C.A. Sharp We have met the enemy and he is us. --Pogo Within a year and a half of obtaining my first Aussie for show and breeding, I slammed up against the reality of canine genetic disease. I remember standing in the vet’s office staring at the first set of hip x-rays I’d ever seen as he explained that Patte was dysplastic. He pointed out features that demonstrated the problem, then asked if I still wanted it sent to OFA. Patte had pre-limed “Good” at a year. I sent them in hoping the vet was wrong. He wasn’t. I got Patte when her first owners gave her back to the breeder because the father lost his job. The breeder thought the 8-month-old had potential and, knowing I wanted an Aussie I could show, placed her with me on condition that she got a litter before I got the papers. She found a stud and had the preliminary OFA x-ray done. I helped with transport to the distant stud and took care of Patte and the litter, so the breeder let me keep one of the pups, expanding my kennel-to-be to two breeding-quality bitches. In anticipation of having a litter all my own, I’d booked Patte to a well-respected stud. Then OFA’s hammer fell. I called the breeder, who was also my mentor. She was very sorry Patte had failed OFA and agreed that breeding her again was out of the question. When I expressed my distress at having to call the stud owner to say why I couldn’t bring Patte to her male, the breeder’s tone changed. "You can’t tell anybody about this. It will ruin your reputation and nobody will have anything to do with you.. It will also ruin mine." She went on to tell me that it could ruin Patte’s litter, the sire of that litter and even the dog to which I had booked her. She made it very clear that no one should ever know what was wrong with Patte. I knew so little and I thought she knew so much. I trusted her guidance, but her advice left me numb. I called the stud owner and made a lame excuse to cancel the breeding. I don’t remember what I said, but I know it was a lie. I could tell the stud owner knew I wasn’t being straight with her. I felt dirty. This happened to me many years ago, but genetic disease continues to inspire a range of negative human behavior, wrapping the subject in a shroud of secrecy and denial. Today, I am a breed health advocate and lay genetic counselor. I frequently find myself in the middle of situations like the above. Intimidation to enforce silence, the fear of speaking out, and inability to face facts, not to mention outright lies, are in my opinion the biggest problem breeders face in the attempt to control genetic disease in purebred dogs. There are many conditions for which science still has too few answers. The expense of testing can be prohibitive. Some diseases occur so late in a dog’s career, it will already have puppies and maybe grand-puppies on the ground. All of these pale beside our too-frequent refusal to be honest with ourselves and each other. Those of us who consider ourselves to be truly dedicated to the preservation of purebred dogs must make a dispassionate analysis of the human behavior surrounding canine genetic disease and realize what it is doing, not only to our dogs, but to ourselves. The Incorrigibles You all know them. The ones who put winning above all other goals. “It doesn’t matter as long as the dog wins,” is their mantra. Their dogs must win, as must their dogs’ offspring, and woe betide anyone who stands in their way as they pursue greater breed—and personal—glory. The full range of the Incorrigibles’ ego-driven behavior is beyond the scope and purpose of this article, but it clearly affects genetic disease control. If a genetic problem isn’t apparent, they will ignore it. If it can be fixed, they will. If it can’t, they will employ some variant on “shoot, shovel and shut-up,” or recoup their losses by shipping the dog a long ways away, preferably across an ocean or two. If someone else knows about the problem, the Incorrigible will use any means at his disposal to shut that person up, ranging from veiled threats and rumor-mongering to blatant bully-tactics and threatened legal action. Nothing can be done to change these people. They are who they are and it is unlikely that any act of man or God will alter their course. However, the rest of us can alter our behavior toward them. The most effective manner of dealing with a bully is to refuse to be bullied. It is hard to keep this in mind when an Incorrigible is threatening you with death, destruction and lawyers. This is especially so if the Incorrigible has a Big Name and you are Nobody (of which status the Incorrigible will frequently remind you.) She will rally her hangers-on to harass and snub you. It hurts to be treated like this, but take a deep breath, give your dog a hug and remember that people who act this way were never your friends in the first place. If La Incorrigible is upset, that is her problem not yours. In very few cases can an Incorrigible really do anything to you other than attempt to make you miserable, though if you’ve made the mistake of getting into contractual agreements with such a person you might do well to get a little legal advice on what you can and cannot do in the situation. An ounce of lawyer ahead of time is worth 175 pounds of lawyer in court. You may find that the Incorrigible’s legal threats are groundless. One thing that has always amazed me about Incorrigibles is how many people will speak among themselves about how unprincipled and ruthless they are and yet these same people will do business with them without the blink of an eye. If a person has a reputation as a jerk or dubious honesty, why deal with him? If he has treated others poorly, why would you think it would be different for you? "Ah, but their dogs win!" If this is your rejoinder, may I humbly suggest you re-evaluate your priorities. Do so with the picture firmly in mind of a child who has just been told his beloved dog has to be euthanized because it has a devastating hereditary disease. The Ostrich Syndrome We have trained ourselves to fear genetic disease in our dogs. Rather than approaching it as just another obstacle a breeder must overcome on the path to producing quality dogs, we react as if we have come caught a socially unacceptable disease. “Love me, love my dog” mutates to “my dog’s disease, my disease.” The normal first reaction of anyone confronted with a bad situation is denial: “This can’t be happening to me!” But this phase should soon give way to emotions better suited to deal with the problem at hand. Unfortunately, some people get stuck at the denial stage. I have long referred to this as “the Ostrich Syndrome.” The Ostrich will find numerous excuses and justifications for not performing screening tests. He will promise faithfully to get screening done, then fail to do so. He will make no effort to follow-up on indications that something may have occurred in a dog he produced. But ignorance is not bliss for those who have dogs from an Ostrich with a hereditary disease in his line. An example of the Ostrich Syndrome gone malignant can be found in my own breed, the Australian Shepherd. Epilepsy is a growing problem. It is a difficult disease to diagnose and many things other than epilepsy can cause seizures. Unfortunately, this gives a dedicated Ostrich plenty of maneuvering room. There are many Ostriches who have or have produced epileptic Aussies, but the testing doesn’t get done, they won’t cooperate with an on-going research project, and what “really” happened is the dog hit it’s head/got into ant poison/had heat stroke and so on. Apparently these dogs hit their heads, eat poison or overheat every three to four weeks. A person stuck in denial can be difficult to dislodge. If someone you know is exhibiting Ostrich tendencies, try to reason with them. Avoid public discussion of the Ostrich’s weak spot and don’t be confrontational or accusing in your approach, as this will probably encourage the Ostrich to shove her head farther into the sand. Always be alert for Ostrich tendencies in yourself. If a health situation comes up in one of your dogs, do your best to put your emotional reaction aside, think about the facts and consult with vets and others who may give you factual insight to the situation. If you find yourself saying, “I can’t deal with this” or “it can’t be true,” you may be on the way to Ostrich status. Circling the Wagons and Feeding Frenzies Fear of genetic disease can spur group behavior. If someone does something to point out a possible genetic problem in a line or family of dogs, owners and breeders of those dogs may “circle the wagons” to fend off the perceived attack. A united front can be a very effective defense. Sometimes the defenders will be camp-followers of a big name with whom they wish to curry favor, but more often than not they are people who are threatened by unsolicited and unpleasant news. The latter is an example of group Ostrich Syndrome, a firing squad for the messenger being more comfortable than facing facts. The more pernicious examples of “circle the wagons” behavior include things like the suppression of health survey results and the stifling or outright cancellation of informative articles in club publications. Every so often, some brave soul will make a very public statement about hereditary disease in specific dogs. Often this is done by placing an ad listing the names and perhaps pedigrees of affected dogs or posting them on a breed discussion list or website. Angry private and public attack often ensues, building to a feeding frenzy in the letter columns and chat lists. I’ve watched the scenario unfold several times in my own breed and heard of it happening in others. Negative reaction from some who own relatives of the affected dog is not surprising, but even those with no personal stake in the matter sometimes feel it necessary join the attack. The public confessor will be accused of lying or being misinformed, even if he has thorough veterinary documentation of the disease. Sometimes the protest boggles the mind, as in a letter to a breed magazine excoriating the confessor because she had placed a proven disease carrier in a pet home! The feeding frenzy is that which most discourages otherwise honest people from speaking out. Standing up under the brunt of public and rancorous attack is difficult. Not everyone has the emotional or moral strength to do so. The confessor can feel isolated and very, very vulnerable. However, a reverse on the “circle the wagons” technique may help. In most cases, if your dog develops a hereditary disease you will not be the only person it has happened to. A number of years ago Collie Eye Anomaly was a hot-button topic among Australian Shepherd people. A group of breeders with affected dogs went public together, taking out an ad in the Aussie Times listing their names and the names of their affected dogs. They did a follow-up a few months later after they had instituted a test-mating program to clear unaffected relatives. Public comment was positive, though the silence from some quarters was deafening to those in the know. By uniting publicly, they avoided the feeding frenzy that had greeted earlier CEA confessors. Honest Sam’s Used Dogs There was a time when sexually transmitted diseases were not to be discussed in polite society. Sometimes it seems canine genetic disease is still there. People will go on at great length about the minutiae of coat color, roundly condemn purely aesthetic “faults,” and at the same time refuse to discuss other genetic situations which have a clear impact on a dog’s health and soundness. More than one person seeking my input has bemoaned his inability to get any useful information about hereditary disease issues out of people from whom he wants to buy a dog or whose stud he is considering. Since there is no such thing as a 100% genetically “clean” line, these potential customers are justified in their frustration. Think about the process of buying a car. You like the way it looks and have read extensively on its performance triumphs. You may even have taken it for a spin and been impressed with the way it handles. But when you ask the salesman about its background, he knows nothing and swears it’s never needed so much as the tires rotated or the oil changed. You decide to do a little independent research before you commit, but consumer reports on the car don’t exist. You can’t find any on other models by that manufacturer. In fact, you can’t find anything but glowing promotional accounts of the manufacturer’s past history, usually generated by an in-house marketing staff. Dealing in dogs can leave you with much the same experience. It is very difficult for the newcomer who has no connections or frame-of-reference, but even the experienced can find themselves floundering in a sea of non-information. While the actions of others in this regard are beyond your control, how do you behave when you are the “car salesman?” Within a couple years of my experience with Patte’s hip dysplasia, I decided I wasn’t going to lie. When discussing my dogs with others, both in the process of doing business and casual conversation, I was up front about Patte’s problem. And I certainly appreciated the breeders who were open with me about the weaknesses along with the strengths of their dogs. We all need to muster the strength of character to bring genetic disease out of the closet. Be willing to say, “When I did this cross, I got that problem in two of six puppies.” No breeder can make good choices when the facts are hidden. If problems occur, the fault lies with the person who neglected to inform the breeder of the potential. There would be far less problem with inherited diseases if everyone would approach them with the same attitude we take with faults in conformation or performance. These issues are openly discussed at great length. Informed breeders will know that if they cross to dogs from that kennel they may lose some intensity in the trial arena or bring out the straight stifles that lurk in their own dogs’ background. This can be weighed against the positive attributes that kennel can bring them. Genetic disease should be a similarly open book. The Face in the Mirror Ultimately, the responsibility for controlling genetic disease belongs to each of us, individually. I hated living a lie in regard to Patte’s hip dysplasia. I finally realized that if I wanted to be able to look myself in the eye when I happened upon a mirror, I had to quit lying about it. Stand yourself squarely in front of that mirror and ask, “Am I in denial? Have I done anything to gang up on those who have been outspoken about genetic problems? Have I done anything to aid and abet an Incorrigible? Have I committed “sins of omission” when dealing with my fellow breeders?” Only you and the face in the mirror know the true answers to these questions. Only you know if the face you see there is friend or foe in the fight against canine genetic disease. Copyright 2000 C. A. Sharp

I just love it when something like this turns up in someones purebred breeders litter. I can just about guarantee the owner of the bitch will say it must have come from the sire. The owner of the sire will say it has come from the bitch. both owners are posative their darling is the victum in this AND anyone that hears of it will say,,,,,,INBREEDING did it... such fun. oddly enough we dont hear about this happening in x bred litters. maybe because its not encouraged for someone whelping a x bred litter to talk about on purebred forums. thanks for posting. although I have related previously the three samoyed x Labradors all with hip displacia that a friends family bought egged on by the garden gnome convincing them that designer is the only way to go if its a sound puppy you want. If you are wondering, yes i have a very warped sense of humour. all the finger pointing that goes on when mother nature decides to pop up disasters and no one looks at the fact that every conception is a huge genetic gamble along with the building blocks can get mixed up in the process and absorb or abort, many conceptions never make it through to birth. even.

I think you could bet your bippy on that one.

of course not...only unethical breeders have problems like that dont they? actually i only now finished reading this page... certainly food for thought re breeds and closed stud books. Very interesting reading, enjoy http://www.akhalteke.info/genetic-de...s-1-70-en.html haven’t checked out the rest of the site yet. Gee that herda is horrible..their skin comes off???????? "Omertà - or the Conspiracy of Silence The expression "conspiracy of silence" relates to a condition or matter which is known to exist, but by tacit communal unspoken consensus is not talked about or acknowledged. Conditions considered shameful or disadvantageous by society or a certain group of people result in avoidance of recognition of some problem in order to officially bury or hide it and thus prevent accusations, investigations or liability. A conspiracy of silence in some field has effects at many levels: those who are directly suffering, or causing others to suffer, perpetuate their cycle of harm and suffering, those who have suffered have their suffering extended by being having their condition ignored or minimized, and are not considered seriously or redressed appropriately, lessons that might be learned for the future are not learned, conditions are exacerbated or even this way allowed to become entrenched in the first place. Conspiracy of silence is a well-known and much executed behaviour among many if not most modern breeders. Unlike breeders of former times, who had to present animals well able to perform and had no problem with destroying those individuals which were showing faults or defects, especially as their livelihood usually depended on their good name in this respect, many if not most modern breeders are more or less hobbyists or - if themselves professionals - selling mainly to hobbyists. Unless they are selling directly to the meat market that is. These hobby breeders usually feel that the name of their breeding is riding on the health state of their animals, or indeed often considerable amounts of money invested are riding on the trust customers and fellow breeders place in them or they do not wish to start over rsp. are unable to buy new breeding stock. In view of the fact that since roughly 100 to 150 years ago studbooks of most pet breeds are closed as a rule and in view of the advent of pure showbreeding also among many if not most pet animal species, decisive and relentless culling has become more necessary than ever. As can be seen in nearly every pet breed which deviated from breeding for practical work, the assault (on genetic and general health) of inbreeding, genetic load, popular sire syndrome and omertà has led to genetic diseases cropping up and spreading through the genepools, as well as a general loss of health values. While horse breeds are not affected as fastly as small pet breeds due their larger generation span, they most certainly are not immune to this mechanism. Quarterhorses with HYPP, HERDA or EPSM, Arabians with LFS, SCID or CA, or Friesians with hydrocephalus or dwarfism, these are just a few examples for genetic diseases spreading like wildfire through either closed genepools or genepools bred heavily for show and perusing largely popular sires to do that. In all of these cases, in every one of them, the conspiracy of silence has seen to it, that the silence of breeders and owners alike allowed the initially but few cases of grave genetical diseases to spread throughout the whole breed, in some cases to the extent that so many individuals are carriers that culling becomes impossible. Only when so many animals are touched by the relevant problem, that at one or other point affected horses get sold to people unwilling to keep silent about it, a grudging acceptance takes place. Rescue measures at that stage then come much too late and the usual testing frenzy is more often than not just windowdressing. An additional problem is that in small, closed genepools even with testing there soon comes a point when the genepool consists of so many carriers that finding good, fitting breeding pairs is a major difficulty. The longer a disease is not talked about and not taken into calculation, the sooner that state will be achieved. E.g. among Friesians this already has resulted in semi-opening of the before firmly closed studbook and strict rules as to lower inbreeding coefficients. This, one needs to say it clearly, is a breed with way more than 10,000 breeding individuals worldwide and still it was discovered to not be sufficient to cull within the closed genepool only. The situation for the Akhal Teke with its much, much lower amount of breeding animals, may quickly become much more serious. Already today the genetic diversity of the breed is insanely low, an AVK of 30-50% (instead of at least 85%) in modern horses should ring any breeder's alarm bells long and hard. Next comes the fact that we already know that several of the extremely popular sires were or must have been carriers of the lethal recessive "Hairless Foal Syndrome". Such horses as 943 Arslan, 736 Keymir or 1054 Gilkuyruk, cases leading back to the immensely influental 448 Kir Sakar, 44 Bek Nasar Dor or 244 Toporbay, can be found by now in every single horse pedigree. That general genetic load and inbreeding depression also is by now taking its toll, should not be negated either, with a major lowering of the average life expectancy of the more recently born horses and the cropping up of such potentially polygenetic diseases as Wobbler Syndrome, Kissing Spine, ringbone, allergies, DLSD or OCD. There is but one way to deal with this for buyers, especially when on the brink of acquiring very expensive horses: • have the horse thoroughly checked by a vet, not the stable vet of the breeder, choose your own vet and make absolutely sure that he is not connected to the breeder! • tell this vet about the potential problems he needs to carefully check up on: Kissing Spine, Wobbler Syndrome, OCD, DSLD, skeletal problems related to early work and overfeeding/pushing of foals • if an independant vet cannot be engaged on place, make the sale and payment of the horse dependant on a thorough check-up done by your own stable vet. Arrange escrow of the payment with a trustworthy firm until the health of the horse has been cleared to your satisfaction. • ask the breeder about such ancestors in the pedigree which may be or have been carriers of the Hairless Foal Syndrome and demand an evaluation by the studbook management prior to the sale. Have this evaluation checked by an independant geneticist! • ask for a calculation of ancestor loss and inbreeding of your horse and if the intention is breeding, have the potential partners of it evaluated for pairing and the values possible foals will achieve. • do not take the simple word of a breeder as being fact. The Akhal Teke may be a rare breed, it however is not different from any other animal species. If claims are made as to potential performance and abilities, ask for direct proof of what the direct ancestors of that horse actually and provenly achieved in those fields. The most important thing to remember is the age-old saying: CAVEAT EMPTOR! As the buyer, you are the one who has to beware. Hopefully critical customers of these horses will eventually force breeders to see the sense in breeding for healthy workable horses, in becoming aware and open about the genetical problems the breed is facing and in using modern methods and knowledge where they can help avoid or combat genetic diseases and genetic load." the really interesting thing about this article is the comments re the closing of stud books being a part of the problem. Thus the problem now will be even worse since most horse registeries mandatory dna has been brought in, this was done because it was known that "some" breeders were introducing "outside" blood, but how to stop them without "everyone else finding out and devaluing the breed" now of course that cannot happen anymore. wonder if it was such a great idea after all? my husband pointed out an interesting fact we seem to be overlooking. the cane toad in australia has a completly closed studbook. apparently the billions of the buggers now inhabiting this country are descended from less than 128 original cane toads. re rabbits "The current infestation appears to have originated with the release of 12 wild rabbits by Thomas Austin on his property, Barwon Park, near Winchelsea, Victoria, in October 1859 for hunting purposes." how many actually were released is pure speculation but considering the stud book was certainly closed there are billions of them now. the australian possum was released in new zealand. again only a few were imported, there are now millions of them all descended from a closed stud book. as for the deer in new zealand...again millions of them from a very small importation. again a closed stud book? something does not make sense here? any idea's? looks to me like mother natures playing ducks and drakes with us all right.

i prefer the barker to the attacker. decades ago we were given a 24/7 barker, nothing worked so gave him to a car yard in an industrial area. they never had a break in over the 10 + years he was on patrol. he was one big dog and looked agressive. little did they know only the volume would have done the damage. one of my ACD's was a silent and used to worry me, as she would dive out of sight and only come out and stare them down when they knocked on the door. always worried what if , while i was out. found out one day. had come home acros the paddock and she didnt know i was home. a gent was knocking on the back door as i came in the front. before i could call out or get to the door i could see her through the window she came out stared at him and he made a run for his car. she went in slow motion after him. giving him time to make it to his car, then she went into high speed. hit the door with her paws doubling its speed in slamming shut and began barking and growling at the window. at least i now knew she wouldnt bite just for the sake of getting someone. although scaring the daylights out of a +70 wasnt a good idea either.

sad how shabbily both she and her dogs have been treated... how disgusting to remove the colour from the standard especially since it had been there 100 years. but then it is pretty typical of the fanitics that seem to think they and their dogs are more special than others. n as she notes has reduced the gene pool in the process.

Because it's a well-known fact that cows can't breathe through their mouths. The point of baiting wasn't to kill the bull by suffocation, the pinning of the nose was to bring the bull down, where it is less capable of defending itself by kicking or crushing the dogs. And as someone already pointed out, that was bulldogs anyway. You'd think they'd check statements made by "experts" and edit them from the story if the "expert" turned out to be a mouth-breathing moron. Kind of makes me wonder why you never hear bulldogs being accused of attacks.. :rofl: O my ... well for starters maybe its because their legs are too short to reach past anyones ankles unless they fell first. then because if they are going to it will be a lick em to death experience????????

Yet this breeder would most definately be branded unethical n puppy farmer here anyway. http://whitedobermanpuppies.com/index.html

spotted this on a puppy website. agree with the owner of the site. definately required reading. When I was a puppy, I entertained you with my antics and made you laugh. You called me your child and despite a number of chewed shoes and a couple of murdered throw pillows, I became your best friend. Whenever I was "bad," you'd shake your finger at me and ask "How could you?" - but then you'd relent and roll me over for a belly rub. My house training took a little longer than expected, because you were terribly busy, but we worked on that together. I remember those nights of nuzzling you in bed, listening to your confidences and secret dreams, and I believed that life could not be any more perfect. We went for long walks and runs in the park, car rides, stops for ice cream (I only got the cone because "ice cream is bad for dogs," you said), and I took long naps in the sun waiting for you to come home at the end of the day. Gradually, you began spending more time at work and on your career, and more time searching for a human mate. I waited for you patiently, comforted you through heartbreaks and disappointments, never chided you about bad decisions, and romped with glee at your homecomings, and when you fell in love. She, now your wife, is not a "dog person" - still I welcomed her into our home, tried to show her affection, and obeyed her. I was happy because you were happy. Then the human babies came along and I shared your excitement. I was fascinated by their pinkness, how they smelled, and I wanted to mother them, too. Only she and you worried that I might hurt them, and I spent most of my time banished to another room, or to a dog crate. Oh, how I wanted to love them, but I became a "prisoner of love." As they began to grow, I became their friend. They clung to my fur and pulled themselves up on wobbly legs, poked fingers in my eyes, investigated my ears and gave me kisses on my nose. I loved everything about them, especially their touch - because your touch was now so infrequent - and I would have defended them with my life if need be. I would sneak into their beds and listen to their worries and secret dreams. Together we waited for the sound of your car in the driveway. There had been a time, when others asked you if you had a dog, that you produced a photo of me from your wallet and told them stories about me. These past few years, you just answered "yes" and changed the subject. I had gone from being your dog to "just a dog," and you resented every expenditure on my behalf. Now you have a new career opportunity in another city and you and they will be moving to an apartment that does not allow pets. You've made the right decision for your "family," but there was a time when I was your only family. I was excited about the car ride until we arrived at the animal shelter. It smelled of dogs and cats, of fear, of hopelessness. You filled out the paperwork and said "I know you will find a good home for her." They shrugged and gave you a pained look. They understand the realities facing a middle-aged dog or cat, even one with "papers." You had to pry your son's fingers loose from my collar as he screamed "No, Daddy! Please don't let them take my dog!" And I worried for him and what lessons you had just taught him about friendship and loyalty, about love and responsibility, and about respect for all life. You gave me a goodbye pat on the head, avoided my eyes, and politely refused to take my collar and leash with you. You had a deadline to meet and now I have one, too. After you left, the two nice ladies said you probably knew about your upcoming move months ago and made no attempt to find me another good home. They shook their heads and asked "How could you?" They are as attentive to us here in the shelter as their busy schedules allow. They feed us, of course, but I lost my appetite days ago. At first, whenever anyone passed my pen, I rushed to the front, hoping it was you - that you had changed your mind - that this was all a bad dream...or I hoped it would at least be someone who cared, anyone who might save me. When I realized I could not compete with the frolicking for attention of happy puppies, oblivious to their own fate, I retreated to a far corner and waited. I heard her footsteps as she came for me at the end of the day and I padded along the aisle after her to a separate room. A blissfully quiet room. She placed me on the table, rubbed my ears and told me not to worry. My heart pounded in anticipation of what was to come, but there was also a sense of relief. The prisoner of love had run out of days. As is my nature, I was more concerned about her. The burden which she bears weighs heavily on her and I know that, the same way I knew your every mood. She gently placed a tourniquet around my foreleg as a tear ran down her cheek. I licked her hand in the same way I used to comfort you so many years ago. She expertly slid the hypodermic needle into my vein. As I felt the sting and the cool liquid coursing through my body, I lay down sleepily, looked into her kind eyes and murmured "How could you?" Perhaps because she understood my dog speak, she said "I'm so sorry." She hugged me and hurriedly explained it was her job to make sure I went to a better place, where I wouldn't be ignored or abused or abandoned, or have to friend for myself - a place of love and light so very different from this earthly place. With my last bit of energy, I tried to convey to her with a thump of my tail that my "How could you?" was not meant for her. It was you, My Beloved Master, I was thinking of. I will think of you and wait for you forever. If you are not crying now you can not have one of our pups! Never take one of our pups to a shelter or rescue! Bring them back to us, we will care for them and find them new homes... They are our babies and we will never abandon them!

my aunt used to breed bull terriorists, LOL. yep scary dogs all right, help the burgler carry out the furniture that lot.

since the topic is roos, i dont think your thoughts are too OT. I dont understand how that roo with the broken neck was kept alive. thats no quality of life for him. ooo if you want a good laugh, (yes off topic) go to the dairy display at any show and what the reactions and whats said by the kids seeing a cow milked for the first time... particuly if offered some of the milk to taste..... absolutely amazing how many didnt know and as one said "grossed out"

having a friend who took up roo harvesting/roo shooter. went out with them for a week. ye gads. had nightmares for years. every shot landed just behind n slightly below the ear. clean kill every time. n im talking hundreds. only once did they accidently hit one with a joey in the pouch and it was tiny. and put down immediatly. the realisation what these men could do if they went nutters like the strathfield massacre scared me witless. as for why do they cull. most of the stations we went through there were more roos per paddock than sheep. no wonder the farmers are having it tough, in the droughts its even worse. plant crops for your stock and its a sea of roos every night. those who think the eastern grey or the big fellas are endangered need a trip out coonamable way. to me i felt pretty sorry for the farmers. they supply the feed and water, pay the rates and the roo shooters harvest a crop on their land and pocket the proceeds... nice job if you have the talent and it sure is a talent. i couldnt shoot that straight night after night like that. also. they never took small ones.. always the biggest...so considering the majorty of a mob are mid age and younger there wasnt any culling of the females unless they were really big ones . no no reduction in next generation. so little relief for the farmer long term anyway.

interesting he says dogs dont pass it on? not what the family who were pressured into putting their kelpie down dont need to find out after the fact

I know how disappointed when a old time breeder sold me a "brood bitch" 12 months old knowing she had grade 4 luxating patella. being a novice i didnt have a clue what i was looking at, but sure learned fast. if there were photos of the different grades walking, newbies would know on the spot what they were looking at. who knows, maybe even that old breeder didnt realise what it was. my vet sure did.

if breeders got off their collective butts and began addressing reducing the incidence of breathing , walking, u name it problems that puppy buyers find in their pets...... surely a breed that needs constant vet care needs reevaluating by the breeders long before a doco like "pedigree dogs exposed " ever got the chance to be made? its been a long time comming. now the pidgeons have come home to roost and there is more butt covering than proacting.. pity

now you are on the mark. everyone and anyone can become interested in becoming a registered breeder. just as there are billions of people now on this planet there are equally billions with very different ideas. the big mistake members of the canine bodies made was decide to begin witchhunts for "backyard/puppy farmers" among the registered breeder ranks. instead of witchhunts in which as usual no one can even agree on what that actually constitutes. why couldnt it intead be an education program.. on the lines of.. What are you looking for in a Pedigreed puppy. educate puppy buyers what to look for! bright eyes, clean coat, health checked parents etc etc learn the breeds strong points and the problem points. do you mind if your puppy's parents have 3 hernia's as long as they are australian champions.? do you mind if the parents never saw a show but look lovely AND dont have hernia's? the list can get pretty long but isnt educating a buyer what to look for themselves going to help? always ask can you return the pup if your vet finds something not right? if the answer is no, keep looking. ... does mum and dad walk normally, do their eyes look normal? what does their mouth look like? if they look odd then the puppys could too. surely this would sort out things far better and less damage to the membership than witch hunting? i asked this question a very looooooong time ago and no one seems to be learning much and look where its got them. running scared because now all registered breeders risk being branded...just like they were warned in the first place. told u so has a nice ring to it.

There is a heck of a lot of confusion. ive friends who have told me they have bought a "registered" dog or puppy. when they show me the "registration" its their microchip papers for council registration????? so to many people "registered" is assumed to mean pedigree but they have no idea what they are supposed to receive for that. In these cases all they have is a lifetime registration with the council one word can sure have a lot of different meanings cant it?