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< Back Nia ACK/CKC Moyen Poodle 40lb / 21" Tall OFA Hip-Good/elbows-normal Eye CERF- Good / * v Wd-clear Heart -Clear / *OFA Thyroid-Clear

Family run dog breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Our Family Our Family- Family is not always born but brought together by God in Love. We have 10 children and 16 Grandchildren and 7 Grandchildren not by name by Love from our Former Foster Daughters. We live in the rural/resort area of Deep Creek Lake, MD. We love to Ski, Boat, Hike, Bike and Swim. Our Children range from 38 to 6 years of age. And our Grandchildren range from 14 years of age to 1 year old. All About Me TLC’s promise to you: We strive to raise a very socialized, friendly and most importantly a healthy puppy. We do all we can to guarantee you a healthy, happy puppy. Our puppy's parents are Health tested to assure to the best of our ability that you receive a happy puppy. We have been breeding standard poodles since 2005. Goldendoodle and Sheepadoodle since 2010. Bernedoodle since 2018 We have many in the agility, and show rings, but our pride is the ones that are serving in therapy and service work. We are State/County AKC Licensed and inspected. VIEW OUR FACILITIES View Here

Family run dog breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. ABOUT US Learn about our family READ HERE! Our Team Learn about our facilities READ HERE! Meet our staff READ HERE! To play, press and hold the enter key. To stop, release the enter key. Dog Breeder, Poodle Puppies for Sale, Doodle Puppies for sale

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Payment Puppy Deposit Puppy Pampering Personal Checks will not be accepted at pickup. Personal checks must be received up to a week before delivery. Confirm your Purchase and Secure the Puppy of your choice by filling out a Puppy Application! A final copy of the Sales/Health contract with signatures be sent to you by E-signature. If your puppy is being shipped by flight nanny, we will ratify the contract through email along with full payment including shipping costs before the puppy flys out. We accept PayPal, Venmo, Apple Pay, and Zelle, allowing you to use your credit or debit card if you wish to place a deposit to hold a particular puppy (minimum $350) or to be put on Deposit wait list. We have been a verified PayPal member since 2005. All deposits (up to but not exceeding $350) are non-refundable, Non transferable to another person but transferable to future litter, to cover the cost of care and re-advertising, etc. Visit our payment page HERE . 3.5% is added to cover the PayPal processing fee. Venmo, Zelle nor Apple pay will not charge you a 3.5% fee. Deposit of $350.00 to hold a pup for you for 3 days after pup turns 8 wks or on older pups one week after deposit is made at which time the balance is due. If you are unable to Pick up your puppy at the time it is ready you need to move to another litter or arrange for a puppy pampering week or a puppy boot camp. Cash, cashier check, PayPal or Credit card at which time pick up/delivery needs to be arranged. A fee of $26.00 a day will be assessed if the puppy is not picked up by 9wks of age. We also can set up payment arrangements up until the puppy is 8wks, and pickup/delivery of the pup when paid in full! We accept Paypal plus a 3.5% Paypal fee, or Venmo or Apple pay, Post Office Money Orders, Cash or Cashiers check ! We collect 6% MD State tax NO EXCEPTION Make Checks (No personal checks will be accepted at delivery but may be malied to TLC at least one week before delivery) or Money orders/cashiers checks(accepted at pickup) payable to: TLC By the Lake 1886 Mosser Rd McHenry, MD 21541 301-501-1818 How to pay final invoice Paypal To make final payment on Paypal We can Send you a Paypal.Me/TLCbytheLake/$ Link Paypal.me/TLCbythelake/$(insert invoice amount) Here's how to send a payment using PayPal.Me with the app: Tap the PayPal.Me link you were given or enter it into your browser. Tap Send. Enter the final invoice amount, add a note (optional), and tap Continue. If available, choose “Sending to a friend” or “Paying for an item or service(buyer protection Fee 3.5% will be added by TLC on invoice.” Choose your payment method and tap Next. Review the details and tap Send Payment Now. How to pay final invoice with Zelle To make final payment on Zelle (free of fees) Go to Zelle App and use 301-501-1818 Trudy Pickrel To Make Final Payment on Venmo Go to Venmo and enter Trudy-Pickrel How to pay final invoice with Venmo TLC Contracts View all of TLC's Contact here! TLC Contracts View all of TLC's Contact here! TLC Breeding Information and Resources Breeder Mentorship Program View TLC Stud Males Male Poodles Male Sheepadoodle Male OES Male Goldendoodle Male Bernedoodle To play, press and hold the enter key. To stop, release the enter key. View our shop Shop Now TLC Breeding Information and Resources Breeder Mentorship Program View TLC Stud Males Male Poodles Male Sheepadoodle Male OES Male Goldendoodle Male Bernedoodle

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Mia and Tucker Mini Bernedoodles Learn more about Bernedoodle here! Read More Puppies Available APPLY Selection Day Sept 26, 2024 First Appointment at 12:00 pm Please Note Times may change right up until night before selection day due to families high up on list picking early or families dropping off at last minute. Please watch here for changes. 1. Deposit Received , A. Stevens, VA, Mini M 12:15-1:45 blue Male 2. Deposit Received, T. Robilotto, NY, F/M 12:30-1:15 Teal Male 3. Deposit Received, A. McCray, MD F, 1:00--1:45 Pink Female 4. Deposit Received, E. P. Marlow, F Selecting This Week 5. Available Red collar Male Appointment in order of Deposit Date These are only estimated START time for your Appt. These Times can change right up to night before Selection day Parents Mom and Dad Read about Mia/Nia Read about Tucker Mia's Males APPLY Mia's Unavailable Puppies APPLY #2 Male-Red Collar- Not Available Born 9/24/24 15.1 oz Ready 11/18/2024 #1 Female- Purple Collar Not Available Born 9/24/24 15.1oz Ready 11/18/2024 #2 Female- Teal Collar-Tri Color Not Available Born 9/24/24 14.8oz Ready 11/18/2024 #3 Female- Pink Collar- Not Available Born 9/24/24 13.6oz Ready 11/18/2024 #1 Male- Blue Collar-Tri color Not Available Born 9/24/24 14.9oz Ready 11/18/2024 APPLY Pick up/delivery day Mia's Litter Nov 18, 2024 10:30- 11:00 AM 417 S. Jefferson St., Frederick, MD Nov 18th 11:00am, McHenry, MD Please confirm with us if you will be picking up Frederick or McHenry. Pittsburgh airport pick up for those flying out, MUST be arranged with TLC before making flight arrangements. Previous Puppies Not for Sale

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Hotels by TLC Nestled in the Alleghany Mountains of Western Maryland, Deep Creek Lake is a convenient drive from a number of major metropolitan areas. 1886 Mosser Rd, McHenry, Md 21541 Hotels near TLC Lake Star Motel 2 miles away from TLC 2001 Deep Creek Drive, 4.5 Stars McHenry, MD 21541 301-387-5596 | 301-387-6775 Reservations@LakeStarLodge.com http://dclhotel.com/ Inn at Deep Creek- 6 miles from TLC by the Lake 4 star Hotel & Motel 19638 Garrett Hwy, Oakland, MD · (301) 387-5534 Boardroom Motel- 16 miles from TLC Hotel & Motel 12678 Garrett Hwy, Oakland, MD · (301) 334-8266 The Garrett Inn 1 room for Pets only- 8 miles from TLC Hotel & Motel 17848 Garrett Hwy, Oakland, MD · (301) 387-6696 Cherry Creek Inn- 13 miles from TLC Oakland, MD 301-334-8686 Hotels-Not Dog friendly Quaint Inn-5 minutes away 1 Stars 2704 Deep Creek Dr Mchenry,MD 21541 301-387-4200 Yough Valley Motel-10 minutes away 4 Stars 138 Walnut Street Friendsville, MD 21531 Lodges at Sunset Village-5 minutes away 4.5 stars 23900 Garrett Hwy McHenry, MD 21541 301-387-2227 Casselmen Inn-20 minutes away 4 Stars 113 Main Street Grantsville, MD 21536 301-895-5055 Comfort Inn-20 minutes away 3.5 Stars 2541 Chestnut Ridge Rd. Grantsville, MD 21536 301-895-5993

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. TLC Chewy Top Picks! Shop Chewy for ALL your puppy needs! These are items we use here at TLC that we get from Chewy.com Dog Breeder, Poodle Puppies for Sale, Doodle Puppies for Sale Deal Bones & Chews Made in USA Steer Stick View Here! Cleaning Items VIEW MORE! Wellness Soft Puppy Bites Lamb & Salmon View Here! Cleaning Items VIEW MORE! Lamb Chop Squeaky Plush Dog Toy View Here! Cleaning Items VIEW MORE! Frisco Two Door Top Load Plastic Dog Kennel View Here! Cleaning Items VIEW MORE! Salmon Bites Salmon Skin & Coat Supplement View Here! Cleaning Items VIEW MORE! KONG Classic Dog Toy View Here! Cleaning Items VIEW MORE! Purina Pro Plan Puppy Sensitive Skin View Here! Cleaning Items VIEW MORE! Fold & Carry Double Door Collapsible Crate View Here! Cleaning Items VIEW MORE! Nature's Miracle Urine Destroyer View Here! Cleaning Items VIEW MORE! Knuckle Bones View Here! Cleaning Items VIEW MORE! FREE Toy or Bowl with Purchase View Here! Cleaning Items VIEW MORE! Deal “This post contains affiliate links and I will be compensated if you make a purchase after clicking on my links.” Shop Affiliate Link HERE View our shop Shop Now

< Back Ruby-2023 Mom Old English Sheepdog Eye CERF-Clear *Penn Hips-Clear / *Heart-Clear

< Back SnowFlake Hi Trudy, Snowflake has been wonderful. My children love her very much. She has been traveling with us and bring joy to everyone in the family. Snowy sleeps through the night and rarely has accident. Thank you so much for your wonderful breeding... Previous Next

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Acerca de TLC Health Testing Health Testing Poodles and Doodles We use health testing to make sure we are producing the healthiest puppies possible. These are a list of tests that should be done when breeding Poodles and Doodles. At TLC, we perform all the below tests on the parent breeds before they are entered into our breeding program. These tests consist of DNA tests, X-rays, and heart and eye exams, as well as physical exams. Please do your research and make sure breeders are performing the testing below. Tests required for breeding of Bernese Mountain Dogs: Hips – OFA, PennHip, or OVC Eyes – CERF Elbows – OFA Heart – OFA Degenerative Myelopathy (SOD1-A and SOD1-B) – Paw Prints Von Willebrand’s Disease – PawPrints Patellas – OFA Tests required for breeding of Golden Retrievers: Hips – OFA, PennHip, or OVC Eyes – CERF Elbows– OFA Degenerative Myelopathy (SOD1-A) – pawprints Heart – OFA Patellas – OFA PRA (GR-PRA1) – pawprints PRA (GR-PRA2) – pawprints Tests required for breeding of Standard Poodles: Hips – OFA, PennHip, or OVC: Eyes – CERF Elbows – OFA Von Willebrand’s Disease – pawprints Sebaceous Adenitis – OFA Degenerative Myelopathy (SOD1-A) – VetGen Heart – OFA Patellas – OFA PRA (rcd4) – VetGen MTC – pawprints NEWS – pawprints Tests required for breeding of Miniature and Toy Poodles: Hips – OFA, PennHip, Eyes – CERF Elbows – OFA Von Willebrand’s Disease – pawprints Sebaceous Adenitis – OFA Degenerative Myelopathy (SOD1-A) – pawprints Heart – OFA Patellas – OFA MTC – pawprints Tests required for breeding of Bernedoodles: Hips – OFA, PennHip, Eyes – CERF Elbows – pawprints Von Willebrand’s Disease – pawprints Sebaceous Adenitis – pawprints Degenerative Myelopathy (SOD1-A and SOD1-B) – pawprints Heart – pawprints Patellas –pawprints PRA (rcd4) – pawprints MTC – pawprints NEWS – pawprints Tests required for breeding of Goldendoodles: Hips – OFA, PennHip, or OVC Eyes – CERF Elbows – OFA Von Willebrand’s Disease – pawprints Sebaceous Adenitis – OFA Degenerative Myelopathy (SOD1-A) – pawprints Heart – OFA Patellas – OFA PRA (rcd4) – pawprints MTC – Pawprints NEWS – Pawprints PRA (GR-PRA1) – Pawprints PRA (GR-PRA2) – Pawprints For Poodles: Degenerative Myelopathy, GM2 Gangliosidosis, Neonatal Encephalopathy with Seizures, Osteochondrodysplasia, Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration, Von Willebrand disease I, Von Willebrand disease II, Hip Dysplasia, Elbow Dysplasia, and Heart Disease. For breeding of Bernese Mountain Dogs: Hips – OFA, PennHip, or OVC, Eyes, Elbows, Heart , Degenerative Myelopathy (SOD1-A and SOD1-B), Von Willebrand’s Disease , Patellas For Goldendoodles: Degenerative Myelopathy, Ichthyosis, Neonatal Encephalopathy with Seizures, Progressive Retinal Atrophy – Golden Retriever Type 1, Progressive Retinal Atrophy – Golden Retriever Type 2, Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration, Von Willebrand disease I, Von Willebrand disease II, Hip Dysplasia, Elbow Dysplasia, and Heart Disease. DM, ICH, NEWS, PRA-1, PRA-2, PRA-PRCD, vWD I and II, OCD, GM2, SAN and DEB are all DNA tests, so we can know with assurance whether or not puppies will be affected by any of these disorders. Hip Dysplasia, Elbow Dysplasia and Heart disease on the other hand are not as easy to eliminate from a breeding program. Hips and Elbows are checked by taking x-rays of their hips and having them evaluated by a professional, whether that be through Penn Hip, Dr. Wallace or OFA. These are very subjective tests, that can come out with different results depending on who takes the films. They are still useful to eliminate obvious hip issues, but are not the only tool that breeders use to evaluate a dog hip wise. You can breed two Excellent rated dogs together and get a dysplastic puppy, this is why you should evaluate an entire pedigree for hips, not just the parents. All of our dogs will either have their hips rated and passed or will have at least 4 generations of all Good and Excellent rated hips. Same goes for Elbows. It is important to know that only 25% of hip dysplasia is genetic, most often it is environmental. This is why it is so important to keep your dogs slim and not overweight! Descriptions of these Diseases: Degenerative Myelopathy Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi , and boxer dog , though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier , Chesapeake Bay retriever , Rhodesian ridgeback , and Cardigan Welsh corgi .[1] [2] Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord. One proposed cause of degenerative myelopathy is that the immune system attacks this sheath, breaking it down. This results in a loss of communication between nerves in lower body of the animal and the brain. Affected dogs usually present in adulthood with gradual muscle Atrophy and loss of coordination typically beginning in the hind limbs due to degeneration of the nerves. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. Affected medium to large breed dogs, such as the golden retriever, can be difficult to manage and owners often elect euthanasia when their dog can no longer support weight in the hind limbs. Dystrophic Epidermolysis Bullosa: Dystrophic epidermolysis bullosa (DEB) syndrome is a group of immune-mediated sub-epidermal blistering skin diseases that result from defects in the dermal-epidermal attachment structures and characterized by flaccid bullae that soon rupture, leaving glistening, flat erosions. Although recognized in dogs for many years, until recently, these diseases were group into a category of bullous pemphigoid. In recent years, advanced diagnostic methods have allowed categorization based on immunohistochemistry developments. Epidermolysis bullosa is now categorized depending upon the level of intracutaneous cleavage into three major subgroups: simplex, junctional, and dystrophic epidermolysis bullosa, which contain more than 20 genetically and clinically distinct subtypes. These diseases are an immune-mediated disease directed against junctional basement-membrane laminin, triggered by autoantigens. Although the etiology of these diseases is unknown, a strong genetic predisposition in some breeds suggests a defect in autoantigen regulation. Affected dogs usually present with crusting, ulcerated lesions, alopecia and pigmentation on the face, trunk and extremities, together with dystrophic nails[13] . Bilateral symmetrical erosions and ulcers are often seen affecting several mucous membranes in mucous membrane pemphigoid, the presence of characteristic eosinophil-rich sub-epidermal vesicles in bullous pemphigoid, and blisters and erosions affecting friction areas and footpads in epidermolysis bullosa acquisita. Diagnosis is usually based on histological examination of skin biopsy samples. A differential diagnosis would include dermatomyositis , cutaneous asthenia , ringworm and demodicosis [14] . Successful treatment has been reported with the use of prednisolone , azathioprine , colchicine , intravenous infusion of immunoglobulins[15] and doxycycline -niacinamide combinations[ Affected dogs typically present with symptoms of neurologic disease around 9 to 12 months of age. Symptoms include vision loss, difficulties walking, loss of balance, head tremors and vomiting. Once an affected dog begins to show signs of the disease, the disease progression is rapid and dogs usually die between the ages of 18 and 23 months. Neonatal Encephalopathy with Seizures: NEWS-is a recessive developmental brain disease. Affected pups exhibit extreme weakness, and those that survive the first week generally develop progressively worse ataxia, or inability to move properly. This is often accompanied by severe seizures. None have survived to 7 weeks of age. The mutation which causes this disease was identified by a research team at the University of Missouri led by Drs. Gary Johnson, and Dennis O'Brien. The test offered by Vetgen is based on their discovery. Animals with no copies of the mutation (clear), and those with only one copy (carriers) show no signs of the disease. This disease known to affect Standard Poodles. Affected puppies are smaller than litter mates at birth, have difficulty nursing after a few days of life, and often die by 1 week of age. By 3 weeks of age, surviving puppies present with neurologic symptoms including muscle weakness, tremors, inability to walk, wide-based stance and frequent falling. The disease quickly progresses to severe seizures that become non-responsive to treatment. Affected dogs typically die or are euthanized by 7 weeks of age. Osteochondrodysplasia : Osteochondrodysplasia is an inherited Musculoskeletal disease affecting Standard Poodles. skeletal dysplasia is a general term for a disorder of the development (dysplasia ) of bone ("osteo") and cartilage ("chondro"). Osteochondrodysplasias are rare diseases . About 1 in 5,000 babies are born with some type of skeletal dyspepsia. Affected dogs typically present at about 3 weeks of age with stunted growth. Puppies often walk differently than unaffected litter mates and stand with their feet turned out and hind legs splayed. Their legs are short and bent with enlarged joints and clubbed feet. They also have flatted rib cages and under bites, which can affect their ability to nurse and breathe. While affected dogs can survive for many years with supportive care, they will develop arthritis and will likely have breathing difficulty due to their deformed rib cages. Progressive Retinal Atrophy – Golden Retriever Type 1: Progressive Retinal Atrophy (PRA) is an inherited disease of the retina (the “film in the camera”) in dogs, in which the rod cells in the retina are programmed to die. PRA occurs in both eyes simultaneously and is non painful. There are many different types of inherited retinal degenerative diseases in purebred dogs, and discussing these are beyond the scope of this article. PRA occurs in most breeds of dogs and also occurs in mixed breeds. It is repressively inherited in all breeds studied, with the following exceptions: PRA is dominantly inherited in Golden Retriever and Goldendoodle, and is sex-linked and found primarily in male dogs in Siberian Husky and Samoyed breeds. Because PRA makes rods die, and rods are responsible for vision in dim light (“night vision”), the first clinical signs that the owner often notices are night-blindness (poor vision in dim light) and that the pupils are dilated; owners often notice a “glow” and increased “eye shine” from the eyes. Clinical signs in dogs with PRA vary from the dog first becoming night blind in the early stage of PRA, to the entire visual field in all light levels becoming affected in advanced PRA. In the final stage of PRA, the dog is completely blind. The natural course of the disease, if specific daily antioxidant supplementation is not given, is that all dogs with PRA will become blind within one year of diagnosis. Sadly, some affected dogs are already completely blind by the time a veterinary ophthalmologist first examines them. PRA reduces vision in most affected dogs and cannot be cured, but in the opinion of many veterinary ophthalmologists, including Dr. McCalla, PRA is no longer a hopeless disease that always leads to complete blindness. Progressive Retinal Atrophy – Golden Retriever Type 2: Progressive retinal atrophy Golden Retriever type 2 (GR2-PRA) is one form of progressive retinal atrophy (PRA) affecting Golden Retrievers. Until now, in Golden Retrievers there have been identified three different forms of PRA caused by 3 different mutations. Progressive retinal atrophy (PRA) comprises autosomal repressively inherited diseases that lead to degeneration of retinal photo-receptor cells in dogs and other pets. There are more than 20 mutations responsible for specific forms of PRA, and some breeds, including Golden Retrievers, can be affected by more than only one form of PRA. Other than that, some forms of PRA are common to multiple dog breeds, while others are recognized in just a single breed. It has been identified in most dog breeds, but also in mixed breed dogs. In general, forms of PRA are characterized by disturbance of dark vision, visual field defects, and abnormalities in the electroretinogram. The electroretinogram (ERG) is a diagnostic test used to measure the electrical activity of cells in the retina in response to a light stimulation. PRA is a progressive disorder and can progress into blindness. It appears in both eyes simultaneously. The age of onset and rate of retinal degeneration varies between the different forms of the conditions. Affected dogs begin showing clinical symptoms related to retinal degeneration at around 4 to 5 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progressive Retinal Atrophy – Progressive Rod-Cone Degeneration: Progressive retinal Atrophy, progressive Rod-cone degeneration (PRA-prcd) is a late onset, inherited eye disease affecting Golden Retrievers. PRA-prcd occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Evidence of retinal disease in affected dogs can first be seen on an Electroretinogram around 1.5 years of age for most breeds, but most affected Golden Retrievers will not show signs of vision loss until 5 to 6 years of age or later. The rod type cells are affected first and affected dogs will initially have vision deficits in dim light (night blindness) and loss of peripheral vision. Over time affected dogs continue to lose night vision and begin to show visual deficits in bright light. Other signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam. Although there is individual and breed variation in the age of onset and the rate of disease progression, the disease eventually progresses to complete blindness in most dogs. Other inherited disorders of the eye can appear similar to PRA-prcd. Genetic testing may help clarify if a dog is affected with PRA-prcd or another inherited condition of the eye. Von Willebrand disease I : Von Willebrand’s disease (vWD) is a blood disease caused by a deficiency of von Willebrand Factor (vWF), an adhesive glycoprotein in the blood required for normal platelet binding (i.e., clotting) at the sites of small blood vessel injuries. In addition, vWF is a carrier protein for coagulation Factor VIII (necessary for blood to clot). A lack of vWF impairs platelet stickiness and clumping. Similar to hemophilia in humans, this condition can lead to excessive bleeding following an injury, due to the lack of clotting. VWF is an autosomal (non-sex-linked) trait, which both males and females express and transmit genetically and with equal frequency. The expression pattern of the severe forms (Types 2 and 3 vWD) is recessive while the milder form (Type 1 vWD) appears to be recessive or incompletely dominant. This is the most common hereditary blood clotting disorder in dogs, occurring with more frequency in some breeds, including, standard poodles, and golden retrievers. Sensory Ataxic Neuropathy: Sensory ataxic neuropathy is an autosomal-recessive genetic neurological disorder of Golden Retrievers. The disease is caused by a missense base-pair deletion mutation in the mt tRNATyr gene that results in mitochondrial dysfunction, specifically reduced ATP production in isolated muscle mitochondria. Affected dogs are usually young (under 6 months of age) and present with slowly progressive postural reaction deficits and reduced or absent spinal reflexes. Clinical pathology, radiography, and electrophysiology of motor systems are frequently within reference values. Electrophysiological examination usually reveals reduced conduction velocities of nerve impulses in sensory nerves. Histopathology of muscle tissues are usually unremarkable although histochemical staining for cytochrome c oxidase and succinate dehydrogenase shows marked reduction in their activity in affected dogs. A differential diagnosis would include ceroid lipofuscinosis and pyruvate dehydrogenase phosphatase 1 deficiency . There is no known treatment for this condition and approximately 50% of affected dogs are euthanized before three years of age. Hip Dysplasia: In dogs, hip dysplasia is an abnormal formation of the hip socket that, in its more severe form, can eventually cause crippling lameness and painful arthritis of the joints. It is a genetic (polygenic) trait that is affected by environmental factors. It is common in many dog breeds, particularly the larger breeds, and is the most common single cause of arthritis of the hips. Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation. The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint’s lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal’s body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint’s range of motion decreases. No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame. Elbow Dysplasia: Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include: Pathology involving the medial coronoid of the ulna (FCP) Osteochondritis of the medial humeral condyle in the elbow joint (OCD) Ununited anconeal process (UAP) Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased. Heart Disease: Heart failure is a clinical syndrome that occurs secondary to severe, overwhelming cardiac disease. It occurs because the heart is no longer able to maintain normal venous/capillary pressures, cardiac output, and/or systemic blood pressure. It is most commonly caused by a chronic disease that results in a severe decrease in myocardial contractility, severe regurgitation or shunting, or severe diastolic dysfunction. However, it is common to have all three abnormalities present simultaneously (but with one predominating). By far, the most common clinical manifestations seen with heart failure are directly due to edema and effusion (congestive or backward heart failure). Much less commonly, animals present because of signs referable to a decrease in cardiac output (forward heart failure). Very rarely, they present in cardiogenic shock (low blood pressure due to decreased cardiac output). This occurs because the cardiovascular system operates under a system of priorities. Its three primary functions are to maintain a normal blood pressure and normal cardiac output, both at a normal venous/capillary pressure. When the system is overwhelmed, it allows venous/capillary pressure to increase first (and so allows edema or effusion to form) and then allows cardiac output to fall. Only after cardiac output has fallen remarkably does cardiogenic shock occur. In acute heart failure, before any compensation has occurred, cardiogenic shock may predominate, but even in this situation, acute chordal rupture is the most common cause of acute heart failure in animals and results in an increased left atrial pressure and thus pulmonary edema. While Doodles tend to be healthier than their parent breeds, they can still be prone to conditions such as hip and elbow dysplasia and certain eye problems. Skin problems, such as hot spots and allergies, are also seen. Genetic testing can reduce the risk of many diseases. A reputable breeder will perform a number of tests and will provide evidence of the successful results. It’s important for prospective buyers to understand that breeders invest a great deal of money upfront in finding healthy breeding stock and doing the required testing. This investment is reflected in the higher cost of the puppy for the buyer. A higher upfront cost will most likely reduce vet bills down the road. To play, press and hold the enter key. To stop, release the enter key.

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Interested in having TLC train your puppy? Extend your new puppies stay by 1-2 weeks to set your puppies off on the right paw $650 a week. First week includeds 2nd Physical and shot at vet. A $100-$200 value LEARN MORE HERE Heading 3 Other Training Videos to help with First week or problem training areas View our shop Shop Now

Family run breeder of AKC/CKC Standard and Moyen Poodle, Standard and Mini Sheepadoodle, Standard and Mini Bernadoodle, Medium and Mini Goldendoodle. Acerca de TLC Old English Sheep Dog Learn about Old English Sheep Dogs READ HERE! Our TLC Adult OES Dogs FEMALE MALE Future Litters Sept 2023 We only breed one OES litter per year Sapphire/Romeo , AKC OES, Pregnant, Sept 3-5th View Wait List Please remember we cannot promise any timeline . We breed but God and nature take it from there. Waiting List started Application if you are interested in any of the above litters, please fill out the contact us form in the bottom right of the screen. If you are ready to move forward you can fill our Application and submit with Deposit . Your questions will be answered promptly (If you do not hear from us in 24hrs please call or email again.) We do not want anyone's email to be lost in junk mail. If you have further questions and would like someone to call you, please include your number when you email us. We have one waiting list for each Breed that we raise. When a litter is born, we go down the list and contact the families in the order the deposits are received. Each family we email is then asked if they want to go with the newborn litter or wait for the next opening, and to reply ASAP within 48hrs so we can move on to next family if they do not want to go with that litter. The Timeline is the Time the family wants a puppy 1. Breeders Choice - Female 2. Breeders Choice - Female 3. Breeders Choice - Male Examples: ASAP- Family wants from next available litter/puppy Spring 2023- Family will not be ready for puppy till 2023 Fall 2022- That Deposit/Family will not be ready for a puppy till Fall 2022 so they will be skipped over until a Fall 2022 litters Apply Here View Future Parents Sept 2023 Sapphire Romeo To play, press and hold the enter key. To stop, release the enter key.