HEALTH TESTING
As a Level 2 Breeder with the American Morkshire Terrier Club, there are required health clearance tests that must be completed on your breeding dogs. The following are 6 tests and 5 are required out of 6. *NEW* 9/2019 the AMTC has now added 2 more tests. Making a total of 8 health clearance tests. The last 3 tests are optional at this time.
- AMTC works with GenSol (for Disease Clearance Tests), Animal Genetics (for DNA Profiling and Disease Clearance Tests), Viaguard (canine genetics lab) and now with Wisdom Health - established in 2020 for analyzing canine DNA and identifying the most useful DNA SNP markers to distinguish between different dog breeds, detect disease mutations, analyze traits and inform on diversity within breeds).
- Visit GenSol Diagnostics to order your Hyperuricosuria (HU) test and all genetic tests.
- Visit Viaguard for purebred status of the American Morkshire Terrier to order your DNA verification kit at www.dogsbreeddna.com.
- Visit Wisdom Health - Optimal Selection to order your canine DNA kit for the American Morkshire Terrier at www.optimal-selection.com.
- *NEW* Effective September 16, 2019 - AMTC now offers DNA Combination Kit's with Animal Genetics. Two Kit's available: 1-combines the DNA profile with the HU test. 2-combines the DNA, HU, PLL and prcd-PRA test.
- PLL and prcd-PRA are NEW tests.
OFA TESTING
As a Level 2 Breeder, there are tests that must be completed by OFA Certifications for ALL Breeding Dogs regardless of Breed! The following are OFA tests that are a requirement of AMTC.
- Heart and Patella test can be performed by your veterinarian who is familiar with OFA testing.
- OFA eye test must be performed by an OFA certified opthamoligist. OFA offers health clinics and you can visit: www.caninehealthclinics.org/ for health clinics in your area that offer all OFA testings.
OFA-Cardiac Guidelines for Breeders- All AMTC breeding dogs must have OFA Cardiac ausculation certification.
A careful clinical examination that emphasizes cardiac auscultation is the most expedient and cost-effective method for identifying Congenital Heart Disease in dogs. While there are exceptions, virtually all common congenital heart defects are associated with the presence of a cardiac murmur. Consequently, it is recommended that cardiac auscultation be the primary screening method for initial identification of CHD and the initial classification of dogs. Murmurs related to CHD may at times be difficult to distinguish from normal, innocent (also called physiologic or functional) murmurs. Innocent cardiac murmurs are believed to be related to normal blood flow in the circulation. Innocent murmurs are most common in young, growing animals. The prevalence of innocent heart murmurs in mature dogs (especially in athletic dogs) is undetermined. A common clinical problem is the distinction between innocent murmurs and murmurs arising from CHD.
Types of Cardiac Exams:
OFA Database is for dogs 12 months and over.
A careful clinical examination that emphasizes cardiac auscultation is the most expedient and cost-effective method for identifying Congenital Heart Disease in dogs. While there are exceptions, virtually all common congenital heart defects are associated with the presence of a cardiac murmur. Consequently, it is recommended that cardiac auscultation be the primary screening method for initial identification of CHD and the initial classification of dogs. Murmurs related to CHD may at times be difficult to distinguish from normal, innocent (also called physiologic or functional) murmurs. Innocent cardiac murmurs are believed to be related to normal blood flow in the circulation. Innocent murmurs are most common in young, growing animals. The prevalence of innocent heart murmurs in mature dogs (especially in athletic dogs) is undetermined. A common clinical problem is the distinction between innocent murmurs and murmurs arising from CHD.
Types of Cardiac Exams:
- Auscultation (listening with a stethoscope) this test can be performed by your licensed veterinarian or an OFA cardiac specialist.
- Echocardiograms- this test is performed if your licensed veterinarian detects any abnormalities.
OFA Database is for dogs 12 months and over.
OFA-Companion Animal Eye Registry (CAER)- All AMTC breeding dogs need to have CEAR certification.
The purpose of the Companion Animal Eye Registry (CAER) is to provide breeders with information regarding canine eye diseases so that they may make informed breeding decisions in an effort to produce healthier dogs. CAER certifications will be performed by board certified (ACVO) veterinary ophthalmologists.
CAER Number Eligibility
Conditions that prevent eligibility for an OFA CAER Number: There are currently ten disorders for which there is an unequivocal recommendation against breeding in all breeds. These diagnoses are ineligible for OFA Eye Registry certifications. These are conditions which frequently result in blindness and for which there is definite evidence of heritability in one or more breeds.
*Note: The prudent approach to these disorders is to assume they are hereditary except in cases specifically known to be associated with trauma, other causes of ocular inflammation, specific metabolic diseases or nutritional deficiencies.
OFA Database is for dogs 12 months and over.
AMTC breeding dogs need to be tested at 1 year and again at 3 years of age.
The purpose of the Companion Animal Eye Registry (CAER) is to provide breeders with information regarding canine eye diseases so that they may make informed breeding decisions in an effort to produce healthier dogs. CAER certifications will be performed by board certified (ACVO) veterinary ophthalmologists.
CAER Number Eligibility
Conditions that prevent eligibility for an OFA CAER Number: There are currently ten disorders for which there is an unequivocal recommendation against breeding in all breeds. These diagnoses are ineligible for OFA Eye Registry certifications. These are conditions which frequently result in blindness and for which there is definite evidence of heritability in one or more breeds.
*Note: The prudent approach to these disorders is to assume they are hereditary except in cases specifically known to be associated with trauma, other causes of ocular inflammation, specific metabolic diseases or nutritional deficiencies.
- Keratoconjunctivitis sicca (KCS) – Breeding is not recommended for any animal demonstrating keratitis consistent with KCS. The prudent approach is to assume KCS to be hereditary except in cases suspected to be non-genetic in origin. See above note.
- Cataract – Breeding is not recommended for any animal demonstrating partial or complete opacity of the lens or its capsule unless the examiner has also checked the space for “significance of above cataract unknown” or unless specified otherwise for the particular breed. See above note.
- Lens luxation or subluxation – See above note.
- Glaucoma – See above note.
- Persistent hyperplastic primary vitreous (PHPV)
- Retinal detachment – See above note.
- Retinal dysplasia – geographic or detached forms – See above note.
- Optic nerve coloboma
- Optic nerve hypoplasia
- Progressive Retinal Atrophy (PRA) – Breeding is not advised for any animal demonstrating bilaterally symmetric retinal degeneration (considered to be PRA unless proven otherwise).
OFA Database is for dogs 12 months and over.
AMTC breeding dogs need to be tested at 1 year and again at 3 years of age.
OFA-Patellar Luxation- All breeding ATMC dogs must have a Patellar Luxation Evaluation.
What is Patellar Luxation?
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position. Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are eight weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb. Patellar luxations fall into several categories:
Patellar Luxation Grades
Grade 1: Manually the patella easily luxates at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is a very slight rotation of the tibia. Flexion and extension of the stifle are in a straight line with no abduction of the hock.
Grade 2: There is frequent patellar luxation, which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed. Especially under anesthesia, it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released. As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially the hock is slightly abducted. If the condition is bilateral, more weight is shifted onto the forelimbs. Many dogs with this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial trochlear ridge of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.
Grade 3: The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi-flexed position. The trochlea is very shallow or even flattened.
Grade 4: The tibia is medially twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane. The patella is permanently luxated. The patella lies just above the medial condyle and space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex. The limb is carried, or the animal moves in a crouched position, with the limb flexed.
OFA Database is for dogs 12 months and over.
Evaluation of dogs under 12 months of age is encouraged if the owner desires to breed at this age but, is not accepted by OFA until dog reaches 12 months and over.
What is Patellar Luxation?
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position. Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are eight weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb. Patellar luxations fall into several categories:
- Medial luxation (toy, miniature, and large breeds)
- Lateral luxation (toy and miniature breeds)
- Lateral luxation (large and giant breeds)
- Luxation resulting from trauma (various breeds, of no importance to the certification process)
Patellar Luxation Grades
Grade 1: Manually the patella easily luxates at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is a very slight rotation of the tibia. Flexion and extension of the stifle are in a straight line with no abduction of the hock.
Grade 2: There is frequent patellar luxation, which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed. Especially under anesthesia, it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released. As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially the hock is slightly abducted. If the condition is bilateral, more weight is shifted onto the forelimbs. Many dogs with this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial trochlear ridge of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.
Grade 3: The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi-flexed position. The trochlea is very shallow or even flattened.
Grade 4: The tibia is medially twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane. The patella is permanently luxated. The patella lies just above the medial condyle and space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex. The limb is carried, or the animal moves in a crouched position, with the limb flexed.
OFA Database is for dogs 12 months and over.
Evaluation of dogs under 12 months of age is encouraged if the owner desires to breed at this age but, is not accepted by OFA until dog reaches 12 months and over.
HYPERURICOSURIA (HU)- DNA test- All AMTC breeding dogs need to have this genetic test done.
This disease is characterized by the excretion of uric acid leading to the formation of urinary calculi (stones) which may then require surgery. If a dog from a breed susceptible to this disorder is seen to experience problems urinating freely, then veterinary advice should be sought immediately. HU is inherited as a simple autosomal recessive defect. Dogs that carry two copies of the disease will be affected and susceptible to develop bladder/kidney stones.
This disease is characterized by the excretion of uric acid leading to the formation of urinary calculi (stones) which may then require surgery. If a dog from a breed susceptible to this disorder is seen to experience problems urinating freely, then veterinary advice should be sought immediately. HU is inherited as a simple autosomal recessive defect. Dogs that carry two copies of the disease will be affected and susceptible to develop bladder/kidney stones.
Dog DNA Fingerprint- All AMTC breeding dogs must have a DNA-profile done. Level 1 after 3rd litter and Level 2 prior to any breeding and must be done through AMTC.
The powerful tool of DNA testing now addresses questions relating to the true identity of dogs.
The “DNA profile”, or “DNA fingerprint” of a dog is unique (except for identical twins). The same technology is used by law enforcement agencies throughout the world to accurately identify suspects of crime.
Many breeding associations throughout the world are now relying on DNA profiles to ensure the accuracy of their registries.
The powerful tool of DNA testing now addresses questions relating to the true identity of dogs.
The “DNA profile”, or “DNA fingerprint” of a dog is unique (except for identical twins). The same technology is used by law enforcement agencies throughout the world to accurately identify suspects of crime.
Many breeding associations throughout the world are now relying on DNA profiles to ensure the accuracy of their registries.
- DNA profile testing DOES NOT determine the following:
- breed of the dog or whether the dog is purebred
- genetic health
- coat color
Serum Bile Acid Disease- This genetic test is optional for AMTC breeding dogs.
The purpose of the serum bile acid test is to provide a phenotypic screening tool for liver shunts (PSVA – portosystemic vascular anomaly) and MVD (microvascular dysplasia). The two conditions are believed to be both related and congenital. Normal bile acid levels provide a sensitive test to indicate the absence of either of these inherited conditions, giving breeders valuable information in making informed breeding decisions.
Bile acids are compounds that are made in the liver, stored in the gall bladder and help with the digestion of foods. During digestion, the gall bladder contracts and pushes the bile acids into the small intestine where they mix with the foods and break down fats into smaller particles for easier absorption. When digestion is finished, the bile acids are absorbed by the intestine, passed into the blood stream, and returned to the gall bladder where they are stored for the next meal.
Elevated bile acids indicate there is a problem with the liver, but do not provide specific diagnostic information regarding cause, severity, or reversibility of the problem. Dogs with elevated bile acids should be monitored at a minimum, and may require additional diagnostic testing such as an ultrasound or liver biopsy to determine an appropriate course of action.
The purpose of the serum bile acid test is to provide a phenotypic screening tool for liver shunts (PSVA – portosystemic vascular anomaly) and MVD (microvascular dysplasia). The two conditions are believed to be both related and congenital. Normal bile acid levels provide a sensitive test to indicate the absence of either of these inherited conditions, giving breeders valuable information in making informed breeding decisions.
Bile acids are compounds that are made in the liver, stored in the gall bladder and help with the digestion of foods. During digestion, the gall bladder contracts and pushes the bile acids into the small intestine where they mix with the foods and break down fats into smaller particles for easier absorption. When digestion is finished, the bile acids are absorbed by the intestine, passed into the blood stream, and returned to the gall bladder where they are stored for the next meal.
Elevated bile acids indicate there is a problem with the liver, but do not provide specific diagnostic information regarding cause, severity, or reversibility of the problem. Dogs with elevated bile acids should be monitored at a minimum, and may require additional diagnostic testing such as an ultrasound or liver biopsy to determine an appropriate course of action.
Primary Lens Luxation (PLL) - This genetic test is optional for AMTC breeding dogs.
The lens of the eye normally lies immediately behind the iris and the pupil, and is suspended in place by a series of fibers. It functions to focus light rays on the retina, in the back of the eye.
When partial or complete breakdown of these fibers occur, the lens may become partially or fully dislocated from its normal position. Lens luxation can occur for several different reasons:
*Note: Not all cases of a luxated lens are from Primary Lens Luxation. Dogs that are genetically clear of the mutation could potentially experience this event at some point. This could be from an injury, other eye disorders, or infection. Therefore, making this an optional test for AMTC breeders.
The lens of the eye normally lies immediately behind the iris and the pupil, and is suspended in place by a series of fibers. It functions to focus light rays on the retina, in the back of the eye.
When partial or complete breakdown of these fibers occur, the lens may become partially or fully dislocated from its normal position. Lens luxation can occur for several different reasons:
- Primary lens luxation is a heritable disease in many breeds.
- Spontaneous luxation of the lens occurs in early adulthood (most commonly 3-6 years of age) and often affects both eyes, although not necessarily at the same time.
*Note: Not all cases of a luxated lens are from Primary Lens Luxation. Dogs that are genetically clear of the mutation could potentially experience this event at some point. This could be from an injury, other eye disorders, or infection. Therefore, making this an optional test for AMTC breeders.
Progressive Retinal Atrophy - (PRA-prcd) - This genetic test is optional for AMTC breeding dogs.
Progressive Rod-Cone Degeneration, or PRA-prcd, is a form of Progressive Retinal Atrophy (PRA) in which the cells in the dog's retina degenerate and die. PRA for dogs is similar to retinitis pigmentosa in humans. Most affected dogs will not show signs of vision loss until 3-5 years of age. Complete blindness can occur in older dogs. Progressive Rod-Cone Degeneration is a form of PRA known to affect over 40 different breeds.
The retina is a membrane located in the back of the eye that contains two types of photoreceptor cells. These cells take light coming into the eyes and relay it back to the brain as electrical impulses. These impulses are interpreted by the brain to "create" images. In dogs suffering from PRA-prcd:
PRA-prcd is inherited as an autosomal recessive disorder. A dog must have two copies of the mutated gene to be affected by PRA. A dog can have one copy of the mutation and not experience any symptoms of the disease. Dogs with one copy of the mutation are known as carriers, meaning that they can pass on the mutation to their offspring. If they breed with another carrier, there is a 25% chance that the offspring can inherit one copy of the mutated gene from each parent, and be affected by the disease.
*This can also be detected with an eye exam performed by an OFA Ophthalmologist.
Progressive Rod-Cone Degeneration, or PRA-prcd, is a form of Progressive Retinal Atrophy (PRA) in which the cells in the dog's retina degenerate and die. PRA for dogs is similar to retinitis pigmentosa in humans. Most affected dogs will not show signs of vision loss until 3-5 years of age. Complete blindness can occur in older dogs. Progressive Rod-Cone Degeneration is a form of PRA known to affect over 40 different breeds.
The retina is a membrane located in the back of the eye that contains two types of photoreceptor cells. These cells take light coming into the eyes and relay it back to the brain as electrical impulses. These impulses are interpreted by the brain to "create" images. In dogs suffering from PRA-prcd:
- The photoreceptors begin to degenerate, causing an inability to interpret changes in light.
- This results in a loss of vision.
- Rod cells, which normally function in low-light or nighttime conditions, begin to degenerate first.
- This leads to night-blindness.
- The cone cells, which normally function in bright-light or daytime conditions, will deteriorate next. This often leads to complete blindness over a period of time.
PRA-prcd is inherited as an autosomal recessive disorder. A dog must have two copies of the mutated gene to be affected by PRA. A dog can have one copy of the mutation and not experience any symptoms of the disease. Dogs with one copy of the mutation are known as carriers, meaning that they can pass on the mutation to their offspring. If they breed with another carrier, there is a 25% chance that the offspring can inherit one copy of the mutated gene from each parent, and be affected by the disease.
*This can also be detected with an eye exam performed by an OFA Ophthalmologist.
If you have any questions regarding the above requirements you can email us at: info@amtcusa.com
NOTE: *If your dog has already been tested prior to July 15, 2019* - you can send those results to us by mail at: AMTC Registrar P.O. BOX 433, Edneyville, NC 28727. *If not, you can obtain a DNA-profile Kit above*
We accept results from these AMTC approved labs for health testings:
Animal Genetic Testing and Research Lab
Department of Veterinary Science
108 Gluck Equine Research Center,
University of Kentucky
Lexington KY 40546-0099
Ph: 859-218-1193 Fax: 859-257-5169
Auburn University
Mary Boudreaux, DVM, PhD
Dept. of Pathobiology, College of Veterinary Medicine
166 Greene Hall
Auburn University, AL 36849
Ph: (334) 844-2692 Email: boudrmk@auburn.edu
Cornell University
Goldstein Molecular and Genetics Laboratory
Richard E. Goldstein, DVM, Dip ACVIM, Dip ECVIM-CA
Ph: 607-253-4480 Fax: 607-253-3534
E-mail: phpt@cornell.edu
Embark
186 Lincoln St., 6th Floor
Boston, MA 02111
E-mail: howdy@embarkvet.com
HealthGene
2175 Keele St.
Toronto, ON M6M 3Z4 Canada
Toll Free: 1-877-371-1551
Email: info@healthgene.co
Jefferson Medical College
Dept. of Neurology -Dr. David Wenger
1020 Locust St, 394
Philadelphia, PA 19107
Email: david.wenger@mail.tju.edu
Laboratory of Veterinary Genetics (LABGENVET)
University of Montreal
Faculty of Veterinary Medicine
David W. Silversides DVM, PhD.
3200 Sicotte, CP5000 St-Hyacinthe, Quebec, Canada J2S 7C6
Tel. 450-773-8521 x8464
David.w.silversides@umontreal.ca
Michigan State University
Laboratory of Comparative Medical Genetics
2209 Biomedical Physical Sciences
East Lansing, MI 48824
Laboratory of Canine Genetics and Molecular Medicine
567 Wilson Rd, BPS Bldg, MSU
East Lansing, MI 48824
Ph: (517) 884-5350
North Carolina State University
Veterinary Genetics Lab
1060 William Moore Drive RB 228
Raleigh, NC 27607
Ph: 919-513-3314 Email: vcgl@lists.ncsu.edu
NYU Medical Center – Neurogenetics Laboratory
Attn: Dr. Bai Jin Zeng NYU Medical Center
400 East 34th St. (Room RR210)
New York, NY 10016 Ph: 212-263-2943
OptiGen, LLC
Cornell Business & Technology Park
767 Warren Road, Suite 300
Ithaca, NY 14850
Ph: 607-257-0301 Fax: 607-257-0353
Email: genetest@optigen.com
Orivet Genetic Pet Care
20 Church Street
Mezzanine Level
Hartford, CT 06103
Ph: 860-952-3407
Email: USA@Orivet.com
Orthopedic Foundation for Animals
2300 E Nifong Boulevard
Columbia, Missouri, 65201-3806
Ph: (573) 442-0418 Fax: (573) 875-5073
Email: ofa@offa.org
Paw Prints Genetics
220 E Rowan, Suite 220
Spokane, WA 99207
Ph: 855-202-4889 Email: askus@pawprintgenetics.com
PennGEN Laboratories
3850 Spruce Street
Philadelphia, PA 19104-6010
Ph: (215) 898-3375
ProjectDog
636 San Pablo Ave
Albany, CA 94706
Ph: (510) 900-3899 Email: dogdna@projectdog.org
University of California – Davis Veterinary Genetics Laboratory
PO Box 1102
Davis, CA 95617-1102
Ph: (530) 752-2211
University of Minnesota – Canine Genetics Laboratory
College of Veterinary Medicine, University of Minnesota 295 AS/VM
1988 Fitch Ave
St. Paul, MN 55108
Ph: (612) 624-5322 Email: cgl@umn.edu
University of Missouri College of Vet Medicine
320 Connaway Hall
Columbia, MO 65211
Ph: (573) 884-3712 E-mail: HansenL@missouri.edu
University of Pennsylvania Section of Medical Genetics
School of Veterinary Medicine
Ryan Veterinary Hospital, Room 4018
3900 Delancey St.
Philadelphia, PA 19104
Ph: (215) 898-8076 Email: casalml@vet.upenn.edu
Veterinary Diagnostics Center (DDC)
225 Corporate Court
Fairfield, OH 45014
Toll-Free: (800) 625-0874 Email: contact@vetdnacenter.com
VetGen
3728 Plaza Drive, Suite One
Ann Arbor, MI 48108
Ph: 800-483-8436
VetNostic
www.vetnostic.com
Ph: (877) 255-9208
Washington State University–Veterinary Clinical Pharmacology Lab (WSU-VCPL)
PO Box 609
Pullman, WA 99163-0609
Ph: 509-335-3745 Fax: 509-335-6309
Email: VCPL@vetmed.wsu.edu
Wisdom Health
PO Box 87586
Vancouver, WA 98687
Toll Free: 1-888-K9 PET TEST (597-3883) Email: info@wisdomhealth.com
NOTE: *If your dog has already been tested prior to July 15, 2019* - you can send those results to us by mail at: AMTC Registrar P.O. BOX 433, Edneyville, NC 28727. *If not, you can obtain a DNA-profile Kit above*
We accept results from these AMTC approved labs for health testings:
Animal Genetic Testing and Research Lab
Department of Veterinary Science
108 Gluck Equine Research Center,
University of Kentucky
Lexington KY 40546-0099
Ph: 859-218-1193 Fax: 859-257-5169
Auburn University
Mary Boudreaux, DVM, PhD
Dept. of Pathobiology, College of Veterinary Medicine
166 Greene Hall
Auburn University, AL 36849
Ph: (334) 844-2692 Email: boudrmk@auburn.edu
Cornell University
Goldstein Molecular and Genetics Laboratory
Richard E. Goldstein, DVM, Dip ACVIM, Dip ECVIM-CA
Ph: 607-253-4480 Fax: 607-253-3534
E-mail: phpt@cornell.edu
Embark
186 Lincoln St., 6th Floor
Boston, MA 02111
E-mail: howdy@embarkvet.com
HealthGene
2175 Keele St.
Toronto, ON M6M 3Z4 Canada
Toll Free: 1-877-371-1551
Email: info@healthgene.co
Jefferson Medical College
Dept. of Neurology -Dr. David Wenger
1020 Locust St, 394
Philadelphia, PA 19107
Email: david.wenger@mail.tju.edu
Laboratory of Veterinary Genetics (LABGENVET)
University of Montreal
Faculty of Veterinary Medicine
David W. Silversides DVM, PhD.
3200 Sicotte, CP5000 St-Hyacinthe, Quebec, Canada J2S 7C6
Tel. 450-773-8521 x8464
David.w.silversides@umontreal.ca
Michigan State University
Laboratory of Comparative Medical Genetics
2209 Biomedical Physical Sciences
East Lansing, MI 48824
Laboratory of Canine Genetics and Molecular Medicine
567 Wilson Rd, BPS Bldg, MSU
East Lansing, MI 48824
Ph: (517) 884-5350
North Carolina State University
Veterinary Genetics Lab
1060 William Moore Drive RB 228
Raleigh, NC 27607
Ph: 919-513-3314 Email: vcgl@lists.ncsu.edu
NYU Medical Center – Neurogenetics Laboratory
Attn: Dr. Bai Jin Zeng NYU Medical Center
400 East 34th St. (Room RR210)
New York, NY 10016 Ph: 212-263-2943
OptiGen, LLC
Cornell Business & Technology Park
767 Warren Road, Suite 300
Ithaca, NY 14850
Ph: 607-257-0301 Fax: 607-257-0353
Email: genetest@optigen.com
Orivet Genetic Pet Care
20 Church Street
Mezzanine Level
Hartford, CT 06103
Ph: 860-952-3407
Email: USA@Orivet.com
Orthopedic Foundation for Animals
2300 E Nifong Boulevard
Columbia, Missouri, 65201-3806
Ph: (573) 442-0418 Fax: (573) 875-5073
Email: ofa@offa.org
Paw Prints Genetics
220 E Rowan, Suite 220
Spokane, WA 99207
Ph: 855-202-4889 Email: askus@pawprintgenetics.com
PennGEN Laboratories
3850 Spruce Street
Philadelphia, PA 19104-6010
Ph: (215) 898-3375
ProjectDog
636 San Pablo Ave
Albany, CA 94706
Ph: (510) 900-3899 Email: dogdna@projectdog.org
University of California – Davis Veterinary Genetics Laboratory
PO Box 1102
Davis, CA 95617-1102
Ph: (530) 752-2211
University of Minnesota – Canine Genetics Laboratory
College of Veterinary Medicine, University of Minnesota 295 AS/VM
1988 Fitch Ave
St. Paul, MN 55108
Ph: (612) 624-5322 Email: cgl@umn.edu
University of Missouri College of Vet Medicine
320 Connaway Hall
Columbia, MO 65211
Ph: (573) 884-3712 E-mail: HansenL@missouri.edu
University of Pennsylvania Section of Medical Genetics
School of Veterinary Medicine
Ryan Veterinary Hospital, Room 4018
3900 Delancey St.
Philadelphia, PA 19104
Ph: (215) 898-8076 Email: casalml@vet.upenn.edu
Veterinary Diagnostics Center (DDC)
225 Corporate Court
Fairfield, OH 45014
Toll-Free: (800) 625-0874 Email: contact@vetdnacenter.com
VetGen
3728 Plaza Drive, Suite One
Ann Arbor, MI 48108
Ph: 800-483-8436
VetNostic
www.vetnostic.com
Ph: (877) 255-9208
Washington State University–Veterinary Clinical Pharmacology Lab (WSU-VCPL)
PO Box 609
Pullman, WA 99163-0609
Ph: 509-335-3745 Fax: 509-335-6309
Email: VCPL@vetmed.wsu.edu
Wisdom Health
PO Box 87586
Vancouver, WA 98687
Toll Free: 1-888-K9 PET TEST (597-3883) Email: info@wisdomhealth.com
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*This material may not be published, rewritten, or redistributed. Unauthorized use is prohibited and protected by exclusive rights.
