About the Test The PSSM1 DNA test verifies the presence of the affected allele at the GYS1 locus responsible for Polysaccharide Storage Myopathy Type 1 (PSSM1). Sample Collection Hair Roots: 20 to 30 roots. Tape them onto the printable submission form. Blood Sample: 5 mL in a K3 EDTA tube. Send with the printable submission form. Turnaround Time 5 working days after sample arrival at the laboratory. Why Test? This test allows breeders to make informed decisions to prevent the birth of affected foals. While PSSM1 cannot be cured, symptoms are manageable through dietary adjustments and consistent exercise routines. Learn More Results Description n/n: Negative for PSSM1. n/P1: Positive heterozygous (Carrier). 50% chance of passing to progeny. P1/P1: Positive homozygous. 100% chance of passing to progeny. Additional Information PSSM1 is a hereditary muscle disease caused by a mutation in the GYS1 gene, leading to abnormal glycogen accumulation. Check our FAQs FAQs What breeds are affected? Many breeds, including Quarter Horses, Belgian Drafts, and Warmbloods. How is it inherited? Autosomal dominant. Even one copy (n/P1) can cause symptoms. Visit our full FAQ page.

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DNA test The DNA test verifies the presence of the chromosomal inversion.  The Tobiano coat pattern usually involves some white on all four legs and rounded white spots on the body with sharp, clean edges. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? This genetic test can confirm is the horse is heterozygous (To/N) or homozygous (To/) for the Tobiano gene. For breeding purposes, homozygous Tobiano horses are highly desirable as they are guaranteed to produce Tobiano foals regardless of their mate. Since Tobiano is only responsible for the white markings of a so called “colored” horse, the test does not determine the horse’s base-color. This is determined using the extension test. The two tests in conjunction not only verify the likelihood of Tobiano being passed to foals, but also the likelihood the foals will be piebald or skewbald. Results description The DNA test verifies the presence of the chromosomal inversion and presents results as one of the following: N/ – Non-tobiano horse. To/N – Positive for the dominant Tobiano gene mutation, carrier of a single inherited copy of Tobiano. Horse’s base color may be modified to varying degrees by the Tobiano markings. To/ – Positive for dominant Tobiano gene mutation, carrying two inherited copies of Tobiano. Will always pass Tobiano to foals. For breeding purposes, homozygous Tobiano horses are highly desirable as they are guaranteed to produce Tobiano foals regardless of their mate. Additional information The Tobiano coat pattern usually involves some white on all four legs and rounded white spots on the body with sharp, clean edges. The head of the horse is usually colored and will not have white caused by the Tobiano gene. The white on the body will generally cross the top-line of the horse. Although white often incorrectly referred to as adding color it is actually a deletion of color. Tobiano is the result of a chromosomal inversion, affecting regulatory regions of the KIT gene. The Tobiano coat pattern is governed by the dominant KIT gene. Only one copy of Tobiano gene (To/N) is required to express Tobiano coat pattern. Homozygosity of the Tobiano gene (To/) may show visual clues (“ink spots” or “paw prints”) but only genetic testing will tell you more conclusively that the horse is homozygous for the Tobiano gene. When there is no presence of the Tobiano gene (N), the Tobiano coat pattern is not possible.  

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Express delivery with door-to-door pick-up service. We can imagine you want to take great care in making sure your sample is handled, transported and delivered by a trusted specialist. Therefore we can arrange a pickup to ensure sample integrity and speedy delivery to the lab.  The pick-up is included for purchases over 200 Euros. In these cases, you do not need to pay for this service.    EXPRESS SHIPPING DELIVERY FOR EUROPEAN COUNTRIES FROM NON REMOTE REGIONS. Check here to know if you are in a remote European region. For remote regions EXTRA fees are applied.  If your purchase order is less than 200 Euros but you want to request an express pick-up please purchase this item or send us an email to support@equigerminal.pt.   We'll be glad to take care of all the logistics for you.

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8 panel genetic test for coat colour with results in 5 to 10 working days.   Includes 8 coat colour genetic markers:  2 base colour - Agouti, Extension; 5 dilutions - Cream, Pearl, Champagne, Silver and Dun (D, nd1, nd2) and the Grey* (G/G, G/N or N/N) depigmentation gene. Our Grey test in panels provide the number of copies of the Grey gene (G/G, G/N, N/N) A Genetic Colour Certificate - Coat Genotype and Offspring Prediction of coat colour is provided Sample type: 30 to 40 hair roots  or 5 mL of blood  (K3 EDTA tube) Turnaround time 5 to 10 working days   Additional information DNA tests for coats can be an important tool for selection, elimination of coat-related diseases and enhancing your stud farm. There are various coat colours and tones in the horse species. Judging coat colour by eye is always subjective and can be influenced by a number of environmental factors (light exposure, time of year and feeding) and it doesn’t allow us to predict with any confidence that the “colour” will be passed down. Genetic determination of coat colour can be done correctly in a laboratory using DNA tests. This method allows us to determine with rigour and objectivity the horse´s coat colour and also forecast the potential transmission of “colour” to offspring. Currently more than 16 gene variants have been identified that can influence this phenotypic characteristic.  

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DNA test The DNA test verifies the presence of the dominant (PATN1) mutation.  Sample 20 to 30 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Results description The DNA test verifies the presence of the dominant (PATN1) mutation and presents results as one of the following: N/ - Negative for PATN1.  Absence of the dominante PATN1 gene - non spotted horse. PATN1/N - Positive heterozygous for PATN1 (Dominant). Presence of one copy of the dominant PATN1 gene responsible spotted coat. The horse can pass the PATN1 variant to 50% of their progeny when bred. PATN1/ -  Positive homozygous for PATN1 (Dominant). Presence of two copies of the dominant PATN1 gene responsible for spotted coat.  The horse will pass the PATN1 gene to 100% of its offspring.   Additional information

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DNA test The DNA test verifies the presence of the grey mutation. Grey is the dominant gene responsible for the gradual and progressive de-pigmentation (fading) of the carrying horse. Sample 5 mL - blood - K3 EDTA tube Turnaround time  5-10  working days Why test? This genetic test can help breeders that are interested in specifically breeding grey foals. Homozygous grey specimens are ideal as they will always transmit the grey gene when bred, thus guaranteeing eventual grey progeny. For the breeder that wants to  “breed-out” the grey modifier to gain non-fading foals may hope for heterozygous grey horses. Some breed-types have a large percentage of grey stock which through historical lineage may harbour colours and dilutions that are ‘hidden’ by the masking effect of the grey. Insight into a foal’s potential to fade: since grey may cause slow de-pigmentation, it may not be visually apparent whether or not a newborn foal will eventually fade to grey. The de-pigmentation process may take many years and therefore DNA testing is useful in the cases whereby a foal is born of one or more grey parents and verification of the presence of grey is necessary. Results description The DNA test verifies the presence of the grey mutation and presents results as one of the following: N/ – Non-grey horse. Negative for grey. Horse will not turn grey. G/N - Grey horse. Positive for dominant grey gene, carrying a single inherited copy. Carrier’s coat modified and will eventually become de-pigmented. Heterozygous grey horses are statistically likely to pass the gene to 50% off their progeny when bred. G/ - Grey horse. Positive for dominant grey gene, carrying two inherited copies. Carrier’s coat modified and will eventually become de-pigmented. Homozygous grey horses are genetically bound to pass the gene to 100% of their progeny when bred, so all foals will receive grey and fade-out. Additional information Grey is the dominant gene responsible for the gradual and progressive de-pigmentation (fading) of the carrying horse. Grey cannot be considered a base-color, or a dilution, but rather a gene which slowly removes pigment from the coat.  This gene is considered to be the ‘strongest’ of all coat modifiers, and acts upon any base-color regardless of the carrying horse’s phenotype. The fading process itself may last for years, but once hair is de-pigmented, the horse’s original colouring will never return. Since grey is a dominant gene, where it is present it is expressed. However, the final phenotype of the carrier will vary from horse to horse. Some grey horses fade to full de-pigmentation (almost pure white) whereas others may be ‘fleabitten’. Fleabitten refers to grey horses with tiny non-faded spots or ‘fleabites.’  Equine melanomas occur most often in grey horses, and it is expected that at least 80% of grey horses will develop melanoma.

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About the Test The qPCR test detects the genome (DNA) of Streptococcus equi subspecies equi, the pathogen responsible for Strangles. Sample Nasopharyngeal swab (dry swab). See AAEP guidelines. Nasal swabs or draining lymph nodes. Guttural pouch washes. Turnaround Time 2 to 5 working days after sample receipt. What is Strangles? A highly contagious upper respiratory infection caused by S. equi. Transmitted via inhalation or contact with contaminated surfaces (e.g., water buckets). Colonizes tonsils/pharynx and causes abscesses in lymph nodes. View More Info For more detailed information, visit our website. How It Works 🛒 Purchase: Buy the test online. 📄 Download Form: Submission Form 📮 Send Samples: Equigerminal Lab, Coimbra, PORTUGAL. FAQs View FAQs How does the qPCR test work? Detects DNA with high sensitivity and specificity. What to do if positive? Isolate the horse, apply biosecurity, and consult a vet.  

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Pathogen test  This is one of the internationally imposed tests in the import/export of live equines or semen/ova and embryos intended for assisted reproduction. PTE029/7 AGID test (Coggins test) to detect antibodies against equine infectious anemia  Equine Infectious Anaemia is a disease listed in the OIE Terrestrial Animal Health Code and countries are obligated to report the occurrence of the disease according to the OIE Code. Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is Equine Infectious Anemia? Equine infectious anemia is a very old viral disease that affects horses, asses, mules and hinnies worldwide. It is subject to tight controls in the import/export of live equines and their products Clinical signs This infection may have an acute, chronic or sub-clinical (silent) phase. The acute phase characterised by intermittent fever associated with depression, lethargy, increased heart and breathing rates, haemorrhaging, diarrhoea with blood, bleeding wounds that won’t heal, lack of coordination and rapid weight loss. It can also cause petechial haemorrhages of the mucous membranes and general oedema more evident in the legs and jaundice. The chronic phase characterised by recurrent episodes of fever, anaemia and thrombocytopenia (decrease of blood platelets) interspersed with periods of normality. These episodes will be spread out over time. This disease is often fatal during the acute or chronic phase. Should the animal survive the acute and chronic phase, it enters a silent phase with no evident signs of illness for the remainder of its life. In this silent phase the virus persists but the clinical signs are only manifest if the immune system is weakened by another disease, stress or the administration of corticosteroids. Transmission EIA is caused by a lentivirus of the HIV family, the equine infectious anaemia virus. The virus can be passed from one horse to another through fly, or more rarely, mosquito bites, or by direct contact with blood or blood derivative products (serum and/or plasma). Such as, for example, by: sharing objects contaminated with infected blood (needles, branding tools, etc). The virus can also be passed down from mare to foal via the placenta or, more rarely, in the mother’s colostrum or milk. Potentially, the virus can be transmitted by semen. Prevention There is no treatment, cure or vaccine for this infection. Prevention is crucial to avoid it being passed on. Serological tests for EIA must be done for any horse with anaemia and thrombocytopenia of unknown origin. Regular tests must be done on a yearly basis to keep the holding free from EIA. It is advisable to test studs and brood mares every 90 days in the breeding period.    

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Equine Piroplasmosis is a serious tick-borne disease caused by Babesia caballi and Theileria equi. As a national reference laboratory, Equigerminal is dedicated to providing the most accurate diagnostic services following ISO17025 standards. Our facility offers reliable cELISA tests to detect antibodies, ensuring compliance with international trade standards. PTE019/6 cELISA test to detect antibodies against Babesia caballi PTE020/6 cELISA test to detect antibodies against Theileria equi Test Details Pathogens Detected: Antibodies against Babesia caballi and Theileria equi. Sample Requirements: 5 mL of blood, serum, or plasma collected in a dry or EDTA tube. Turnaround Time: 2-5 working days after sample receipt. When to Choose the cELISA Test The cELISA test is ideal for detecting chronic or inapparent infections, routine screening, and ensuring compliance with international trade regulations. It detects antibodies (IgG) 21 days post-exposure. How It Works How It Works 🛒 Purchase: Buy online and receive instructions. ✨ Collection: Veterinarian collects the sample. 📄 Download Form: Download submission form here. 📮 Send: To Equigerminal Lab, Rua Pedro Nunes, IPN Incubadora, Edifício C, 3030-199 Coimbra. More Info View More Info For more details, visit our detailed diagnosis page. FAQs View FAQs How does cELISA work? Detects specific antibodies with high sensitivity for chronic infections. Samples? 5 mL blood in dry or EDTA tube. Turnaround? 2-5 working days.

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DNA Test Bundle: PSSM1 & WFFS Discover Peace of Mind with Precision Equine Genetics. Our bundle offers comprehensive screening for PSSM1 and WFFS, empowering you with essential information for the wellbeing of your horse. Tests Included PSSM1: Detects the GYS1 mutation affecting muscle metabolism. WFFS: Identifies the PLOD1 mutation related to fragile connective tissue. Sample Collection Hair: 20-30 roots. Tape to the submission form. Blood: 5 mL in EDTA tube. Send with the submission form. Turnaround Time Standard: 5 working days. Premium: 2 working days (includes express courier; contact support@equigerminal.pt). Learn More Results Description PSSM1: Results range from n/n (clear) to n/P1 (heterozygous) and P1/P1 (homozygous). WFFS: Results range from n/n (clear) to n/WFFS (carrier) and WFFS/WFFS (affected). Check our FAQs FAQs Why test? Testing is vital to inform breeding decisions and manage the health of your horse through specific dietary and exercise protocols. Visit our full FAQ page.  

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Buy a Base colour test and find out if your horse's base colour is Black, Bay or Chestnut. Results within 24 h are available. DNA test for the Agouti and Extension loci that controls distribution of Black and Red pigment throughout the coat. Sample 30 to 40  hair roots  or 5 mL - blood - K3 EDTA tube Turnaround time Standard processing - Results in 3-5 working days after sample arrival at the laboratory. Clients organize and support the costs of sending the samples to the laboratory. PREMIUM processing - Results in 1 day after sample arrival. Includes free express delivery** . The laboratory organizes Express shipping with pick-up of the package at the client's address and delivery at the laboratory. ** PREMIUM SERVICES INCLUDE AN EXPRESS SHIPPING DELIVERY FOR EUROPEAN COUNTRIES FROM NON-REMOTE REGIONS. Check here to know if you are in a remote European region. For remote/outreach regions EXTRA fees are applied.      Why test? Horses have only three base colours: Bay, Black or Chestnut These different colours are controlled by 2 loci, the Extension  (Red/Black) and Agouti. The Extension locus controls the production of black or red pigment throughout the coat. The allele for black color (E) is dominant over the red allele (e), so a horse only needs one copy of the black allele to appear black-based. But if the horse has two alleles (e/e) he will appear Chestnut. The Agouti locus can then modify black pigment by pushing it the horse's points, creating a Bay. The Agouti A allele is dominant, so a black pigmented horse only needs one copy (heterozygous) of the A allele to appear Bay. The Agouti (a) allelle is recessive, thus, a horse needs two copies (homozygous) of the recessive allele (a) at the Agouti locus to appear Black. Agouti has no effect on red pigment, but the red allele (e) is dominant over the (a) allele. This means a Chestnut horse (e/e) can carry one or two copies of the Agouti recessive (a) allele and will look no different from chestnut horses with  Agouti dominant alleles (e/e a/a, e/e A/a,  e/e A/A).   Results description Base Colour Extension Agouti Bay E/E or E/e A/A or A/a Black E/E or E/e a/a Red e/e A/A, A/a or a/a   References Rieder, S., Taourit, S., Mariat, D., Langlois, B., & Guérin, G. (2001). Mutations in the agouti (ASIP), the extension (MC1R), and the brown (TYRP1) loci and their association to coat color phenotypes in horses (Equus caballus). Mammalian genome : official journal of the International Mammalian Genome Society, 12(6), 450–455. https://doi.org/10.1007/s003350020017  Marklund, L., Moller, M. J., Sandberg, K., & Andersson, L. (1996). A missense mutation in the gene for melanocyte-stimulating hormone receptor (MC1R) is associated with the chestnut coat color in horses. Mammalian genome : official journal of the International Mammalian Genome Society, 7(12), 895–899. https://doi.org/10.1007/s003359900264

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MIM (PSSM2) DNA Test Ensure the Health and Performance of Your Horses with Accurate MIM Testing. Our DNA test identifies genetic variants associated with Muscle Integrity Myopathy (MIM), formerly known as PSSM2, which affects muscle function and structure. Sample Requirements 30 to 40 hair roots (envelope) Alternatively, 5 mL blood (K3 EDTA tube) Turnaround Time Up to 15 working days Results Description The DNA test identifies six genetic variants that predispose horses to MIM symptoms: P2: Myotilinopathy P3: Filaminopathy P4: Myozenin-3-Myopathy P8: PYROXD1-Myopathy Px: CACNA2D3-Myopathy K1: COL6A3-Myopathy Learn More Additional Information MIM is a genetic disorder that disrupts muscle structure. While not curable, management through tailored diet and exercise helps mitigate symptoms, allowing horses to lead better lives. Check our FAQs FAQs What breeds are affected? Almost any breed, common in Quarter Horses, Warmbloods, and Thoroughbreds. How is it managed? Through optimized feeding and exercise protocols tailored to the horse's genetic status.

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DNA test DNA test for Hereditary Equine Regional Dermal Asthenia (HERDA). This test verifies the presence of the recessive HERDA gene. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? This DNA test helps breeders to identify horses that carrying the HERDA recessive mutation. Informed choices can be made for breeding selections, and prevent the born of affected foals. Results description  The DNA test verifies the presence of the recessive HERDA gene and presents results as one of the following: N/ - Negative for HERDA. Absence of the defective gene responsible for HERDA. N/HERDA - Carrier - Positive heterozygous for HERDA. Presence of one copy of the allele responsible for HERDA.  The horse is a carrier for HERDA and can pass on a copy of HERDA allele to their progeny when bred. HERDA/ - Positive Homozygous for HERDA. Presence of two copies of the allele responsible for HERDA.  The horse is affected by  HERDA disorder and can pass the HERDA allele to 100% of their progeny when bred. Additional information Hereditary equine regional dermal asthenia (HERDA) is a genetic skin disease predominantly found in the American Quarter Horse. Within the breed, the disease is prevalent in particular lines of cutting horses. HERDA is characterised by hyper-extensible skin, scarring, and severe lesions along the back of affected horses. Affected foals rarely show symptoms at birth. The condition typically occurs by the age of two, most notably when the horse is first being broke to saddle. There is no cure, and the majority of diagnosed horses are euthanised because they are unable to be ridden and are inappropriate for future breeding. HERDA has an autosomal recessive mode of inheritance and affects stallions and mares in equal proportions.

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DNA test 2 DNA tests that can help to predict the possible type of incidence for developing  dermal melanomas on grey horses. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? This 2 DNA tests for melanoma confirms if the grey horse is heterozygous (G/N) or homozygous (G/) for the Grey gene and if is Homozygous for non-agouti (a/a).The results can predict the type incidence for developing dermal melanomas.   Results description The genetic profile test verifies the genotype of the Grey and Agouti genes, and presents results as one of the following:  Melanoma incidence risk G/N + A/a or A/A – Moderate incidence of dermal melanomas. G/N + a/a – Moderate to high incidence of dermal melanomas. G/G + A/a or A/A – High incidence of dermal melanomas. G/G + a/a – Very high incidence of dermal melanomas.   Additional information Most melanomas found in horses are benign. Once present these benign types of melanoma are not aggressive in their growth and may progress over several years requiring little treatment. A melanoma is one of the most common skin tumors seen in a horse or pony. Grey horses have a high incidence of dermal melanomas that are commonly seen around the tail and head. Over 80% of Grey horses older than 15 years will develop melanoma. Grey homozygotes are more likely to develop melanoma than heterozygotes. Grey horses that are homozygous for non-agouti (aa) genotype at the Agouti locus, also have a higher risk for melanoma. Many Grey horses show depigmentation of the skin around the eyes, mouth and anus but there are no health risks associated with this condition. Malignant melanomas in horses can cause severe problems and can be life-threatening. Problems develop when melanomas are present internally or if they become so large that they ulcerate, bleed and become infected. Equine melanomas sometimes grow so large that they can cause severe weight loss and/or colic. If a melanoma is situated on the head in an area where a bridle, saddle, head collar or rug might rub, it will be uncomfortable for the horse, potentially causing behavioural problems. Infections can also occur.  

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Pathogen test  The PCR test detects the genome (DNA) of Burkholderia mallei, the bacteria responsible for Glanders in equines. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Glanders? Glanders is a contagious and fatal disease of horses, donkeys, and mules, caused by infection with the bacterium Burkholderia mallei.The pathogen causes nodules and ulcerations in the upper respiratory tract and lungs. A skin form also occurs, known as ‘farcy’. Control of glanders requires testing of suspect clinical cases, screening of apparently normal equids, and elimination of positive reactors. As B. mallei can be transmitted to humans, all infected/contaminated or potentially infected/contaminated material must be handled in a laboratory with appropriate biosafety and biosecurity controls following a biorisk analysis. Glanders is an OIE listed disease as described in the Terrestrial Animal Health Code of the World Organisation for Animal Health (OIE). As indicated in the OIE Terrestrial Animal Health Code any occurrence of glanders must be notified to the OIE. Clinical signs The disease causes nodules and ulcerations in the respiratory tract and lungs in animals. A skin form, known as ‘farcy’, also occurs. Both acute and chronic forms of the disease have been described. Acute forms occur most frequently in donkeys and mules, with high fever and respiratory signs. In horses, glanders generally takes a more chronic course and they may survive for several years. There are four recognised clinical presentations of glanders: nasal, pulmonary, cutaneous and asymptomatic carrier. These different forms of glanders are usually referred to according to the location of the initial infection. The nasal and pulmonary forms tend to be more acute while the cutaneous form is a chronic process. Inflammatory nodules and ulcers develop in the nasal passages and give rise to a sticky yellow discharge. Stellate scarring follows upon healing of the ulcers. The formation of nodular abscesses in the lungs is accompanied by progressive debility, coughing and may also be accompanied by diarrhoea. In the cutaneous form (“farcy’), the lymph vessels are enlarged; nodular abscesses form along their course, which then ulcerate and discharge yellow pus. Nodules are regularly found in the liver and spleen, leading to wasting and death. Transmission The most common source of infection is ingestion of contaminated food or water. Contaminated aerosols (produced by coughing and sneezing), and contaminated fomites brought to the animals via grooming equipment and tack may also be a source of infection. The bacteria can also enter the body through contact with lesions or abrasions of the skin or through mucosa. In this case, a local infection with ulceration may develop spreading to other parts of the body in the course of the disease. Poor husbandry and feeding conditions as well as animal transport can be predisposing factors. Unsanitary conditions and over-crowded stables are risk factors. Prevention To date, no treatment with veterinary drugs is capable to cure the infection. Control of glanders requires early detection and diagnostic testing of suspected clinical cases, screening of apparently normal equids, and elimination of positive cases. For glanders-free countries, there are recommendations on importing equines. An international veterinary certificate is required attesting that the animals showed no clinical signs of glanders and were kept in an exporting country free of the disease for at least 6 months prior to shipment.

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Parameter Anti-Müllerian Hormone (AMH)  Sample 5 mL - blood - serum tube  Turnaround time 2 to 5 working days

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 DNA test The cream dilution gene has varying effects on different base colours. To obtain the exact ‘type name’ of cream dilute of the horse it is recommended to run this test in conjunction with Extension and Agouti genes. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days   Why test? Testing is useful where genetic confirmation is required or to define cream dilute horses aside from other genes with similar effects (such as champagne dilution and grey). Running this test will confirm if a horse is cream dilute. As mentioned the cream dilution gene has varying effects on different base colours. To obtain the exact ‘type name’ of cream dilute of the horse (eg. Buckskin, Palomino, Cremello…) it is recommended to run this test in conjunction with red factor and agouti. Results description The DNA test verifies the presence of the Cream dilution gene and presents results as one of the following: N/ - Non-dilute. Basic colours are black, bay or chestnut, in the absence of other modifying genes. N/Cr – Dilute. Heterozygous, one copy of the Cream (Cr) allele. Chestnut is diluted to palomino; bay is diluted to buckskin and black is diluted to smoky black. These colours can be further modified by the actions of other genes. Cr/ - Double dilute, two copies of the Cream (Cr) allele. Chestnut is diluted to cremello; bay is diluted to perlino and black is diluted to smoky cream. Additional information The cream dilution gene affects both red and black pigment and is responsible for ‘diluting’ the carrying horse to lighter coat shades and colours. In many breeds this is often considered a highly desirable trait. Cream dilution is the gene responsible for palominos, buckskins, cremellos and many more. Horses which carry one copy of the cream gene are identified as single dilutes; they are heterozygous for the cream dilution gene. In the simplest case, a bay horse with a single copy of cream is known as a buckskin, a single dilute black horse is known as a smoky black and a single dilute chestnut or sorrel horse is known as a palomino. Single dilute horses have a 50% chance on passing the cream gene on to its offspring. Horses which carry two copies of the cream gene are referred to as double dilutes; they are homozygous for the cream dilution gene. A bay horse with two copies of cream is known as a perlino. A black horse with two copies of cream is known as a smoky cream and a chestnut or sorrel horse that carries two copies of cream is known as a cremello. Double dilute horses will always pass on a copy of the cream gene to its foals.      

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Adrenocorticotropic hormone - ACTH  ACTH levels are seasonal in horses  Increased ACTH levels could indicate Pituitary Pars Intermedia Dysfunction PPID, also known as Equine Cushing’s Disease. For more information about PPID please check the 2021  EEG recommendations on diagnosis and management of pituitary pars intermedia dysfunction (PPID).   Sample requirements 5 mL of blood in EDTA tube Separate the plasma by centrifugation or gravity and freeze plasma at -20ºC (in a regular freezer).  Send freeze plasma to lab ASAP in a refrigerated package.  Turnaround time 2 to 5 working days

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Pathogen test  The PCR test detects the genome (DNA) of  Trypanosoma equiperdum, the pathogen responsible for Dourine. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Dourine? Dourine is a chronic or acute contagious disease of breeding equids that is transmitted directly from animal to animal during coitus. The causal organism is Trypanosoma equiperdum. Dourine is the only trypanosomosis that is not transmitted by an invertebrate vector. Trypanosoma equiperdum differs from other trypanosomes in that it is primarily a tissue parasite that is rarely detected in the blood. There is no known natural reservoir of the parasite other than infected equids. Clinical signs Dourine is characterised mainly by swelling of the genitalia, cutaneous plaques and neurological signsThe symptoms vary with the virulence of the strain, the nutritional status of the horse, and stress factors. The clinical signs often develop over weeks or months. They frequently wax and wane; relapses may be precipitated by stress. This can occur several times before the animal either dies or experiences an apparent recovery.Genital edema and a mucopurulent discharge are often the first signs. Mares develop a mucopurulent vaginal discharge, and the vulva becomes oedematous; The genital region, perineum and udder may become depigmented. Abortion can occur with more virulent strains. Stallions develop edema of the prepuce and glans penis, and can have a mucopurulent discharge from the urethra. In stallions, the swelling may spread to the scrotum, perineum, ventral abdomen and thorax. Neurological signs can develop soon after the genital edema, or weeks to months later. Restlessness and weight shifting from one leg to another is often followed by progressive weakness, incoordination and, eventually, paralysis. Facial paralysis, which is generally unilateral, may be seen in some animals. Conjunctivitis and keratitis are common, and in some infected herds, ocular disease may be the first sign of dourine. Anemia and intermittent fever may also be found. In addition, dourine results in a progressive loss of condition, predisposing animals to other diseases. Transmission Unlike other trypanosomal infections, dourine is transmitted almost exclusively during breeding. Transmission from stallions to mares is more common, but mares can also transmit the disease to stallions. T. equiperdum can be found in the vaginal secretions of infected mares and the seminal fluid, mucous exudate of the penis, and sheath of stallions. Periodically, the parasites disappear from the genital tract and the animal becomes noninfectious for weeks to months. Non infectious periods are more common late in the disease. Male donkeys can be asymptomatic carriers. Rarely, infected mares pass the infection to their foals, possibly before birth or through the milk. Infections are also thought to occur through mucous membranes such as the conjunctiva. Other means of transmission may also be possible; however, there is currently no evidence that arthropod vectors play any role in transmission. Sexually immature animals that become infected can transmit the organism when they mature. Prevention To prevent dourine from being introduced into a herd or region, new animals should be quarantined and tested by serology. When dourine is found in an area, quarantines and the cessation of breeding can prevent transmission while infected animals are identified. Dourine can be eradicated from a herd, using serology to identify infected equids. Infected animals are euthanised. In some cases, stallions have been castrated to prevent disease transmission; however, geldings can still transmit the disease if they display copulatory behavior. Successful treatment with trypanocidal drugs has been reported in some endemic areas. However, therapeutic regimes have not been thoroughly investigated, and treatment is usually discouraged due to fears that the organism will persist inapparently. Good hygiene should be used at assisted matings. No vaccine is available.

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Canine DNA Profiling and Parentage Analysis Introduction Ordering and utilizing our canine genetic tests is a straightforward process designed to provide you with valuable insights into your dog's health and lineage. Simply follow the instructions provided in the kit to collect a DNA sample from your dog and send it back to our laboratory for analysis. Benefits Verified Parentage: Understand your dog's unique genetic heritage and confirm their parentage, ensuring their pedigree. Verified Identity: Secure a unique genetic ID for your dog, invaluable for breeders, registration, and in case of loss. Procedure Follow the instructions provided in the kit to collect a DNA sample from your dog and send it back to our laboratory for analysis. Results Results are typically available within 2-3 weeks and include a detailed report on the genetic status of your dog. FAQs How do I collect the sample? Follow the instructions provided in the kit to collect a DNA sample. How long does it take to get results? Results are typically available within 2-3 weeks from the time we receive the sample. What should I do if my dog tests positive for a genetic predisposition? If your dog tests positive, consult with your veterinarian to create a management plan tailored to your dog's needs.

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Pathogen profile Screening of 5 pathogens responsible for respiratory disease in equines: EHV-1, EHV-4, Equine Influenza, Rhodococcus equi (Pneumonia), and Streptococcus equi (Strangles). Our lab is approved by the FEI for EHV-1 testing. Sample 1 nasopharyngeal swab (see AAEP guidelines) 5 mL blood (K3 EDTA tube) Turnaround time 2 to 5 working days

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DNA test DNA test for the Malignant hyperthermia (MH). This test verifies the presence of the dominant MH gene and presents results as one of the following: Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Results description The DNA test verifies the presence of the dominant MH gene and presents results as one of the following: N/ - Negative for MH.  Absence of the allele responsible for Malignant Hyperthermia (MH). MH/N - Affected - Positive heterozygous for MH. Presence of one copy of the allele responsible for MH. The horse is affected with the MH disorder and can pass the MH allele  to 50% of their progeny when bred. MH/ - Affected - Positive homozygous for MH. Presence of two copies of the allele responsible for MH.  The horse is affected with the MH disorder and will pass the MH allele to 100% of its offspring. Additional information Malignant Hyperthermia or MH is a genetic muscle disorder that affects Quarter Horses and related breeds. Horses with the MH mutation may not show any physical signs of the disorder until triggered by exposure to anaesthesia or extreme exercise or stress. Symptoms can include high temperature, increased heart rate, high blood pressure, sweating, acidosis, and muscle rigidity. Symptoms develop rapidly, and if not treated quickly, this condition can be fatal. MH is inherited as an autosomal dominant trait, so the disorder can be passed on even if only one parent has the defective gene. The mutation can be present along with PSSM and if a horse also has PSSM, the symptoms associated with MH can be more severe. Therefore, testing for both PSSM and MH is recommended for Quarter Horse breeds. Although this condition is rare, testing for MH is recommended in case a horse must undergo anaesthesia. Horses that are known to have the MH mutation can be given medication prior to administering anaesthesia to help reduce the severity of the symptoms.

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DNA test DNA test for the Glycogen Branching Enzyme Deficiency (GBED). This DNA test verifies the presence of the recessive GBED allele. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? This DNA test identify inapparent carriers of the GBED fatal disorder.  In breeding selection is recommended to avoid the crossbreeding of two GBED inapparent carriers to prevent in utero abortion of foetus and the birth of foals affected by GBED.  To confirm GBED in affected foals. DNA testing provide important tools for informed choices about breeding selections to prevent abortion and the birth of affected foals.    Frequency and affected breeds More frequent in Paint Horses and Quarter horses related breeds. A prevalence of  7,1% and 8,3% in the Paint and Quarter Horse breeds, respectively (Wagner et al., 2006).   Results description The DNA test verifies the presence of the recessive GBED alleles and presents results as one of the following:  N/ - Negative for GBED. Absence of the defective allele responsible for GBED. GBED/N - Carrier - Positive heterozygous for GBED. Presence of one copy of the allele responsible for GBED.  The horse is a carrier for GBED and can pass on a copy of GBED allele to their progeny when bred. GBED/ - Affected - Positive Homozygous for GBED. Presence of two copies of the allele responsible for GBED.  The animal is affected by GBED disorder. GBED is lethal causing abortion and/or  neonatal mortality.   Additional information Glycogen Branching Enzyme Deficiency (GBED) fatal condition caused by an autosomal recessive genetic disorder that results in the bodies' inability to properly store sugar in the glycogen form. In a normal horse, the body stores sugar as energy by converting glucose to glycogen. This genetic disorder  affects the production of the enzyme needed to branch the glycogen structure, preventing the horse from being able to adequately store sugar in the glycogen form. This means that the horse will not be able to store enough energy to fuel important organs, such as the muscles and brain. Unfortunately, GBED is always fatal.  GBED often causes the foetus to be aborted in utero. When born most affected foals will die in the first weeks of age.  Research studies showed that as many as 2,5% of aborted Quarter Horse foetus were homozygous for the GBED mutation (Wagner et al., 2006).  Foals born which are affected by GBED suffer from a range of clinical signs associated with this lack of sugar, such as low energy, weakness and difficulty rising.  Other clinical signs include low body temperature, contracted muscles, seizures, and sudden death.   REFERENCES Tryon RC, Penedo MC, McCue ME, Valberg SJ, Mickelson JR, Famula TR, Wagner ML, Jackson M, Hamilton MJ, Nooteboom S, Bannasch DL. Evaluation of allele frequencies of inherited disease genes in subgroups of American Quarter Horses. J Am Vet Med Assoc. 2009 Jan 1;234(1):120-5. doi: 10.2460/javma.234.1.120. PubMed PMID: 19119976.DOI: 10.2460/javma.234.1.120 Wagner ML, Valberg SJ, Ames EG, Bauer MM, Wiseman JA, Penedo MC, Kinde H, Abbitt B, Mickelson JR. Allele frequency and likely impact of the glycogen branching enzyme deficiency gene in Quarter Horse and Paint Horse populations. J Vet Intern Med. 2006 Sep-Oct;20(5):1207-11. PubMed PMID: 17063718.DOI: 10.1892/0891-6640(2006)20[1207:afalio]2.0.co;2

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DNA test for the Hyperkalemic Periodic Paralysis Disease (HYPP). This DNA test verifies the presence of the recessive HYPP gene.  Sample requirements  30 to 40 hair roots  or 5 mL of blood in K3 EDTA tube Turnaround time 2 to 5  working days Why test? This genetic test helps breeders to identify horses that carrying the HYPP recessive gene. Informed choices can be made for breeding selections, and prevent the born of affected foals. All offspring of Impressive should be tested for HYPP. Because HYPP is dominant disorder, the effects of it can also be transposed to other breeds of horses when intermixing occurs. This test is important in preserving the inherited health of all horses. Horses with suspicious symptoms of the disease should also be tested. Results description  The DNA test verifies the presence of the recessive HYPP gene and presents results as one of the following: N/ –  Normal - Absence of the allele responsible for HYPP. N/H – Affected - Positive heterozygous for HYPP. Presence of one copy of the allele responsible for HYPP. The horse is affected with the HYPP disorder and there is a 50% chance this horse will pass a HYPP allele to its offspring. H/ – Affected- Positive homozygous for HYPP. Presence of two copies of the allele responsible for HYPP. The horse is affected with the HYPP disorder and there is a 100% chance this horse will pass a HYPP allele to its offspring. Additional information Hyperkalemic Periodic paralysis (HYPP) is an inherited disease of the muscle, which is caused by an inherited genetic mutation. A point mutation in DNA exists in the sodium channel gene, which codes for an abnormal channel to be expressed in skeletal muscle. This mutation is passed on to offspring. Sodium channels are “pores” in the muscle cell membrane which control contraction of the muscle fibers. When the defective sodium channel gene is present, the channel becomes “leaky” and makes the muscle overly excitable and contract involuntarily. The channel become “leaky” when potassium levels fluctuate in the blood. This may occur with fasting followed by consumption of a high potassium feed such as alfalfa. Hyperkalemia, which is an excessive amount of potassium in the blood, causes the muscles in the horse to contract more readily than normal. This makes the horse susceptible to sporadic episodes of muscle tremors or paralysis. Severity of attacks varies from unnoticeable to collapse or sudden death. The cause of death is usually respiratory failure and/or cardiac arrest. This genetic defect has been identified in offspring of the American Quarter Horse sire, Impressive. To date, confirmed cases of HYPP have been restricted to descendants of this horse.  HYPP is a dominant disorder meaning both homozygous positive (HH) and heterozygous (nH) horses will be affected. Only homozygous negative (nn) horses are not affected by HYPP.

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