MIM (PSSM2) DNA Test Ensure the Health and Performance of Your Horses with Accurate MIM Testing. Our DNA test identifies the presence of 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 developing symptoms of Muscle Integrity Myopathy: P2: Myotilinopathy P3: Filaminopathy P4: Myozenin-3-Myopathy P8: PYROXD1-Myopathy Px: CACNA2D3-Myopathy K1: COL6A3-Myopathy Genetic Inheritance Muscle Integrity Myopathy (MIM) is caused by a hereditary predisposition involving multiple genetic variants. These variants disrupt the structure and function of muscle fibers, leading to symptoms such as muscle stiffness, unexplained lameness, and difficulty building muscle. Clinical Signs and Affected Breeds Symptoms of MIM can vary widely among horses and include unexplained lameness, muscle stiffness, difficulty with gait changes, reluctance to move, muscle atrophy, and behavioral changes. Almost any breed can be affected, with common occurrences in breeds like Quarter Horses, Warmbloods, and Thoroughbreds. Why Test? Testing for MIM is crucial for breeders and owners to make informed decisions. By identifying carriers of the genetic variants, breeding choices can be optimized to prevent the spread of these disorders. Additionally, knowing a horse's genetic status can help manage and mitigate symptoms through tailored exercise and feeding protocols. Learn More Detailed Results Description The DNA test results will indicate the presence of the following genetic variants: P2: Myotilinopathy P3: Filaminopathy P4: Myozenin-3-Myopathy P8: PYROXD1-Myopathy Px: CACNA2D3-Myopathy K1: COL6A3-Myopathy Additional Information Muscle Integrity Myopathy (MIM) is a genetic disorder that disrupts muscle function and structure, leading to various clinical signs. While it is not possible to cure genetic disorders, optimized management through diet and exercise can help mitigate symptoms, allowing horses to lead normal lives. References Generatio. Muscle Integrity Myopathy in HorsesEquiSeq. Polysaccharide Storage Myopathy type 2 (PSSM2) Check our FAQs for more information FAQs What breeds are affected by MIM? Almost any breed can be affected by MIM, with common occurrences in breeds like Quarter Horses, Warmbloods, and Thoroughbreds. How is MIM inherited? MIM is caused by multiple genetic variants that disrupt muscle structure and function. These variants are inherited and can predispose horses to developing symptoms of exertional myopathy. How can MIM be managed? While genetic disorders cannot be cured, their symptoms can often be managed through optimized feeding and exercise protocols. Identifying genetic variants through testing allows for tailored management strategies to mitigate symptoms. Visit our full FAQ page for more details.

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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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 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 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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Pathogen test  The qPCR test detects the genome (DNA) of  Equine Herpesvirus Type 4 (EHV-4). Molecular detection of EHV-4 by PCR is the most sensitive, specific and accurate tool in assessing the infectivity of an affected horse Sample 1 nasal or nasopharyngeal swab ( see AAEP guidelines)  and 5 mL - K3 EDTA tube 20 gr - placental or foetal tissue - sterile flask Turnaround time 2 to 5 working days   What is Herpesvirus Type 4? Equine Herpesvirus Type 4 (EHV-4) is a health risk to equine populations worldwide. Disease severity depends on multiple factors and may be latent in normal horses. And because clinical signs are similar to other respiratory diseases, it is difficult to make a definitive diagnosis from clinical presentation alone. Clinical signs EHV-4 infections are restricted to respiratory tract epithelium and associated lymph nodes, Infection of pregnant mares with EHV-4 strains rarely results in abortion. Like EHV-1 the EHV-4 establish latent infection in the majority of horses, which do not show clinical signs but may experience reactivation of infection and shedding of the virus when stressed. Transmission EHV-4 spread via aerosolised secretions from infected coughing horses, by direct and indirect (fomite) contact with nasal secretions. The most common way for EHV-4 to spread is by direct horse-to-horse contact. This virus is shed from infected horses via the respiratory tract. Horses may appear to be perfectly healthy yet spread the virus via the secretions from their nostrils. It is important to realize that EHV-4 can also be spread indirectly through contact with physical objects contaminated with infectious virus. The air around a horse that is shedding the virus can also be contaminated with infectious virus. Prevention Herd elimination of equine herpesviruses is virtually impossible because of the pervasiveness of the carrier state. Disease prevention, rather than treatment or attempts at eradication, offers the most effective means for controlling herpesvirus and its potential sequelae. Strategies aimed at reducing the economic and welfare impact associated with EHV-1 and EHV-4 respiratory infections include (1) prophylactic immunisation and (2) the implementation of preventive herd management practices. Subdivide horses into the small epidemiologically isolated closed groups. Minimize risks of exogenous and endogenous (stress induced viral reactivation) introduction of EHV-1. Maximize herd immunity through vaccination. Important measures in the case of an EHV-4 outbreak: Disinfection of areas contaminated by virus from the aborted foetus and placental membranes. Isolation of affected horses. Submission of clinical samples to a diagnostic laboratory. Implementation of hygienic procedures to prevent spread of infection (biosecurity).  

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 Pathogen test  The iELISA test detects specific antibodies to Streptococcus equi subs. equi, the pathogen (bacteria) responsible for Strangles. Sample 5 mL, blood in a serum tube Turnaround time 2 to 5 working days   What is Stranglers? Strangles is a highly contagious upper respiratory infection of horses caused by the bacteria Streptococcus equi subspecies equi (S. equi). It is transmitted by inhalation or direct contact with contaminated surfaces (for example horses sharing water buckets). The bacteria colonize the horse’s tonsils and pharynx within hours of infection, and then infect the lymph nodes under and behind the jaw resulting in abscessation of these structures days later. Horses develop a fever initially, but are typically not contagious during the initial 48-72 hours. Rarely, infection spreads to other parts of the body resulting in abscesses in other organs such as the intestines, kidneys, lungs, spleen or liver. This is often called “bastard strangles” or metastatic abscessation. A few horses may develop a hypersensitivity reaction to the bacteria with repeated exposure either in the form of infection or vaccination otherwise known as purpura hemorrhagica. Horses that develop classic clinical signs and are not treated with antibiotics have the potential to develop immune protection up to five years. Clinical signs Classic clinical signs include a fever (often >103°F or 39.5°C) first, followed by one or more of the following symptoms: depression, thick nasal discharge and lymph node enlargement under the jaw and/or in the throat latch region. The abscessed lymph nodes may drain externally or into the guttural pouches (blind-end sacs connected to the throat in horses) resulting in nasal discharge. Horses that have been vaccinated for strangles or horses that have previous partial immunity may develop milder signs of upper respiratory tract infection. Bastard strangles cases may develop colic signs, fever, and/or weight loss with or without a history of previous strangles disease or exposure. Horses with purpura hemorrhagica may develop edema of the head, trunk, and/or legs; and broken blood vessels or bruising of the mucous membranes of the mouth, eyes and nose. Additional signs can include fever, severe depression, and muscle tightness. The severity of symptoms in purpura hemorrhagica cases ranges from mild to life-threatening. Transmission Strangles is caused by oral exposure of a horse to S. equi bacteria. Once within the oral cavity, the bacteria invade the tonsils and subsequently colonize the lymph nodes. Bacteria can be transmitted through contact with pus or nasal discharges from an infected horse, or from contaminated bedding or barn equipment (water troughs, buckets, etc.). Flies may also act as vectors, spreading the bacteria from horse to horse. Under the right conditions, S. equi can survive in the environment for weeks or months. Exposure of a horse to S. equi does not necessarily mean that it will come down with strangles. Factors that influence the risk of disease include dose of bacteria (poor sanitation and direct contact with nasal secretions and pus increase the chance of disease); immune status of horse. Previously exposed horses are often immune to the disease, or do not get as sick as unexposed horses. During the first three to six months of life, foals are often protected by maternal antibodies. Vaccination can also increase resistance to the disease; stress (poor nutrition, overcrowding, lengthy transportation or pre-existing diseases increase the risk of strangles). Strangles may be transmitted by “silent shedders” who do not display signs of disease. These horses commonly carry the strangles organism in the guttural pouch, an air sac at the back of the horse’s throat. Detection of these animals requires guttural pouch endoscopy (passing an endoscope via the horse’s nose into the guttual pouch). Strangles is most commonly transmitted by acutely ill or recovering horses that are still shedding bacteria in their nasal secretions. Bacterial culture results have a turnaround time of 2 to 3 days. The DNA test known as Polymerase Chain Reaction (PCR) takes less than a day. However, it may take an additional 1 to 2 days to send samples to the laboratory. Prevention Biosecurity on the farm is necessary to prevent spread of disease. Isolate new horses for three weeks prior to introducing them to the rest of the population. Isolate any horse with a fever and signs of strangles. Do not share tack or equipment between sick horses and others Perform twice daily monitoring of rectal temperatures of all horses in an outbreak to identify new cases. Stop all movement of horses to and from farm when strangles is identified. Disinfect water buckets daily. Use strict hygiene between horses to reduce spread of the disease. Ideally, three throat flush samples are obtained from recovering horses and any horses who were in contact with sick horses at approximately weekly intervals and tested for S. equi subsp equi by PCR and culture. Identification of strangles bacteria in clinically recovered horses may mean the guttural pouches have retained some infection. Endoscopy of the guttural pouches provides visualisation of any pus or dried debris (chondroids) that harbor the bacteria. A small number of horses will recover from strangles and continue to shed bacteria from the guttural pouch, causing recurrent farm outbreaks. Detection and treatment of these “silent carriers” (S. equi bacteria in guttural pouches) via endoscopy and PCR is essential for preventing disease recurrence on a farm. Discuss vaccination types and recommendations with your veterinarian. Vaccination does not provide 100% immunity against S. equi infection. Vaccination is not recommended during or within two years of a strangles outbreak due to the increased risk of purpura hemorrhagica.

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Non-invasive allergy testing to different allergens. Mites and moulds allergens  Results are given as (reactive 0 to 5) for each of the 2 classes of allergens, with identification of the specific allergen in each class.  1 - Testing for Six different Mite allergens : - Dermatophagoides (D.) farinae - D. pteronyssinus - Tyrophagus putrescentiae - Acarus siro  - Glycophagus domesticus  - Lepidoglyphus destructor PLUS 2 - Testing for different Mould allergens, such as  :  - Alternaria alternata - Aspergillus fumigatus - Aspergillus niger - Cladosporium herbarum  - Epicoccus nigrum - Helmintosporum sativum - Penicillium notatum - Fusarium spp. - Ustilago  - Rhizopus    Sample 5 mL serum or 4 mL of blood collected in a serum tube   Turnaround time 7  working days   Why test? Equine allergies are common and can affect any breed, age or sex of horse. Symptoms involving the skin, respiratory and gastrointestinal systems can occur for a number of reasons with the diagnosis of allergy being made by systematically ruling out other common conditions. Once diagnosed, knowing what allergens your horse is sensitive to allows you to manage their condition in a way that is specific to their individual needs. Key points: Rapid and easy identification of potential offending allergens Non-invasive and not influenced by most medications Standardised procedure with excellent reproducibility  

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Pathogen test  Two qPCR test, one that detects the genome (DNA) of  Equine Herpesvirus Type 1 (EHV-1) and one that detects the genome (DNA) of Equine Herpesvirus Type 4 (EHV-4). Sample 1 nasal or nasopharyngeal swab ( see AAEP guidelines)  and 5 mL - K3 EDTA tube Turnaround time 2 to 5 working days 24-48h - please contact lab  Our lab is approved by FEI for EHV-1 testing. What is Herpesvirus Type 1? more info here What is Herpesvirus Type 4? more info here

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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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Pathogen profile Screening of 5 pathogens responsible for respiratory disease in equines: EHV-1, EHV-4, Equine Influenza, Rhodococcus equi (Pneumonia) and Streptococcus equi (Stranglers).  Our lab is approved by 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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