Pathogen test  This test determines the NEV viral load of your horse by a molecular test that identifies the NEV genome in circulating blood. This test doesn’t determine the NEV status of your horse. An  undetectable viral load doesn't mean that your horse is free of infection.  Sample 5 mL - blood - K3 EDTA tube or 5 mL - Liquor (CSF). Turnaround time 5 to 10 working days Knowing the NEV status and viral load of your horse can help keep your horse - and others - safe Key points The New Equine Virus (NEV) is a horse lentivirus distinctive from Swamp fever virus (EIAV) and similar to HIV-1. Like in HIV infected humans NEV attacks the immune system and natural defence against illness.  A horse infected with NEV will get weaker and weaker until it can no longer fight off life threatening infections and diseases. The rate at which NEV progresses varies depending on age, general health and genetic background.    Learn more about NEV Explore results If NEV viral load is undetectable - No risk of transmitting NEV An undetectable viral load means that the NEV level in the blood is too low to be detected by a viral load test. NEV positive horses can show undetectable viral loads. Horses with NEV who maintain and undetectable viral load have effectively no risk of transmitting NEV to NEV  negative horses.  If NEV viral load is detectable - Risk of transmitting NEV A detectable viral load means that the NEV level in the blood is high to be detected by a viral load test. Horses with NEV who maintain and detectable viral load have effectively a risk of transmitting NEV to NEV  negative horses.    Take Action - Find the suggested next steps based on results. If your horse has a NEV detectable viral load begin by talking to your veterinarian about therapies to boost the immune system of your horse as well about antiretroviral therapy (ART). Monitoring of NEV viral load levels is crucial to evaluate disease progression and risk.  Like with HIV, ART can’t cure NEV, but can help your horse to live a longer and healthier life. The main goal of ART is to reduce your horse’s viral load to an undetectable level. Learn more about ART here

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Pathogen test   This diagnostic profile determines the NEV status of a horse, as well the transmitting with a viral load test.  Includes a serological test for NEV - to determine NEV status and a molecular test to determine the NEV viral load.  Sample 5 mL - blood - serum tube and 5 mL - blood - K3 EDTA tube or 5 mL - Liquor (CSF). Turnaround time 5 to 10 working days   Knowing the NEV status and viral load of your horse can help keep your horse - and others - safe Key points The New Equine Virus (NEV) is a horse lentivirus distinctive from Swamp fever virus (EIAV) and similar to HIV-1. Like in HIV infected humans NEV attacks the immune system and natural defence against illness.  A horse infected with NEV will get weaker and weaker until it can no longer fight off life threatening infections and diseases. The rate at which NEV progresses varies depending on age, general health and genetic background.  Learn more about NEV  Explore results If your horse is NEV negative : Testing shows that your horse doesn’t have NEV. Continue taking steps to keep your horse safe from getting NEV  If your horse is NEV positive : Testing shows that your horse does have NEV, but you can still take steps to protect your horse´s health. NEV viral load test indicates the transmitting risk. An undetectable viral load means that the NEV level in the blood is too low to be detected by a viral load test. Horses with NEV who maintain and undetectable viral load have effectively no risk of transmitting NEV to NEV  negative horses.  Learn more about NEV viral load Take action - Find the suggested next steps based on results If your horse is NEV positive Begin by talking to your veterinarian about therapies to boost the immune system of your horse as well about antiretroviral therapy (ART). Monitoring of NEV viral load levels is crucial to evaluate disease progression and risk.  Like with HIV, ART can’t cure NEV, but can help your horse to live a longer and healthier life. The main goal of ART is to reduce your horse’s viral load to an undetectable level. Learn more about ART here.

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  Certified DNA Disorder-Free Lines Ensure your horse's lineage is free from genetic disorders with our comprehensive DNA testing panel. Certify your horse against 10 genetic disorders: SCID, LFS, CA, PSSM1, HYPP, GBED, HERDA, MH, CM, WFFS. Sample Collection Hair Roots: 30 to 40 hair roots. Blood Sample: 5 mL blood in a K3 EDTA tube. Turnaround Time Standard Processing: Results in 5 to 10 working days after sample arrival at the laboratory. Clients organize and cover the costs of sending the samples. Why Test? Our Certified DNA Disorder-Free Lines test helps breeders, purchasers, and studbook certifiers ensure that horses are free from genetic disorders. This guarantees healthier horses, informed breeding decisions, and enhanced peace of mind. Learn More Results Description The DNA test results will be one of the following: n/n: Negative. No affected allele present. n/P1: Positive heterozygous. One mutated allele present. The horse can pass the allele to 50% of its progeny. P1/P1: Positive homozygous. Two mutated alleles present. The horse will pass the allele to 100% of its offspring. Additional Information Polysaccharide Storage Myopathy (PSSM1) is a hereditary muscle disease that affects many breeds. The condition is caused by a mutation in the GYS1 gene, leading to an abnormal accumulation of glycogen in the muscles. This can cause symptoms such as muscle tremors, stiffness, reluctance to move, and excessive sweating. Management of PSSM1 includes dietary changes and regular exercise to help mitigate symptoms. Check our FAQs for more information FAQs Why is genetic testing important for horse breeders? Genetic testing is essential for breeders to make informed breeding decisions and to ensure that their horses do not carry alleles for genetic disorders. This helps in maintaining the health and performance of the breed. What breeds are affected by SCID and LFS? SCID and LFS are commonly found in Arabian horses and breeds influenced by Arabian bloodlines. Testing is crucial for breeding and purchasing decisions to ensure the health of the horses. How prevalent are genetic disorders in certain horse breeds? Genetic disorders can have significant frequencies in specific breeds. For example, HERDA is prevalent in Quarter Horses, while WFFS often affects Warmbloods. Regular testing helps in identifying carriers and making informed decisions. How do genetic disorders impact horse health? Genetic disorders such as SCID, LFS, PSSM1, HYPP, and others can significantly impact the health, performance, and longevity of horses. Early detection through genetic testing allows for better management and breeding practices to ensure healthier future generations. Visit our full FAQ page for more details. How it Works ✨ Purchase the Test: Select and buy the DNA test online. 📄 Receive Instructions: After payment confirmation, receive instructions for hair root collection and a printable submission form. ✂️ Collect Hair Roots: Pluck hair roots, tape them on the submission form, place it in an envelope or sealed plastic bag. 📬 Send Samples: Send to our lab by regular mail or express delivery to: Equigerminal LabRua Eduardo Correia, Nº133030-504 Coimbra, PORTUGAL 📧 Receive Results: Get the result certificate by email. If you need assistance, contact us at support@equigerminal.pt. ♻️ Note: No need for a sample collection kit, enhancing sustainability by reducing waste and plastic use.

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DNA test for the Congenital Myotonia (CM). This test verifies the presence of the recessive cm gene. Sample  30 to 40 hair roots or 5 mL of blood in a K3 EDTA tube Turnaround time 2 to 5  working days Why test? This genetic test helps breeders to identify horses that carrying the cm 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 cm gene and presents results as one of the following: N/ - Normal for Congenital Myotonia (CM).  Absence of the affected variant responsible for Congenital Myotonia N/cm - Carrier of Congenital Myotonia (CM). Presence of one copy of the genetic variant causative of Congenital Myotonia. The horse is clinical healthy and can pass the genetic variant responsible for CM to 50% of their progeny when bred. cm/ - Affected by CM. Presence of two copies of the genetic variant causative of Congenital Myotonia. The horse is affected with Congenital Myotonia and will pass genetic variant to 100% of its offspring. Additional information Congenital Myotonia is an inherited neuromuscular disorder characterised by the slow relaxation of muscles after voluntary contraction or electrical stimulation. This disorder has been identified in New Forest ponies and it is caused by an autosomal recessive mutation, which is responsible for the function of chloride ion channels in the skeletal muscle. Carriers of the mutation appear normal, but when two carriers are mated, a 25 percent chance exists that an affected foal will be produced.  Affected foals appear normal at birth. The first symptoms are recurrent episodes of recumbency and difficulty rising to its feet as a result of muscle stiffness. They occur during the first weeks of age and usually increase in the following months. Picking up the limbs is not possible because of the muscle rigidity. The eye-bulb may be retracted due to the myotonia.

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DNA test DNA test for the Severe Combined Immunodeficiency (SCID). SCID is an inherited disease seen in pure and part-bred Arab horses. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? The DNA test for SCID helps breeders to identify the animals that are carriers of the SCID mutation. This information allows breeders to prevent two carriers from breeding, which reduce the chances of producing an SCID foal. Continued breeding of horses that are carriers of the SCID gene is now possible without the worry of producing SCID foals. For example, carrier stallions that possess highly desirable traits can now be selectively bred to clear (homozygous normal) mares (and vice versa). The resulting foals would have an equal chance of being a carrier or clear of SCID, but would definitely not be affected. The foals could be tested anytime after birth to determine their SCID genotype and future matings could be rationally planned. Results description The DNA test verifies the presence recessive SCID mutation and presents results as one of the following: nn – Non-carrier of the SCID gene.Tested negative for the SCID mutation. nSCID – Heterozygous horse for SCID gene, both the normal and SCID alleles were detected. The horse is a carrier of SCID genetic disorder and there is a 50% chance this horse will pass a SCID allele to its offspring SCID SCID – Carrier of two copies of the SCID gene. Homozygous horse for SCID mutation. The horse is affected with the SCID genetic disorder. Additional information Severe Combined Immunodeficiency Disease (SCID) is an inherited disease seen in pure and part-bred Arab horses. Animals with this inherited condition have an enhanced susceptibility to infection and first show signs of disease at between two days and eight weeks of age. Clinical diagnosis of the disease is not straightforward as the symptoms, such as raised temperature, respiratory complications and diarrhoea, are typical of new-born foals with a range of infections. Foals affected by SCID always die from the disorder within the first six months of life. This happens regardless of the level of veterinary care. SCID is therefore a distressing condition for the effected animal and the owners or caregivers, and results in financial loss due to dead foals and veterinary expenses. The disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene to suffer from the disease. Consequently both the sire and the dam must possess at least one copy of the mutated gene in order for the offspring to be afflicted. Offspring born with one copy of the defective gene and one non-defective copy are considered a carrier and have a 50% chance of passing the defective gene on. A number of studies have attempted to estimate the frequency of SCID carriers in the Arab horse population. Most sources speculate that the percentage of Arab foals which die of SCID is 2-3%. If breeding is random then it would imply that roughly 28-35% of Arab horses are carriers. However, most breeding is rather selective, making the true frequency of carriers in the population somewhat unclear.

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DNA test The DNA test verifies the presence of 2 mutations of the TBX3 gene responsible for Dun dilution and primitive markings.  Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? The DNA test that will provide information for both dun dilution (D) and the primitive markings (nd1, nd2).  Results description D/ - Homozygous for Dun. The basic coat colour will be diluted by Dun and primitive markings expressed. The Dun genetic variant will be passed on 100% of the offspring. D/nd1 - 1 copy of Dun and one copy of nd1. The basic coat colour will be diluted by Dun and primitive markings expressed. Horse can pass on Dun dilution (50%) or primitive markings without dilution (50%). D/nd2 - 1 copy of Dun and one copy of nd2. Horse will have Dun dilution and express primitive markings. The Dun genetic variant will be passed  with a 50% chance to the offspring nd1/nd1 - Homozygous for nd1. The basic coat colour will not be diluted but primitive markings are expressed in varying levels. The primitive markings will be passed on 100% of the offspring. nd1/nd2 - 1 copy of nd1 and one copy of nd2. The basic coat colour will not be diluted but primitive markings are expressed in varying levels. The primitive markings will be passed on 50% of the offspring. nd2/nd2 - Negative for Dun Dilution and primitive markings. Additional information Dun is a dominant dilution gene of equines characterised by lightening of the body color, leaving the head, lower legs, mane and tail undiluted. Dun is also typically characterised by “primitive markings” consisting of a dark dorsal stripe and sometimes leg barring, shoulder stripes and concentric marks on the forehead. Dun is present in many breeds of horses including (but not limited to) Appaloosa, Bashkir Curly, Iberian horse breeds, Icelandic Horse, Mustang, Norwegian Fjord, Paint, Paso Fino, Peruvian Paso, Quarter Horse and several of the pony breeds  

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DNA test The DNA test verifies the presence of the champagne mutation. Champagne  is a coat dilution modifier. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? Equigerminal offers testing for the dominant champagne gene-mutation. DNA testing may be useful in cases whereby a horse has previously tested negative for cream or silver dilutions, but appears to have a lightened-coat. Testing is also used to determine Homozygosity of the champagne gene.  Results description The DNA test verifies the presence of the champagne mutation and presents results as one of the following: N/ – Non-champagne horse. N/Ch – Positive for dominant champagne gene, possessing one inherited copy. Coat will be diluted accordingly. Will pass champagne gene to approximately 50% of the offspring. Ch/ – Positive for dominant champagne gene, possessing two inherited copies. Coat will be diluted accordingly. Additional information Champagne dilution is caused by a dominant gene, meaning that a horse with a single copy of the Champagne gene will have Champagne characteristics. The Champagne dilution gene lightens a horse’s coat color by diluting the pigment. The specific color produced will depend on the horse’s base color: bay coats to a golden brown, black coats can lighten to a dark brown, and chestnut coats to an apricot or gold. A horse can carry more than one dilution gene which can further affect coat color. Unlike cream dilution, there are no visual differences between a horse with one copy or two copies of Champagne. Although similar to the cream, pearl and dun dilutions, the Champagne gene has certain characteristics that distinguish it from other dilutions. Common characteristics of a Champagne horse include pinkish freckled or mottled skin, a shiny coat that is often slightly darker in the winter, and a hazel eye color. Champagne horses are typically born with a blue eye color that evolves to a hazel or an amber colour and pink skin that becomes darker and more freckled over time, especially around the eyes and muzzle. A homozygous Champagne horse will always pass one copy of the Champagne gene to its foal. Heterozygous horses have a 50% chance of passing the gene on to its foals.

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DNA test The genetic test verifies the presence of the Silver coat dilution modifier. The Silver genetic variant is associated with Multiple Congenital Ocular Abnormalities (MCOA) in some breeds.   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 silver gene and presents results as one of the following: N/ – Negative for Silver - No evidence of the genetic variant for Silver. No risk to develop Multiple Congenital Ocular Abnormalities (MCOA) associated to Silver. Z/N - Heterozygous for Silver - The Black and Bay basic coat colour will be diluted by Silver. Black-based horses will be chocolate with flaxen mane and tail. Bay-based horses will have pigment on lower legs lightened and flaxen mane and tail. No effect on chestnut color. Moderate risk to develop MCOA. Z/ – Homozygous for Silver - Two copies of altered sequence detected. Black-based horses will be chocolate with flaxen mane and tail. Bay-based horses will have pigment on lower legs lightened and flaxen mane and tail. No effect on chestnut color, but will pass the variant on to 100% of offspring.  Higher risk to develop severe MCOA. Additional information The Silver dilution behaves as a coat colour dominant trait on bay and black base coat colours. While chestnut base colour is not affected by the Silver dilution and can pass the variant silently to the offspring.  In short, the Silver dilution variant (Z) will only affect coat colour phenotype of black pigmented horses (E/e or E/E) and has no effect on red pigmented horses (e/e).  In addition, the eye disorders associated to Silver genetic variant are incomplete autosomal dominant:  homozygous horses (with two copies of Z)  may be at higher risk of developing severe Multiple Congenital Ocular Abnormalities (MCOA), while heterozygous (with one copy of Z) may develop a milder form of MCOA.   The effects of the silver dilution on coat colour gene can vary widely. The agouti gene affects the coat colour by controlling the distribution of the black pigment whereas the Silver dilution variant dilutes areas of the black pigment. Dilution by the Silver variant on a horse with a uniform black base typically involves lightening of the mane and tail and a dilution of the body to a chocolate color, often dappled as well. A Bay horse carrying the Silver gene will usually have a lightened mane and tail, as well as lightened lower legs. It is important to know that although a red horse (e/e) will not be diluted by the silver variant, it can be a carrier of the genetic variant and thus potentially pass the gene on to its offspring. Silver dilution has been identified in a number of horse breeds including the Quarter horse, the Rocky Mountain horse, the Icelandic horse, Morgans, Shetland ponies and the Miniature horse. References: Brunberg, E., Andersson, L., Cothran, G., Sandberg, K., Mikko, S., Lindgren, G.: A missense mutation in PMEL17 is associated with the silver coat color in the horse. BMC Genetics 7:46, 2006. Andersson, L.S., Wilbe, M., Viluma, A., Cothran, G., Ekesten, B., Ewart, S., Lindgren, G.: Equine Multiple Congenital Ocular Anomalies and Silver Coat Colour Result from the Pleiotropic Effects of Mutant PMEL. PLoS One 8:e75639, 2013.

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DNA test The DNA test is designed to verify the presence of the pearl allele (Prl), a coat color dilution modifier discovered in horses of Iberian origin. This variant produces dilutions of the base color, introducing golden tones to the coat.   Sample requirements  20 to 30 hair roots, or 5 mL of blood in a K3 EDTA tube.   Turnaround time The results are available within 2 to 5 working days. Why test? Purpose of the Test Pearl is a rare variant that dilutes the base coat colors in a less pronounced manner than the cream variant (Cr). It can complement the effect of the Cream variant, leading to very diluted coats similar to Cream double dilutes when both are present in heterozygosity. Testing is crucial for breeding purposes, as heterozygous Pearl horses can produce diluted offspring when bred with another Pearl carrier or a Cream dilute horse. The impact of the Pearl dilution varies based on the horse's base color, affecting the phenotype differently across different base colors.    Interpretation of Results for the Pearl Locus  N/N - Negative for Pearl The horse is genetically negative for the pearl allele, meaning it does not have any copies of this genetic variant. Its phenotype reflects the natural, unaltered base coat color. This horse will not pass the pearl dilution trait to its offspring, ensuring the continuation of the base coat color in the lineage. N/Prl – Positive Heterozygous  The horse is positive for the Pearl allele in a heterozygous state, indicating it carries one copy of the pearl variant. This configuration subtly dilutes the base coat color, infusing it with golden tones, although in some instances, the dilution effect may not be visually apparent.  As a heterozygous carrier, there's a 50% probability that it will transmit this dilution trait to its offspring, potentially leading to varied coat colors among the progeny. Prl/Prl -  Positive Homozygous  The horse is positive for the pearl allele in a homozygous state, carrying two copies of this genetic variant. This genotype manifests in a more noticeable dilution of the coat color, even in the absence of other dilution genes. Being homozygous, the horse will invariably pass the pearl allele to all of its offspring, ensuring the trait's propagation and contributing to the diversity of coat colors in future generations.   Additional insights The interplay between the Cream and Pearl genes subtly yet significantly affects horse coat colors, particularly evident in horses heterozygous for both genes (N/Cr + N/Prl). These horses often resemble double cream dilutes but can be distinguished by slightly darker eye colors and a marginally darker coat. Unlike double cream dilutes, the combined dilution effect of heterozygous Cream and Pearl genes might not be as pronounced, requiring careful observation or genetic testing for accurate identification.Homozygous Pearl horses (Prl/Prl) exhibit a more noticeable dilution, displaying pronounced golden tones in their coats compared to their homozygous Cream counterparts (Cr/Cr), whose phenotype is lighter. Interestingly, the eye and skin colors in foals—typically blue and pinkish, respectively—tend to darken with age, while the coat lightens.The subtle dilution effects of a single Pearl allele (N/Prl) often go undetected without genetic analysis, as they minimally alter the horse's appearance. However, the presence of two Pearl alleles (Prl/Prl) significantly enhances the dilution, affecting not just the coat but also the eye color, with amber or green hues depending on the base coat color.Identified in Iberian breeds like the Purebred Lusitano (PSL) and Purebred Spanish Horse (PRE), and speculated in the Spanish Mustang, the Pearl gene's inclusion in genetic discussions highlights its broad impact across equine breeds. This genetic diversity, particularly when Pearl intersects with Cream, underscores the complexity of equine coat colors and the value of genetic testing for breeders. 

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 DNA test DNA test for the Extension gene that controls the production of black or red pigment throughout the coat. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? The DNA testing for the Extension gene can be used to identify those black horses for which neither pedigree nor breeding records is informative for identifying carriers of the recessive red factor. Since red is inherited as a recessive trait, it is relatively easy to start up a breeding program that will produce only red horses. It has been more difficult to initiate a black breeding program as black (Ee) horses can produce red foals.  Results description The DNA test for Extension gene verifies the base coat color and presents results as one of the following: E/E - Dominant Homozygous for Extension - Black, Bay or Brown - Only the black factor is expressed. The horse can only transmit the (E) allele E/E to it offspring. It cannot have foals with basic coat colour Chestnut or Sorrel foals regardless of the color of the mate. The Agouti gene will determine if the basic coat color will be black, bay or brown, unless modified by other color modifying genes. E/e - Heterozygous for Extension - Black, Bay or Brown - Both red and black factor are expressed. It can transmit either (E) or (e) allele to its offspring. The Agouti gene will determine if the basic coat color will be black, bay or brown, unless modified by other color modifying genes. e/e - Recessive homozygous for Extension - Chestnut or Sorrel - Only the red pigment is expressed. The basic coat color is chestnut or sorrel unless modified by other color modifying genes. Additional information Equine coat color is built on one of two possible base pigments: red or black. The Extension gene controls the production of this base pigment (red or black). All horses will have the genetics for black or red pigment, regardless of their physical appearance. There are a number of dilutions patterns and modifiers, which a horse can carry that affect the base pigment of a horse. The Extension gene (red factor) has two alternative states (alleles). The dominant allele (E) produces black pigment in the coat. The recessive allele (e) produces red pigment. Red horses (chestnuts, sorrels, palominos…) are homozygous, that is they have two alleles, for the recessive red allele (e/e). Black pigmented horses (black, bay, brown, buckskin…) have at least one (E) allele. They can be homozygous (E/E) or heterozygous (E/e). A horse that is homozygous (E/E) will not produce red offspring, regardless of the color of the mate.  

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DNA test DNA test for the Lavender Foal Syndrome (LFS) – Pure and part-bred Arab horses. This test verifies the presence of the recessive LFS 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 genetic test determines LFS clear, carrier or affected status. 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 LFS gene and presents results as one of the following:  N/ – Non-carrier of the LFS gene. Tested negative for the LFS gene. N/LFS - Heterozygous horse for LFS, both the normal and LFS alleles were detected. The horse is a carrier of LFS genetic disorder and there is a 50% chance this horse will pass a LFS allele to its offspring LFS/ – Homozygous horse for LFS, carrier of two copies of the LFS gene. The horse is affected with the LFS genetic disorder. Additional information Lavender Foal Syndrome (LFS) is a recessive genetic disorder. Affected foals born with the unique diluted coat color that can appear to be pale lavender, pale pink or silver. This foals-often have a difficult delivery, problems standing at birth and usually have episodes where they rigidly extend their limbs, neck and back. These episodes tend to resemble a seizure, although the affected foal does not seem normal between episodes. All affected foals are usually euthanised within days or weeks of birth. LFS is rare and is considered to be an autosomal recessive trait. “Autosomal” means that there is no sex linkage, so both males and females can be equally affected. “Recessive” means that in order for a foal to be affected, it must have received two copies of the mutated gene, inheriting one copy from each parent. Horses that have one copy of the mutated gene, in combination with one copy of the normal gene, are physically normal but are considered carriers and have a 50% probability, each time they are bred, of passing the mutation along to their offspring. The SNP mutation that causes LFS has not been detected in other breeds.  Testing for this mutation in horses with no Arabian blood lines is not recommended. However, in cases where pedigree is not known, testing could be a useful tool to prevent possible affected foals.

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DNA test DNA test for the Overo gene that is associated with the Lethal White Foal Syndrome (LWFS). Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? The relationship between Lethal White Foal Syndrome (LWFS) and the frame overo coat pattern is not always straightforward. Usually carriers of LWFS are frame overo in pattern, and have 1 copy of the mutated allele (nL). But not all frame overo horses carry the mutated allele, some have the genotype (nn). And some horses with other coat patterns (including solid coloured paints and tobiano) have been found to carry the mutated allele. It should also be remembered that not all white foals have the genotype (LL) ,and may not be affected by LWFS. Results description The DNA test verifies the presence of the mutation associated to the Overo and presents results as one of the following:  N/ – Non-Overo or ‘solid’ horse O/N – Frame Overo horse. Horse carries just a single copy of frame Overo. Since frame Overo is a dominant gene, the coat pattern should be present in all horses with a single copy of the mutated gene. O/ – A Lethal White Foal Syndrome (LWFS). Foal carries two copies, homozygous for frame Overo. Since no living frame Overo horse more than a week old will test as being homozygous, it applies only to horses in the Lethal White condition. Additional information Frame Overo is a highly desirable white pattern gene. All Frame Overo horses carry a single inherited copy of the Ile118Lys EDNRB mutation. This mutation causes pigment loss, producing white markings on certain areas of the horse. While the mutation produces visually desirable horses, it is also linked to a fatal condition known as Lethal White Foal Syndrome (LWFS), whereby a foal is born almost pure white in appearance, and dies within its first few days of life. Correct breeding can avoid this occurrence.  LWFS occurs when a horse inherits two copies of the mutated gene, one from both parents. Whereas horses with just one copy of the gene will live normally and exhibit the desirable pattern. A horse with two copies of the mutated gene will suffer intestinal abnormalities caused by undeveloped nerves of the foal’s digestive system. These animals die within the first 72 hours of being born and are typically euthanized sooner for humane reasons. Frame Overo horses which carry just a single copy of the gene, will pass one copy of it to their foals approximately 50% of the time when bred. Therefore, when breeding an Overo horse to a solid non-Overo horse, the foal can only inherit one copy. However, if two Overo horses are bred together they could potentially both pass the Overo gene to the foal, meaning it inherits two copies. Horses which inherit two copies of Frame Overo will suffer the Lethal White condition. Proper mating must be carried out to ensure that two frame Overo horses do not breed. This will prevent any risk of the foal inheriting two copies of the mutated gene.

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Metabolic profile - Liver function Metabolic profile with 5 parameters: AST Gama-GT Bilirubines (total, direct and indirect) Alkaline Phosphatase Albumin Sample 5 mL - blood - Serum tube Turnaround time 1 working day   Metabolic Profile Reference Intervals Parameter Low High Units AST 222,00 489,00 U/L Gama-GT 8,00 33,00 U/L Total Bilirubine 0,50 2,10 mg/dL Direct Bilirubine 0,10 0,55 mg/dL Indirect Bilirubine 0,30 2,00 mg/dL Alkaline Phosphatase 88 268 U/L Albumin 2,9 3,60 g/dL

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 Culture Mycological examination (direct and culture)  Sample fur  skin other  Turnaround time 15 to 30 days

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Pathogen test  The RT-qPCR test detects the genome (RNA) of Indiana and Jersey virus strains responsible for Vesicular Stomatitis. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Vesicular Stomatitis? Vesicular Stomatitis (VS) is a contagious disease that afflicts horses, livestock, wildlife and even humans. The disease is caused by a virus, which although rarely life threatening, can have significant financial impact on the horse industry. Vesicular Stomatitis is a reportable disease. Equestrian event organisers may also choose to cancel horse shows, and other equestrian activities in the surrounding area. Interstate and international movement of horses may also be restricted.  Clinical signs When vesicular stomatitis occurs in horses, blister-like lesions usually develop on the tongue, mouth lining, nose or lips. In some cases, lesions can develop on the coronary bands, or on the udder or sheath. When VS is suspected, an exact diagnosis should be obtained by testing the blood for virus-specific antibodies or by testing swabs from the lesions to identify the presence of the virus. Testing is necessary to rule out the possibility that the lesions are caused by photosensitivity (sunburn), irritating feeds or weeds, or toxicity from non-steroidal anti-inflammatory medications like phenylbutazone.  The disease generally runs its course within two weeks, although it may take as long as two months for the sores to entirely heal. Live virus can often be isolated from the lesions for up to a week after the lesions appear.  During this time, the horse remains infective and the potential remains for the disease to spread to other animals. Transmission There are still some questions regarding how vesicular stomatitis is transmitted and why it only occurs sporadically in the U.S. The disease is distributed only in North, Central, and South America, with a greater incidence in warmer regions. Due to the seasonal occurrence of VS during summer through early fall, it is believed that insects such as biting flies and midges contribute to maintaining the lifecycle of the virus.  Black flies, sand flies, and midges are known to transmit the virus, but there may be other insect vectors that have not yet been identified. VS also can be passed from horse to horse by contact with saliva or fluid from ruptured blisters. Physical contact between animals, or contact with buckets, equipment, housing, trailers, feed, bedding, shared water troughs or other items used by an infected horse can provide a ready means of spread.  Prevention By observing the following guidelines you can help prevent the occurrence of VS:  Healthy horses are more disease resistant so provide good nutrition, regular exercise, deworming and routine vaccinations.  Isolate new horses for at least 21 days before introducing them into the herd or stable. Observe your horse closely. Immediately isolate any horse that shows signs of infection and contact your veterinarian. Implement an effective insect control program. Keep stabling areas clean and dry. Remove manure and eliminate potential breeding grounds (standing water, muddy areas) for insect vectors. Use individual rather than communal feeders, waterers, and equipment. Clean and disinfect feed bunks, waterers, horse trailers and other equipment regularly. Be sure that your farrier and other equine professionals who come into direct contact with your animals exercise due care so as not to spread the disease from one horse or facility to the next. On farms where VS has been confirmed, isolate any animals with lesions away from others and handle healthy animals first, ill animals last. Handlers should then shower, change clothing and disinfect equipment to prevent exposing others. Anyone handling infected horses should implement proper biosafety methods, including wearing latex gloves and washing hands after handling animals with lesions. If you are sponsoring an event during an outbreak, require a more recent health certificate on every horse entering the venue and consider having a veterinarian visually inspect all horses at check-in.  Work with your event veterinarian to establish isolation and response procedures that can be implemented quickly if a suspect case is identified at the venue.   

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Pathogen test  The PCR test detects the genome (DNA) of the Salmonella serovar abortus-equi, the bacteria responsible for Salmonellosis and abortion in equines. Sample 1 genital swabs - sterile swab       and/or 20 gr - placental or foetal tissues - sterile flask      and/or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Salmonellosis? Contagious and zoonotic bacterial infection caused by Salmonella spp, of which there are >2500 serotypes. Clinical signs   Abortion with infection by Salmonella serovar abortus-equi.   Clinically normal horses can transiently shed Salmonella, with shedding more common during: Concurrent illness: antibacterial usage, physiological disturbance Stress: transportation, social, nutritional Gastrointestinal disturbance: motility (especially colic), feed change  Diarrhoea (soft feces to projectile, watery diarrhoea) is most common, however, horses may have normal feces Fever (patient may have normal temperature, especially if treated with NSAIDs) Lethargy Anorexia Colic Localised infection (e.g. joint or bone infection) Sepsis/septic shock Laminitis as a common sequel to enterocolitis   Foals are commonly more seriously affected when compared to older horses, with profound systemic illness including: Hemorrhagic diarrhoea Pneumonia Meningitis Physitis Septic arthritis Transmission Fecal-oral spread Ingestion of contaminated material (pasture, roughage, feed or water) Fomites are a significant means of indirect transmission of infection Intermittent shedding by subclinically infected horses Aerosol transmission has been suspected in other species; evidence of this route in horses is lacking Prevention Measures Biosecurity Guidelines Quarantine horses that develop diarrhoea and/or fever. If a separate stall or paddock is not available, establish barrier precautions at their current location Isolate horses following significant colic episodes, impactions (notably small colon), or colic surgery to reduce environmental contamination and potential exposure of other horses should Salmonella subsequently be recovered on fecal culture Prevent horses that have come in contact with known infected or clinical cases from mixing with the general population Contaminated stall and equipment should have all organic material removed. Dispose of organic matter in a manner which prevents contamination of the facility (do not spread on pastures). Disinfection can be performed after all organic matter has been removed and the surfaces cleaned. Pressure washers or hoses should not be used as they can aerosolise Salmonella, potentially contaminating other parts of the facility or infecting a susceptible horse or human No commercially available validated vaccine is currently marketed. For animals with positive cultures while clinically ill: Before removing restrictions, following resolution of clinical signs, conduct a series of fecal cultures (see Diagnostic Sampling, Testing and Handling) to determine if all negative Where culture is not performed, isolation up to 30 days may be required to minimize risk of exposure of other horses from convalescent shedding of previously infected horses following the cessation of clinical signs (fever, diarrhoea). • Isolate horse for 30 days from resident horses Obtain 5 consecutive negative fecal cultures prior to releasing horse into the general population Prior to entry into the general population the horse should be housed in an environment that can be thoroughly cleaned and disinfected If the horse is turned out in a paddock, manure should be promptly removed and appropriately disposed of in a manner that avoids potential contamination of other areas of the facility. Caretakers should wear personal protective equipment. After the horse is released, the paddock should be harrowed to encourage drying and kept unused for 30 days  

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Pathogen test  The PCR test detects the genome (DNA) of the Clamydia psittaci, the bacteria responsible for Chlamydiosis. Sample 1 genital swabs - sterile swab 20 gr - placental or foetal tissues - sterile flask 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Chlamydiosis? Chlamydia psittaci is a bacterium carried by birds. It can cause a respiratory disease in people called Psittacosis and has also been linked to abortion in mares.    

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Screening of 3 pathogens responsible for Contagious Equine Metritis (CEM): Taylorella equigenitalis by culture over 14 days Pseudomonas aeruginosa by culture  Klebsiela pneumonia by culture Sample requirements 2 or 3 genital swabs in Amies transport  medium with charcoal. Clitoral fossa – use standard swab with Amies culture and transport system Clitoral sinuses swabbed – use Minitip Amies culture and transport system. Openings to the sinuses are on the dorsum of the clitoris - the central one is usually always present whereas the lateral sinuses may be multiple or not be present. Swab all that are present. Either cervical (closed cervix if pregnant or mid-cycle) or endometrial (while in estrus or true anestrus) swab – use guarded 25” swab. NOTE: Schedule all CEM culture submissions in advance with the laboratory. Multiple culture instances are often required and timing is critical. Official CEM testing generally involves multiple sets of samples taken on multiple days. Exact sampling schedules need to be confirmed with appropriate regulatory agencies in advance of testing. Horses cannot be tested while being treated and for a period of time after treatment with antibiotics. Turnaround time 14  working days   What is Contagious Equine Metritis? Contagious equine metritis is an inflammatory disease of the proximal and distal reproductive tract of the mare caused by Taylorella equigenitalis, which usually results in temporary infertility. It is a nonsystemic infection, the effects of which are restricted to the reproductive tract of the mare. Clinical signs When present, general clinical signs include endometritis, cervicitis and vaginitis of variable severity and a slight to copious mucopurulent vaginal discharge. In mares there are two states of infection: The active state in which the main outward sign is a vulval discharge, which may range from very mild to extremely profuse. The carrier state in which there are no outward signs of infection. However, the mare remains capable of transmitting infection because the bacteria are established on the surface of the clitoris, the clitoral fossa and sinuses and, in the case of pneumoniae and P. aeruginosa, sometimes in the urethra and bladder. In stallions: (‘stallion’ means mating stallions, teasers and stallions used for AI) Infected stallions do not usually show clinical signs of infection but the bacteria are present on their penis, sheath and. These stallions can infect mares during mating, teasing or AI. Occasionally, the bacteria may invade the stallion’s sex glands, causing pus and bacteria to contaminate the semen. Transmission Direct venereal contact during natural mating presents the highest risk for the transmission of equigenitalis from a contaminated stallion or an infected mare. Direct venereal transmission can also take place by artificial insemination using infective raw, chilled and possibly frozen semen. Indirectly, infection may be acquired through fomite transmission, manual contamination, inadequate observance of appropriate biosecurity measures at the time of breeding and at semen- collection centres. Stallions can become asymptomatic carriers of equigenitalis. The principal sites of colonisation by the bacterium are the urogenital membranes (urethral fossa, urethral sinus, terminal urethra and penile sheath). The sites of persistence of equigenitalis in the majority of carrier mares are the clitoral sinuses and fossa and infrequently the uterus. Foals born of carrier mares may also become carriers. The organism can infect equid species other than horses, e.g. donkeys. Prevention If infection with equigenitalis is suspected in any mare, stallion or teaser on the basis of clinical signs, all breeding activities must cease immediately. The affected horse(s) should be isolated and swabbed by the attending veterinary surgeon. Arrange swabbing of any at risk horse. Disinfect all equipment used for breeding procedures. Inform all owners of mares booked to the stallion, including any which have already left the premises; Inform people to whom semen from the stallion has been sent; Arrange for one straw from every ejaculate of stored semen from infected and at risk stallions to be tested by a laboratory. If a straw from any ejaculate is infected, all straws from that ejaculate should be destroyed; Any at risk pregnant mare must be foaled in isolation. The placenta must be incinerated. Foals born to these mares should be swabbed three times, at intervals of not less than seven days, before three months of age. Any mares with an abnormal vaginal exudate, or returning to oestrus prematurely, should be investigated and managed as though infected with equigenitalis until results of laboratory testing prove otherwise. If carriers of equigenitalis are detected, the organism can be eliminated by treatment with systemic and/or local antibiotics combined with antiseptic washing of the sites of persistence in the mare and the stallion.

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Screening of 3 pathogens responsible for Contagious Equine Metritis (CEM): Taylorella equigenitalis by Culture over 7 days Pseudomonas aeruginosa, Culture  Klebsiela pneumonia, Culture   Sample 2 or 3 genital swabs in swab Amies transport medium with charcoal. Clitoral fossa – use standard swab with Amies culture and transport system Clitoral sinuses swabbed – use Minitip Amies culture and transport system. Openings to the sinuses are on the dorsum of the clitoris - the central one is usually always present whereas the lateral sinuses may be multiple or not be present. Swab all that are present. Either cervical (closed cervix if pregnant or mid-cycle) or endometrial (while in estrus or true anestrus) swab – use guarded 25” swab. NOTE: Schedule all CEM culture submissions in advance with the laboratory. Multiple culture instances are often required and timing is critical. Official CEM testing generally involves multiple sets of samples taken on multiple days. Exact sampling schedules need to be confirmed with appropriate regulatory agencies in advance of testing. Horses cannot be tested while being treated and for a period of time after treatment with antibiotics. Turnaround time 7  working days   What is Contagious Equine Metritis? Contagious equine metritis is an inflammatory disease of the proximal and distal reproductive tract of the mare caused by Taylorella equigenitalis, which usually results in temporary infertility. It is a nonsystemic infection, the effects of which are restricted to the reproductive tract of the mare. Clinical signs When present, general clinical signs include endometritis, cervicitis and vaginitis of variable severity and a slight to copious mucopurulent vaginal discharge. In mares there are two states of infection: The active state in which the main outward sign is a vulval discharge, which may range from very mild to extremely profuse. The carrier state in which there are no outward signs of infection. However, the mare remains capable of transmitting infection because the bacteria are established on the surface of the clitoris, the clitoral fossa and sinuses and, in the case of pneumoniae and P. aeruginosa, sometimes in the urethra and bladder. In stallions: (‘stallion’ means mating stallions, teasers and stallions used for AI) Infected stallions do not usually show clinical signs of infection but the bacteria are present on their penis, sheath and. These stallions can infect mares during mating, teasing or AI. Occasionally, the bacteria may invade the stallion’s sex glands, causing pus and bacteria to contaminate the semen. Transmission Direct venereal contact during natural mating presents the highest risk for the transmission of equigenitalis from a contaminated stallion or an infected mare. Direct venereal transmission can also take place by artificial insemination using infective raw, chilled and possibly frozen semen. Indirectly, infection may be acquired through fomite transmission, manual contamination, inadequate observance of appropriate biosecurity measures at the time of breeding and at semen- collection centres. Stallions can become asymptomatic carriers of equigenitalis. The principal sites of colonisation by the bacterium are the urogenital membranes (urethral fossa, urethral sinus, terminal urethra and penile sheath). The sites of persistence of equigenitalis in the majority of carrier mares are the clitoral sinuses and fossa and infrequently the uterus. Foals born of carrier mares may also become carriers. The organism can infect equid species other than horses, e.g. donkeys. Prevention If infection with equigenitalis is suspected in any mare, stallion or teaser on the basis of clinical signs, all breeding activities must cease immediately. The affected horse(s) should be isolated and swabbed by the attending veterinary surgeon. Arrange swabbing of any at risk horse. Disinfect all equipment used for breeding procedures. Inform all owners of mares booked to the stallion, including any which have already left the premises; Inform people to whom semen from the stallion has been sent; Arrange for one straw from every ejaculate of stored semen from infected and at risk stallions to be tested by a laboratory. If a straw from any ejaculate is infected, all straws from that ejaculate should be destroyed; Any at risk pregnant mare must be foaled in isolation. The placenta must be incinerated. Foals born to these mares should be swabbed three times, at intervals of not less than seven days, before three months of age. Any mares with an abnormal vaginal exudate, or returning to oestrus prematurely, should be investigated and managed as though infected with equigenitalis until results of laboratory testing prove otherwise. If carriers of equigenitalis are detected, the organism can be eliminated by treatment with systemic and/or local antibiotics combined with antiseptic washing of the sites of persistence in the mare and the stallion.

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This culture test detects the presence Taylorella equigenitalis by culturing, the most common bacteria responsible for the Contagious Equine Metritis. Sample requirements 2 or 3 genital swabs - swab Amies transport with charcoal. Clitoral fossa – use standard swab with Amies culture and transport system Clitoral sinuses swabbed – use Minitip Amies culture and transport system. Openings to the sinuses are on the dorsum of the clitoris - the central one is usually always present whereas the lateral sinuses may be multiple or not be present. Swab all that are present. Either cervical (closed cervix if pregnant or mid-cycle) or endometrial (while in estrus or true anestrus) swab – use guarded 25” swab. NOTE: Schedule all CEM culture submissions in advance with the laboratory. Multiple culture instances are often required and timing is critical. Official CEM testing generally involves multiple sets of samples taken on multiple days. Exact sampling schedules need to be confirmed with appropriate regulatory agencies in advance of testing. Horses cannot be tested while being treated and for a period of time after treatment with antibiotics. Turnaround time 14  working days   What is Contagious Equine Metritis? Contagious equine metritis is an inflammatory disease of the proximal and distal reproductive tract of the mare caused by Taylorella equigenitalis, which usually results in temporary infertility. It is a nonsystemic infection, the effects of which are restricted to the reproductive tract of the mare. Clinical signs When present, general clinical signs include endometritis, cervicitis and vaginitis of variable severity and a slight to copious mucopurulent vaginal discharge. In mares there are two states of infection: The active state in which the main outward sign is a vulval discharge, which may range from very mild to extremely profuse. The carrier state in which there are no outward signs of infection. However, the mare remains capable of transmitting infection because the bacteria are established on the surface of the clitoris, the clitoral fossa and sinuses and, in the case of pneumoniae and P. aeruginosa, sometimes in the urethra and bladder. In stallions: (‘stallion’ means mating stallions, teasers and stallions used for AI) Infected stallions do not usually show clinical signs of infection but the bacteria are present on their penis, sheath and. These stallions can infect mares during mating, teasing or AI. Occasionally, the bacteria may invade the stallion’s sex glands, causing pus and bacteria to contaminate the semen. Transmission Direct venereal contact during natural mating presents the highest risk for the transmission of equigenitalis from a contaminated stallion or an infected mare. Direct venereal transmission can also take place by artificial insemination using infective raw, chilled and possibly frozen semen. Indirectly, infection may be acquired through fomite transmission, manual contamination, inadequate observance of appropriate biosecurity measures at the time of breeding and at semen- collection centres. Stallions can become asymptomatic carriers of equigenitalis. The principal sites of colonisation by the bacterium are the urogenital membranes (urethral fossa, urethral sinus, terminal urethra and penile sheath). The sites of persistence of equigenitalis in the majority of carrier mares are the clitoral sinuses and fossa and infrequently the uterus. Foals born of carrier mares may also become carriers. The organism can infect equid species other than horses, e.g. donkeys. Prevention If infection with equigenitalis is suspected in any mare, stallion or teaser on the basis of clinical signs, all breeding activities must cease immediately. The affected horse(s) should be isolated and swabbed by the attending veterinary surgeon. Arrange swabbing of any at risk horse. Disinfect all equipment used for breeding procedures. Inform all owners of mares booked to the stallion, including any which have already left the premises; Inform people to whom semen from the stallion has been sent; Arrange for one straw from every ejaculate of stored semen from infected and at risk stallions to be tested by a laboratory. If a straw from any ejaculate is infected, all straws from that ejaculate should be destroyed; Any at risk pregnant mare must be foaled in isolation. The placenta must be incinerated. Foals born to these mares should be swabbed three times, at intervals of not less than seven days, before three months of age. Any mares with an abnormal vaginal exudate, or returning to oestrus prematurely, should be investigated and managed as though infected with equigenitalis until results of laboratory testing prove otherwise. If carriers of equigenitalis are detected, the organism can be eliminated by treatment with systemic and/or local antibiotics combined with antiseptic washing of the sites of persistence in the mare and the stallion.

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Pathogen test The culture test detects the presence of Taylorella equigenitalis, the most comum bacteria responsible for the Contagious Equine Metritis. Sample 3 genital swabs - swab Amies transport with charcoal. Clitoral fossa – use standard swab with Amies culture and transport system Clitoral sinuses swabbed – use Minitip Amies culture and transport system. Openings to the sinuses are on the dorsum of the clitoris - the central one is usually always present whereas the lateral sinuses may be multiple or not be present. Swab all that are present. Either cervical (closed cervix if pregnant or mid-cycle) or endometrial (while in estrus or true anestrus) swab – use guarded 25” swab.   NOTE: Schedule all CEM culture submissions in advance with the laboratory. Multiple culture instances are often required and timing is critical. Official CEM testing generally involves multiple sets of samples taken on multiple days. Exact sampling schedules need to be confirmed with appropriate regulatory agencies in advance of testing. Horses cannot be tested while being treated and for a period of time after treatment with antibiotics. Turnaround time 7  working days   What is Contagious Equine Metritis? Contagious equine metritis is an inflammatory disease of the proximal and distal reproductive tract of the mare caused by Taylorella equigenitalis, which usually results in temporary infertility. It is a nonsystemic infection, the effects of which are restricted to the reproductive tract of the mare. Clinical signs When present, general clinical signs include endometritis, cervicitis and vaginitis of variable severity and a slight to copious mucopurulent vaginal discharge. In mares there are two states of infection: The active state in which the main outward sign is a vulval discharge, which may range from very mild to extremely profuse. The carrier state in which there are no outward signs of infection. However, the mare remains capable of transmitting infection because the bacteria are established on the surface of the clitoris, the clitoral fossa and sinuses and, in the case of pneumoniae and P. aeruginosa, sometimes in the urethra and bladder. In stallions: (‘stallion’ means mating stallions, teasers and stallions used for AI) Infected stallions do not usually show clinical signs of infection but the bacteria are present on their penis, sheath and. These stallions can infect mares during mating, teasing or AI. Occasionally, the bacteria may invade the stallion’s sex glands, causing pus and bacteria to contaminate the semen. Transmission Direct venereal contact during natural mating presents the highest risk for the transmission of equigenitalis from a contaminated stallion or an infected mare. Direct venereal transmission can also take place by artificial insemination using infective raw, chilled and possibly frozen semen. Indirectly, infection may be acquired through fomite transmission, manual contamination, inadequate observance of appropriate biosecurity measures at the time of breeding and at semen- collection centres. Stallions can become asymptomatic carriers of equigenitalis. The principal sites of colonisation by the bacterium are the urogenital membranes (urethral fossa, urethral sinus, terminal urethra and penile sheath). The sites of persistence of equigenitalis in the majority of carrier mares are the clitoral sinuses and fossa and infrequently the uterus. Foals born of carrier mares may also become carriers. The organism can infect equid species other than horses, e.g. donkeys. Prevention If infection with equigenitalis is suspected in any mare, stallion or teaser on the basis of clinical signs, all breeding activities must cease immediately. The affected horse(s) should be isolated and swabbed by the attending veterinary surgeon. Arrange swabbing of any at risk horse. Disinfect all equipment used for breeding procedures. Inform all owners of mares booked to the stallion, including any which have already left the premises; Inform people to whom semen from the stallion has been sent; Arrange for one straw from every ejaculate of stored semen from infected and at risk stallions to be tested by a laboratory. If a straw from any ejaculate is infected, all straws from that ejaculate should be destroyed; Any at risk pregnant mare must be foaled in isolation. The placenta must be incinerated. Foals born to these mares should be swabbed three times, at intervals of not less than seven days, before three months of age. Any mares with an abnormal vaginal exudate, or returning to oestrus prematurely, should be investigated and managed as though infected with equigenitalis until results of laboratory testing prove otherwise. If carriers of equigenitalis are detected, the organism can be eliminated by treatment with systemic and/or local antibiotics combined with antiseptic washing of the sites of persistence in the mare and the stallion.

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Pathogen test  This PCR test detects the genome (DNA) of Taylorella equigenitalis the most comum bacteria responsible for the Contagious Equine Metritis. Sample 3 genital swabs - swab Amies transport with charcoal. Clitoral fossa – use standard swab with Amies culture and transport system Clitoral sinuses swabbed – use Minitip Amies culture and transport system. Openings to the sinuses are on the dorsum of the clitoris - the central one is usually always present whereas the lateral sinuses may be multiple or not be present. Swab all that are present. Either cervical (closed cervix if pregnant or mid-cycle) or endometrial (while in estrus or true anestrus) swab – use guarded 25” swab. Turnaround time 2 to 5  working days   What is Contagious Equine Metritis? Contagious equine metritis is an inflammatory disease of the proximal and distal reproductive tract of the mare caused by Taylorella equigenitalis, which usually results in temporary infertility. It is a nonsystemic infection, the effects of which are restricted to the reproductive tract of the mare. Clinical signs When present, general clinical signs include endometritis, cervicitis and vaginitis of variable severity and a slight to copious mucopurulent vaginal discharge. In mares there are two states of infection: The active state in which the main outward sign is a vulval discharge, which may range from very mild to extremely profuse. The carrier state in which there are no outward signs of infection. However, the mare remains capable of transmitting infection because the bacteria are established on the surface of the clitoris, the clitoral fossa and sinuses and, in the case of pneumoniae and P. aeruginosa, sometimes in the urethra and bladder. In stallions: (‘stallion’ means mating stallions, teasers and stallions used for AI) Infected stallions do not usually show clinical signs of infection but the bacteria are present on their penis, sheath and. These stallions can infect mares during mating, teasing or AI. Occasionally, the bacteria may invade the stallion’s sex glands, causing pus and bacteria to contaminate the semen. Transmission Direct venereal contact during natural mating presents the highest risk for the transmission of equigenitalis from a contaminated stallion or an infected mare. Direct venereal transmission can also take place by artificial insemination using infective raw, chilled and possibly frozen semen. Indirectly, infection may be acquired through fomite transmission, manual contamination, inadequate observance of appropriate biosecurity measures at the time of breeding and at semen- collection centres. Stallions can become asymptomatic carriers of equigenitalis. The principal sites of colonisation by the bacterium are the urogenital membranes (urethral fossa, urethral sinus, terminal urethra and penile sheath). The sites of persistence of equigenitalis in the majority of carrier mares are the clitoral sinuses and fossa and infrequently the uterus. Foals born of carrier mares may also become carriers. The organism can infect equid species other than horses, e.g. donkeys. Prevention If infection with equigenitalis is suspected in any mare, stallion or teaser on the basis of clinical signs, all breeding activities must cease immediately. The affected horse(s) should be isolated and swabbed by the attending veterinary surgeon. Arrange swabbing of any at risk horse. Disinfect all equipment used for breeding procedures. Inform all owners of mares booked to the stallion, including any which have already left the premises; Inform people to whom semen from the stallion has been sent; Arrange for one straw from every ejaculate of stored semen from infected and at risk stallions to be tested by a laboratory. If a straw from any ejaculate is infected, all straws from that ejaculate should be destroyed; Any at risk pregnant mare must be foaled in isolation. The placenta must be incinerated. Foals born to these mares should be swabbed three times, at intervals of not less than seven days, before three months of age. Any mares with an abnormal vaginal exudate, or returning to oestrus prematurely, should be investigated and managed as though infected with equigenitalis until results of laboratory testing prove otherwise. If carriers of equigenitalis are detected, the organism can be eliminated by treatment with systemic and/or local antibiotics combined with antiseptic washing of the sites of persistence in the mare and the stallion.  

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Pathogen test  This RT-qPCR test detects the genome (RNA) to Equine Viral Arteritis (EVA) virus. Sample 5 mL - blood - K3 EDTA blood 10 mL - semen - sterile tube Turnaround time 2 to 5 working days   What is Equine Viral Arteritis? Equine viral arteritis (EVA) is an economically important viral disease of equids. Stallions can become long term carriers of the virus, and transmit it during breeding. Although carrier stallions can be bred if precautions are taken, the need to mate them with seropositive or vaccinated mares decreases their desirability as breeders. Acute illness also occurs in some horses. Although deaths are very rare in healthy adults, pregnant mares that become infected may abort, and very young foals may die of fulminating pneumonia and enteritis. Equine viral arteritis has recently increased in prevalence, possibly due to increased transportation of horses and semen. Clinical signs Most EAV infections, especially those that occur in mares bred to long-term carriers, are asymptomatic. The clinical signs are generally more severe in old or very young animals, and in horses that are immunocompromised or in poor condition. Fulminant infections with severe interstitial pneumonia and/ or enteritis can be seen in foals up to a few months of age. Systemic illness also occurs in some adults. In adult horses, the clinical signs may include fever, depression, anorexia, limb edema (particularly in the hindlimbs), and dependent edema of the prepuce, scrotum, mammary gland and/or ventral body wall. Conjunctivitis, photophobia, periorbital or supraorbital edema and rhinitis can also be seen. Abortions or stillbirths can occur in mares that are pregnant when they are exposed. Abortions are not necessarily preceded by systemic signs. Temporary decreases in fertility, including reduced quality sperm and decreased libido, may be seen in stallions during the acute stage of the disease. Transmission Equine Arteritis Virus (EAV) can be transmitted by the respiratory and the venereal routes. Acutely affected horses excrete the virus in respiratory secretions; aerosol transmission is common when horses are gathered at racetracks, sales, shows and other events. This virus has also been found in urine and feces during the acute stage. It occurs in the reproductive tract of acutely infected mares, and both acutely and chronically infected stallions. In mares, EAV can be found in vaginal and uterine secretions, as well as in the ovary and oviduct, for a short period after infection. Mares infected late in pregnancy may give birth to infected foals. Stallions shed EAV in semen, and can carry the virus for years. Transmission from stallions can occur by natural service or artificial insemination. Some carriers may eventually clear the infection. True carrier states have not been reported in mares, geldings or sexually immature colts; however, EAV can occasionally be found for up to six months in the reproductive tract of older prepubertal colts. Equine arteritis virus can be transmitted on fomites including equipment, and may be spread mechanically by humans or animals. Semen remains infectious after freezing. Prevention Acutely infected horses should be isolated to prevent transmission in secretions and excretions. Precautions should also be taken to avoid spreading the virus on fomites. EAV is readily inactivated by detergents, common disinfectants and lipid solvents. No specific treatment is available; however, most healthy horses other than young foals recover on their own. Good nursing and symptomatic treatment should be used in severe cases. Vaccination can also help contain outbreaks. Venereal transmission can be controlled by good management and vaccination. To protect pregnant mares from abortion, they should be separated from other horses and maintained in small groups according to their predicted foaling dates. Newly acquired horses should be isolated for 3 to 4 weeks. Vaccination appears to prevent uninfected stallions from becoming long term carriers. Stallions that are not carriers should be vaccinated before the start of the breeding season. Prepubertal colts are given the vaccine when they are 6-12 months old. Carrier stallions are identified and bred only to well vaccinated or naturally seropositive mares. Similarly, semen that contains EAV should be used only in these mares. Because first-time vaccinates may shed field viruses for a short time after exposure, these mares should be isolated from seronegative horses, particularly pregnant mares, for three weeks after breeding. Naturally infected mares and those that are not first-time vaccinates are isolated for 24-48 hours, to protect other horses from the viruses present in semen. Carrier stallions should be housed where they can be physically separated from uninfected horses; in one case, stallions apparently became infected by indirect exposure to semen. However, this appears to be rare. EAV is sensitive to sunlight and low humidity, and uninfected stallions have been kept near carriers for years without infection. Excellent hygiene and decontamination of fomites should be practiced when breeding infected horses or collecting semen.

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Pathogen test  This ELISA test detects antibodies to Equine Viral Arteritis (EVA) virus. Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is Equine Viral Arteritis? Equine viral arteritis (EVA) is an economically important viral disease of equids. Stallions can become long term carriers of the virus, and transmit it during breeding. Although carrier stallions can be bred if precautions are taken, the need to mate them with seropositive or vaccinated mares decreases their desirability as breeders. Acute illness also occurs in some horses. Although deaths are very rare in healthy adults, pregnant mares that become infected may abort, and very young foals may die of fulminating pneumonia and enteritis. Equine viral arteritis has recently increased in prevalence, possibly due to increased transportation of horses and semen. Clinical signs Most EAV infections, especially those that occur in mares bred to long-term carriers, are asymptomatic. The clinical signs are generally more severe in old or very young animals, and in horses that are immunocompromised or in poor condition. Fulminant infections with severe interstitial pneumonia and/ or enteritis can be seen in foals up to a few months of age. Systemic illness also occurs in some adults. In adult horses, the clinical signs may include fever, depression, anorexia, limb edema (particularly in the hindlimbs), and dependent edema of the prepuce, scrotum, mammary gland and/or ventral body wall. Conjunctivitis, photophobia, periorbital or supraorbital edema and rhinitis can also be seen. Abortions or stillbirths can occur in mares that are pregnant when they are exposed. Abortions are not necessarily preceded by systemic signs. Temporary decreases in fertility, including reduced quality sperm and decreased libido, may be seen in stallions during the acute stage of the disease. Transmission Equine Arteritis Virus (EAV) can be transmitted by the respiratory and the venereal routes. Acutely affected horses excrete the virus in respiratory secretions; aerosol transmission is common when horses are gathered at racetracks, sales, shows and other events. This virus has also been found in urine and feces during the acute stage. It occurs in the reproductive tract of acutely infected mares, and both acutely and chronically infected stallions. In mares, EAV can be found in vaginal and uterine secretions, as well as in the ovary and oviduct, for a short period after infection. Mares infected late in pregnancy may give birth to infected foals. Stallions shed EAV in semen, and can carry the virus for years. Transmission from stallions can occur by natural service or artificial insemination. Some carriers may eventually clear the infection. True carrier states have not been reported in mares, geldings or sexually immature colts; however, EAV can occasionally be found for up to six months in the reproductive tract of older prepubertal colts. Equine arteritis virus can be transmitted on fomites including equipment, and may be spread mechanically by humans or animals. Semen remains infectious after freezing. Prevention Acutely infected horses should be isolated to prevent transmission in secretions and excretions. Precautions should also be taken to avoid spreading the virus on fomites. EAV is readily inactivated by detergents, common disinfectants and lipid solvents. No specific treatment is available; however, most healthy horses other than young foals recover on their own. Good nursing and symptomatic treatment should be used in severe cases. Vaccination can also help contain outbreaks. Venereal transmission can be controlled by good management and vaccination. To protect pregnant mares from abortion, they should be separated from other horses and maintained in small groups according to their predicted foaling dates. Newly acquired horses should be isolated for 3 to 4 weeks. Vaccination appears to prevent uninfected stallions from becoming long term carriers. Stallions that are not carriers should be vaccinated before the start of the breeding season. Prepubertal colts are given the vaccine when they are 6-12 months old. Carrier stallions are identified and bred only to well vaccinated or naturally seropositive mares. Similarly, semen that contains EAV should be used only in these mares. Because first-time vaccinates may shed field viruses for a short time after exposure, these mares should be isolated from seronegative horses, particularly pregnant mares, for three weeks after breeding. Naturally infected mares and those that are not first-time vaccinates are isolated for 24-48 hours, to protect other horses from the viruses present in semen. Carrier stallions should be housed where they can be physically separated from uninfected horses; in one case, stallions apparently became infected by indirect exposure to semen. However, this appears to be rare. EAV is sensitive to sunlight and low humidity, and uninfected stallions have been kept near carriers for years without infection. Excellent hygiene and decontamination of fomites should be practiced when breeding infected horses or collecting semen.

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