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

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

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

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DNA test DNA test for the Cerebellar Abiotrophy (CA) – Pure and part-bred Arab horses. This test verifies the presence of the recessive CA mutation. 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 determines CA clear, carrier or affected status. Informed choices can be made for breeding selections, and prevent the born of affected foals. CA is sometimes confused with Wobbler’s syndrome, Equine Protozoal Myeloencephalitis (EPM) and injury-related problems, such as a concussion, so this DNA test could help on the diagnostic. Results description  The DNA test verifies the presence of the recessive CA mutation and presents results as one of the following: N/ – Negative for CA. Absence of the allele responsible for CA. N/CA – Carrier - Positive heterozygous for CA. Presence of one copy of the allele responsible for CA.  The horse is a carrier for CA disorder and can pass on a copy of CA allele to 50% of their progeny when bred. CA/– Affected - Positive Homozygous for CA. Presence of two copies of the allele responsible for CA.  The horse is affected by  CA disorder and can pass the CA allele to 100% of their progeny when bred. Additional information Cerebellar Abiotrophy (CA), is a genetic neurological disease in certain species of animals. The disorder manifests itself when Purkinje cells, the neurons that affect balance and coordination, are present in the cerebellum of the brain. This condition known to affect Arabian horses as well as Miniature horses, the Gotland Pony and possibly the Oldenburg. In most cases, foals appear normal at birth, and symptoms generally become noticeable after four months. There have been reported cases where the condition was observed shortly after birth, while others report symptoms developing after the first year. Horses affected with CA tend to startle easily and often fall. Common symptoms include head tremor, a lack of balance and other neurological issues. Affected horses may develop a wide-based stance of the forelegs and difficulty rising from a reclining position. In horses, CA is believed to be linked to an autosomal recessive gene. This means that it is not sex-linked and the allele has to be carried and passed on by both parents in order for an affected animal to be born. Horses that only carry one copy of the gene may pass it on to their offspring, despite being perfectly healthy themselves and having no symptoms of the disease. Because the disorder is recessive, the allele for CA may pass through multiple generations before it is expressed.

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DNA test The DNA test verifies the presence of the dominant LP gene.  The LP gene is associated to high risk of Equine Recurrent Uveitis (ERU) and Congenital Stationary Night Blindness (CSNB). Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Results description The DNA test verifies the presence of the dominant LP Gene (designated LP) and presents results as one of the following:                                                             N/ - Negative for LP. Absence of the dominante LP gene, non spotted horse. Lower risk to develop Equine Recurrent Uveitis (ERU) and Congenital N/ Stationary Night Blindness (CSNB) associated to Leopard. LP/N - Positive heterozygous for LP. Presence of one copy of the incomplete dominant LP gene responsible spotted coat (Appaloosa coat pattern). Horses have high risk to develop Equine Recurrent Uveitis (ERU). The horse can pass the LP gene to 50% of their progeny when bred. LP/ - Positive homozygous for LP. Presence of two copies of the incomplete dominant LP gene responsible for spotted coat (Appaloosa coat pattern). Additionally horses have highest risk to develop Equine Recurrent Uveitis (ERU) and Congenital Stationary Night Blindness (CSNB). The horse will LP/LP pass the LP gene to 100% of its offspring. Risk for ERU associated to LP is evaluated LP/LP > LP/N > N   Additional information The white patterns called Leopard Complex (LP), also know as Appaloosa spotting, has an high variable expression ranging from absent to extreme white patterning.  The expression of Leopard Complex includes several effects on the horse's coat: speckled/mottled skin around the eyes, muzzle, anus, genitalia, and eyes, and progressive roaning (varnish roan) of pigmented coat areas with age. White spotting may also be present, with pigmented leopard spots tending to occur on the white spotting background of heterozygous horses. The inheritance of this coat colour trait is incomplete dominant. The amount of white present is not dosage related, such that homozygous horses can have minimal expression of white patterning. The variability in the amount of white on leopard complex patterned horses is controlled by other genes, one of which is Pattern 1.  /PATN1, the coat pattern spotting.    Horses that are homozyous for the Leopard Complex  develop Congenital Stationary Night Blindness (CSNB) which is the inability to see in low to no-light conditions. Equine Recurrent Uveitis (ERU), also known as moon blindness, is also associated to the LP genetic variant. ERU is characterised by repeated episodes of inflammation of the iris, ciliary body, and choroid. The cumulative effects of the immune mediated process can lead to glaucoma, cataracts, and complete loss of vision.  ERU is the most common cause of blindness in horses. The LP test is the most effective genetic test to ascertain risk for ERU.  Risk for ERU based on this genetic test can be evaluated as LP/LP > LP/N > N/N.  Horses homozygous for LP mutation are the highest risk of developing ERU. Horses heterozygous for LP mutation are at higher risk of developing ERU than those with the mutation. The LP variant is closely identified to the Appaloosa breed, though has indicated has a very ancient genetic variant. European cave paintings have recorded spotted horses and archaegenetic studies have identified the LP genetic variant in European horses of the Pleistocene and Copper Age. The LP genetic variant can be found in many different breeds such as pony of Americas breeds, British Spotted Pony, Knabstrupper, Noriker, Tannu Tuva Pony, American Miniature Horse, Mustang breeds and Tiger horses .  References Bellone, R.R., Holl, H., Setaluri, V., Devi, S., Maddodi, N., Archer, S., Sandmeyer, L., Ludwig, A., Foerster, D., Pruvost, M., Reissmann, M., Bortfeldt, R., Adelson, D.L., Lim, S.L., Nelson, J., Haase, B., Engensteiner, M., Leeb, T., Forsyth, G., Mienaltowski, M.J., Mahadevan, P., Hofreiter, M., Paijmans, J.L., Gonzalez-Fortes, G., Grahn, B., Brooks, S.A.: Evidence for a retroviral insertion in TRPM1 as the cause of congenital stationary night blindness and leopard complex spotting in the horse. PLoS One 8:e78280, 2013.  Bellone RR. Genetic Testing as a Tool to Identify Horses with or at Risk for Ocular Disorders. Vet Clin North Am Equine Pract. 2017;33(3):627–645. doi:10.1016/j.cveq.2017.08.005 Pruvost M. et al.. Genotypes of predomestic horses match phenotypes painted in Paleolithic works of cave art. Proc. Natl. Acad. Sci. 108, 18626–18630 (2011). [PMC free article] [PubMed] [Google Scholar]  

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DNA test The DNA test verifies the presence of the mutation associated to the Overo.   Frame Overo is a highly desirable white pattern gene. 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 horse. O/N - Frame Overo horse. Horse is heterozygous for the dominant gene causative of frame Overo. A characteristic Overo coat pattern is present in O/N all horses with a copy of frame Overo and will pass this allele to 50% of offspring. Matting two Frame Overo horses has a 50% chance to generate Lethal White foals and should be avoided. O/ – A Lethal White Foal Syndrome (LWFS). Homozygous for frame Overo are lethal and newborns survive less than a week old. 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 euthanised 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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  WFFS DNA Test Ensure the Health and Future of Your Horses with Accurate WFFS Testing. Our DNA test verifies the presence of the affected allele at the PLOD1 locus responsible for Warmblood Fragile Foal Syndrome (WFFS), also known as Fragile Foal Syndrome (FFS). Sample Requirements 30 to 40 hair roots - envelope Alternatively, 5 mL blood - K3 EDTA tube Turnaround Time 2 to 5 working days Results Description The DNA test verifies the presence of the affected allele at the PLOD1 locus responsible for WFFS and presents results as one of the following: n/n: Negative for WFFS. No affected allele present. The horse is not a carrier of the WFFS mutation. n/WFFS: Carrier, heterozygous for WFFS. One mutated allele present. The horse can pass the WFFS allele to 50% of its progeny when bred. WFFS/WFFS: Positive, homozygous for WFFS. Two mutated alleles present. The foal will exhibit severe clinical signs and must be euthanized shortly after birth due to the untreatable nature of the disease. Genetic Inheritance Warmblood Fragile Foal Syndrome (WFFS) is an inherited autosomal recessive disorder caused by a single mutation in the PLOD1 gene. Clinical Signs and Affected Breeds The disease is present at birth. Affected foals have skin that lacks tensile strength, characterized by tearing, ulceration, and other lesions from normal contact. Lesions are most noted on pressure points, gums, and other oral cavity mucous membranes. Limb joints are lax and hyper-extensible, making it difficult for affected foals to stand normally. WFFS/FFS is similar to Ehlers Danlos Syndrome (EDS) in humans. The mutation has been reported in Warmblood breeds (11-30% carriers) and at low frequency in Thoroughbreds (2.75% of Irish Thoroughbreds), as well as in Hanoverian, Selle Français, KWPN, Oldenburg, and Westphalians. Why Test? Testing for WFFS is crucial for breeders to make informed decisions. By identifying carriers and avoiding breeding two carriers together, the risk of producing affected foals can be minimized. This helps ensure the health and wellbeing of future generations of horses. Learn More Detailed Results Description The DNA test results will be one of the following: n/n: Negative for WFFS. No affected allele present. The horse is not a carrier of the WFFS mutation. n/WFFS: Carrier, heterozygous for WFFS. One mutated allele present. The horse can pass the WFFS allele to 50% of its progeny when bred. WFFS/WFFS: Positive, homozygous for WFFS. Two mutated alleles present. The foal will exhibit severe clinical signs and must be euthanized shortly after birth due to the untreatable nature of the disease. Additional Information Warmblood Fragile Foal Syndrome (WFFS) is a fatal genetic defect of connective tissue, resulting from a mutation in the PLOD1 gene. WFFS is characterized by hyperextensible, fragile skin and mucous membranes, leading to severe lesions and often resulting in euthanasia of affected foals shortly after birth. This condition significantly impacts a horse's health and performance, making genetic testing an essential tool for breeders and buyers. References References: Ablondi, M., et al. (2022). Performance of Swedish Warmblood fragile foal syndrome carriers and breeding prospects. Genet Sel Evol 54, 4. Rowe, Á., et al. (2021). Warmblood fragile foal syndrome causative single nucleotide polymorphism frequency in horses in Ireland. Ir Vet J 74, 27. Dias, N. M., et al. (2019). Warmblood Fragile Foal Syndrome causative single nucleotide polymorphism frequency in Warmblood horses in Brazil. Vet J 248, 101–102. Hoelzle, L., et al. (2020). Distribution of the Warmblood Fragile Foal Syndrome Type 1 Mutation (PLOD1 c.2032G>A) in Different Horse Breeds from Europe and the United States. Genes 11(12), 1518. Check our FAQs for more information FAQs What breeds are affected by WFFS? WFFS primarily affects Warmbloods but has also been detected in breeds like Thoroughbreds, Knabstruppers, Haflingers, and American Sport Ponies. How is WFFS inherited? WFFS is inherited as an autosomal recessive trait, requiring two copies of the mutated gene (WFFS/WFFS) for the disease to manifest. Affected foals with two copies of the WFFS mutation will not survive to adulthood and must be euthanized shortly after birth. How can WFFS be managed? Unfortunately, there is no cure for WFFS. The condition is lethal, and affected foals exhibit severe clinical signs shortly after birth. The best management strategy is through genetic testing to inform breeding decisions and avoid producing affected foals. Why is it important to test for WFFS? Testing for WFFS is crucial for breeders to make informed decisions. By identifying carriers and avoiding breeding two carriers together, the risk of producing affected foals can be minimized. This helps ensure the health and wellbeing of future generations of horses. Visit our full FAQ page for more details.

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Pathogen test  The ELISA test detects antibodies to the African Horse Sickness Virus (AHSV). Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is African Horse Sickness? African Horse Sickness (AHS) is a serious, often fatal disease of horses, mules, and donkeys. The virus is spread by infected insects (biting midges) and causes fever and, heart and respiratory (breathing) problems in affected animals. Death is common and can occur suddenly. The disease primarily occurs in Africa, but outbreaks have been reported in Egypt, parts of the Middle East, Spain, Portugal, Morocco, Pakistan and India. African horse sickness has not occurred in the United States. AHS does not affect humans, so there are no human or public health implications. Clinical signs African Horse Sickness can cause respiratory (lung) disease, cardiac (heart) disease, or a cyclic fever. Death rates can be as high as 95% for some forms of the disease. The pulmonary or respiratory form occurs rapidly (within days). Signs of disease include fever, difficulty breathing, coughing, sweating, and frothy discharge from the nostrils. Death usually occurs within a few hours after illness is seen. The cardiac form of the disease causes fever and swelling (edema) around the eyes, lips, cheeks, tongue, and neck. Death usually occurs due to heart failure. Some affected animals may have both pulmonary and cardiac signs of disease. Some animals may only develop a cyclic fever (high in the afternoon, gone in the morning). These animals may also have depression and a decreased appetite. Animals with this horse sickness fever form of AHS will typically recover. Transmission AHS virus cannot be transmitted directly from horse to horse (or directly between any equine animals). Virus transmission between horses, donkeys and zebras occurs via small insect vectors known as midges (Culicoides species). The virus can also be mechanically transmitted through transfusion of infected blood products or through unhygienic practices (e.g. use of contaminated surgical equipment or hypodermic needles). It is unknown whether AHS can be transmitted by semen or ova from infected animals. Dogs can become infected with AHS through eating meat from an infected horse, donkey or zebra. Prevention The best way to protect animals from AHS is to decrease their exposure to biting midges and other insects (e.g., mosquitoes and biting flies). Stabling horses in insect-proof housing, particularly between dusk and dawn when the insects are most active, can help prevent exposure. Insect repellents and insecticides may also be useful. Monitor your horse’s temperature. Horses with fevers should be examined by your veterinarian. There is no comercial vaccine for any serotype of AHS currently available in Europe. A vaccine bank is being developed by the European Commission that will hold 100,000 doses of vaccine against seven different AHS serotypes. This vaccine will only be used in a strictly controlled manner in an emergency situation

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  Screening of 3 pathogens responsible Contagious Equine Metritis (CEM):  Taylorella equigenitalis, qPCR Pseudomonas aeruginosa, qPCR Klebsiela pneumonia, qPCR Sample requirements 2 or 3 genital swabs -  use standard swab in dry swabs or transport media for molecular biology Clitoral fossa swab Clitoral sinuses swab. 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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Agouti locus controls distribution of black pigment throughout the coat. This DNA test determine if a horse is A/A, A/a or a/a for the Agouti.  To determine base colour Extension and Agouti testing are needed.   Buy the Base colour test and get DNA tests for Agouti (A) and Extension (E) loci. Sample requirements  and submission form 30 to 40  hair roots or 5 mL of blood in a K3 EDTA tube    Get the sample submission form here   Turnaround time Standard processing - Results in 3-5 working days after sample arrival at the laboratory. Clients organize and support the costs of sending the samples to the laboratory. PREMIUM processing - Results in 1 days after sample arrival. Includes free express delivery** . The laboratory organizes Express shipping with pick-up of the package at the client's address and delivery at the laboratory. ** PREMIUM SERVICES INCLUDE AN EXPRESS SHIPPING DELIVERY FOR EUROPEAN COUNTRIES FROM NON-REMOTE REGIONS. Check here to know if you are in a remote European region. For remote/outreach regions EXTRA fees are applied.    Why test? Agouti is not shown physically on red (e/e) horses. Therefore, a breeder might want to test a chestnut base horse to see if it is an Agouti carrier. Testing bay horses might be desired to see whether the horse carries one (A/a) or two (A/A) copies of the Agouti allele. A homozygous Agouti (A/A) horse will always pass Agouti to its offspring whereas a heterozygous (A/a) horse will have a 50% chance of passing on the gene. Another reason to test for Agouti might be if there is some doubt whether a black horse is truly black or a very dark bay. The effects of other genes might also make it hard to tell if Agouti is present or not. Results description A/A - Bay or Brown - Dominant Homozygous for Agouti. Black pigment restricted to the points. The horse cannot have black foals regardless of the coat color of the mate. The basic coat color will be bay or brown in the absence of other color modifying genes. A/a - Bay or Brown - Heterozygous for Agouti. Black pigment distributed in point pattern. The horse can transmit either (A) or (a) allele to its offspring. The basic coat color will be bay or brown unless modified by other coat color modifying genes. a/a - Black - Recessive homozygous for Agouti. Black pigment distributed uniformly. The basic coat color will be black in the absence of other coat color modifying genes.   Additional information The Agouti gene controls the distribution of black pigment. This pigment can be either uniformly distributed or distributed to “points” of the body (ear rims, lower legs, mane, tail). Agouti has been linked to a deletion of 11 nucleotides in the Agouti locus. The 11 nucleotide deletion of this gene is the recessive form of the gene. Only when the agouti gene is homozygous for the deletion (aa) is the black pigment evenly distributed. Heterozygous (A/a) or homozygous for the absence of the 11 nucleotide deletion (A/A) results in point distribution of black pigment. Agouti has no effect on homozygous positive red factor (ee) horses as there has to be black pigment present for agouti to have an effect.    

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Ensure your horse's high health and performance with our comprehensive diagnostic profile. This profile includes three tests that follow ISO17025 standards, ensuring the highest level of accuracy and reliability. Tests Included Equine Infectious Anemia Virus (EIAV), AGID - Coggins Test Babesia caballi, C-ELISA Theileria equi, C-ELISA Test Details Pathogens Detected: EIAV, Babesia caballi, and Theileria equi. Sample Requirements: 5 mL of blood, serum, or plasma collected in a dry or EDTA tube. Turnaround Time: Standard Processing: Results within 2-5 working days after sample receipt. Why Choose This Profile? This diagnostic profile is essential for maintaining high health and performance in horses. It includes comprehensive testing for Equine Infectious Anemia Virus, Babesia caballi, and Theileria equi, ensuring early detection and management of these critical health conditions. How It Works How It Works 🛒 Purchase the Test: Select and buy the test online. 📧 Receive Instructions: After payment confirmation, receive instructions for sample collection. ✨ Sample Collection: Your veterinarian collects the sample. 📄 Download Submission Form: Download the printable submission form here. 📮 Send Samples: Send to our lab by regular mail or express delivery to:Equigerminal LabRua Eduardo Correia, Nº133030-507 Coimbra, PORTUGAL 📄 Receive Results: Get the result certificate by email. If you need assistance, contact us at support@equigerminal.pt. More Info View More Info For more detailed information on this diagnostic profile, including sample collection and submission instructions, please visit our website or contact our support team. Visit our detailed diagnosis page for more information. FAQs View FAQs How do the tests work? The profile includes the AGID (Coggins) test for EIAV, and cELISA tests for Babesia caballi and Theileria equi, following ISO17025 standards for high accuracy and reliability. What types of samples are required for the tests? 5 mL of blood, serum, or plasma collected in a dry or EDTA tube. How long does it take to get the test results? The turnaround time is 2-5 working days after the sample is received in the laboratory. What should be done if a horse tests positive? Horses that test positive should be isolated to prevent the spread of the disease. Follow biosecurity measures and consult with a veterinarian for appropriate treatment and management. How can these diseases be prevented? Prevention involves regular testing, controlling tick exposure, using repellents, acaricides, and regular inspections, and following biosecurity measures.  

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Breeding stallion profile includes 3 accredited tests:  Coggins test for Equine Infectious Anemia (EIA), AGID (accredited test) Equine Viral Arteritis (EVA) test by RT-qPCR Taylorella equigenitalis (CEMO),test by qPCR Sample requirements Test Sample type Collection Volume (mL) Coggins test Serum/ Whole blood Serum tubes 1 EVA PCR EDTA blood K3 EDTA tube  1 CEMO PCR 3 genital swabs (foreskin, urethra, glans fossa) Synthetic swab without media N.A Turnaround time 2 to 5  working days

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Breeding mare Profile includes 2 tests:  Coggins Test (accredited test for AIE) Taylorella equigenitalis (CEMO) testing by qPCR Sample requirements Test Sample type Collection Volume (mL) Coggins test Serum/ Whole blood Serum tubes 1 EVA PCR EDTA blood K3 EDTA tube  1 CEMO PCR 2 genital swabs: clitoral fossa and clitoral sinuses Synthetic swab without media N.A   Turnaround time 2 to 5  working days

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Pathogen test  The RT-qPCR test detects the genome (RNA) of the Equine Infectious Anaemia Virus (EIAV). This method is used when there are positive/conflicting results on serologic tests. Confirmation of early infection, before serum antibodies to EIAV develop. Equine Infectious Anaemia is a disease listed in the OIE Terrestrial Animal Health Code and countries are obligated to report the occurrence of the disease according to the OIE Code. Sample 5 mL - blood - K3 EDTA tube 1 mL - frozen semen or others Turnaround time 2 to 5 working days   What is Equine Infectious Anemia? Equine infectious anemia is a very old viral disease that affects horses, asses, mules and hinnies worldwide. It is subject to tight controls in the import/export of live equines and their products Clinical signs This infection may have an acute, chronic or sub-clinical (silent) phase. The acute phase characterised by intermittent fever associated with depression, lethargy, increased heart and breathing rates, haemorrhaging, diarrhoea with blood, bleeding wounds that won’t heal, lack of coordination and rapid weight loss. It can also cause petechial haemorrhages of the mucous membranes and general oedema more evident in the legs and jaundice. The chronic phase characterised by recurrent episodes of fever, anaemia and thrombocytopenia (decrease of blood platelets) interspersed with periods of normality. These episodes will be spread out over time. This disease is often fatal during the acute or chronic phase. Should the animal survive the acute and chronic phase, it enters a silent phase with no evident signs of illness for the remainder of its life. In this silent phase the virus persists but the clinical signs are only manifest if the immune system is weakened by another disease, stress or the administration of corticosteroids. Transmission EIA is caused by a lentivirus of the HIV family, the equine infectious anaemia virus. The virus can be passed from one horse to another through fly, or more rarely, mosquito bites, or by direct contact with blood or blood derivative products (serum and/or plasma). Such as, for example, by: sharing objects contaminated with infected blood (needles, branding tools, etc). The virus can also be passed down from mare to foal via the placenta or, more rarely, in the mother’s colostrum or milk. Potentially, the virus can be transmitted by semen. Prevention There is no treatment, cure or vaccine for this infection. Prevention is crucial to avoid it being passed on. Serological tests for EIA must be done for any horse with anaemia and thrombocytopenia of unknown origin. Regular tests must be done on a yearly basis to keep the holding free from EIA. It is advisable to test studs and brood mares every 90 days in the breeding period.

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  Pathogen test  The ELISA test it can, in some cases, replace the Coggins Test, the official test required for trade/import/ export of horses. PTE018/2 ELISA test to detect antibodies against equine infectious anemia virus   Equine Infectious Anaemia is a disease listed in the OIE Terrestrial Animal Health Code and countries are obligated to report the occurrence of the disease according to the OIE Code. Sample 5 mL of blood collected in a dry tube or 2 mL of sera.   Turnaround time Standard processing - Results in 2-5 working days after sample arrival at the laboratory. Clients organise and support the costs of sending the samples to the laboratory. PREMIUM processing - Results in 5 hours after sample arrival. Includes free express delivery** . The laboratory organises Express shipping with pick-up of the package at the client's address and delivery at the laboratory. ** PREMIUM SERVICES INCLUDE AN EXPRESS SHIPPING DELIVERY FOR EUROPEAN COUNTRIES FROM NON REMOTE REGIONS. Check here to know if you are in a remote European region. For remote regions EXTRA fees are applied.  What is Equine Infectious Anemia? Equine infectious anemia is a very old viral disease that affects horses, asses, mules and hinnies worldwide. It is subject to tight controls in the import/export of live equines and their products Clinical signs This infection may have an acute, chronic or sub-clinical (silent) phase. The acute phase characterised by intermittent fever associated with depression, lethargy, increased heart and breathing rates, haemorrhaging, diarrhoea with blood, bleeding wounds that won’t heal, lack of coordination and rapid weight loss. It can also cause petechial haemorrhages of the mucous membranes and general oedema more evident in the legs and jaundice. The chronic phase characterised by recurrent episodes of fever, anaemia and thrombocytopenia (decrease of blood platelets) interspersed with periods of normality. These episodes will be spread out over time. This disease is often fatal during the acute or chronic phase. Should the animal survive the acute and chronic phase, it enters a silent phase with no evident signs of illness for the remainder of its life. In this silent phase the virus persists but the clinical signs are only manifest if the immune system is weakened by another disease, stress or the administration of corticosteroids. Transmission EIA is caused by a lentivirus of the HIV family, the equine infectious anaemia virus. The virus can be passed from one horse to another through fly, or more rarely, mosquito bites, or by direct contact with blood or blood derivative products (serum and/or plasma). Such as, for example, by: sharing objects contaminated with infected blood (needles, branding tools, etc). The virus can also be passed down from mare to foal via the placenta or, more rarely, in the mother’s colostrum or milk. Potentially, the virus can be transmitted by semen. Prevention There is no treatment, cure or vaccine for this infection. Prevention is crucial to avoid it being passed on. Serological tests for EIA must be done for any horse with anaemia and thrombocytopenia of unknown origin. Regular tests must be done on a yearly basis to keep the holding free from EIA. It is advisable to test studs and brood mares every 90 days in the breeding period.    

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Pathogen test  The PCR test detects the genome (DNA) of  Borrelia burgdorferi, the pathogen responsible for the Lyme disease or Borreliose. For animals with clinical signs. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Lyme disease? Lyme disease is a tickborne illness that results from infection with members of the Borrelia burgdorferi sensu lato complex. These organisms are maintained in wild animals, but they can affect humans and some species of domesticated animals, like horses. Lyme disease has been reported in North America, Europe, Australia and parts of Asia. Clinical signs Clinical signs appear in less than 10% of horses infected with the bacteria. Signs include: Lameness (usually of larger joints) that shifts from limb to limb; Generalised stiffness; Soreness in the large joints and back; Low-grade fever (which may or may not be present); Behavioural changes such as reluctance to work and irritability; Laminitis (occasionally associated with Lyme disease) Horses do not show a skin rash with Lyme disease. Swelling around a tick bite in a horse is generally due to a reaction to the tick’s saliva, not Lyme disease. Transmission The ticks become infected when they feed on rodents such as the white-footed mouse that carry the bacteria. The tick can then pass on this infection when it feeds on another host, such as a horse or deer. The bacteria migrate from the tick to the horse after 12 to 24 hours of attachment. In areas where the incidence of disease is high among people, only about 50% of horses are likely to become infected. Of these horses, less than 1 in 10 develops clinical signs of the disease. The remaining horses either have subclinical infection (carry the antibodies against the bacteria but remain clinically healthy) or their immune systems fight off the bacteria (and these horses carry the antibodies to Lyme disease for up to a year). People can also be infected with Lyme disease, but there is no risk of the disease being transmitted from horses to humans. Prevention Since there is no vaccine available, prevention is focused on control of the tick population: Perform a daily tick examination. Remember that it takes 12 to 24 hours of attachment for bacteria to migrate from the tick to the host. Treat turned out horses with permethrin-based insect repellents during peak adult deer tick seasons: early spring, late summer, and fall. Minimize habitat for ticks and their hosts.  

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Pathogen test  The PCR test detects the genome (DNA) of  Trypanosoma evansis, the pathogen responsible for Surra. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Surra? Trypanosoma evansi causes a trypanosomosis known as ‘surra’.This parasite, which has been reported in domestic and wild mammals, can cause considerable economic losses. The trypanosomes reproduce in the blood of the vertebrate host, and the trypomastigote forms are transmitted mechanically by bloodsucking insects from infected to uninfected animals. Surra is the most commonly reported disease in some continents due to the favorable environment for insects. In recent years, several outbreaks or isolated cases have been reported in certain European countries, an atypical region for the disease. Clinical signs The general clinical signs of evansi infections: pyrexia directly associated with parasitaemia together with a progressive anaemia, loss of condition and lassitude are not sufficiently pathognomonic for diagnosis. Recurrent episodes of fever and parasitaemia occur during the course of the disease. Oedema, particularly of the lower parts of the body, urticarial plaques and petechial haemorrhages of the serous membranes are sometimes observed in horses. Abortions have been reported in buffalos and camels. Nervous signs are common in horses. The disease causes immunodeficiencies that may be of high impact when interfering with other diseases or vaccination campaigns. Trypanosomiasis caused by evansi can be clinically confused with other diseases, including equine protozoal myeloencephalitis in the chronic stages. Where surra is suspected, it is important to rule out other causes of equine neurologic disease. Transmission Surra is a non-contagious disease, transmitted only mechanically by several different genera of haematophagous flies. The efficiency of vector transmission is dependent on high intensity of fly challenge, the presence of high numbers of the parasite in the blood of horses, and the close herding of animals that maintains short intervals between successive feeds. The infectivity of a fly is highest within minutes of feeding and drops quickly thereafter, with the loss of ability to reinfect when feeding intervals exceed 8 hours. Wild carnivores and dogs can be infected by ingestion of meat from parasitaemic animals. In Central and South America, The vampire bat can also act as a vector. The disease can be reproduced experimentally by blood inoculation. Prevention There is no vaccine against trypanosomiasis. Therefore, conventional disease control measures are based on the use of curative and preventive drugs to combat the parasite and interventions to control fly populations. Control and eradication of surra from an area is usually depends upon the detection and treatment of infected animals. Protection of susceptible animals from biting flies by smoking and using flies repellants.  

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 Pathogen test  The qPCR test detects the genome (DNA) of Anaplasma phagocytophilum, the bacterium (formerly known as Ehrlichia phagocytophila and Ehrlichia equi)  responsible for the Equine Anaplasmosis. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Equine Anaplasmosis? Anaplasmosis is a tick-borne disease caused by the bacterium Anaplasma phagocytophilum that infects white blood cells. The disease is transmitted by ticks. The risk of transmission to people is unclear at this time. Although horses and people appear to be infected with strains of the same bacteria, it is believed that people also acquire the infection from tick bites, and not directly from infected horses. Clinical signs The severity of signs varies with the age of the animal and duration of the illness. Signs may be mild. Horses less than 1 year old may have a fever only; horses 1 to 3 years old develop fever, depression, mild limb swelling, and lack of coordination. Adults exhibit the characteristic signs of fever, poor appetite, depression, reluctance to move, limb swelling, and jaundice. Fever is highest during the first 1 to 3 days of infection, but may last for 6 to 12 days. Signs become more severe over several days. Any existing infection (such as a leg wound or respiratory infection) can be made worse. Transmission The disease is transmitted by ticks. Immature ticks pick up the bacterium from rodents who serve as reservoirs, maintain it as they mature, and then transmit it to the horse they feed off of as adults. It is unknown how long the tick has to be attached before transmission occurs. It takes approximately 2-3 weeks after disease transmission for the horse to develop clinical signs of Anaplasmosis, meaning that by the time signs are noticed the tick is long gone. Phagocytophilum organisms infect neutrophils and eosinophils in the blood. Prevention The disease is easily treated in the early stages using appropriate antibiotics. The severity of the disease is variable; many horses recover after 14 days without treatment. However, rare fatalities have occurred that are believed to be associated with secondary infections. Horses with severe signs and neurologic signs may benefit from injectable corticosteroids. Recovered horses develop immunity for at least 2 years and are not carriers. Tick control measures are mandatory for control of the disease. There is no vaccine.

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Pathogen test  The PCR test detects the genome (DNA) of Leptospira interrogans, the pathogen responsible for Leptospirosis. Sample 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5 working days   What is Leptospirosis? Leptospirosis is a bacterial infection that can result in abortion, chronic uveitis, and/or kidney failure in horses and can also infect humans,  pets, and other livestock. Clinical signs Some horses with leptospirosis appear completely normal. Others might show generalised flulike signs. More serious cases present as mid- to late-term abortions, chronic uveitis (an eye disease that’s the leading cause of blindness in horses), or renal (kidney) disease. Foals from infected dams born alive might suffer from malnutrition, jaundice, pulmonary haemorrhage, or severe respiratory distress—all of which can be fatal. If you can start treatment immediately—before the infection damages eyes or organs—horses with leptospirosis generally have good prognoses. And, you can protect the rest of your herd (and yourself and other animals) by isolating infected horses, treating your other horses with preventive antibiotics or, depending on the species involved, vaccinating. Transmission Leptospirosis is caused by spiral-shaped bacteria called spirochetes, specifically leptospires, that enter an animal’s body through mucous membranes in areas such as the nostrils, lips, eyes, trachea, stomach, genitals, or anus, or through broken skin. In addition to mammals (horses, humans, squirrels, voles, and scores more), amphibians (such as frogs) and reptiles (including snakes) can become infected with and pass on the disease-causing bacteria. In horses, foals can become infected in utero. Leptospires most commonly live and multiply in the renal tubules (where urine collects in the kidneys) of reservoir or carrier hosts such as rodents, wildlife, and domestic animals. In addition to spreading in urine, leptospires can be transmitted via infected blood or tissues or by infected urine splashing into eyes or the mouth. When an infected reservoir host urinates, the leptospires pass out of its body in the urine and contaminate the surrounding ground and/or water. In fact, exposure to standing water, such as ponds or floodwaters, is the biggest risk factor for leptospirosis infection. Occasionally, says Carter, animals (horses, livestock, etc.) inhale leptospires, ingest them with feed, or transmit them via wounds or bites. Prevention Humans who work with animals or have frequent exposure to them are at a higher risk of contracting leptospirosis. The leptospirosis is now classified as a re-emerging disease. Worldwide, the incidence is increasing, which may be due to increased episodes of flooding. According to the CDC, most human leptospirosis symptoms are flulike and include: high fever; headache; chills; muscle aches; vomiting; jaundice (yellow skin and eyes); red eyes; and abdominal pain. Treatment is fairly straightforward. The emphasis now is on rapid diagnostics so the disease can be diagnosed quickly and treatment started. Prevention is characterised differently for different risk groups. For occupational exposure (for example, veterinarians and animal caretakers that might be exposed to the disease), appropriate PPE (personal protective equipment, including protective gloves and glasses) is important. For recreational exposure, preventing contact of mucous membranes and broken skin with contaminated water is advised.

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Pathogen test  This ELISA test detects antibodies to Equine Herpesvirus Type 1 (EHV-1) and to Equine Hespesvirus type 4 (EHV-4), the 2 agents responsible for Rhinopneumonitis. ELISA test with ab tritation. Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is Rhinopneumonitis? Equine Rhinopneumonitis (ER) is a collective term for any one of several highly contagious, clinical disease entities of equids that may occur as a result of infection by either of two closely related herpesviruses, equid herpesvirus-1 and -4 (EHV-1 and EHV-4). Infection by either EHV-1 or EHV-4 is characterised by a primary respiratory tract disease of varying severity that is related to the age and immunological status of the infected animal. Infections by EHV-1 in particular are capable of progression beyond the respiratory mucosa to cause the more serious disease manifestations of abortion, perinatal foal death, or neurological dysfunction. Clinical signs The incubation period (period of time from exposure to development of first clinical signs) ranges from 2 to 10 days. Respiratory signs for EHV-1 and EHV-4 include high temperature that lasts for 1-7 days, coughing, depression, inappetence (going off feed), and nasal discharge. Abortion usually occurs between months 7 and 11 of gestation, about 2-12 weeks after infection. There is no evidence that the mare’s reproductive tract is damaged, and it does not affect her ability to conceive in later pregnancies. Signs of neurologic disease for EHV-1 and EHV-4 include mild incoordination, hindlimb paralysis, recumbency (lying down and being unable to get up), loss of bladder and tail function, and loss of sensation to the skin around the tail and hindlimb areas. Transmission Transmission occurs when infected and uninfected horses come in either direct (nose to nose contact) or indirect (through buckets, clothing, blankets that are contaminated) contact with nasal discharges of infected horses. The virus can travel via aerosol (in the air) for short distances. The virus may also be transmitted by contact with aborted foetuses, placental fluids, or placentas from infected horses. Also, following infection, horses may become latent carriers of EHV; virus may be reactivated after stress or high doses of corticosteroids. Upon detection of clinical signs suggestive of EHV, the veterinarian may choose to take a nasopharyngeal (nose and throat) swab of the horse, blood sample, or tissue from the aborted foetus for detection of virus in the tissues.  Paired blood samples for detection of antibody trites (levels) may also be taken. Treatment involves supportive care and treatment of the symptoms.  Non-steroidal anti-inflamatory drugs are commonly used to reduce fever, pain and inflammation. In uncomplicated cases, complete recovery will occur in a few weeks. Horses with neurological disease have variable recovery rates depending on severity of the clinical signs.  The prognosis is poor if the horse is recumbent (unable to stand) for an extended period of time. The horse should be rested until fully recovered and gradually returned to work. Prevention Transmission occurs when infected and uninfected horses come in either direct (nose to nose contact) or indirect (through buckets, clothing, blankets that are contaminated) contact with nasal discharges of infected horses. The virus can travel via aerosol (in the air) for short distances. The virus may also be transmitted by contact with aborted foetuses, placental fluids, or placentas from infected horses. Also, following infection, horses may become latent carriers of EHV; virus may be reactivated after stress or high doses of corticosteroids. Upon detection of clinical signs suggestive of EHV, the veterinarian may choose to take a nasopharyngeal (nose and throat) swab of the horse, blood sample, or tissue from the aborted foetus for detection of virus in the tissues.  Paired blood samples for detection of antibody triers (levels) may also be taken. Treatment involves supportive care and treatment of the symptoms.  Non-steroidal anti-inflamatory drugs are commonly used to reduce fever, pain and inflammation. In uncomplicated cases, complete recovery will occur in a few weeks. Horses with neurological disease have variable recovery rates depending on severity of the clinical signs.  The prognosis is poor if the horse is recumbent (unable to stand) for an extended period of time. The horse should be rested until fully recovered and gradually returned to work.

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Pathogen test  The qPCR test detects the genome (DNA) of  Equine Herpesvirus Type 3 (EHV-3), the pathogen responsible for the Equine Coital Exanthema. Molecular detection of EHV-3 by PCR is the most sensitive, specific and accurate tool in assessing the infectivity of an affected horse Sample 5 mL - blood - K3 EDTA tube 1 genital swab - dry swab 20 gr - placental or foetal tissue - sterile flask Turnaround time 2 to 5 working days   What is Equine Coital Exanthema?  Equine Herpesvirus type 3 (EHV-3) causes coital exanthema, a contagious genital infection (vulva in mares, penis and scrotum in stallions), spread venereally and characterised by numerous small blisters or spots, sometimes called ‘the pox’. Clinical signs The clinical presentation of equine coital exanthema (ECE) is characterised by the presence of superficial lesions on the skin of the external genitalia of mares or stallions. The progress of each cutaneous lesion follows a well-defined and predictable course. Transmission Infection by EHV-3 occurs via direct cutaneous contact either during the act of coitus or by the transfer of virus-containing secretions from contaminated objects, such as hands, gloves, instruments, palpation sleeves, sponges and the lips or nose of a horse. The virus is easily transmitted by simple contact with the skin; the epidermal surface need not be damaged for infection to be established. Prevention There is no commercial vaccine against EHV-3. A stringent code of practice should be implemented within breeding sheds following observation of a case of ECE. The three priorities necessary for successful ECE control are: Cessation of breeding of clinically affected animals; Heightened vigilance on the part of personnel for early recognition of new clinical cases; Strict adherence to breeding shed hygiene procedures designed to eliminate mechanical transmission of the virus.

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Pathogen test  This ELISA test detects antibodies to Equine Influenza Virus Type A. Equine Influenza is a disease listed in the OIE Terrestrial Animal Health Code and countries are obligated to report the occurrence of the disease according to the OIE Code. Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is Equine Influenza? Equine Influenza (EI) is a highly contagious though rarely fatal respiratory disease of horses, donkeys and mules and other equidae. The disease has been recorded throughout history, and when horses were the main draft animals, outbreaks of EI crippled the economy. Nowadays outbreaks still have a severe impact on the horse industry. EI is caused by two subtypes of influenza A viruses: H7N7 and H3N8, of the family Orthomyxoviridae. They are related to but distinct from the viruses that cause human and avian influenza. Once introduced into an area with a susceptible population, the disease, with an incubation period of only one to three days, spreads quickly and is capable of causing explosive outbreaks. Crowding and transportation are factors that favour the spread of EI. Clinical signs In fully susceptible animals, clinical signs include fever and a harsh dry cough followed by a nasal discharge. Depression, loss of appetite, muscle pain and weakness are frequently observed. The clinical signs generally abate within a few days, but complications due to secondary infections are common. While most animals recover in two weeks, the cough may continue longer and it may take as much as six months for some horses to regain their full ability. If animals are not rested adequately, the clinical course is prolonged. Transmission Highly contagious, EI is spread by contact with infected animals, which in coughing excrete the virus. Animals can begin to excrete the virus as they develop a fever before showing clinical signs. It can also be spread by mechanical transmission of the virus on clothing, equipment, brushes etc carried by people working with horses. Prevention Vaccination is practiced in most countries. However, due to the variability of the strains of virus in circulation, and the difficulty in matching the vaccine strain to the strains of virus in circulation. Vaccination does not always prevent infection although it can reduce the severity of the disease and speed recovery times. Act immediately if you see flulike signs in your horse, especially if you have multiple animals housed together. Being proactive can help halt disease spread and save money and time. Call your veterinarian and have him or her take nasal swab samples first to determine what pathogen you are dealing with (several diseases can cause similar signs in infected horses) and treat accordingly. Immediately place the horse in question in a quarantine area and thoroughly clean and disinfect any areas or equipment he has been in contact with. Because horses with influenza do not show signs right away, quarantine other horses that have been housed close to the sick one, as they are most likely already infected. Flu’s incubation period, or time that a horse is infectious before showing signs of illness, is about three days. Management techniques can also help reduce disease spread, including designating one person to handle/treat the sick horse, treating the horse at the end of the day/shift (when the handler won’t be coming into contact with other horses), and setting up foot baths with disinfectant solution for handlers to dip their shoes in as they enter and exit the premises. Disinfecting equipment such as buckets and hoses as well as tack can also prevent disease spread. Regardless of your disinfection protocol, be sure to dedicate a separate water bucket and hose for the sick horse.    

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Pathogen test  The qPCR test detects the genome (DNA) of  Equine Herpesvirus Type 2 (EHV-2).  Serological detection of EHV-2 is of limited use to determine the re-activation of this herpesvirus. EHV-2 can remain latent in affected animals while shedding at levels adequate to infect other horses. Molecular detection of EHV-2 by qPCR is the most sensitive, specific and accurate tool in assessing the infectivity of an affected horse. Sample 1 nasopharyngeal swab - dry swab 5 mL - K3 EDTA tube 5 mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Herpesvirus Type 2? Equine Herpesvirus Type1 2 (EHV-2) was recently classified within the Gammaherpesvirinae subfamily. EHV-2 is widely spread in horse populations and it has been isolated from healthy animals as well as from horses with different clinical signs.  EHV-2 is able to establish persistent infections. Various observations indicate that EHV-2 should not be neglected as a pathogen in equids. There are convincing results indicating that EHV-2 has a role as a predisposing factor for Rhodococcus equi invasion in the respiratory tract. Also as been suggested that EHV-2 may play a role in transactivation and reactivation of latent EHV-1 and EHV-4 infections. Clinical signs EHV-2 infection occurs most frequently in young foals, and the most common symptoms are keratoconjunctivitis, respiratory disease with pneumonia and pharyngitis, fever, enlarged lymph nodes, inappetence/anorexia, general malaise, and poor performance. There is no evidence that EHV-2 has abortigenic potential. Transmission The prowess of EHV-2 as a successfully adapted viral parasite of the horse is substantiated by seroepidemiological and virological studies which indicate almost universal acquisition of viral infection by young foals. The limited data collected supports the scenario that EHV-2, in aerosolised infective material excreted from the respiratory tract of another virus-shedding horse, enters the new host through the upper respiratory tract where it infects and replicates first in the respiratory mucosal epithelium. Prenatal infection with EHV-2 has not been recorded, and the virus has not been detected in colostrum or milk. Experimental infection of a mid-gestational equine foetus in utero resulted in normal term delivery, although the foal showed mild rhinitis and conjunctivitis, with nasal shed- ding of EHV-2. Prevention On the basis of evidence suggesting that EHV-2 infection can play an etiological role in predisposing foals to subsequent R. equi pneumonia, both passive immunisation with hyperimmune equine serum against EHV-2 and active immunisation with an vaccine containing EHV-2 glycoprotein antigens have been used, with reported success, for the prophylactic treatment of annual reoccurrences of this highly fatal foal disease. Ocular disease in foals associated with infection by EHV-2 on breeding farms has been successfully treated with ophthalmic ointments containing either idoxuridine or trifluridine together with antibiotics and non-steroidal anti-inflammatory agents.

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