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.

Read more less

  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.

Read more less

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

Read more less

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

Read more less

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

Read more less

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

Read more less

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.

Read more less

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.    

Read more less

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

Read more less

  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.  

Read more less

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

Read more less