Pathogen profile This profile includes 10 qPCR tests that detects 10 pathogens responsible for  neurological disease in horses such as: EHV-1, EPM, EEE, EEV, VEE, JEV, WEE, WNV, RBV, Hendra. Sample 5 mL - blood ( K3 EDTA tube) and/or 5mL - liquor (CSF) in a sterile tube Turnaround time 2 to 5  working days  

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  DNA test kit DNA test to predict the genetic potential for being a small, medium or tall height horse. Sample 30 to 40 hair roots - envelope or 5 mL of blood  - K3 EDTA tube Turnaround time 5 to 8  working days Why test?  Confidently predict the expected mature height at withers of a young foal. Identify horses that are 70% likely to be within the specific height range desired by the owner. Produce horses of a desired height more consistently. Results description The DNA test verifies the presence of the (C) allele associated to tall height horses, and presents the results as one of the following:  C/C – Tall physical height. This genotype, with two copies of the (C) allele,  is associated with large horses, (169+/-4 cm height at the withers). This genotype can be found in draught horses, Westphalians (31%), Oldenburgs (29%), Hanoverians (28%), Holsteiners (18%) and Pureblood Lusitanos (4%). T/C – Medium physical height. This genotype, with one copy of the (T) allele and another of the (C) allele,  is associated with medium-sized horses (164+/-5 cm height at the withers). This genotype can be found in the Holsteiner (64%), Westphalian (60%), Hanoverian (56%) and Pureblood Lusitano (29%). T/T – Small physical height. This genotype, with two copies of the (T) allele, is associated with smaller horses (159 +/- 4 cm height at the withers) and ponies (<148 cm height at the withers). This genotype can be found in the majority of ponies, Arabs (100%) and Pureblood Lusitanos (67%).                                 Additional information The development of the skeletal apparatus is regulated by the expression of the gene LCORL. Recent studies have identified a variation of a simple nucleotide base (Single Nucleotide Polymorphism) in the promoter of this gene. The replacement of a thymine (T) with a cytosine (C) varies the expression of the LCORL gene. This variation in the expression influences the horse’s dimension. Consequently, if the expression of the LCORL gene is diminished the resulting horse has a larger body dimension (bones are longer).

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

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

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

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DNA test The genetic test verifies the presence of the Silver coat dilution modifier. The Silver genetic variant is associated with Multiple Congenital Ocular Abnormalities (MCOA) in some breeds.   Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Results description The DNA test verifies the presence of the silver gene and presents results as one of the following: N/ – Negative for Silver - No evidence of the genetic variant for Silver. No risk to develop Multiple Congenital Ocular Abnormalities (MCOA) associated to Silver. Z/N - Heterozygous for Silver - The Black and Bay basic coat colour will be diluted by Silver. Black-based horses will be chocolate with flaxen mane and tail. Bay-based horses will have pigment on lower legs lightened and flaxen mane and tail. No effect on chestnut color. Moderate risk to develop MCOA. Z/ – Homozygous for Silver - Two copies of altered sequence detected. Black-based horses will be chocolate with flaxen mane and tail. Bay-based horses will have pigment on lower legs lightened and flaxen mane and tail. No effect on chestnut color, but will pass the variant on to 100% of offspring.  Higher risk to develop severe MCOA. Additional information The Silver dilution behaves as a coat colour dominant trait on bay and black base coat colours. While chestnut base colour is not affected by the Silver dilution and can pass the variant silently to the offspring.  In short, the Silver dilution variant (Z) will only affect coat colour phenotype of black pigmented horses (E/e or E/E) and has no effect on red pigmented horses (e/e).  In addition, the eye disorders associated to Silver genetic variant are incomplete autosomal dominant:  homozygous horses (with two copies of Z)  may be at higher risk of developing severe Multiple Congenital Ocular Abnormalities (MCOA), while heterozygous (with one copy of Z) may develop a milder form of MCOA.   The effects of the silver dilution on coat colour gene can vary widely. The agouti gene affects the coat colour by controlling the distribution of the black pigment whereas the Silver dilution variant dilutes areas of the black pigment. Dilution by the Silver variant on a horse with a uniform black base typically involves lightening of the mane and tail and a dilution of the body to a chocolate color, often dappled as well. A Bay horse carrying the Silver gene will usually have a lightened mane and tail, as well as lightened lower legs. It is important to know that although a red horse (e/e) will not be diluted by the silver variant, it can be a carrier of the genetic variant and thus potentially pass the gene on to its offspring. Silver dilution has been identified in a number of horse breeds including the Quarter horse, the Rocky Mountain horse, the Icelandic horse, Morgans, Shetland ponies and the Miniature horse. References: Brunberg, E., Andersson, L., Cothran, G., Sandberg, K., Mikko, S., Lindgren, G.: A missense mutation in PMEL17 is associated with the silver coat color in the horse. BMC Genetics 7:46, 2006. Andersson, L.S., Wilbe, M., Viluma, A., Cothran, G., Ekesten, B., Ewart, S., Lindgren, G.: Equine Multiple Congenital Ocular Anomalies and Silver Coat Colour Result from the Pleiotropic Effects of Mutant PMEL. PLoS One 8:e75639, 2013.

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

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DNA test DNA test for the Lavender Foal Syndrome (LFS) – Pure and part-bred Arab horses. This test verifies the presence of the recessive LFS gene. Sample 30 to 40 - hair roots - envelope or 5 mL - blood - K3 EDTA tube Turnaround time 2 to 5  working days Why test? This genetic test determines LFS clear, carrier or affected status. Informed choices can be made for breeding selections, and prevent the born of affected foals. Results description The DNA test verifies the presence of the recessive LFS gene and presents results as one of the following:  N/ – Non-carrier of the LFS gene. Tested negative for the LFS gene. N/LFS - Heterozygous horse for LFS, both the normal and LFS alleles were detected. The horse is a carrier of LFS genetic disorder and there is a 50% chance this horse will pass a LFS allele to its offspring LFS/ – Homozygous horse for LFS, carrier of two copies of the LFS gene. The horse is affected with the LFS genetic disorder. Additional information Lavender Foal Syndrome (LFS) is a recessive genetic disorder. Affected foals born with the unique diluted coat color that can appear to be pale lavender, pale pink or silver. This foals-often have a difficult delivery, problems standing at birth and usually have episodes where they rigidly extend their limbs, neck and back. These episodes tend to resemble a seizure, although the affected foal does not seem normal between episodes. All affected foals are usually euthanised within days or weeks of birth. LFS is rare and is considered to be an autosomal recessive trait. “Autosomal” means that there is no sex linkage, so both males and females can be equally affected. “Recessive” means that in order for a foal to be affected, it must have received two copies of the mutated gene, inheriting one copy from each parent. Horses that have one copy of the mutated gene, in combination with one copy of the normal gene, are physically normal but are considered carriers and have a 50% probability, each time they are bred, of passing the mutation along to their offspring. The SNP mutation that causes LFS has not been detected in other breeds.  Testing for this mutation in horses with no Arabian blood lines is not recommended. However, in cases where pedigree is not known, testing could be a useful tool to prevent possible affected foals.

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

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

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

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

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

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Pathogen test  The RT-cPCR test detects the genome (RNA) of Hendra virus. Sample 5 mL - blood - K3 EDTA tube and/or 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Hendra virus? Hendra virus (HeV) infection is a rare emerging zoonosis that causes severe and often fatal disease in both infected horses and humans. The natural host of the virus has been identified as being fruit bats of the Pteropodidae Family, Pteropus genus. Clinical signs The clinical signs in horses can include:  frothy nasal mucus high temperature rapid heart rate sweating muscle spasms and twitching muscle weakness balance difficulties rapid deterioration. Transmission Hendra virus can be transmitted from flying fox to horse, horse to horse and horse to human. The exact route of transmission is not known, but it is thought that horses become infected via contact or droplet transmission of the virus.This may occur by ingesting material contaminated by infected flying fox body fluids and excretions. While Hendra virus is present in flying fox populations periodically, the likelihood of horses becoming infected is low. Hendra virus can spread from horse to horse through direct contact with infectious body fluids, or through indirect contact via equipment contaminated with infectious body fluids. The few cases of Hendra virus infection in people occurred following high-level exposure to respiratory secretions (e.g. mucus) and/or blood and other body fluids from an infected horse. Other people have reported having some contact with infected horses but have remained well, and their blood tests have shown no evidence of Hendra virus infection. There is no evidence of Hendra virus spreading from person to person or from flying foxes to humans. The scientific information available on the disease is not complete. Research continues so that we can learn more about Hendra virus—particularly about how it is transmitted from flying foxes to horses. Prevention How to reduce the risk of horses becoming infected: A Hendra virus vaccine is available for horses. Vaccination is the single most effective way of reducing the risk of Hendra virus infection in horses. Discuss the option of vaccination with your veterinarian. See Vaccination in this brochure for more information. Remove horse feed and water containers from under trees. If possible, place feed and water containers under a shelter. Remove your horses from paddocks where flowering/fruiting trees may be attracting flying foxes. Return the horses only after the trees have stopped flowering/fruiting and the flying foxes have gone. If the horses cannot be removed from the paddock, consider fencing (temporary or permanent) to restrict access to flowering/fruiting trees. Clean up any fruit debris underneath the trees before returning the horses. If it is not possible to remove your horses from paddocks for long periods, try to temporarily remove your horses during times of peak flying fox activity (usually at dusk and during the night). Clean and disinfect gear exposed to any body fluids from horses before using it on another horse. This includes items like halters, lead ropes and twitches. Talk to your veterinarian about which cleaning agents and disinfectants to use. When cleaning contaminated equipment, wear gloves, cover any cuts or grazes and wash your hands thoroughly afterwards. If your horse becomes sick, isolate it from other horses, other animals and people until a veterinarian’s opinion is obtained.  

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Pathogen test  The qPCR test detects the genome (DNA) of Rabies virus. Sample 1 swab - saliva - dry swab 5mL - blood - K3 EDTA tube 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Rabies?  Rabies is a virus that causes a neurological disease that can affect all mammals. When an animal is bitten, the virus migrates to the brain where it causes inflammation, known as encephalitis. It is rapidly progressive and invariably fatal. The incubation period – the time between the virus’ entry into the body and the onset of clinical signs – averages 2 to 9 weeks, but may be as long as 15 months. Clinical signs Clinical signs can be subtle and could include: Sudden change in behaviour (depression to manic); Lameness or being unable to rise; Head-pressing and circling; Pain or difficulty urinating; Muscle tremors or convulsions; Persistent and painful erection in absence of sexual interest; Loss of appetite; Appearance of choke; Neurologic signs such as incoordination and paralysis; and Sudden death can also be seen on occasion. Transmission We see an increased incidence of rabies infections in horses and other livestock in the late summer and fall when wildlife populations peak. Horses contract rabies through the bite of an infected (rabid) animal, such as a raccoon, fox, skunk or bat. A horse’s curiosity can get the best of him, with bites typically occurring on the horse’s face and muzzle or lower limbs. Most exposures aren’t noticed and most bite wounds aren’t found. Since wildlife may enter barns (especially at night), both horses in stalls and those on pasture are at risk of exposure. Due to the serious threat for human exposure when handling a horse with rabies, any suspected case of equine rabies should be handled as if it were positive until proven otherwise. You may become infected with the rabies virus through contact with saliva or brain/nervous system tissue from a rabid animal. Individuals who have been in contact with a horse since the onset of clinical signs should immediately consult with their physician regarding medical treatment. Prevention Horse owners can take advantage of some basic husbandry practices and good common sense to help reduce the risk factors that can contribute to disease incidence. One thing that all of us can do is to keep our feed storage areas neat and clean. Untidy areas with spilled feed invites unwanted guests such as opossums.  Keep your feed in sealed or closed containers. Cover your hay storage area if possible. Keep rodents under control on your property. Discourage visits by opossums. Check with local authorities with respect to trapping and relocating opossums or eliminating them. Properly dispose of any animal carcasses that you may see on or near your property. Clean your equine water sources on a regular basis. Do not feed on the ground. When transporting horses, make them as comfortable as possible.   

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Pathogen test  The RT-qPCR test detects the genome (RNA) of Japanese Encephalitis virus (JEV). Sample 5 mL - blood - K3 EDTA tube 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Japanese Encephalitis Virus? Japanese encephalitis occurs throughout most of Asia, including India, China and Japan. In temperate areas, infection usually occurs in late summer and autumn, when mosquitoes are more active. Infection builds up in water birds and then spreads by mosquitoes to pigs during late spring and early summer and finally to humans and horses. Cases in humans and horses tend to be sporadic or occur in small clusters, but serious outbreaks could occur in a large, susceptible population exposed to infected mosquitoes. Infected horses are dead-end hosts as there is not enough of the virus in their blood to infect mosquitoes. Clinical signs These include: vary from a passing fever through to violent neurological signs and death mild cases: off feed, sluggish and reddened or jaundiced (yellow) mucous membranes (gums) more serious cases: lethargic with a fluctuating fever, difficulty swallowing, jaundice (yellow), pinpoint haemorrhages in mucous membranes (gums) nervous signs such as lack of coordination, staggering, falling, aimless wandering and unpredictable behaviour may occur in serious cases severe cases: blindness with profuse sweating and muscle trembling before collapsing and dying. Transmission Japanese encephalitis is caused by a virus related to West Nile virus and Murray Valley encephalitis virus. The virus cycles naturally between water birds (herons and egrets) and mosquitoes. Pigs can also be infected and spread disease causing abortions in pregnant sows and neurological signs in piglets. Humans and horses may suffer severe disease from the virus, but they do not spread the disease. Infections without recognisable signs occur in other livestock and animals. The disease has an incubation period of 8–10 days. Prevention Sanitary prophylaxis Housing animals in-doors in screened stabling can provide protection from mosquitoes o Especially during active JE outbreaks and during peak vector activity (usually dawn to dusk) o Insecticides, repellents and fans also provide protection. Vector control reduces transmission. Vaccine is available for horses .  Vaccine protects horses from clinical disease and possible sequelae.

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 Pathogen test  The RT-qPCR test detects the genome (RNA) of Western Equine Encephalitis (WEE) virus. Sample 5 mL - blood - K3 EDTA tube 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Western Equine Encephalitis? Western equine encephalitis (WEE) is a viral disease carried by mosquitoes. WEE occurs in the western parts of the United States, including Iowa and Canada. WEE causes “sleeping sickness” in horses. Clinical signs WEE viruses affect the nervous system, so affected animals will have fever, depression and changes in behaviour. Signs of infection may also include impaired vision, muscle twitches, circling or head pressing behaviours, the inability to swallow, paralysis and convulsions. Survival rates of horses infected with WEE is 70-80%.  Transmission The virus is transmitted to people and horses by bites from infected mosquitoes and birds during wet, summer months Prevention Vaccines for WEE are available for horses. Measures to control mosquito populations and minimize mosquito exposure will decrease chances of infection.

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Pathogen test  The ELISA test detects antibodies to the West Nile Virus (WNV). Sample 5 mL - blood - serum tube Turnaround time 2 to 5 working days   What is West Nile Virus? West Nile virus (WNV) is a zoonotic mosquito-transmitted viral disease that cause can cause encephalitis or meningitis, infection of the brain and the spinal cord or their protective covering. Most horses bitten by carrier mosquitoes do not develop disease. Of those that do, approximately one-third develop severe disease and die or are so affected that euthanasia is required. The time between the bite of an infected mosquito and when clinical signs appear, ranges from three to 14 days. Clinical signs In horses that do become clinically ill, the virus infects the central nervous system and causes symptoms of encephalitis.  Clinical signs of encephalitis in horses include loss of appetite and depression, in addition to any combination of the following signs: fever, weakness or paralysis of hind limbs, muscle fasciculations or muzzle twitching, impaired vision, ataxia (incoordination), head pressing, aimless wandering, convulsions, inability to swallow, circling, hyper-excitability, or coma. It is important to note that not all horses with clinical signs of encephalitis have West Nile encephalitis. Other diseases, including rabies, botulism, equine protozoal myeloencephalitis (EPM), and other mosquito-borne viral encephalitic diseases of horses caused by Eastern,Western, and Venezuelan encephalitis viruses, can cause a horse to have symptoms similar to WNV. Only laboratory tests can confirm the diagnosis of West Nile encephalitis. Transmission WNV is spread by the bite of an infected mosquito. Mosquitoes become infected when they feed on infected birds. Horses cannot spread the disease to humans, but humans are susceptible to the disease if bitten by a carrier mosquito. There is no evidence that horses can transmit WNV to other horses, birds, or people. WNV may cross the placenta from mother to gestating foal. No transfusion related horse illnesses have been reported. However, human to human transmission via blood transfusions have been confirmed, so this method of transmission is possible in horses. Prevention There is no specific treatment for West Nile encephalitis in horses, supportive veterinary care is recommended. Currently, there are some vaccines available against West Nile Virus. It is imperative that horses are vaccinated according to the label on the vaccine. Horses vaccinated against Eastern, Western, and Venezuelan equine encephalitis are not protected against West Nile Virus. There are some easy steps you can take to prevent mosquitoes from affecting your horses: House horses indoors during peak periods of mosquito activity (dusk and dawn). Avoid turning on lights inside the stable during the evening and overnight (mosquitoes are attracted to lights). Place incandescent bulbs around the perimeter of the stable to attract mosquitoes away from the horses. Remove all birds, including chickens, that are in or close to the stable. Look around the property periodically for dead birds, such as crows. Any dead birds should be reported to the local health department. Use rubber gloves to handle dead birds or use an implement, such as a shovel. Eliminate areas of standing water on your property. Shallow standing water, used tires, manure storage pits, and drainage areas with stagnant water are ideal mosquito breeding places. Topical preparations containing mosquito repellents are available for horses. Read the product label before using and follow all instructions. Use fans on the horses while in the stable to help deter mosquitoes. Fog stable premises with a pesticide in the evening to reduce mosquitoes. Read directions carefully before using.

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 Pathogen test  The RT-qPCR test detects the genome (RNA) of West Nile Virus (WNV). Sample 5 mL - blood - K3 EDTA tube 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is West Nile Virus? West Nile virus (WNV) is a zoonotic mosquito-transmitted viral disease that cause can cause encephalitis or meningitis, infection of the brain and the spinal cord or their protective covering. Most horses bitten by carrier mosquitoes do not develop disease. Of those that do, approximately one-third develop severe disease and die or are so affected that euthanasia is required. The time between the bite of an infected mosquito and when clinical signs appear, ranges from three to 14 days. Clinical signs In horses that do become clinically ill, the virus infects the central nervous system and causes symptoms of encephalitis.  Clinical signs of encephalitis in horses include loss of appetite and depression, in addition to any combination of the following signs: fever, weakness or paralysis of hind limbs, muscle fasciculations or muzzle twitching, impaired vision, ataxia (incoordination), head pressing, aimless wandering, convulsions, inability to swallow, circling, hyper-excitability, or coma. It is important to note that not all horses with clinical signs of encephalitis have West Nile encephalitis. Other diseases, including rabies, botulism, equine protozoal myeloencephalitis (EPM), and other mosquito-borne viral encephalitic diseases of horses caused by Eastern,Western, and Venezuelan encephalitis viruses, can cause a horse to have symptoms similar to WNV. Only laboratory tests can confirm the diagnosis of West Nile encephalitis. Transmission WNV is spread by the bite of an infected mosquito. Mosquitoes become infected when they feed on infected birds. Horses cannot spread the disease to humans, but humans are susceptible to the disease if bitten by a carrier mosquito. There is no evidence that horses can transmit WNV to other horses, birds, or people. WNV may cross the placenta from mother to gestating foal. No transfusion related horse illnesses have been reported. However, human to human transmission via blood transfusions have been confirmed, so this method of transmission is possible in horses. Prevention There is no specific treatment for West Nile encephalitis in horses, supportive veterinary care is recommended. Currently, there are some vaccines available against West Nile Virus. It is imperative that horses are vaccinated according to the label on the vaccine. Horses vaccinated against Eastern, Western, and Venezuelan equine encephalitis are not protected against West Nile Virus. There are some easy steps you can take to prevent mosquitoes from affecting your horses: House horses indoors during peak periods of mosquito activity (dusk and dawn). Avoid turning on lights inside the stable during the evening and overnight (mosquitoes are attracted to lights). Place incandescent bulbs around the perimeter of the stable to attract mosquitoes away from the horses. Remove all birds, including chickens, that are in or close to the stable. Look around the property periodically for dead birds, such as crows. Any dead birds should be reported to the local health department. Use rubber gloves to handle dead birds or use an implement, such as a shovel. Eliminate areas of standing water on your property. Shallow standing water, used tires, manure storage pits, and drainage areas with stagnant water are ideal mosquito breeding places. Topical preparations containing mosquito repellents are available for horses. Read the product label before using and follow all instructions. Use fans on the horses while in the stable to help deter mosquitoes. Fog stable premises with a pesticide in the evening to reduce mosquitoes. Read directions carefully before using.

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 Pathogen test  The RT-qPCR test detects the genome (RNA) of Venezuelan Equine Encephalitis (VEE) virus. Sample 5 mL - blood - K3 EDTA tube 5mL - liquor (CSF) - sterile tube Turnaround time 2 to 5 working days   What is Venezuelan Equine Encephalitis? Venezuelan equine encephalitis virus is a mosquito borne viral pathogen that causes Venezuelan equine encephalitis or encephalomyelitis (VEE). VEE can affect all equine species, such as horses, donkeys and zebras.  After infection, equines may suddenly die or show progressive central nervous system disorders. Humans also can contract this disease.  Clinical signs WEE viruses affect the nervous system, so affected animals will have fever, depression and changes in behaviour. Signs of infection may also include impaired vision, muscle twitches, circling or head pressing behaviours, the inability to swallow, paralysis and convulsions. For VEE, death rates are variable but can be as high as 90%. Transmission The virus is transmitted to people and horses by bites from infected mosquitoes and birds during wet, summer months. Prevention Vaccines for EEE are available for horses. Measures to control mosquito populations and minimize mosquito exposure will decrease chances of infection.

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Pathogen test  The PCR test detects the genome (DNA) of the Rhodococcus equi, the pathogen responsible for Pneumonia. Sample 1 nasopharyngeal swab - dry swab  Turnaround time 2 to 5 working days   What is Pneumonia? Rhodococcus equi, a Gram‐positive facultative intracellular pathogen, is one of the most common causes of pneumonia in foals. Rhodococcus equi is a very well recognized pathogen in horses – it is a common cause of pneumonia in foalsbetween the ages of 1-6 months, and infection is also sometimes associated with other problems such as diarrheas, swollen joints and abscesses in other parts of the body. The infection can be very difficult to treat because the bacteria are able to live inside white blood cells, which helps protect them from the body’s immune system, and because they often cause abscesses to form, which are difficult for antibiotics to penetrate. Rhodococcus equi infection in foals has been studied extensively, but there’s still a lot we don’t know how the body defends itself against this organism.  Clinical signs The most common clinical manifestation of R. equi infections in foals is bronchopneumonia. Early clinical signs may only include a slight increase in respiratory rate and a mild fever. These subtle clinical signs are often either missed or ignored, allowing the condition to progress. As the disease progresses, clinical signs might include: • Decreased appetite • Lethargy • Fever • Tachypnea • Increased effort of breathing characterised by nostril flaring and increased abdominal effort Cough and bilateral nasal discharge are inconsistent finding. Because ultrasonographic screening for early detection has become routine practice at some farms endemic for pneumonia caused by R. equi (see below), the most frequently recognised form of R. equi infection at those farms is a subclinical form in which foals develop sonographic evidence of peripheral pulmonary consolidation or abscessation without necessarily manifesting clinical signs. Extrapulmonary manifestations of rhodococcal infections are common. Extrapulmonary disorders might occur concurrent with or independent of pneumonia. Abdominal lesions (see necropsy below) are present in approximately 50% of foals that die from infections caused by R. equi. However, the majority of foals with abdominal lesions do not show clinical signs of abdominal disease. Polysynovitis is present in approximately 25–30% of cases with clinical R. equi infections. In some foals, lameness might be the result of septic arthritis or, more commonly, osteomyelitis caused by R. equi. Uveitis is not uncommon and might result in blepharospasm, ocular discharge, and blindness in severely affected foals. Occasionally, R. equi can cause infections of a variety of other extrapulmonary tissues or organs. Although rare, clinical signs resulting from abdominal infection with R. equi might include fever, diarrhoea, weight loss or failure to thrive, and colic. Transmission Inhalation of virulent R. equi is the major route of pulmonary infection in foals. Ingestion of the organism is an important route of exposure, and likely of immunisation, but rarely leads to hematogenously acquired pneumonia unless a foal has multiple exposures to extremely large numbers of bacteria. Prevention In the absence of an effective vaccine, control and prevention of the disease at farms endemic for infections caused by R. equi have relied on passive immunisation and screening to promote earlier recognition of the disease. There are no isolation requirements for foals with this disease. Foals with pneumonia caused by R. equi shed higher numbers of R. equi in their feces than healthy foals or foals with subclinical lesions. Therefore, pneumonic foals might be an important source of contamination of the environment with virulent R. equi but there is no evidence that R. equi infection is contagious among foals and exposure to virulent R. equi is widespread in the environment of foals. Thus, currently no environmental management practice or biosecurity measure has sufficient evidence on which to base recommendations for controlling and preventing R. equi pneumonia. Zoonotic Potential R. equi can occasionally cause severe pulmonary or systemic infections in immunosuppressed people. Infections with R. equi are extremely rare and typically less severe in immunocompetent individuals.

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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 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 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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