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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