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Watch this video of a presentation on equine colic by Dr. Danica Wolkowski. (Be sure to turn up your sound!) Related resources you may also be interested in: “Equine Colic: What to Expect,” by Nora Grenager, VMD “Enteroliths: A Rock and a Hard Place,” by Timothy G. Eastman, DVM, DACVS, MPVM “Colic in Horses: What You Should Know,” by Timothy G. Eastman, DVM, DACVS, MPVM “Colic Questions Answered,” by Lindsay Berreth, published in Chronicle of the Horse “Colic Updates and Prevention,” by Dr. Nancy Loving, published by American Association of Equine Practitioners (AAEP) “Colic: Minimizing Its Incidence and Impact in Your Horse,” published by American Association of Equine Practitioners (AAEP)

Watch this video of a presentation on nuclear scintigraphy by Dr. Jacquelyn Dietrich. (Be sure to turn up your sound!) Learn more about Nuclear Scintigraphy at Steinbeck Peninsula Equine Clinic...

By Nora Grenager, VMD, DACVIM Equine gastric ulcer syndrome (EGUS) is prevalent in our equine population and can be a cause of a huge variety of clinical signs ranging from suboptimal performance and behavioral issues to poor appetite and mild colic. It has been estimated that 50 to 100 percent of adult horses have gastric ulcers depending on level of work and management practices. Unlike in humans, a horse’s stomach continuously secretes gastric acid because horses were designed to graze throughout the day. The equine stomach is divided into two parts — a smaller upper squamous portion (about one third) and a larger lower glandular portion (about two thirds) — separated by a raised border of tissue called the “margo plicatus.” The upper squamous portion is like a continuation of the esophagus; the lower glandular portion is where acid is produced. EGUS occurs when there is an imbalance between gastric acid secretion and the stomach’s normal protective mechanisms. Types of Gastric Ulcers There are two syndromes of EGUS that have different predisposing factors, signs, and treatments — gastric ulceration in the squamous portion and gastric ulceration in the glandular portion. The glandular portion of the stomach secretes acid and other compounds. It has intrinsic protective mechanisms to deal with acid and is accustomed to acid exposure. Ulceration in this portion is likely due to both an increased acid exposure as well as a decrease in its protective mechanisms. Gastric ulcers in the squamous portion is likely due to the fact that this region is not accustomed to, nor equipped for, acid exposure. The majority of gastric ulcers in the squamous portion of the stomach occur along the margo plicatus, which is closest to the glandular acid-producing portion. Risk Factors Factors that likely predispose horses to glandular ulceration include stress and administration of nonsteroidal anti-inflammatory drugs, called “NSAIDs,” such as phenylbutazone (Bute™), flunixin meglumine (Banamine™), and less commonly firocoxib (Equioxx™). Stress decreases the stomach’s natural protective mechanisms. NSAIDs also decrease the stomach’s natural protective mechanisms, more often with high doses or long duration of treatment. Factors that predispose horses to squamous ulceration include infrequent feedings, high concentrate diets, and intensive training. Stress and NSAID administration can augment these processes in this region as well. Feed deprivation or infrequent feeding has been found to cause gastric ulcers because when the stomach is small and contracted the squamous portion of the stomach is exposed to acid. The byproducts from fermentation of high concentrate diets can also cause acid injury of the squamous portion. Consuming hay and the salivation that accompanies eating (because saliva contains natural buffers) help to buffer stomach acid. Intense exercise potentially increases intra-abdominal pressure and delays gastric emptying time, which increases the exposure of the squamous portion to acid. Clinical Signs Many instances of gastric ulceration probably go unrecognized. Interestingly, the severity of a horse’s clinical signs does not correlate with the degree of gastric ulceration. Horses with EGUS may have poor or picky appetite, weight loss, rough hair coat, poor performance, poor body condition, sore back, “girthy” behavior, or changes in attitude (the horse may seem “grumpy”). A horse with EGUS can present with excessive teeth grinding or excessive salivation, mild recurrent colic or even a more severe acute colic episode, though this is uncommon. Diagnosis Suspicion of EGUS may be based on history and clinical signs, but evaluation of the stomach with an endoscope (a procedure called “gastroscopy”) is the only way to confirm the presence, type, and severity of EGUS. This procedure can be performed at the barn or at a referral veterinary facility. The procedure is usually done in the morning after an overnight fast (the horse must be fasted for a minimum of 12 hours prior to gastroscopy so that the stomach is empty for evaluation). The horse is typically sedated and the endoscope is passed through the nostril down the esophagus into the stomach. The presence, severity, chronicity, and type of gastric ulceration is determined. Unfortunately, there is no blood or fecal test available that can accurately diagnose EGUS. Treatment Several types of drugs are available and commonly used to treat EGUS, and it depends on whether ulceration is present in the squamous, glandular, or both parts of the stomach. Treatment duration usually lasts 4–8 weeks. The gold standard treatment for squamous ulceration is omeprazole (Gastrogard™), a proton-pump inhibitor drug that directly blocks acid secretion. It is formulated as a flavored oral paste given once daily and has been proven to most effectively cure gastric ulceration. Ideally this is given on an empty stomach, 30–60 minutes prior to feeding (so usually first thing in the morning or just before lunch). Antacids (such as aluminum or magnesium hydroxide and calcium carbonate) can help relieve immediate clinical signs, but do not effectively treat the ulceration. Antacids also have a short duration of effect and need to be administered orally every 2–3 hours so they are not convenient for long-term treatment. The typical treatments for glandular gastric ulceration include sucralfate and misoprostol, sometimes along with Gastrogard™. Sucralfate coats ulcerated areas and stimulates the GI tract’s own local protective mechanisms. It is sometimes used alone, or in conjunction with Gastrogard™ for mild to moderate cases of glandular ulceration. Misoprostol is used for moderate to severe glandular ulceration (usually in conjunction with sucralfate +/- Gastrogard™). It increases the body’s own protective mechanisms against glandular ulceration. It cannot be used in pregnant mares and it can occasionally cause transient cramping at the start of administration. Therapy is typically tapered off rather than stopped cold turkey. We usually recommend repeat gastroscopy at the end of the treatment interval to assess the response to treatment. Most cases of squamous ulceration respond well to appropriate treatment, but glandular ulceration is less predictable. Some cases respond well to one month of treatment, while others require longer; unfortunately, it is difficult to predict into which category a horse will fall. Last but certainly not least, it is widely believed that EGUS does not occur in a vacuum. There is typically something else driving the condition — be it musculoskeletal pain, other GI pain, stress, or feed changes. It is very important to try to home in on any other potential causes to maximize the efficacy of your treatment and prevent recurrence. Prevention Gastrogard™ given at a quarter dose once daily (called Ulcergard™ — available over the counter) is effective at preventing the formation of gastric ulcers. This is often recommended around times of stress or NSAID administration in horses at risk for EGUS. Corn oil added to the feed has also been shown to help increase gastric pH (i.e., decrease the amount of acid), although some horses can become “hot” with corn oil supplementation. It has been shown that supplements containing pectin and lecithin can help prevent EGUS, and mineral-rich calcified marine algae helps prevent squamous ulceration. Most importantly, prevention of EGUS involves recognition of situations that may predispose a horse to gastric ulceration. Horses on high doses of NSAIDs or long-term treatment with NSAIDs are theoretically at higher risk for EGUS. Horses in training or who are fed high concentrate meals without access to roughage are at an increased risk. Performance horses are not the only horses at risk for EGUS, as severe ulceration has been diagnosed in recreational and retired horses in seemingly calm environments. It is important to keep EGUS in mind if a horse is being exposed to potential stresses, particularly those horses that have had EGUS in the past. Recognition of clinical signs with appropriate diagnosis and treatment of EGUS improves attitude, performance, and quality of life for our horses.

Watch this video of a presentation on pigeon fever by Dr. Nora Grenager. (Be sure to turn up your sound!) Related resources you may also be interested in: “Pigeon Fever” by Nora Grenager, VMD, DACVIM and Tim Eastman, DVM, DACVS, MPVM AAEP Infectious Disease Guidelines: Pigeon Fever EDCC (Equine Disease Communication Center)

Watch this video of a presentation on EHM by Dr. Nora Grenager. (Be sure to turn up your sound!) Related resources you may also be interested in: California Department of Food and Agriculture (CDFA): Equine Herpes Myeloencephalopathy (EHM) Fact Sheet California Department of Food and Agriculture (CDFA): Equine Herpes Myeloencephalopathy (EHM) FAQ American Association of Equine Practitioners (AAEP): Equine Herpes Virus Resources American Association of Equine Practitioners (AAEP): Equine Herpes Virus FAQ

In this video, Dr. Danielle Price shows you how to securely wrap a bandage around a horse’s lower leg. (Be sure to turn up your sound!)

Your veterinarian may recommended a foot poultice to treat a sole bruise, foot abscess or other condition. (Note that if your horse is shod, the shoe will need to be removed to place the poultice. Your veterinarian will advise you regarding shoe removal.) Wrapping a bandage around your horse’s hoof to keep the poultice in place can be tricky. In this video, Dr. Jacquelyn Dietrich shows you how to place a foot poultice and securely wrap a bandage around the hoof. (Be sure to turn up your sound!)

About EHV-1 Equine herpesviruses (EHV) are found in the majority of horses. Most horses have been exposed to the virus and have had no clinical signs or side effects. There are nine EHVs that we have been able to identify worldwide, but EHV 1, 3, and 4 are the strains that have caused clinical disease in horses. EHV-1 specifically has multiple manifestations of disease in horses: neurological form, respiratory form, and can cause abortion and neonatal death. There is also some evidence that it may cause chorioretinopathy (a disease process in the eye). Research has shown that greater than 80% of horses may be latently infected with the EHV-1 virus, but not all horses will develop clinical signs. The Science Behind EHM EHV-1 myeloencephalopathy (EHM) is still being studied today and we are constantly acquiring new information. There are multiple reports of theories describing how the virus causes neurological disease. A single point mutation in the DNA polymerase gene has been associated with neurological disease, causing the presence of aspartic acid (D) or asparagine (N) at position 752. AAEP reports that 80-90% of neurological disease cases are caused by D752 isolates, and 10-20% by N752 isolates. Recently, there has also been a proven association with a single nucleotide polymorphism at position 2254 in the DNA polymerase gene and the occurrence of EHM. The virus can become reactivated and furthers cell-associated viremia delivering the virus to endothelial cells in the uterus and central nervous system. Clinical signs occur due to the vasculitis and cellular damage caused by the virus. Infection of Horses Horses are affected through contact with respiratory secretion, aborted fetuses/placentas, or by fomites (infected objects, such as grooming tack). Following infection, a viremia is established as the virus circulates the body in infected cells. Following this, virus-infected cells are latently infected. Horses can shed virus in nasal secretions as early as day 1 of infection, and can continue to shed the virus for approximately 28 days. The virus can cause disease in infected horses or can re-activate from latency causing clinical disease in the horse. The virus can typically survive in the environment for up to 7 days, but this can vary based on the environmental conditions. Signs of EHM The incubation period of EHV is typically 4-6 days, but has the potential to be longer. Some clinical signs associated with the neurological disease may include: Fever Nasal discharge Hindlimb weakness Incoordination Loss of tail tone Lethargy Urine dribbling Head tilt Inability to rise Diagnosing EHM Clinical signs (neurological signs and fever) and isolation of the virus are how we confirm EHM. Isolation of the virus can be done using quantitative polymerase chain reaction (qPCR) from nasal swabs and blood collection. Treating and Preventing EHM After confirming EHM, implementing a strict quarantine and biosecurity measures under supervision of local and state veterinarians is key. Treatment options include anti-inflammatories and supportive care. Vaccination and biosecurity protection are the two ways to help avoid disease outbreak. No current EHV-1 vaccine has a claim to prevent EHM. Some EHV-1 vaccines can reduce nasal shedding and possibly viremia. By vaccinating your horses, you induce a strong immune response to the virus without inducing clinical disease. It is important to clean tack, equipment and the environment to inactivate the virus. Cleaning first with a detergent or soap to allow for removal of organic material (such as soil) is recommended in order to prevent disinfectants becoming inactive when they make contact with organic material. There are multiple effective disinfectants that will kill the virus, including 1:10 dilution of bleach to water. Other key points for understanding EHM prevention include: Immunity following infection or vaccination offers limited protection Boosting (routine vaccination) contributes to herd immunity to help protect individual horses It is difficult for the body to establish immunity due to “evasion” properties of this virus Early recognition and diagnosis is key Quarantine and close monitoring of suspected cases is important Exposed horses should have their temperature taken twice daily Please note that this virus is still being investigated and new research is constantly being release as we try to better understand EHM. Additional resources: AAEP: Equine Herpesvirus Resources California Department of Food and Agriculture: Equine Herpes Virus References: Allen GP. Risk factors for development of neurologic disease after experimental exposure to equine herpesvirus-1 in horses. American Journal of Veterinary Research 69,         1595–600, 2008 Diallo IS, Hewitson G, Wright L, Rodwell BJ, Corney BG. Detection of equine herpesvirus type 1 using a real-time polymerase chain reaction. Journal of Virological Methods          131, 92–8, 2006 Diallo IS, Hewitson G, Wright LL, Kelly MA, Rodwell BJ, Corney BG.            Multiplex real-time PCR for the detection and differentiation of equid herpes- virus 1 (EHV-1)          and equid herpesvirus 4 (EHV-4). Veterinary Microbiology 123, 93–103, 2007 Dunowska M. A review of equid herpesvirus 1 for the veterinary practitioner. Part A: Clinical presentation, diagnosis and treatment. New Zealand Veterinary Journal, 62,         171–78, 2014a Dunowska M. A review of equid herpesvirus 1 for the veterinary practitioner. Part B: Pathogenesis and epidemiology. New Zealand Veterinary Journal, 62, 179– 88, 2014b Equine Herpesvirus (Rhinopneumonitis). (n.d.) Retrieved March 7 2016, from http://www.aaep.org/-i-173.html Goodman LB, Loregian A, Perkins GA, Nugent J, Buckles EL, Mercorelli B, Kydd JH, Palu G, Smith KC, Osterrieder N, Davis-Poynter N. A point mutation in a herpesvirus      polymerase determines neuropathogenicity. PLoS Pathogens 3, e160, 2007 Pusterla, N., & Hussey, G. (2014). Equine Herpesvirus 1 Myeloencephalopathy. Veterinary Clinics of North America: Equine Practice, 30(3), 489-506.

San Mateo County Large Animal Evac (SMLAEG) provides evacuation services and shelter for large/farm animals in the event of disaster, such as wildfire or flood, or in other emergencies. These efforts include the evacuation of animals, caring for the animals in holding areas after evacuation, and facilitating the return of animals to their owner/agent. SMCLAEG is activated by the San Mateo County Office of Emergency Services, or other first responders, and its efforts are staffed by SMCLAEG's core team members and volunteers. SMCLAEG is an all-volunteer 501c3. The group also provides preparedness workshops and site inspections upon request. HOW TO CONTACT SMCLAEG: In an emergency, call 911. Tell dispatch that you need the services of the San Mateo Large Animal Evacuation Group. BE PREPARED! Visit https://smclaeg.org/preparation to learn more... Steinbeck Equine Veterinary Clinics works with SMCLAEG as their primary veterinary contact to advise on planning evacuations and during emergency evacuations. LARGE ANIMAL EVACUATION RESOURCES: • Monterey County • Santa Clara County • Santa Cruz County • San Mateo County

By Nora Grenager, VMD, DACVIM and Tim G. Eastman, DVM, DACVS, MPVM Many horse owners in central California may have heard of “Pigeon Fever” — and if not, now’s the time to learn about it. Although also seen throughout the southern United States, California is particularly well known for having a high incidence of this disease, especially during the late summer and early fall. The more arid parts of our state are hit harder by Pigeon Fever. Some years the prevalence seems to be much higher than others, with almost a cyclic nature. Pigeon Fever is caused by a bacteria called Corynebacterium pseudotuberculosis that can survive for long periods of time in the soil. The bacteria is likely to penetrate the skin through abrasions, small wounds, or enter by fly bites (most common). Once the bacteria has entered the horse, it proliferates in these warm, moist cutaneous environments. Pigeons actually have nothing to do with the disease, but it historically causes abscesses and dramatic swelling in the pectoral region of the horse, making the horse’s chest resemble that of a pigeon. Other names for the condition include “Dryland Distemper,” “Pigeon Breast Fever,” “Dryland Strangles,” and its bacterial name, Corynebacterium pseudotuberculosis. The typical signs of Pigeon Fever include abscesses anywhere along the ventral midline (i.e., especially where flies bite!) including the chest, sheath/mammary glands, or in small chains along the lymphatic channel of a leg. However, abscesses can develop anywhere on the horse (see facial abscess image). Large plaques of ventral edema are also frequently present adjacent to the abscesses (ventral edema causes sponge-like swelling on the underbelly of horses)(see edema image). Pigeon fever abscesses usually take several weeks to mature, open, and drain, but rarely the infection may be long-lasting and recurrent for over a year. Pigeon Fever should be considered at the top of the differential list in any horse that has a swelling or abscess in a typical location. The diagnosis can be confirmed by culturing fluid taken from an abscess and growing the bacteria in the lab. Uncommonly, C. pseudotuberculosis can instead cause an internal abscess (less than 3% of all cases). Horses with internal abscesses present with fever, weight loss, depression, and sometimes lameness. If a veterinarian suspects an internal abscess, there is also an antibody blood test that can be performed to help rule in or rule out the disease. This blood test is performed at the University of California at Davis and is very affordable. Treatment of Pigeon Fever can vary depending on the severity and the body system(s) involved. Draining the abscess is the mainstay of treatment (see drainage image) but should not be performed until the abscess is mature. If done prematurely, drainage can be painful and the abscess is more likely to recur. The maturity of an abscess can be assessed by palpation (they generally get soft in the middle when they are mature) and/or by ultrasound. Ultrasound is also helpful in determining if there are multiple pockets of fluid and in identifying deep abscesses. Once opened, the abscess cavity should remain open and it should be flushed daily with an antiseptic solution like povidone-iodine or chlorhexidine. Most horses will be completely over the disease within 3 weeks of the abscess being drained. Again, rare horses will have recurrent abscesses. Use of antibiotics is controversial in horses with Pigeon Fever. Many veterinarians recommend against administering antibiotics for external abscesses because of the potential to delay abscess maturation. However, in cases involving internal abscesses, those involving the lymph channels of a leg (“lymphangitis”), or with very deep abscesses that are difficult to drain and are causing the horse extreme discomfort, long-term antibiotics are generally prescribed. While horses affected with external abscesses have an excellent prognosis, internal abscesses have a more guarded prognosis. Once a Pigeon Fever abscess matures and the condition resolves, over 90% of horses will remain immune to the disease in the future. In those rare instances where the disease recurs, it is unknown whether recurrence is due to re-infection or relapse of the original disease. It is possible it is more likely to recur, or even occur in the first place, in horses with somewhat compromised immune systems. Prevention is centered on good sanitation practices and fly control. Quarantine of affected individuals is not generally recommended due to the long distances that insects carrying the bacteria can travel. A vaccine has recently become available from Boehringer-Ingelheim and may be advisable in naive horses at high-risk for disease. The use of this vaccine should be a discussion between each owner and his/her veterinarian. Related resources: Pigeon Fever Presentation Video by Dr. Nora Grenager

Published by the American Association of Equine Practitioners (AAEP) When an emergency or natural disaster occurs, it is always in the best interest of the horses for both the equine practitioner and the horse owner to be prepared. Foreign animal disease outbreaks or other catastrophic events can adversely affect the health and well-being of horses. Preparation is a key part of making sure your horses are safe and taken care of in a crisis situation. One must understand who the other resources are and what their plan is in order for a coordinated response to result. The American Association of Equine Practitioners (AAEP) has collected helpful links to make sure you, the horse owner, have vital information available before a disaster strikes. Learn more...

The Equine Disease Communication Center (EDCC) is an industry-driven initiative which works to protect horses and the horse industry from the threat of infectious diseases in North America. The communication system is designed to seek and report real time information about diseases similar to how the Centers for Disease Control and Prevention (CDC) alerts the human population about diseases in people.