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The AAEP Vaccination Guidelines are intended to be a reference for veterinarians who utilize vaccines in their respective practices. They are neither regulations nor directives and should not be interpreted as such. It is the responsibility of attending veterinarians, through an appropriate veterinarian-client-patient relationship, to utilize relevant information coupled with product availability to determine optimal health care programs for their patients. Based on the professional judgment of those involved with the development of these guidelines, the recommendations for vaccine administration in this document may differ from the manufacturer’s recommendation. However, it is incumbent on each individual practitioner to reach a decision on vaccine usage based on the circumstances of each unique situation and his or her professional experience. Information provided in these guidelines addresses only those products licensed by the United States Department of Agriculture (USDA) for use in horses (including draft and pony breeds). There are limited data regarding the use of vaccines in other equidae (i.e. asses, donkeys, mules, miniature horses, and zebra); vaccination of these animals is at the discretion of the attending veterinarian.

By Matt Durham, DVM, DACVSMR Published in Bay Area Equestrian Network February 2007 In the scenic foothills of the Central Coast of California, there lurks a quiet problem that can lead to severe disease in our horses. Commonly known as ‘chalk rock’, this dusty rock form can cause an irreversible lung condition known as silicosis. Silicosis is a well known occupational disease in humans, typically caused by inhaling rock dust created in mining, masonry work, sandblasting, and many other industries where rock is crushed into an easily-inhaled dust. In horses, the disease was first diagnosed in the late 1970s in the Monterey-Carmel area. Before this time, area veterinarians had noted signs of respiratory disease, but had been unsure of its cause. For years, silicosis in horses was believed to be isolated to this small region. But as awareness of the disease increased, cases started to be diagnosed in other parts of the state. What Causes Silicosis? Briefly, silicosis is caused by inhaling silica dust small enough to travel all the way into the smallest airways and air sacs in the lung. Some sources incompletely describe silicosis as a lung disease caused by inhaling quartz dust. As will be discussed in the section titled Silicates, other crystal forms of silica can also cause silicosis. Once the dust particles become lodged in the lung, the body mounts a strong immune reaction. While bacteria or pollen can be broken down and removed from the lung, silicates can not. This causes an ongoing process which can lead to scarring of the lung, and, in people, certain auto-immune disorders. History In humans, silicosis is a fairly well understood but frustrating disease. As an occupational disease, silicosis may have been recognized by ancient Egyptians, and was described well by Agricola in 1556.Even now, there is no cure. Occupational safety measures have dramatically decreased the incidence of the disease, but cases still occur. The most notorious occupational incident occurred in the early 1930s when at least 700 workers died from silicosis. Workers came from all around to tunnel through a mountain in Gauley Bridge West Virginia, eager for any type of work during the Great Depression. The tunnel was to be used to carry water for a new hydroelectric plant. Although it was well understood at the time that silicosis was a risk if dry-drilling was used, the contractors chose this method over the much safer, but slower, wet-drilling technique. Silicates Silicates are crystalline forms of the element silica. By far the most widespread crystal of silicate is quartz, which is present in most rock types. The form which causes silicosis in horses is cristobalite. Cristobalite causes a more severe reaction in the lung than quartz does. This crystal is present in abundance in the Monterey/Carmel Valley areas. Geologists refer to this particular deposit of rock as the Monterey Formation. Although this rock type is common in this region, it is present from Point Reyes to San Onofre in the coastal ranges, with outcroppings in the San Joaquin valley, and as far south as Baja California. The Monterey Formation developed in shallow seabeds during the Miocene epoch (between 5 and 20 million years ago) from deposits of microorganisms known as diatoms. Diatoms have a non-crystalline form of silica in their structure which, over millions of years, becomes compressed into crystalline forms. Initially, the crystal formed is cristobalite, but with more time, quartz can be formed. Many of the soils of the Monterey Formation have high levels of cristobalite. These soils are often referred to as ‘chalk rock’ locally, as they tend to be dusty and light. (True chalk is actually limestone, which contains no silica.) Geologists refer to some of the various subsets of the Monterey Formation as porcelanite, chert, siliceous mudstone, and siliceous shale. For the rest of this article, the term siliceous soils will be used. Cristobalite can also be formed through volcanic activity. The Sonoma volcanic soils are a likely source of the cristobalite responsible for silicosis in horses from this region. Exposure Areas with siliceous soils are typically in foothill areas. Often, cases are seen not long after recent construction has disrupted the soil, creating a dusty environment. The horses inhale the dust over days to months or even years. Depending on a variety of factors, affected horses may show no signs or could develop severe respiratory compromise. Rate of exposure and individual immune response probably play the biggest roles in terms of severity of signs. Clinical Signs Affected horses will sometimes develop a cough, an elevated respiratory rate (normal resting rate for a horse is typically around 8-16 breaths per minute), flared nostrils at rest, and/or exercise intolerance. It is very important to remember that these signs are typical of respiratory compromise in general, so are not specific for silicosis. Diagnostics Lung x-rays are the simplest test to perform to diagnose silicosis. Abnormal x-rays exhibit classical signs for silicosis in advanced cases. Early or mild cases may have subtle, non-specific lung x-ray findings. Lung x-ray of a horse, showing severe lung fibrosis from silicosis (normal lung is nearly black on x-rays) Samples of fluid and cells from the lungs can be obtained in two ways: a transtracheal wash, or a bronchoalveolar lavage (BAL). Affected horses may exhibit pink crystals within a type of white blood cell called a macrophage. The crystals are silicate crystals, and the macrophages are the cells that attempt to destroy or remove the particles. At Steinbeck Country Equine Clinic, we typically choose the BAL technique for this diagnosis. Ultrasound is occasionally useful in imaging silicosis cases, particularly with advanced cases. Most silicosis changes are deep within the lung, and the ultrasound beam does not penetrate through the air present within the lung, so less advanced cases do not show up well. Treatment In horses, as in humans, there is no cure for silicosis. Treatment involves removing the horse from the silicate dust as well as from other types of dusty or moldy environments. In mild to moderate cases, short courses of steroids and bronchodilators can get a horse through a flare-up. Affected horses may not be able to regulate their temperature, so it is important during hot weather to provide shade, or other means to create a cool environment. Silicate Associated Osteoporosis In horses living on siliceous soils, certain bone deformities and fractures can develop. Horses with silicate associated osteoporosis can develop signs years after moving away from an area with siliceous soils. This disease typically occurs in horses with a longer-term exposure to silicate dust. The bones develop osteoporosis which, as in people, can predispose to fractures. Horses typically develop bowed shoulders, a swayed back, and often a stiff neck secondary to osteoporosis and secondary arthritis in the cervical spine, although early cases have no obvious outward signs. Horse with silicate associated osteoporosis, showing swayed back and bowing of the shoulder blades. Footing material is siliceous shale. [Image courtesy Dr. Coral Armstrong] Body soreness and exercise intolerance are common in horses with silicate associated osteoporosis, and some horses may develop neurologic signs. Fractures are most common in the spine, ribs, pelvis and shoulder blades. Affected horses may or may not have respiratory signs, but will typically have some degree of respiratory involvement. Diagnosis of silicate associated osteoporosis is simple in advanced cases, where outward signs alone are diagnostic. In mildly affected horses, diagnosis is challenging, because vague lameness or stiffness may be the only signs (as can be seen in countless other disease processes). In these cases, nuclear scintigraphy (bone scan) is very sensitive at detecting the disease. Ultrasound of the shoulder blades and x-ray images of the neck can help define the disease as signs progress, but will often be normal in early cases. Treatment for silicate associated osteoporosis with typical anti-inflammatories such as phenylbutazone is often minimally effective. Sometimes steroids will improve the comfort level, but not always. Intravenous Legend® can help with the arthritis pain in the neck that commonly develops, but does not help with bone pain. Tildren® may help decrease bone pain and possibly stop the progression of osteoporosis. Tildren® is in the same family of drugs as Actonel®, Fosamax®, and Boniva®, which are used to treat osteoporosis in people. Recently, zoledronate (Zometa® or Reclast®) has been used experimentally at UC Davis, with promising results. Prevention of Silicosis Prevention of silicosis requires limiting the amount of inhaled silicate dust. Areas of new construction should be avoided. Dry lot situations should be altered as much as is possible. The ideal solution is to plant grass over the area and irrigate throughout the summer months, but this is often very impractical. Incorporating organic material into the soil can help to retain moisture and minimize dustiness. Wood chips or composted manure are fairly effective and inexpensive methods. Topsoil brought in from an unaffected area may also be effective. Future Directions in Silicosis Study Control of the excessive immune response is the primary direction of research in the human field. In horses, the primary areas of study involve silicate associated osteoporosis. We are currently working in conjunction with researchers at UC Davis on studies to determine the exact nature of the bone disease. Currently, Dr. Murray is studying two blood tests, which appear to be promising in detecting the disease process. With earlier detection and monitoring of bone density, we hope to be able to prevent the catastrophic fractures and other bone-related pain.

By Richard A.Mansmann, Sarah James, Anthony T.Blikslager, Kurtvom Orde Published in the Journal of Equine Veterinary Science (Purchase access to read the complete article) Abstract This study deals with the relationship between long toes in the hind feet and pain in the gluteal region in horses, and the remedial value of trimming/shoeing that moves the breakover point back at the toe. 77 client-owned horses were studied, 67 shod riding horses retrospectively and 10 barefoot broodmares prospectively. The 10 mares were evaluated twice, and 24 of the 67 riding horses were re-evaluated at the next shoeing, for a total of 111 observations. Each horse underwent gluteal palpation and lateral radiographs of both hind feet. Toe length was quantified as breakover distance (BD), the horizontal distance between the tip of the third phalanx and the dorsalmost point at which the wall/shoe was in contact with the ground. The BD was then shortened with trimming +/− shoeing to a length of ≤15mm (shod horses) or ≤20 mm (barefoot horses). The 24 riding horses were re-evaluated 4-6 weeks later and the 10 broodmares 1 week after trimming. The results showed that of the 67 riding horses, 75% were positive for gluteal pain at initial evaluation. The mean BD for the positive and negative horses was 24.2 ± 1.3 mm and 18.8 ± 2.0 mm, respectively (p = 0.04). At the next shoeing, the mean BD was 10.9 ± 2.3 mm and gluteal pain was improved in all 24 horses; 20 horses (83%) were negative and 4 horses (17%) were now only mildly positive. The 10 broodmares were all positive for gluteal pain initially. The mean BD before and after trimming was 23.7 ± 1.2 mm and 10.9 ± 1.1 mm, respectively. One week later, gluteal pain was improved in all 10 mares; 8 mares (80%) were negative, and the other 2 mares (20%) were only mildly positive. The conclusion is that excessive toe length in the hind feet may be accompanied by pain in the gluteal region and, in our experience, may be associated with gait or performance problems. Shortening the toe can alleviate this pain within days or weeks. Aiming for a BD of between 0 and 20 mm probably is appropriate for the average-size horse.

By Verena K. Affolter, Dominic Dawson, Keita Iyori, Koji Nishifuji, Thierry Olivry, Catherine A. Outerbridge, Anna C. Renier, Yu Hsuan Wang, Stephen D. White, and Laramie D. Winfield Published in the Equine Veterinary Journal (Purchase access to read the complete article) Abstract Hypothesis/Objectives: To describe the clinical, histological and immunological findings of an equine case of pemphigus vulgaris, including the demonstration of antidesmoglein (anti-Dsg) autoantibodies. Case Report: The diagnosis of pemphigus vulgaris was confirmed in a 9-year-old Welsh pony stallion with both direct and indirect immunofluorescence and immunoprecipitation studies, the latter identifying circulating anti-Dsg3 IgG. Treatment with immunosuppressive medications was initiated. Lesions were seen in the perineal area, sheath, mane, tail, eyelids, coronary bands and mucosa of the mouth and oesophagus. Initial corticosteroid treatment improved the clinical signs, but the onset of laminitis necessitated a reduction in dosage, which was associated with a recurrence of lesions and development of oral ulcers. A corneal ulcer developed after 60 days of treatment. Despite treatment with azathioprine, gold salts and dapsone, the disease progressed and the pony was euthanized. Postmortem examination showed additional lesions of the cardia of the stomach. Conclusions and Clinical Importance: Pemphigus vulgaris is rarely diagnosed in equids. We describe a case that was substantiated by the demonstration of anti-Dsg3 IgG. Response to treatment was poor, with the best response to high doses of prednisolone. Equine pemphigus vulgaris is likely to carry a poor prognosis and if there is no response to treatment, humane euthanasia is warranted.

By M. Aleman, P. H. Kass, J. E. Madigan, K. G. Magdesian, N. Pusterla, and L. S. Winfield Published in the Equine Veterinary Journal (Purchase access to read the complete article) Abstract Summary: Reasons for performing study There are currently few data available on the prognosis and outcome of recumbent horses. Objectives: To investigate the outcome of hospitalised horses that had been recumbent in the field or hospital and factors affecting their survival within the first 3 days of hospitalisation and survival after 3 days to hospital discharge. Study Design: Retrospective analysis of clinical records. Methods: Records of 148 horses admitted to the William R. Pritchard Veterinary Medical Teaching Hospital, University of California Davis from January 1995 to December 2010 with a history of recumbency or horses that became recumbent while hospitalised were evaluated. Exact logistic regression was used to assess the association between clinical parameters and survival within the first 3 days of hospitalisation and survival to hospital discharge after 3 days. Results: There were 109 nonsurvivors and 39 survivors. Multivariate analysis showed variables associated with an increased odds of death within the first 3 days of hospitalisation included duration of clinical signs prior to presentation, with horses showing clinical signs for over 24 h having increased odds of death (P = 0.043, odds ratio [OR] 4.16, 95% confidence interval [95% CI] 1.04–16.59), the presence of band neutrophils (P = 0.02, OR 7.94, 95% CI 1.39–45.46), the horse not using the sling (P = 0.031, OR 4.22, 95% confidence interval 1.14–15.68) and horses that were unable to stand after treatment (P<0.0001, OR 231.15, 95% CI 22.82–2341.33). Increasing cost was associated with lower odds of death (P = 0.017, OR 0.96, for each additional $100 billed, 95% CI 0.93–0.99). Conclusions: This study demonstrates that the duration of clinical signs, response to treatment and the ability of horses to use a sling are associated with survival to hospital discharge for recumbent horses.

Hemorrhage and blood loss–induced anemia associated with an acquired coagulation factor VIII inhibitor in a Thoroughbred mare By Laramie S. Winfield, DVM and Marjory B. Brooks, DVM Published in the Journal of the American Veterinary Medical Association (Purchase access to read the complete article) Abstract Case Description: A 23-year-old Thoroughbred mare was evaluated because of a coagulopathy causing hemoperitoneum, hematomas, and signs of blood loss–induced anemia. Clinical Findings: The mare had tachycardia, pallor, hypoperfusion, and a large mass in the right flank. The mass was further characterized ultrasonographically as an extensive hematoma in the body wall with associated hemoabdomen. Coagulation testing revealed persistent, specific prolongation of the activated partial thromboplastin time (> 100 seconds; reference interval, 24 to 44 seconds) attributable to severe factor VIII deficiency (12%; reference interval, 50% to 200%). On the basis of the horse’s age, lack of previous signs of a bleeding diathesis, and subsequent quantification of plasma factor VIII inhibitory activity (Bethesda assay titer, 2.7 Bethesda units/mL), acquired hemophilia A was diagnosed. The medical history did not reveal risk factors or underlying diseases; thus, the development of inhibitory antibodies against factor VIII was considered to be idiopathic. Treatment and Outcome: The mare was treated with 2 transfusions of fresh whole blood and fresh-frozen plasma. Immunosuppressive treatment consisting of dexamethasone and azathioprine was initiated. Factor VIII deficiency and signs of coagulopathy resolved, and the inhibitory antibody titer decreased. The mare remained healthy with no relapse for at least 1 year after treatment. Conclusions and Clinical Relevance: Horses may develop inhibitory antibodies against factor VIII that cause acquired hemophilia A. A treatment strategy combining transfusions of whole blood and fresh-frozen plasma and administration of immunosuppressive agents was effective and induced sustained remission for at least 1 year in the mare described here.

By Monica Aleman, Danika L. Bannasch, Carrie J. Finno, Steven R. Hollingsworth, John E. Madigan, Ron Ofri, and Laramie Winfield Published in the Equine Veterinary Journal (Purchase access to read the complete article) Abstract Objective: Neuroaxonal dystrophy (NAD) is a disease characterized by the sudden onset of neurologic signs in horses ranging from 4 to 36 months of age. Equine degenerative myeloencephalopathy (EDM), a disease that has been associated with low vitamin E concentrations, is considered a more advanced form of NAD. The objective of this report is to describe the electrophysiological features of NAD/EDM in American Quarter horses (QHs). Horses: Six NAD/EDM-affected QHs and six unaffected QHs were evaluated by ophthalmic examination and electroretinography. Five of the NAD/EDM-affected QH and five unaffected QHs were also evaluated by electroencephalography (EEG). Results: Ophthalmic examination, ERGs, and EEGs were unremarkable in NAD/EDM cases. Conclusions: Neuroaxonal dystrophy/EDM does not appear to cause clinical signs of ocular disease or functional ERG/EEG deficits in QHs.

Long-term Outcome of Standing Medial Patellar Ligament Splitting to Manage Horses Exhibiting Delayed Patellar Release: 64 Horses By Sarah J. James, Timothy G. Eastman, and Justin D. McCormick Published in the Journal of Equine Veterinary Science (Purchase access to read the complete article) Abstract A standing surgical technique for splitting the medial patellar ligament is described, and the long-term (average 4.5-years) efficacy of the procedure in horses exhibiting delayed patellar release is reported. Medical records of 64 horses that underwent a standing medial patellar ligament splitting surgery performed to treat delayed patellar release were analyzed retrospectively. Horses were sedated in standing stocks. A number 15 scalpel blade was used to percutaneously split the medial patellar ligament from just proximal to its insertion on the tibial tuberosity to its attachment on the parapatellar fibrocartilage, with the goal of inducing a localized desmitis and subsequent thickening of the ligament. Aftercare consisted of oral antibiotics, 14 days stall rest with hand walking, light exercise for 14 days, and full work at 4 weeks. Follow-up information was obtained through telephone calls to owners and/or clinical evaluation by a veterinarian. Results showed that 89% of horses benefitted from the procedure, with complete resolution in 58% of horses and improvement in 31% of horses. A total of 73% of horses were able to perform at the desired level following the procedure; 63% of horses showed signs of improvement or resolution within 30 to 60 days. Two horses had complications following the procedure: 1 horse had an incisional infection, and 1 had a medial patellar ligament rupture. This study shows that standing medial patellar ligament splitting is a successful, long-term surgical option for treatment of delayed patellar release. The procedure has few complications and allows rapid return to desired performance.