Date: [__date__]

Dear [__name__];

Welcome to the August edition of our montly newsletter. This month we take the opportunity to discuss some of the current hot topics in the veterinary world including Hendra virus, new drug withhold times and equine gastric ulcers. We hope you find this edition of our newsletter useful and informative. Please do not hesitate to contact our office if you have any further questions about this months topics.

Hendra Virus

This week Hendra virus was confirmed on a property at Cawarral, about 20km from Rockhampton after the death of a horse on 8 August. Hendra virus was first isolated in 1994 after 13 horses died as a result of infection with the previously unknown disease. During this outbreak two people who had close contact with these horses became infected with the disease and one of these cases was fatal. Since then there have been sporadic outbreaks of disease that have resulted in the deaths of both horses and people. In light of this weeks developments, we thought it was timely to provide our clients with the current information available about Hendra virus.

Fruit bats (Pteropus spp.), commonly known as flying foxes, are the natural host of Hendra virus. Antibodies to Hendra virus have been isolated in all four species of fruit bats occurring in Australia. Since the first outbreak in 1994, more than 30 cases of Hendra virus in horses have been detected on or east of the Great Dividing Range from Cairns to northern New South Wales. However, because antibodies to Hendra virus have been detected in fruit bats in all parts of Australia, Hendra virus could potentially occur wherever there are fruit bats.

Spillover events from fruit bats to horses are rare and have only happened in paddock situations where fruit bats are present. Research has shown that horses, humans, cats and guinea pigs can become infected with Hendra virus. However, to date natural infections have only been reported in horses and humans. Our current understanding is that infection is from bat to horse, from horse to horse and from horse to human. To date, there is no evidence to suggest that human to human or human to horse transmission occurs.

It is suspected that spillover events are associated with pregnancy and lactation in fruit bats and Hendra virus has been identified in the placenta and foetal tissues of experimentally infected fruit bats. Horses are infected via the nasal/oral route. In a stable environment, Hendra virus has the potential to spread from horse to horse through direct contact with infectious body fluids or through indirect contact with contaminated items such as water buckets and feed bins. Human infections have occurred after close contact with blood and other body fluids (especially respiratory secretions, saliva and urine).

Infection with Hendra virus results in the acute onset of disease, fever, respiratory and/or neurological signs with a rapid progression to death, usually within 48 hours. The reported mortality rate in affected horses is in excess of 70%. This clinical presentation, in conjunction with proximity to fruit bats is highly suggestive of Hendra virus infection, however, a lack of fruit bat sightings should not preclude suspicion of Hendra virus infection in these types of cases.

In relation to the risk posed by Hendra virus to Victorian horse owners, our advice is to be aware but not alarmed. We advise isolating horses arriving from Queensland and northern New South Wales from other horses for a period of 48 hours. Take the rectal temperature of these horses twice daily and telephone our office if a high temperature is detected.

Our practice has adopted a policy of wearing personal protective equipment (latex gloves, overalls, face masks) when examining horses with acute onset of fever and severe respiratory or neurological signs, especially if fruit bats have been sighted on the property. In this situation, we will provide our clients with personal protective equipment and help them implement appropriate biosecurity procedures until any risk posed to humans and horses has been properly assessed.

Solu-Cortef - New Withholding Period

New advice has been provided to Equine Veterinarians Australia by Dr John Vine, the Laboratory Director of Racing Analytical Services Ltd. Dr Vine advises that hydrocortisone-hemisuccinate (Solu-Cortef) can be detected in both equine blood and urine. Dr Vine advises against using this substance within 48 hours of competition.

Cyproheptadine - Recent Show Horse Positive Swab

A positive swab to Cyproheptadine (Periactin) has recently resulted in the disqualification of a horse from the EFA RT Edgar Victorian Show Horse State Titles held in October 2008. Cyproheptadine is a human antihistamine and is not registered for use in horses. Cyproheptadine is a prohibited substance under the current FEI Equine Prohibited List. Our practice does not recommend the use of this drug in competition horses under any circumstances.

Equine Gastric Ulcers

Equine gastric ulceration is currently a hot topic amongst horse owners, so we decided to use this issue of our newsletter to provide our clients with a detailed review of the current knowledge available to veterinarians about this syndrome.

Equine gastric ulcer syndrome is a disease complex in horses that is associated with damage to the lining of the oesophagus, stomach and duodenum. Clinical signs are often non-specific and include lack of appetite, weight loss/poor body condition, acute and recurrent colic, loose feces, poor performance and changes in attitude. The non-specific nature of the clinical signs associated with gastric ulceration often leads owners and veterinarians to suspect gastric ulceration as a cause of poor condition and poor performance in horses.

So, why are horses so susceptible to gastric ulcers? The anatomy and physiology of the equine stomach gives us some clues. The equine stomach is divided into two parts, a squamous part (closest to the oesophagus) and a glandular part (closest to the duodenum). Most gastric ulcers occur in the squamous part of the stomach where there are very few defence mechanisms against increased gastric acidity. Gastric acidity is determined by the acidity of the stomach contents, which are a mixture of salivary, gastric, duodenal, biliary and pancreatic secretions.

Saliva plays an important role in decreasing the acidity of the stomach contents and it is thought that low roughage diets may decrease the production of saliva and increase the acidity of the stomach. The horse is also a continuous secretor of gastric acid. This means that acid secretion occurs even without the presence of feed material in the stomach. When horses are stabled for long periods of time and have no access to pasture, they spend less time eating, even when provided with feed ad libitum. It is likely that this decreases the amount of saliva produced and increases the acidity within the stomach.

High grain diets can also play a role in gastric ulceration. Many grains contain high concentrations of fermentable carbohydrates that are converted by bacteria in the stomach to volatile fatty acids. Volatile fatty acids can cause cellular swelling, inflammation and result in gastric ulceration. Concentrations of volatile fatty acids in the stomach are highest 2-6 hours after feeding and decrease as food moves out of the stomach. However, the negative effects of volatile fatty acids can be reduced by feeding grain in conjunction with lucerne hay. Lucerne hay is high in protein and calcium which both help to decrease gastric acidity for up to 6 hours after ingestion.

Other risk factors for gastric ulceration include stress, transport, intermittent feeding, non-steroidal anti-inflammatory drugs, intense exercise and racing. Indeed, one study showed that up to 90% of racehorses in training develop gastric ulcers by the time they have been in work three months! In comparison, the prevalence of gastric ulcers in show and riding school horses is lower with one study demonstrating 23/62 (37%) of these types of horses having endoscopic evidence of lesions. The prevalence of lesions in show horses was shown in another study to increse to 13/23 (56%) after three consecutive days of travel and competition.

In many horses, a presumptive diagnosis of ulcers is often based on clinical signs. Due to the number of studies demonstrating a high prevalence of gastric ulceration in racehorses, preventative therapy for gastric ulcers in racehorses is easily justified and often recommended by our practice. In show, pleasure and performance horses our recommendations often vary on a case by case basis.

Definitive diagnosis of equine gastric ulcers is based upon endoscopic examination of the stomach with a 3m gastroendoscope. At the present time, our practice refers cases to the University of Melbourne Equine Hospital at Werribee for gastroscopy. It is necessary to withhold food for 6-12 hours before the examination. The horse is sedated, twitched and the gastroscope is passed up the nostril, down the oesophagus and into the stomach. The stomach is insufflated with air to allow visualisation of the entire lining. Any lesions are then assessed based on their location and severity and a treatment plan is formulated bearing this information in mind.

The two main drugs we use to treat equine gastric ulcers are histamine H2 receptor antagonists and proton pump inhibitors.

Histamine H2 Receptor Antagonists

These drugs act primarily to inhibit gastric acid secretion. They act in a dose dependent manner and need to be administered at least twice daily. Ranitidine (Ulcerguard) is the most potent H2 receptor antagonist available for use in horses. Studies published in the veterinary literature have been able to demonstrate the prevention of ulcers in adult horses with ranitidine administration. However, there does not appear to be convincing evidence to support ranitidine as an effective treatment for existing gastric ulceration. In light of this, our practice prefers to use ranitidine for prevention, rather than treatment of gastric ulcers.

Proton Pump Inhibitors

These drugs are potent and highly specific inhibitors of gastric acid secretion. They act to inhibit an enzyme that is necessary for the last step in the acid secretory pathway. Omeprazole (Gastrozol, Omoguard) is the proton pump inhibitor available for use in horses. Omeprazole has prolonged antisecretory effects and this allows for once daily dosing. A recent study has shown that treatment with omeprazole at 4mg/kg once daily for 28 days results in a significant improvement in the appearance of gastric ulcers in 92% of treated horses. Other studes have shown that after the initial course of omeprazole, a lower daily dose of omeprazole can be used to prevent the recurrence of ulcers in most horses in training. Our practice routinely uses omeprazole for the treatment of equine gastric ulcers.

We hope you have enjoyed the August edition of our newsletter. Please do not hesitate to contact our office if you have any questions in relation to the above topics. We welcome suggestions for future newsletter topics, so please don't hesitate to send us an email if you have any requests!

Kind Regards,

Tweedie & Associates Equine Veterinary Services.