“JUVENILE medicine” was the theme of a morning session at the BEVA congress in September. The first paper, “Lawsonia intracellularis: managing the individual case and its herdmates” was given by Cormac Feeney of Troytown Grey Abbey Equine Hospital in Kildare.
Lawsonia is an intracellular bacterium that can survive for two weeks in the environment. It is best known as a pig pathogen but it causes equine proliferative enteropathy (EPE) in the horse.
Lawsonia intracellularis was first described in 1982 and by 1986 it was being recovered from individual cases and outbreaks of EPE. It was first diagnosed in Ireland in 2006. It spreads by the faecal-oral route and has reservoirs in wildlife: deer, rabbits, mice, rats and birds.
Cormac has encountered the disease among thoroughbreds between weaning and one year old and considers it as an emerging problem. The first case to present usually dies in spite of intervention.
The disease occurs seasonally on stud farms, typically between August and February, but the risk time varies between farms, so the timing of vaccination can be adjusted to get the first dose given a month before the outbreak is expected and the next a month later, tailored to the known disease pattern on each farm.
Clinical signs can be non-specific: the animal may be a poor doer or it may present with colic, scour and inappetence. This can be complicated by concurrent problems such as parasites or gastric ulcers.
Diagnosis is by clinical signs, complete blood cell counts (these are usually non-specific), blood biochemistry, PCR on faeces, abdominal ultrasonography and serum immunoperoxidase monolayer assay (IPMA) to detect anti-L. intracellularis antibodies.
In a typical case, ultrasonography shows a “cartwheel” appearance of the intestines. Serum IPMA is a good indicator of exposure to the bacteria and low serum albumen levels are the best way of identifying clinical cases.
Bacterial DNA is detectable in faeces with active shedding 12 to 18 days post-challenge. This lasts about 18 to 21 days with the maximum lesion occurring at 21 days. PCR can be negative outside its specific time-frame and the horse may still need antibiotic treatment. If the intestine undergoes the acute necrotising form of infection, the animal will die; survival is determined by intestinal functionality.
Treatment consists of doxycycline 10mg per kg bodyweight given twice daily orally for two weeks or longer if necessary. Most cases can be managed on the farm but animals that are weak, in pain or not eating need hospitalisation. There are no records of spontaneous recovery in clinical cases.
Hospitalised animals receive the full range of supportive treatment: fluids, colloids, anti-inflammatories, plasma transfusion, anabolics and anti-ulcer drugs, parenteral nutrients and nasogastric caloric support. Treatment is labour-intensive and prolonged and it is difficult to predict the outcome. Animals that continue to graze have a good prognosis. Overall, the survival rate is 93%.
On a happier note, per-rectal vaccination using a commercial avirulent porcine vaccine, which is off-licence, has given complete protection for the herdmates of a case diagnosed with EPE. Sick animals were not vaccinated but they were treated with antibiotics.
Cormac considers that EPE is an active threat to the weanling population; he is seeing more cases each year. M. L. Frazer’s study1 observed that weanlings sold for 68% of their expected value though they made up for it when racing, having no loss of earnings.
Ian Cameron, who practices with Rossdale and Partners of Newmarket, took up the theme of ill thrift and difficult diagnosis in young stock with his paper on “Ascarids: a re-emerging threat”.
Many paddocks that are used for young foals are heavily contaminated with ascarids (Parascaris equorum) and the problem is compounded by the fact that ascarids are great survivors, eggs on the ground are resistant to decay and larvae and adults inside the horse are increasingly resistant to anthelmintics.
Ascarids have a complex life-cycle which goes more quickly in warm weather. Adults are prolific egg layers (each one produces many thousand eggs each day) and these eggs survive on pasture for many years; infestation from stables is less important.
It takes around 60 to 70 days for the ingested ascarid egg to develop into an egg-laying adult. By18 months of age the horse develops an effective immune response to the parasite.
The infested foal can present with symptoms which range from ill thrift, rough hair coat, a pot belly or nasal discharge through to colic, peritonitis and even sudden death.
Ultrasound images can be vague, worm egg counts will be negative for the first two months after infestation and antibiotics will have no effect.
The eggs swallowed from the pasture hatch into larvae which migrate into the intestinal wall and travel through the veins to heart, liver and lungs and are coughed up and swallowed to grow to egg-laying maturity in the intestine.
If the foal is very heavily infested, the gut can be perforated by the adult ascarids leading to fatal peritonitis; or if anthelmintic is used, the mass of dead worms can block the intestine: this calls for exploratory laparotomy and, possibly, euthanasia.
Foals infested with ascarids have reduced immunity; they may have ringworm (when the mares do not) or concurrent infection with Lawsonia, rotavirus or rhodococcus.
Faecal worm egg counts (WEC) provide the information which is the foundation for designing a control strategy, even though they are only useful in foals over two months of age. They can be done in-house on stud farms and should be done every one to two months on every individual over four months.
WECs allow appreciation of the pattern of pasture contamination, so that vulnerable young foals can be kept on the cleanest pasture.
Also, WECs used in conjunction with anthelmintic treatment help to reduce anthelmintic use and determine which treatments are effective. In the face of ever-increasing resistance to anthelmintics, such strategy is imperative.
Regular removal of faeces from paddocks, at least twice weekly, is essential. At-risk foals need regular worming from eight weeks old to four months.
Ascarids have become resistant to ivermectins though moxidectin appears to be working but it is not licensed for foals under four months, due to potential neurotoxic effects.
A possible scheme for young foals is to do a WEC followed by treatment with fenbendazole at eight weeks, another WEC followed by treatment with pyrantel at 12 weeks and WEC followed by treatment with moxidectin at four months.
As new wormers are absent, good pasture management based on WEC information with strategic use of our existing wormers is the only way to control the ascarid problem.
1. Frazer, M. L. (2008) Lawsonia intracellularis infection in horses: 2005-2008. J Vet Intern Med 22: 1,243-1,248.