Parasite Burdens In Stabled Horses
In article in the International Journal of Applied Research in Veterinary Medicine looked at the small strongyle parasite burdens in stalled vs. pastured horses with some surprising findings.
The stabled horses studied were adults, dewormed with fenbendazole up to age 1, primarily ivermectin between ages of 1 and 2, and an every two-month rotational deworming program after that, using ivermectin, fenbendazole and pyrantel pamoate. The only pasture access was a small grass paddock, for one hour at a time, about three times a month in the summer.
Three more farms were studied where horses were on year-round turnout with dewormings every two to three months, rotating between ivermectin, fenbendazole and pyrantel pamoate. A few horses also received pyrantel tartrate. The fifth farm dewormed less frequently and horses were under relatively crowded conditions.
As you might expect, the fifth farm had the highest fecal egg counts. However, the counts in the stabled horses weren’t far behind and were significantly higher than those found in horses on the other three farms with year-round pasture turnout and a similar, or less frequent, deworming schedule.
One theory was that the horses had been infected during their brief times on grass, with larvae then becoming dormant until a deworming removed adults from the intestine and triggered the dormant stages to mature. However, parasite eggs can find enough moisture in stalls, from water spills, urine, and inside fresh manure, to mature to infective larvae.
Considering the brief time they had access to a grassy paddock, it’s more likely they were infected in their stalls. This study also found that horses that had been dewormed with ivermectin had a much better response in terms of egg reduction and continued to test negative for longer than horses who received another drug. In the stalled horses, two months was too long to go between deworming treatments if using anything other than ivermectin.
Although pasture crowding was extreme on the fifth farm, in the other three with year round turnout there was a maximum of only one acre per horse available. This was sufficient to keep egg counts low with regular dewormings.
The finding that regularly dewormed stabled horses had much higher parasite burdens than horses on pasture was important since it changes our traditional view of high-risk situations.
Modified Live Vaccines Best For Equine Herpes
The change in case numbers and virus behavior in neurological Herpes over the past few years has caused considerable concern. The solution is going to have to come from better vaccine protection, and a study from Cornell published in Vaccine gives us hope.
Three groups of horses were exposed to a herpes virus isolated from an outbreak. One group was unvaccinated, one vaccinated with a killed virus vaccine and one with a modified live vaccine. Horses vaccinated with the modified live vaccine had lower neutralizing (virus inactivating) antibody titers in their blood, and lower levels of the immunoglobin IgG directed at the virus. However, these horses were protected from neurological disease, while three out of five horses in each of the other two groups developed symptoms. The horses vaccinated with the modified live vaccine also had shorter duration of fever after exposure and shed significantly less.
We’ve been conditioned to think of antibody titers as being synonymous with protection from disease, but this is only part of the story. Some antibodies can ”tie up” invading organisms, others serve to identify infected cells so that immune system cells can dispose of them. However, without a strong response in the cell-mediated, sophisticated arm of the immune system there’s a good chance the infection will not be stopped. Despite antibody production after vaccination actually being lower, only the horses with the modified live vaccination were protected from neurological Herpes. Killed virus vaccines don’t trigger a good cell-mediated immune response.Pfizer’s Rhinomune is a modified live vaccine.
Do Steroids Cause Laminitis’
You may have heard that corticosteroid drugs, e.g. Dexamethasone, cortisone, can cause laminitis. Package inserts for these drugs even contain a precaution to that effect. However, if you asked your vet, you were probably told it’s not true. Vets remain sharply divided on this question. Part of the reason for that is that attempts to induce laminitis experimentally, even with large doses of corticosteroids, have failed, and certainly not every horse that gets corticosteroids develops laminitis. In fact, most don’t. What’s going on’
There’s little scientific study of this issue. In addition to the attempts to produce laminitis with corticosteroids mentioned above, there are sporadic case reports of laminitis following corticosteroid use. There was one study in 1979, reported in the American Journal of Veterinary Research, where researchers used digital (hoof) arteries and veins obtained from horses, studied their responses to naturally occurring substances like epinephrine or histamine that could induce contractions, and found that adding corticosteroids to the mix made them contract more dramatically, especially the veins. This was a particularly interesting finding since laminitis studies implicated contracture/spasm of the veins more than the arteries.
That was basically where things sat, until another article by researchers from Michigan State which just appeared in the Equine Veterinary Journal. They wanted to build on the 1979 study by using thermography, an indirect indicator of blood flow, to study what happened to horses that were given dexamethasone and whether or not it changed their response to vasoconstricting substances. They found that horses treated with dexamethasone had decreased skin temperatures, indicating decreased perfusion/blood flow, and that dexamethasone also either magnified the effect of vasoconstrictors, or was additive to the drop in skin temperature they produced without dexamethasone.
The bottom line here is that laminitis as a side effect of corticosteroids isn’t as simple as ”use the drug, get laminitis.” Corticosteroids have an important place in treating severe inflammatory reactions secondary to injury, even in saving the horse’s life in situations such as shock or purpura reactions to Strangles infections. As with any drug, decision about whether or not to use it should be based on carefully weighing the risks versus the benefits. When it comes to danger of laminitis, horses at highest risk would be those under considerable stress, horses with prior laminitis problems or other compromise to the blood supply to their hoof/hooves. Horses with insulin resistance or Cushing’s disease may be at high risk since these conditions may be associated with poor circulation and/or high corticosteroid levels already.
Lyme Disease Hard To Diagnose Overseas, Too
The Institute of Comparative Tropical Medicine and Parasitology in Munich, Germany, published the results of a survey sent to 118 practicing veterinarians. Over half responded that they felt Lyme disease was a problem for horses, and cited poor performance and orthopedic problems as the most common symptoms.
Serology (antibody testing) was usually used to confirm the diagnosis, treatment being antibiotics and anti-inflammatories. Many of the vets surveyed felt that Lyme was a significant problem and being underdiagnosed, while others felt e xactly the opposite.
That’s pretty much the situation here as well. The problem is that the symptoms are not specific for Lyme, and positive serology only means exposure, not active infection. It’s difficult to get an accurate idea of the true number of horses with Lyme problems, but owners who have gone through this, and vets who have seen responses to treatment, can attest that it’s real.
In addition to vague, shifting lameness that is sometimes suspected to be a neurological problem, owners may report low grade laminitis, behavior changes, depression, sensitivity to touch. Mild elevations of liver enzymes may occur at some stages, or changes in red or white blood cell counts.