The Lessons of Dusty
Published in modified form in "Equus"

Silverado Duster was born in 1996, in a classic old barn in California’s Napa Valley. His mom, Jet, was wonderfully attentive and his irrigated pasture was thick with orchard grass, purple clover and rye. Dusty didn’t have to work very hard and eating was definitely his favorite pastime. He was bred to be a cutter, but he mostly got to play by Soda Creek in the day, eat grass, and head for his bedded stall at night to eat some more.

All that changed on September 1, 2001, when my husband Jim and I sold the veterinary practice we had owned for 24 years and semi-retired to Pagosa Springs, Colorado. After a two-day trip, Dusty, Jet, and his best friend Nellie, were turned out in knee high grass on our 80-acre ranch. The waters of Mill Creek nourished the bottom brome pasture, and snow and rain watered the more delicate woodland meadows near our house and barns. Our pampered California horses learned to dodge tree limbs, navigate downed logs, and escape fall mosquitoes and spring horse flied by running to the barn. They negotiated mountain trails and watched migrating elk with interest, wondering, it seemed, if they were strange cousins.

Jim and I purchased two more geldings to train for trail riding and bred our two mares. The mares both produced beautiful fillies in the late spring of 2003, and we took the three geldings horse camping in the high mountains in the summer. The aspen were spectacular in the fall. We thought our new home was perfect.

Then Jet began to lose weight. We weaned her filly at four months of age and increased Jet’s senior feed. Due to her age and a nosebleed a few weeks back, we tested her for Equine Cushing’s Syndrome and blood clotting deficiency. Both tests were normal but the blood test showed an increase in gamma glytamyl transferase (GGT), a liver specific enzyme. Jet did not have a fever or any elevation in white blood cells or fibrinogen, so we placed liver infection low on our list of differentials. But her high globulin levels indicated that toxins could be a cause of her liver inflammation. We checked for mold in concentrates or hay that could produce aflatoxins. We found none. We checked for blue-green algae in the water, but the creek was running well and all the water troughs were clean. We treated Jet with vitamins, anti-inflammatories, and antibiotics to prevent infection that might travel up her slow bile duct.

Jet improved over the winter and her blood tests looked pretty good. We felt a little better.

In the spring of 2004, runoff soaked the bottom pasture. As the snow pack thinned, we turned the horses out in the upper woodland meadows after their breakfast each morning. Using the instincts of their ancestors, they dug through the remaining snow to forage for the season’s first green shoots. By the first of May, four of our seven horses showed early liver disease on lab testing. Jet seemed to be the worst. We moved the mares and weanlings to the lower brome pasture and put the geldings on the slope above them.

We got out Dr. Tony Knight’s A Guide to Plant Poisoning of Animals in North America and began to read.

Alsike clover is a common pasture legume that has been associated with liver disease. During wet years or when growing in wet areas, it can harbor a toxic fungus. Signs of poisoning can be weight loss, depression, neurologic disturbances, slobbering, photosensitization (blistering of white hair areas) and liver failure. Horses eating toxic alsike clover usually recover if they are removed from the source.

We searched the pasture and found some purple clover near the creek. Alsike clover has a white to whitish pink flower, but we fenced off the creek just to be safe.

We also looked for plants containing saponins—Saponaria, Lantana, panic grasses, tansy mustard and flixweed, that could cause short term liver disease, since Jet had recovered over the winter. We found a few flixweed plants, but the horses avoided these plants. Pictures of the pastures sent to Dr. Knight did not display the poisonous plants we were looking for.

We also read about pyrollizidine alkaloids (PA). These are found in many species of plants and cause progressive liver cell death, scarring, bile duct thickening, inability of the liver to regenerate, and possible damage to small blood vessels in the lungs. The effects are cumulative so horses that eat small amounts of plants containing PA over a long time can be poisoned. Eating twenty-five pounds or more of the toxic plants at one time can be fatal, and there are reported cases of liver toxicity and death in horses inadvertently fed alfalfa hay contaminated with plants containing PA.

Typical signs of PA toxicity are loss of appetite, weight loss, depression, and eventually neurologic symptoms including yawning, compulsive walking, head pressing, and even seizures. Liver cell death and eventually bile duct obstruction lead to jaundice, a yellow color in the gums and the whites of the eyes and even in areas of light skin. Sudden death can occur without prior warnings. Characteristic changes seen on biopsy are large irregular liver cells known as megalocytes, plus liver scarring and enlarged bile ducts.

Worldwide, the most common plants associated with PA poisoning are in the Senecio (renamed Packera) genus and include tansy ragwort, threadleaf groundsel or woolly groundsel, and Riddell’s groundsel. In the West, fiddleneck and houndstongue (Cynoglossum) are associated with PA poisoning, and in the Southeast, Rattlebox has poisoned livestock. Peak levels of PA toxins occur in stems and leaves just before flowers open, and in the seeds and flowers.

Common wisdom holds that horses will not eat PA containing plants if adequate forage is available. Climatic variation such as the recent droughts in Colorado, grazing cattle on leased land in the fall, and time of year certainly affect the amount of available grass. There are also variations in susceptibility to PA and in the forage preferences of individual horses.

In walking all over our upper woodland pastures, we found small, scattered silver-wooly groundsel, Senecio cana, plants usually near pussy toes, a favorite non-toxic plant of the horses. Note the dentate appearance of the tips of leaves in the picture above.

Senecio (Packera) cana is a biannual plant that produces a rosette of leaves in its

second year flowering plant
first year as well as flowering in second year plants. Some of the smallest leaves have a dentate or toothed outer edge and the single tap root may be slightly purple. The rosettes were easy to pull from the ground. The second year plants show flower stalks with a single yellow flower head. These look either like pencil erasers early on or like ray (daily-like) flowers.

The real identifying feature is the single layer of green bracts stacked parallel, but not overlapping, around the flower head. This is the common feature of the Senecio/groundsel family and there are over 3000 species in the family. When we disturbed a first year plant it would often grow back

with smaller leaves and shorter—like it was trying to hide.

The bottom pasture was clean. The horses looked fat and sassy. Throughout the spring Jet remained in excellent spirits. She and Nellie and their fillies were still confined in the lush brome pasture and fed grass hay plus mare/foal concentrates with added minerals and salts. The weaned fillies had a creep feeder. We repeated blood tests on all our horses. The fillies were fine. Our Wyoming bred gelding was perfect, and Dusty and Nellie’s liver enzymes were barely elevated. We check blood on May 28, and with the geldings feeling great, we made trips to Aspen Spur, Echo Canyon, and closest to home, Willow Draw on June 9. The horses were full of enthusiasm and

the air was clear. But biweekly lab checks of Jet’s blood began to show increased levels of GGT once again, an indication of ongoing liver inflammation. Another liver enzyme, aspartate aminotransferase (AST) remained within normal limits. That was good news. Nellie’s tests showed only mild liver reaction. But now the other new gelding had increasing liver enzymes.

We suspected a longer term toxin and the Senecio family of plants were our biggest concern.

We made the decision to ultrasound and biopsy one of the affected horses. Jet’s liver was small on ultrasound, typical of an older horse, and the ultrasound showed increased fibrosis (scarring). So on June 18, 2004, we obtained a biopsy from Hammer, the 4-year-old gelding who had a moderate elevation of GGT at that point, but no clinical signs. His liver ultrasound looked fairly normal in size and texture. We sent samples to our veterinary diagnostic lab and slides were forwarded to the USDA Poisonous Plant Lab in Utah. There, Dr. Bryan Stegelmeier concurred that the damage was caused by pyrollizidine alkaloids, and advised that the plant most likely involved was in fact from the Senecio group. We sent plant samples to the lab. The plants were confirmed to be Senecio (Packera) cana. We treated the gelding as we had treated Jet.

We trailered down to the Red Ryder arena to work on basic maneuvers on July 17, and spent more time habituating the geldings to the white flag monsters along the grandstands. Looking back, maybe Dusty was less reactive than usual, but he still danced away when a crow launched itself from behind a flag, and he had certainly eaten well that morning.

Arriving home, we turned the boys out for some pasture time. That evening, Dusty was not as aggressive as usual about his personal food bucket. By morning, he was definitely too quiet. We brought him up to the barn, checking temp, pulse, borborygmus (intestinal sounds), and gum color and refill; we were looking for colic. Dusty finished his breakfast and dinner but without his usual gusto. The next day we sent in a blood panel. Lab tests confirmed liver failure on July 19. His GGT was at 1008 IU/L, nearly 50 times normal, and his bilirubin was very elevated. We could see jaundice. Ominously, Dusty, always the ager eater, picked at his food.

In the first stall of our main barn we have an IV drip system with a long spiral tube that allows us to provide intravenous nourishment and electrolytes around the clock while giving the horse freedom of movement. We installed a large-bore catheter in Dusty’s jugular vein and began to run IV fluids to attempt to flush his system and hydrate him. Through the catheter we also gave Baytril, an antibiotic, to fight any infection that might have traveled backwards up his sluggish bile duct system. The liver is the main storehouse of vitamins and Dusty’s liver wasn’t storing much of anything, so we gave him doses of these as well. We supported him with IV sugar (dextrose) to let his liver rest from its duty of providing energy. We gave him injectable anti-inflammatories, both steroids and then Banamine (Flunixin meglumine) for discomfort and to decrease the reaction in the liver. Dusty seemed to feel a little better but his appetite remained poor. Repeated blood tests showed slight improvement, but not enough to give us much hope.

We brought Jet, Dusty’s mom, over to the barn. For a few hours each day we would disconnect the IV and let Dusty and Jet out in a small pasture. They would graze and even run and play a little, but it was always Jet who initiated the activity. As the days crept on, Dusty did not improve. He lost weight. We tried every type of food we could encourage him to eat; he would only eat a few treats. We rechecked blood. His liver enzyme levels remained high.

On July 28, Dusty did not eat not even treats or carrots. He wandered aimlessly in the pasture but didn’t really graze. He wanted to stand in the sun. His manure was scant. He didn’t drink. He didn’t want company or comfort. Lab work was discouraging.

On July 29, 2004, I jumped on Jet bareback and slowly led Dusty into the upper pasture. We had chosen a site where the horses loved to run, where we would pass by on Christmas sleigh rides and on cross country skis, where he would be close to those he loved. A friend with a tractor dug his grave. His mom stood quietly, tied at a nearby tree. Dusty had always been good for shots, but I gave him a sedative before I gave him a large dose of a concentrated euthanasia solution. He let go of life with relief and seemed to forgive us for our failure to protect him. A necropsy sample confirmed massive, PA-induced liver failure.

These are the lessons of Dusty:
Horses have an instinct to graze despite available and plentiful feed, excellent nutrition, and body condition. And some may have a preference for a new plant or an increased susceptibility to plant toxins. As near as we can figure now, despite being well fed and having access to grass, sometime with about eight weeks of his clinical illness, Dusty must have found Senecio that is buddies didn’t want, in an area perhaps mixed with clovers or puppytoes, and he must have eaten it all.

Pastures must be managed to encourage grass, control weeds, and remove toxic plants. Guidelines are available from county extension agents, soil conservation offices, and weed control district officers. Weeds should be sprayed during spring growth, toxic plants identified, and pulled after each rain. Native grasses can be reseeded and horses should be kept off of fragile woodland pastures during spring growth of grass (from May 15-June 30 in our area). Horses should be rotated from one pasture to another. We have sprayed areas of our pastures with 2,4 D and Redeem to control clover and Senecio family plants. We mowed all weeds, reseeded and fertilized the grass, and used electric fences to block areas we haven’t inspected and reinspected. We have pulled up all suspect plants in areas where the horses are allowed to graze. We will continue to harrow and fertilize our lower pasture. And we will do it all again, year after year, after year.

A check of plants within 12 inches of Senecio did not show any root transfer of toxins.

I promised that the lessons of Dusty would safeguard the rest of his friends. The gelding we biopsied is full of energy. Our Wyoming gelding and Nellie and the fillies did well. Jet lived to be 22. We check GGT blood levels at least once every year, and so far, in 2010, the horses remain healthy. This was a painful lesson

We know that there are a number of toxic plants in the Pagosa Springs area. Senecio is prevalent in pastures all along the Highway 84 corridor. Recognition of the plant is critical to protect horses in this area.
See Articles:   |   Poisonous Plants in the Pagosa Springs Area  |  

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