DSLD-ESPA in the Veterinary Community

About DSLD-ESPA

noreply@blogger.com (Unknown) — Sat, 13 Aug 2011 17:12:00 +0000

What is DSLD? What is ESPA? Why two names?
©Terry Barrall
Many years ago a pioneering veterinarian began a study of horses with visibly dropped, swollen, painful fetlock joints. The suspensory ligaments of these horses were severely compromised. They did not heal, but degenerated instead; some slowly and some virtually overnight. She named the condition Degenerative Suspensory Ligament Desmitis, or DSLD.

In 2006, Dr. Jaroslava Halper, MD PhD, a professor and research pathologist with the College of Veterinary Medicine at the University of Georgia released a peer-reviewed publication about this equine disease. She determined that affected horses had a body-wide over-accumulation of a certain type of proteoglycan, causing widespread damage throughout the body of the horse. She felt it was important to rename the condition to reflect that it is far more than just a problem of the ligaments of the leg; rather a systemic disorder of connective tissue. Her name, Equine Systemic Proteoglycan Accumulation, or ESPA is still relatively new and not yet as well known as the old name, DSLD. Therefore, you will see both here, frequently shortened to DE.

While there is much yet to be learned, research continues into this devastating disease. There is no cure at this time. However, a veterinarian-led treatment trial, coordinated through the “DSLD-Equine” list on Yahoo Groups, has given many horses relief.

Originally felt to be a disease of Paso gaited horses, DE is now known to be found in many, or most, breeds of horses including purebreds, crossbreds, and mules.

Necropsy results show that DE progresses, and that the long-recognized sign of fallen fetlocks is most probably a late-stage symptom. Horses can be affected in tendons and ligaments of all legs, nuchal ligament, patella, skin and organ fascia, eyes, aorta, and other connective tissues throughout the body. Some horses have shown an iron overload.

Current research at the University of Georgia is concentrating on the biochemical aspects of the disease; and the mechanism(s) that regulate the cellular processes.

DE is believed to be a genetic disorder; it has been shown to pass to offspring with great regularity. For this reason, it is strongly advised to take all affected horses out of the breeding pool so the disease does not get passed on. Unfortunately, many affected animals of breeding age do not show visible symptoms of disease until later in life. Breeding animals can be screened via the Mero Diagnostic Protocol and recording form; however this can only show current condition. It is not predictive, and should be repeated annually for breeding stock.
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This blog wishes to thank Terry Barrall for permission to reproduce copyright material, What is DSLD? What is ESPA? Why two names? © 2010

Differences Between Injury and DSLD-ESPA

noreply@blogger.com (Unknown) — Sat, 06 Aug 2011 22:53:00 +0000

The differences between injury and DSLD are:

1. Injury usually not bilateral, certainly not quadrilateral

2. If there is fetlock dropping, it occurs at the time of the injury, not as a late development

3. Injuries heal by a combination of tendon regeneration and scar tissue. While ultrasound appearance during an acute DSLD flare may improve somewhat as that settles down, they do not heal.

4. The enlargement seen in healed injured tendons and ligaments is from scar tissue and does not increase over time. It usually decreases. With DSLD, enlargement is progressive over time.

5. There is usually no obvious precipitating event with DSLD, such as racing or pasture accident. With injury there always is.

--Eleanor Kellon, VMD

Euthanasia: Necessary? How, When, and Why?

noreply@blogger.com (Unknown) — Sat, 06 Aug 2011 15:35:00 +0000

What Do You Do When There Are No Proven Treatments?
When you work providing care and treatment to horses, it doesn’t take long to realize that there’s only so much that you can do. Medical conditions fall into one of three categories:

Things for which something can be done
Things for which there’s nothing that can be done
Things that get better on their own

When is the Right Time to Say Goodbye?
General advice on how to objectively approach the decision to euthanize.

Equine Euthanasia: How do I Know When it's Time
More guidance on how to approach the decision to euthanize.

Top Four Reasons for Euthanasia
Lameness, weight loss, colic, and equine Cushing's syndrome are the four top reasons for euthanizing an older horse, said Catherine McGowan, BVSc, PhD, RCVS, European specialist in equine internal medicine, who presented research by Thomas McGowan, BSc, DVM, PhD, at the American College of Veterinary Internal Medicine Forum, held June 3-6 in Montréal, Quebec.

HSUS List of Humane Options for Disposal of Horse Remains
The Humane Society of the United States released a national list of humane resources for horse owners making end-of-life arrangements for their equine companions.
"Providing a humane, dignified death for your horse is simply responsible horse ownership," said Keith Dane, The Humane Society of the United States' director of equine protection. "No one likes to think about the death of a beloved companion, but planning ahead is key to understanding your options. This resource list gives horse owners the information they need to plan effectively."

News: Dr Halper available for biopsy tissue diagnosis

noreply@blogger.com (Unknown) — Tue, 26 Jul 2011 21:17:00 +0000

Dr Halper is available for biopsy tissue diagnosis. Please click on the appropriate link for instructions and prices.
--Click here for post-mortem instructions and prices.
--Click here for instructions to take nuchal ligament sample from live horse.

Ono Eagle Joe

noreply@blogger.com (Unknown) — Tue, 26 Jul 2011 01:49:00 +0000

Thoroughbred Gelding, Age: 8

Vet Report:

Veterinarian: Kevin Snekvik, Senior Pathologist
Washington Animal Disease Diagnostic Laboratory

Clinical: Mild to moderate tendon enlargement, deep digital flexor tendons, superficial digital flexor tendons, and suspensory ligaments

Videos: (best viewed with high speed connections)

Photos:

Ultrasound photos:

Necropsy photos:

Necropsy report:

Pathological findings and opinion: Moderately affected. DSLD/ESPA in the tendons and ligaments of all four legs along with nuchal ligament and aorta.

Pathologist: Jaroslava Halper, MD, PhD

==================
Owner Notes:

Eagle, a thoroughbred gelding, gave his life to DSLD/ESPA research in June 2005. He was purchased at an auction and thought to be a Quarter Horse needing a trim.

When given his papers after the sale, I discovered Eagle was a Jockey Club registered TB and had the famous ancestors of Bold Ruler (sire of Secretariat), Native Dancer, War Admiral, Man 'O War, Swing On (dam of Seabiscuit) in his pedigree.

Noticing his dropped rear pasterns, I had him checked by ultrasound and he came back with a positive reading for DSLD/ESPA using Dr Mero's Diagnostic Protocol.

Eagle was then sent to Washington State University and donated to research. Various tissues/organs went to U of GA, U of KY. Tissue diagnosis was done by Dr Halper and confirmed DSLD/ESPA.

Alisandro, Peruvian Paso Gelding

noreply@blogger.com (Unknown) — Mon, 25 Jul 2011 18:00:00 +0000

Age 15
Examining Vet Report:

LH leg-dropped pastern/fetlock.

Pain to palpation across LH SL branches, none on RH.

Owner reported positive to flexions on all 4 limbs. Suspected DSLD. Ultrasound requested 05/19/05.

U.S. exam at LH.

No defects or enlargement at SL body.

Thickening and increased echogenicity at medial branch at insertion and thickening of lateral branch along majority of length, with areas of local hypoechogenicity.

Diagnosis: Suspensory Desmitis of branches of LH limb.

Second opinion by Dr. Mero, after viewing ultrasounds:
Sonograms clearly show increase in size of the suspensory branches and body and a somewhat major lesion (black hole) in the medial branch on one of the views.
Clinical: Enlargement of suspensory branch and body.
Diagnosis: DSLD mid stage

Ultrasound Photos:

Necropsy Report

Pathological findings and opinion: Both left legs showed changes consistent with DSLD in all submitted tendons (superficial and deep digital flexor tendons, suspensory ligaments). In addition, the nuchal ligament showed similar changes. These tissue changes suggest fairly advanced disease. The liver revealed mild siderosis (presence of iron). The skin showed mild irregularities in collagen fibers and almost total absence of elastic fibers. Aorta and lung were normal.
Pathologist: Jaroslava Halper, MD, PhD

Owner Notes:

Alisandro, "Alex", age 15, in late March, 2005, started to exhibit brief lameness and stiffness after getting up from lying down or rolling. He seemed to walk out of it and be ok.By mid April, Alex was stumbling under saddle and dropping on the left hind fetlock as he walked. There was some mild swelling and tenderness in the suspensory of that leg and swelling that came and went in the other hind.
In May, he failed a flex test on all four legs and an ultrasound of the left hind showed enlargement in both body and branches of the suspensory, with a fairly large lesion or "black hole" in the medial branch.
A few weeks later, Alex was clearly swelling and dropping on the right hind as well. There was also some intermittent swelling and hard, lumpy spots on the front suspensories and tendons, though no dramatic dropping.
I also noticed his skin getting looser. He developed multiple, "Char Pei" like wrinkles under his chest by the forelegs. Friends commented on how rapidly he seemed to be aging. I began to see conformational changes in his hind legs and muscle degeneration in his back and hips.
I had to use Bute to manage Alex's pain. Herbal pain relief such as B-L solution didn't seem to work well for him. He was also on MSM. He stabilized briefly at the end of the summer and seemed to be doing better.
In late October, Alex was becoming stiffer and obviously having pain. I increased his Bute to 2 grams/day. On November 29, he was humanely euthanized and tissues sent to Dr. Halper at the University of Georgia.

Impreso, Peruvian Paso Gelding

noreply@blogger.com (Unknown) — Mon, 25 Jul 2011 15:19:00 +0000

Purebred Peruvian Paso Gelding, Age: 11

Vet Report:
August 2005: Colic of unknown origin, shoulder lameness.
Diagnosis: PSSM and arthritis RF and LF.

May 2006: Examining veterinarian noted obscure lameness, fetlock pain, and conformational changes including LF & RF fetlock enlargement, lesser in RR/LR. Suspensory ligament enlargement in all four legs, enlargement in SL branches. Wind puffs in all four fetlocks, change in fetlock angles.
Ultrasound diagnosis: Severe quadrilateral DSLD (confirmed by Dr Mero)

Nov 06: Follow-up Ultrasounds (see before and after images below) on Impreso showed significant improvement almost across the board from May '06 to Nov '06 while on the treatment recommended by Dr Kellon. Palpations showed some mostly minor pain responses in some areas of the suspensories. No pain in the deep & superficial flexors except for very minor in the left rear deep digital flexor. (In May, he was in excruciating pain in all flexor tendons). Vet noted no lesions within tendons/ligaments at this time. Comparison data below from May '06 ultrasounds and Nov '06 ultrasounds:

Area of Concern	May 06	Nov 06
Fetlock Enlargement	Yes, in all	None
Suspensory Ligament (SL) Enlargement	Yes, in all	Yes in LF & LR No in RF Very minimal RR
Wind-puffs	Yes LF & RF, mild Yes in RR & LR	None

Ultrasound Measurements
		LF Leg	RF Leg	RR Leg	LR Leg
Suspensory Body	May	1.75 cm²	2.01 cm²	2.26 cm²	2.01 cm²
Suspensory Body	Nov	1.50 cm²	1.50 cm²	1.75 cm²	1.53 cm²
Lateral Branch	May	1.25 cm²	0 .78 cm²	1.09 cm²	1.09 cm²
Lateral Branch	Nov	1.09 cm²	0.94 cm² *	0.75 cm²	0.94 cm²
Medial Branch	May	1.09 cm²	1.09 cm²	0.87 cm²	1.09 cm²
Medial Branch	Nov	0.87 cm²	0.78 cm²	0.75 cm²	0.94 cm²

*the only leg showing worse
Note: table color added only for reading clarity

Photos and Ultrasounds:

Ultrasound photos (before entering Dr Kellon's study):

Follow up Ultrasounds:

Owner Notes:

Prior symptoms: At age 4, crest tipped and was gelded. I purchased him at age 4 1/2. He was ridden extensively on trail and shown.Age 9: Had muscle spasm in left hip and fell with rider while warming up at a horse-show, got up limping. Previous vet exams showed no problems. Thorough vet exam at veterinary school immediately after the fall showed no problems, nor did vet exams upon return home. Horse was lame and put on pasture rest. After length of time recommended by veterinarian and no longer showing any lameness, horse was returned to light work. He tolerated this well and showed no lameness. However, he experienced severe colic of unknown origin. Treatment at veterinary school consisted of lavage and inpatient stay of three days for monitoring. Recovery was declared successful and he returned home. A month later, returned to light riding, increased as time went on and seemed to tolerate well. No problems noted.Age 10: Onset of migrating lameness. Put on pasture rest again. In the fall of 2005, showed pain nearly everywhere, including all four legs and was diagnosed with PSSM. At that time, he was put on IR diet and improved greatly; however, as pain resolved, lameness became more profound. By early 2006, he was dead lame and moved with a great amount of discomfort. There was still no definitive diagnosis by a number of veterinarians. Due to the pain he was in, we were considering euthanasia.In May of 2006, I discovered the DSLD Equine list and found he fit a number of symptoms, including loose skin. Following exam using Dr. Mero's protocol and ultrasounds, Dr. Mero consulted and confirmed diagnosis of quadrilateral dsld.In late May 2006, Impreso was started on Dr Kellon's supplement / treatment study and supplemented with magnesium citrate and cinnamon. He has steadily shown a decrease in pain and general improvement in attitude, movement, elasticity of skin, and internal status of legs as shown by ultrasounds performed late Nov. 2006. Lameness, which is sometimes evident, is approximately grade 1.

Ehlers-Danlos Syndrome Similar to DSLD-ESPA

noreply@blogger.com (Unknown) — Wed, 20 Jul 2011 01:14:00 +0000

Ehlers-Danlos Syndrome is a human disease similar to DSLD-ESPA in horses.

http://www.bedspa.com/2009/07/video-link-to-eds-ehlers-danlos-syndrome/

What Is Ehlers-Danlos Syndrome?

Ehlers-Danlos Syndrome is a group of inherited connective tissue disorders, caused by faulty collagen (a protein in connective tissue).

Connective tissue helps support the skin, muscles, ligaments and organs of the body. People who have the defect in their connective tissue associated with Ehlers-Danlos Syndrome may have symptoms which include joint hypermobility, skin which is easily stretched and bruised, and fragile tissues. There are six major classifications of Ehlers Danlos Syndrome.

What Are The Six Types of Ehlers- Danlos Syndrome?

Ehlers-Danlos Syndrome has been classified into six types:

Hypermobility
Classical
Vascular
Kyphoscoliosis
Arthrochalasia
Dermatosparaxis

Hypermobility Type of Ehlers-Danlos:

The primary symptom associated with the Hypermobility Type of Ehlers-Danlos Syndrome is generalized joint hypermobility which affects large and small joints. Joint subluxations and dislocations are a commonly recurring problem. Skin involvement (stretchiness, fragility, and bruising) is present but to varying degrees of severity, according to the Ehlers-Danlos Foundation. Musculoskeletal pain is present and can be debilitating.

Classical Type of Ehlers-Danlos :
The primary symptom associated with the Classical Type of Ehlers-Danlos Syndrome is distinctive hyperextensibility (stretchiness) of the skin along with scars, calcified hematomas, and fat-containing cysts commonly found over pressure points. Joint hypermobility is also a clinical manifestation of the Classical Type.

Vascular Type of Ehlers-Danlos:
The Vascular Type of Ehlers-Danlos Syndrome is considered the most serious or severe form of Ehlers-Danlos Syndrome. Arterial or organ rupture can occur which can lead to sudden death. Skin is extremely thin (veins can be seen easily through the skin) and there are distinctive facial characteristics (large eyes, thin nose, lobeless ears, short stature and thin scalp hair). Clubfoot may be present at birth. Joint hypermobility usually only involves the digits.

Kyphoscoliosis Type of Ehlers-Danlos:
Generalized joint laxity (looseness) and severe muscle weakness are seen at birth with the Kyphoscoliosis Type Of Ehlers-Danlos. Scoliosis is observed at birth. Tissue fragility, atrophic scarring (causing a depression or hole in the skin), easy bruising, scleral (eye) fragility and ocular rupture are possible clinical manifestations as well as spontaneous arterial rupture.

Arthrochalasia Type of Ehlers-Danlos:
The distinguishing feature of the Arthrochalasia Type of Ehlers-Danlos is congenital hip dislocation. Severe joint hypermobility with recurrent subluxations are common. Skin hyperextensibility, easy bruising, tissue fragility, atrophic scars, loss of muscle tone, Kyphoscoliosis, and osteopenia (bones which are less dense than normal) are also possible clinical manifestations.

Dermatosparaxis Type of Ehlers-Danlos:
Severe skin fragility and bruising are characteristics of the Dermatosparaxis Type Of Ehlers-Danlos. Skin texture is soft and sagging. Hernias are not uncommon.

Increasing Awareness of Ehlers-Danlos Syndrome :
The types of Ehlers-Danlos Syndromes (EDS) are treated based on the clinical manifestation which is problematic. Skin protection, wound care, joint protection, and strengthening exercises are important to the treatment plan. The debilitating and sometimes fatal condition affects about 1 in 5,000 people. At least 50,000 Americans have EDS. It is estimated that 90% of people who have Ehlers-Danlos syndrome go undiagnosed until an emergency occurs which requires immediate medical attention.

Gomero

noreply@blogger.com (Unknown) — Tue, 19 Jul 2011 13:02:00 +0000

Purebred Peruvian Paso Gelding, Age: 16

Veterinarian: Lisa Gift Krauter, DVM
Clinical: DSLD symptoms and ultrasound in the legs

Pathologist: Jaroslava Halper, MD, PhD
Necropsy report:

Pathological findings and opinion: All three (1 front and 2 rear) legs showed changes consistent with DSLD in all submitted tendons (superficial and deep digital flexor tendons, suspensory ligaments), more in distal (lower) parts. In addition, the nuchal ligament showed similar changes. The aorta appeared normal. The lung revealed the presence of small calcified granulomas, likely due to an allergic reaction or a parasitic infection, though no organisms were identified in the lesions. No organisms identified in lesions using special stains.

Video: Symptoms of irregular gait, landing toe first, hind end tucked under, extreme flex of pasterns in motion.

Full body shot. Note stance.

Close up of legs showing swelling of
fetlock, lumps, enlarged suspensory.

Ultrasounds

Necropsy Photos

Owner Notes:

I owned this guy since Oct 02 so I have a pretty good history including pictures that I took of his leg (inadvertently) since Oct/Nov '03 as I became involved with barefoot at that time. Just as far as basics go.
Spring of '05 I noticed he became very clear that he didn't want me to trim his feet. Time was limited and he would turn and look at me with both eye's as if to say "Please, not today." He also became more and more tender on the rocks (barefoot).
He also seemed off on his right hind after our trail ride in June of '05 but recovered within a week.
It seemed harder this last year to keep weight on him. I had his
teeth checked in Fall of '04 but the vet said they were fine. Wait till next year.
Gomero had some work done in Fall of '03. I rode him on many BCHW rides over the Summer. Long rides up in the Mountains. He fared well till Aug '05 when I took him to Ocean Shores for 4 days (Pacific Beaches). Some-thing was clearly wrong. His canter was very choppy like his feet hurt (on sand?) He was resting his right hind a lot the day we packed up and left.
I brought him home and the next morning he was hurting pretty bad with a pronounced toe than heel first landing on all fours. At this time I did give him Bute. The second day he was worse, he had been sleeping (standing) and as he came up to be fed it was so clear to me what was wrong that further diagnosis for me seemed to be a wasted expense. It was very clear.. One foot, two foot, three foot, four foot. He was using much effort to get those legs to cooperate. And especially at first so gingerly placed each toe down first than slowly to heel on all fours as he walked.
By the end of one week he was moving much better. After two weeks it was harder to see the problem. It was Mid Aug '05 and if you watch real close on the video clip, he is ever so slightly landing toe first on all fours. From that time on he was always resting his right hind though really didn't seem to limp too bad.

donations

noreply@blogger.com (Unknown) — Tue, 19 Jul 2011 00:13:00 +0000

Genetic Research:
Please include memo on check:
Support the DSLD Research of
Dr. E.G. Cothran

Make check payable to:
Texas A&M Foundation

Mail to:
Ms. Merrie Noak
Dept of Veterinary Integrative Biosciences
CVM, TAMU4458
Texas A&M University
College Station, TX 77843

BioChemical Research:

Please include memo on check:

Halper DSLD-ESPA Research
Fund #A912210

Make check payable to:
University of Georgia

Mail to:
University of Georgia,
Dr. Halper
142 Vet Med 1
Athens, GA 30602-7388

Examination: Diagnosis of DSLD-ESPA

noreply@blogger.com (Unknown) — Mon, 11 Jul 2011 01:40:00 +0000

Flex test of fetlock joint. DSLD/ESPA horses will fail in two or more legs.
Palpation: Pain response especially in the suspensory branches and fetlock area. Suspensory may be enlarged. May feel very taut while weight bearing and soft /mushy when not weight bearing.
Ultrasound: Follow Dr Mero's Diagnostic Protocol. Also useful is Dr Mero's exam form for SL measurements.
Tissue diagnosis is available from UGA at necropsy. Tissue samples may include tendon ligament bundle of lower leg, one leg affected and one that looks nonaffected. The aortic arch, eye, liver, lungs and skin.

The amount of harvested tissue can include all tissues or just the legs, depending on the amount of diagnostic information requested by the owner.

News: Iron Study

noreply@blogger.com (Unknown) — Mon, 11 Jul 2011 01:35:00 +0000

Eleanor Kellon, VMD, is conducting an iron/ferritin study of DSLD-ESPA horses since so many are diagnosed with high iron or iron overload.

Please contact Dr Kellon before sending blood sample to University of KS for testing.

Click here for Iron Submission Form.

News: Research Findings

noreply@blogger.com (Unknown) — Mon, 11 Jul 2011 01:34:00 +0000

Dr Halper's research has been published. Click here for the abstract. To read the entire paper, please click here. (requires Adobe Reader)

Dr Halper is available for biopsy tissue diagnosis. Please click on the appropriate link for instructions and prices.

--Click here for postmortem instructions and prices.

--Click here for instructions to take nuchal ligament sample from live horse.

Donations: Genetic Research - Texas A&M

noreply@blogger.com (Unknown) — Fri, 08 Jul 2011 12:46:00 +0000

Important:
Please include memo on check that the donation is to
Support the DSLD Research of Dr. E.G. Cothran

Make checks payable to:

Texas A&M Foundation

Mail to:
Ms. Merrie Noak
Dept of Veterinary Integrative Biosciences
CVM
TAMU4458
Texas A&M University
College Station, TX 77843

Donations: BioChemical Research - UGA

noreply@blogger.com (Unknown) — Fri, 08 Jul 2011 12:42:00 +0000

Important:
Please include memo on check:

Halper DSLD-ESPA Research Fund #A912210

Make check out to:
University of Georgia

Mail to:
University of Georgia,
Dr. Halper
142 Vet Med 1
Athens, GA 30602-7388

Documenting Cases

noreply@blogger.com (Unknown) — Thu, 30 Sep 2010 20:04:00 +0000

If your horse has been diagnosed with DSLD-ESPA (or is symptomatic), please consider signing up for Dr Kellon's treatment/study. The majority of horses on treatment have responded favorably. If you would like to participate in the study, join the DSLD-Equine list. and fill out a treatment study form for your horse(s). To request a form, please contact- dsldinfo@gmail.com.