Elizabeth A. Giuliano, DVM, MS
Hi everyone!
I was researching glaucoma for my Blog and came across this article by Elizabeth A. Giuliano, DVM, MS. She is the woman that is a part of the research study called:
The Mapping and Characterization of Mutations Responsible for Canine Glaucoma – Pending Grant No. 747
The BHCA just donated 20,000 dollars to it. I did a blog on it back on 1-21-08. Here is a portion of it. This information is on the club’s website as well.
……it goes
I found the following motion very interesting. I was very pleased that the board has decided to donate to these grants that will better our beloved-ed breed. So many of us have hounds or have had hounds who have suffered through these types of medical issues. Anything to better our breed’s health is well worth the money spent!
Motion #07-08
I move, “That the BHCA partially support the following grant requests out of the AKC/CHF Basset Hound Donor Advised Fund”:
Pending Grant No. 747: The Mapping and Characterization of Mutations Responsible for Canine Glaucoma
Principal Investigator(s): Elizabeth Giuliano, DVM, MS, DACVO, University of Missouri, Columbia
Sponsor(s): No Sponsors
Grant Amount: $82,080.00 (half paid by AKC/CHF)
Start Date: 10/1/2007 Duration (in yrs): 2
BHCA Amount: $20,000 (BH breed specific)
End
I am very interested in Dr. Giuliano’s efforts and will following them closely. Last night I found this article. It is not dated.
Canine Glaucoma Basics
Elizabeth A. Giuliano, DVM, MS
Diplomate, American College of Veterinary Ophthalmologists
Assistant Professor, University of Missouri, College of Veterinary Medicine
Glaucoma is defined as an increase in pressure within the eye. The increased pressure is the result of a buildup of the intraocular fluid which is known as aqueous humor. In a healthy animal, aqueous humor primarily drains out through a circular filter at the junction of the clear cornea and white sclera, called the iridocorneal angle. Animals with glaucoma have an abnormality in the filter which obstructs outflow, resulting in a buildup of fluid within the eye. An analogy would be a kitchen sink – if the drain is open and the water is running, the sink is operating normally. However, the drain becomes clogged for some reason and the water continues to flow, then the sink fills up with water and overflows!
There are various causes of a defective filter. Dogs of some breeds are often born with abnormal filters and are therefore prone to getting inherited (genetic or primary) glaucoma in both eyes.
(Note from Cat: This is exactly what I am talking about. Never buy a pup with abnomal drainage angles.)
continue article….
Other breeds have a genetic predisposition to developing displaced (luxated) lenses, which block the filters, obstructing the flow of fluid. In both dogs and cats, the filters can be clogged with inflammatory cells if inflammation inside the eye (uveitis) occurs. Intraocular tumors can also lead to glaucoma.
The result of uncontrolled glaucoma is blindness. The increased pressure which occurs in glaucoma quickly destroys the retina and optic nerve, which are essential for vision. If the pressure is not relieved the eye may stretch and enlarge. In order to maintain vision, eyes with glaucoma must be treated early (usually within hours of detecting an ocular problem, as evidenced by an increase in squinting, tearing, rubbing, or redness), before damage to the retina and optic nerve occur and the eye enlarges. The first priority in treating animals with glaucoma is to preserve vision. If a pet has lost vision, the next goal is to keep the pet comfortable.
Treatment for glaucoma: In early cases of glaucoma medical therapy is often instituted. The various medications work, primarily, in two different ways – to decrease production of aqueous humor and to open up the filter to make it more efficient. A pet may be prescribed a variety of topical and oral medications which work in concert to decrease intraocular pressure.
Some cases of glaucoma are resistant to the effects of medications. Surgical treatment of glaucoma may include laser therapy or cryosurgery to reduce aqueous humor production. When vision and comfort are no longer able to be maintained , additional surgical procedures may be recommended including either removal of the entire eye (enucleation) or removal of the ocular contents (evisceration) and placement of a prosthesis (false eye).
In animals that have lost vision in one eye due to primary glaucoma, an important therapeutic goal is to maintain vision in the pet’s other eye. Life-long prophylactic glaucoma therapy for the remaining functional eye may be instituted.
Please contact your local veterinarian or board-certified ophthalmologist immediately if you notice any redness, pain, excessive tearing or cloudiness in your pet’s eye(s). The earlier glaucoma can be diagnosed and treatment instituted, the better the chances are of maintaining vision in a glaucomatous eye.
More research later….Cat, Chaps and our Emma.
Comments(1)
12-7-12
Updated information I wanted to place here.
http://www.akcchf.org/research/funded-research/0747.html
00747: The Mapping and Characterization of Mutations Responsible for Canine Glaucoma
Grant Status: Closed
Grant Amount: $82,080
Dr. Elizabeth Giuliano, DVM, University of Missouri, Columbia
October 1, 2007 – September 30, 2010
Sponsor(s): American Bouvier Des Flaundres Club – Bouvier Health Foundation, American Sealyham Terrier Club, Basset Hound Club of America, Inc., Health & Rescue Foundation of the Petit Basset Griffon Vendeen Club of America, Welsh Terrier Club of America, Inc.
Breed(s): Basset Hound, Bouvier des Flandres, Dandie Dinmont Terrier, Welsh Terrier
Disease(s): Glaucoma
Project Summary
The research used a state-of-the-art procedure known as a genome-wide association study (GWAS) in attempts to find the chromosomal locations of the mutations that cause canine glaucoma. A GWAS is done with a device called a SNPchip which supports the simultaneous analysis of a DNA at tens of thousands or hundreds of thousands of distinct locations spread throughout each of the canine chromosomes. The results obtained from a group of affected dogs (the “cases”) are compared to the results from a group of healthy dogs that should have the same genetic background (the “controls”). In the last three years, the investigators conducted many GWAS. When the disease in most or all of the “cases” is caused by the same single mutation, they have almost always obtained large “case” versus “control” differences in SNPchip results from assays at chromosomal sites near the mutation. By analyzing the genes at these chromosomal sites the investigators can usually, but not always, find the mutation. When they have not obtain large “case” versus “control” differences in SNPchip results, they have interpreted this to mean that the disease in different individuals in the “case” group results from different mutations and/or that the disease results from a combination of mutations and perhaps also from environmental factors. In this project the investigators conducted six GWASs to find the chromosomal locations of mutations responsible for canine glaucoma. The first GWAS involved “case” and “control” DNA samples from Dandie Dinmont Terriers and was conducted in conjunction with Dr. Hannes Lohi’s research group in Helsinki Finland. This study produced moderately strong evidence that appears to have localized the Dandie Dinmont Terrier glaucoma mutation to a specific chromosomal location. The project’s investigators and the Finnish researchers have examined genes from within this chromosomal location; however, they still have not found the mutation responsible for the glaucoma of Dandie Dinmont Terriers. The other five GWASs involved Basset Hounds (three studies), Bouvier des Flandres, and Petit Basset Griffon Vendeens. In each study, they found only small “case” versus “control” differences in SNPchip results which could signal the chromosomal locations of glaucoma-causing mutations but more likely resulted from random variation. The third Basset Hound GWAS involved samples for “cases” and “controls” for this collected by Drs. Markus H. Kuehn, University of Iowa, and Sinisa D. Grozdanic, Iowa State University. An initial evaluation at the University of Missouri revealed a weak but possible association peak. The SNPchip data has been sent to the University of Iowa for further analysis. During this funding period, the investigators conducted a more successful GWAS in which they used Jack Russell Terrier cases and controls to discover the mutation responsible for primary lens luxation in a variety of terrier breeds. Although PLL and primary glaucoma are usually considered to be distinct diseases, this distinction is not clear cut in all cases. Furthermore, PLL can lead to secondary glaucoma and primary glaucoma can lead to secondary lens luxation. They therefore tested for the primary lens luxation mutation in DNA from all dogs in our collection that were diagnosed with primary glaucoma. Glaucomatous representatives from most breeds tested negative for the primary lens luxation mutation. Nonetheless, several Welsh Terriers that were diagnosed with primary glaucoma tested positive for the lens luxation mutation. Furthermore, they found that a Chinese Shar-Pei with a well documented case of primary glaucoma had a different mutation in this same gene. It appears that primary lens luxation and primary glaucoma can sometimes develop concurrently as a disease syndrome in the same dog.
Publication(s)
Farias, Fh, Johnson, Gs, Taylor, Jf, Giuliano, E, Katz, Ml, Sanders, Dn, Schnabel, Rd, Mckay, Sd, Khan, S, Gharahkhani, P, O’leary, Ca, Pettitt, L, Forman, Op, Boursnell, M, Mclaughlin, B, Ahonen, S, Lohi, H, Hernandez-Merino, E, Gould, Dj, Sargan, D and Mellersh, Cs (2010) An ADAMTS17 Splice Donor Site Mutation in Dogs with Primary Lens Luxation. Invest. Ophthalmol. Vis. Sci. 10.1167/iovs.09-5142 http://www.iovs.org/cgi/content/abstract/iovs.09-5142v1