On this page I have attempted to hightlight some of the inherited diseases that can occour in the English Springer, all except Chronic Hepatitis can be tested for and avoided by using clear dogs in breeding programms. A research project for Chronic Hepatitis is underway, so hopefully in time this too will become avoidable. Having said all this, the ESS is generaly a healthy and robust dog.
ALL DOGS IN OUR BREEDING PROGRAMME HAVE BEEN TESTED CLEAR FOR ALL DISEASES THAT CAN BE TESTED FOR AND CAN AFFECT THE ESS
CHRONIC HEPATITIS
Chronic Hepatitis is a disease of the liver and as yet we know very little about its cause, and to date, there is no cure. This disease is very serious and has a poor prognosis. However a research project has been set up at Cambridge University, to look into the cause and hopefully to find a cure.
Below is an article that was published in the Vetinery Record, which explains about the disease and what is known about it.
CHRONIC HEPATITIS IN THE ENGLISH SPRINGER SPANIEL
N.H.Bexfield1, T.J.Scase1, S.M.Warman2, E.Skancke3, W.Farstad3, P.J.Watson1
1Department of Veterinary Medicine, University of Cambridge, Cambridge, UK, 2School of Clinical Veterinary Science, University of Bristol, Bristol, UK, 3Department of Companion Animal Clinical Sciences, Norwegian School of Veterinary Science, Oslo, Norway.
Canine chronic hepatitis (CH) is seen with an increased incidence in certain breeds, including the Bedlington, West Highland White and Skye Terrier, Cocker Spaniel, Doberman, Dalmatian and Labrador Retriever. In some breeds CH is thought to be associated with abnormalities in copper metabolism. In the majority of cases of CH however, the aetiology is poorly understood. The authors have recently noted a previously undocumented increased incidence of CH in the English Springer Spaniel (ESS). The purpose of this study was to describe the history, clinical signs, clinicopathologic abnormalities and outcome in such cases.
ESS presented to referral and general practices in the UK and Norway for investigation of elevated liver enzymes, clinical signs of liver disease and histopathological confirmation of CH were identified. Clinical, laboratory and pathological data were obtained from case records or by contact with the referring veterinarian. Formalin fixed or paraffin embedded liver tissue was obtained for review by one of the authors using a panel of seven liver-specific stains including rubeanic acid.
Thirty four cases were identified. Mean age was 3 years 4 months (range 7 months - 9 years) and 24 female and 10 male dogs were represented. 28/34 dogs had been vaccinated within the proceeding 12 months. Clinical signs at presentation included vomiting, depression, lethargy and anorexia. Pyrexia was documented in 12 dogs and 26 dogs were jaundiced.
Biochemical changes in all cases included moderate to marked elevations in ALP and ALT and mild to moderate elevations in total bilirubin. Other variable findings included, hypocholesterolaemia, hypercholesterolaemia, hypoalbuminaemia, decreased urea, elevated bile acids and prolonged coagulation times. Neutrophilia was documented in 12 of 21 dogs. Results of abdominal imaging were non-specific. Histological examination of liver tissue demonstrated changes consistent with CH including hepatocellular apoptosis or necrosis, a variable mononuclear or mixed inflammatory infiltrate, regeneration and fibrosis. There was no evidence of increased copper accumulation in any dog. Treatment included one or more of dietary modification, antioxidants, antibiotics, ursodeoxycholic acid and corticosteroids. Follow up data was available in 26 dogs and 16 of these died or were euthanased within a mean of 4 months following initial diagnosis. The median survival time of the remaining dogs was 7 months.
This study suggests that the ESS might be predisposed to a type of CH without copper accumulation which carries a poor prognosis. Further investigations in to the aetiology and possible genetic basis of this condition are indicated.
PROGRESSIVE RETINAL ATROPHY (PRA)
This is a genetic, inherited disease of the retina (the "film" in the camera), which occurs in both eyes simultaneously. The disease is nonpainful, and there is no cure for it. The eyes are genetically programmed to go blind. PRA occurs in most breeds of dogs and can occur in mixed breeds also.
Clinical signs vary from the dog first becoming night blind in the early stage of PRA (not able to see in low light surroundings) to the entire visual field in all light levels becoming affected, which is advanced PRA. The pupils are usually dilated, and owners often notice a "glow" and increased "eye shine" from the eyes. All dogs with PRA will eventually develop blindness from advanced PRA, and this time frame until the dog is blind varies considerably from dog to dog, but usually takes at least 6 months from the time of diagnosis, and can rarely take years until the dog is completely blind. Although no treatment for PRA is possible to stop the disease, nutritional antioxidant supplementation for retinal health may help slow the deterioration of the retina to "buy some time" before the blindness inevitably happens.
A DNA test for the Cord 1 mutation is available from the Animal Health Trust, to find out more CLICK HERE
An annual eye test will determin if your dog is clinicaly affected
The disease affects young adults, usually between 18 months and 4 years of age, and is characterised by nervous signs that progress over a period of several months. These signs include inco-ordination and ataxia (loss of control of movement), change in temperament, loss of learned behaviour, loss of balance, apparent deafness, visual impairment and varying degrees of depression. The inco-ordination and ataxia affects all four legs and is mostly evident when affected animals are
walking on slippery surfaces or attempt more complicated movements such as turning. In addition, affected dogs lose weight and may suffer from swallowing difficulties and sometimes regurgitation.
A DNA test for this disease is available from the Animal Health Trust - click the link above.
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