Navigation
Affiliates
Sponsors

 
Google  


  Spartan Dogs - Bull and Terriers - Research 

Categorie: Research, Diseases, Defects, Abnormalities, Bull and Terriers, Articles

Namen Research, Diseases, Defects, Abnormalities
Groep Bull and Terriers

Bull and Terriers - Research

L2HGA:

l-2-Hydroxyglutaric aciduria (l-2-HGA) is een zeldzame, autosomaal recessieve, neurometabolische afwijking geassocieerd met voortschrijdende neurologische symptomen. In honden, zijn deze neurologische symptomen merendeels: cerebellaire ataxia, spierstijfheid, dementie en stuiptrekkingen. Honden met L2HGA, die zich doorgaans melden voor onderzoek bij de dierenarts voordat ze 2 jaar oud zijn geworden, zijn bijna altijd Staffordshire Bull Terriers.

J Comp Pathol. 2008 Feb-Apr;138(2-3):160-4. Epub 2008 Feb 25.

Neuropathological findings in a Staffordshire bull terrier with l-2-hydroxyglutaric aciduria.

Scurrell E, Davies E, Baines E, Cherubini GB, Platt S, Blakemore W, Williams A, Schöniger S.

Department of Pathology and Infectious Diseases, The Royal Veterinary College, UK. escurrell@rvc.ac.uk

l-2-Hydroxyglutaric aciduria (l-2-HGA) is a hereditary neurometabolic disorder reported in human beings and dogs. An 11-month-old Staffordshire bull terrier was suspected to have the disease, on the basis of clinical signs and magnetic resonance imaging findings. l-2-HGA was confirmed by urinary organic analysis and DNA testing and the dog was humanely destroyed. Post-mortem findings consisted only of microscopical lesions in the brain, characterized by marked spongiform changes and predominantly affecting the grey matter of the cerebral cortex, thalamus, cerebellum and brainstem. The spongiform changes were characterized by well-demarcated, clear vacuoles located at perineuronal and perivascular sites. Immunohistochemical and ultrastructural examination confirmed that the affected cells were astrocytes.

PMID: 18295785 [PubMed - indexed for MEDLINE]

Quote from this article:
l-2-Hydroxyglutaric aciduria (l-2-HGA) is a rare, autosomal recessive, neurometabolic disorder associated with progressive neurological signs. In man, l-2-HGA is a progressive neurodegenerative leucoencephalopathy characterized by mental and pyschomotor retardation, cerebellar ataxia and seizures ([Larnaout et al., 1994], [Chen et al., 1996], [D'Incerti et al., 1998], [Seijo-Martinez et al., 2005], [Topcu et al., 2005], [Goffette et al., 2006] and [Shafeghati et al., 2006]). In dogs, the neurological signs, which are similar, include cerebellar ataxia, muscle stiffness, dementia and seizures ([Abramson et al., 2003] and [Garosi et al., 2005]). Affected dogs, which are usually presented for examination within the first 2 years of life, are almost exclusively Staffordshire Bull Terriers (Abramson et al., 2003), although the disorder was also described in a West Highland White Terrier (Garosi et al., 2005). In both human and canine patients the disease is characterized by increased concentrations of the organic acid, l-2-hydroxyglutaric acid (l-2-HG acid), in urine, plasma and cerebrospinal fluid (CSF) ([Gibson et al., 1993], [Hoffmann et al., 1995] and [Abramson et al., 2003]). In human patients, typical magnetic resonance imaging (MRI) findings include diffuse signal changes within the subcortical white matter and basal ganglia, accompanied by cerebellar atrophy and occasional macrocephaly (D'Incerti et al., 1998 L. D'Incerti, L. Farina, I. Moroni, G. Uziel and M. Savoiardo, l-2-Hydroxyglutaric aciduria: MRI in seven cases, Neuroradiology 40 (1998), pp. 727-733. View Record in Scopus ¦ Cited By in Scopus (33)D'Incerti et al., 1998). MRI findings in affected dogs differ somewhat in distribution, having been reported as diffuse signal change within the grey matter of the cerebral cortex, basal ganglia, thalamus, brainstem and cerebellum (Abramson et al., 2003).

Diabetes Mellitus:

J Am Vet Med Assoc. 2000 May 1;216(9):1414-7.

Breed distribution of dogs with diabetes mellitus admitted to a tertiary care facility.

Hess RS, Kass PH, Ward CR.

Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104-6010, USA.

OBJECTIVE: To determine which dog breeds are at low and high risk for developing diabetes mellitus (DM). DESIGN: Cohort study. ANIMALS: Hospital population of 221 dogs with DM and 42,882 dogs without DM during 5.5 years. PROCEDURE: 165 breeds (including a mixed-breed category) were represented in the hospital population. Breed-specific expected numbers of dogs with DM were calculated by multiplying the proportion of all dogs admitted to the hospital that were determined to have DM during the study period by the breed-specific totals during the study period. Breeds or breed groups evaluated in the analysis (n = 20) were restricted to those that had a combined observed and expected count > 5 to document breeds at low and high risk for developing DM. Proportionate changes in the risk of developing DM by breed were calculated and presented using exact odds ratios, 95% confidence intervals, and P values. Mixed-breed dogs were chosen as the reference breed. RESULTS: Samoyeds, Miniature Schnauzers, Miniature Poodles, Pugs, and Toy Poodles were at high risk for developing DM. Dog breeds found to be at low risk for developing DM were German Shepherd Dog, Golden Retriever, and American Pit Bull Terrier. CONCLUSION AND CLINICAL RELEVANCE: The finding that certain dog breeds are at low or high risk for developing DM suggests that some genetic defects may predispose dogs to development of DM, whereas other genetic factors may protect dogs from development of DM.

PMID: 10800511 [PubMed - indexed for MEDLINE]

Chronic Renal diseases:

Aust Vet J. 2002 Jun;80(6):353-61.

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers.

O'Leary CA, Ghoddusi M, Huxtable CR.

Division of Veterinary Pathology and Anatomy, The University of Queensland.

OBJECTIVE: To describe the renal lesions in Bull Terrier polycystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). DESIGN: Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. RESULTS: In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. CONCLUSION: This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously.

PMID: 12153062 [PubMed - indexed for MEDLINE]

Kidney Int. 1995 Mar;47(3):758-65.

Bull terrier hereditary nephritis: a model for autosomal dominant Alport syndrome.

Hood JC, Savige J, Hendtlass A, Kleppel MM, Huxtable CR, Robinson WF.

Section of Pathology, School of Veterinary Studies, Murdoch University, Perth, Western Australia.

Bull terrier hereditary nephritis is inherited as an autosomal dominant disease and causes renal failure at variable ages in affected dogs. The aims of this study were to compare the clinical, ultrastructural and immunohistochemical features of bull terrier hereditary nephritis with the characteristics of the human forms of Alport syndrome. Many animals with bull terrier hereditary nephritis have hematuria, and some have anterior lenticonus. However, deafness is not associated with the renal disease, and affected dogs do not have the large platelets that are occasionally seen in patients with autosomal Alport syndrome. The glomerular capillary basement membrane (GCBM) in affected bull terriers has an identical ultrastructural appearance to that seen in X-linked Alport syndrome, with lamellations and intramembranous electron-dense deposits. However, both the Goodpasture and the Alport antigens, which represent parts of the alpha 3(IV) and alpha 5(IV) collagen chains, respectively, are present in the GCBM of affected dogs. Bull terrier hereditary nephritis represents an animal model for autosomal dominant Alport syndrome, and can be used to further examine how genetic mutations affect a basement membrane protein and the corresponding membrane structure.

PMID: 7752574 [PubMed - indexed for MEDLINE]

Vet Rec. 1990 May 5;126(18):456-9.

Hereditary nephritis in the bull terrier: evidence for inheritance by an autosomal dominant gene.

Hood JC, Robinson WF, Huxtable CR, Bradley JS, Sutherland RJ, Thomas MA.

Division of Veterinary Biology, School of Veterinary Studies, Murdoch University, Western Australia.

A high prevalence of renal failure has been reported in bull terriers in Australia. The pattern of inheritance was analysed in a family of 33 bull terriers in which 10 dogs had renal disease manifested by proteinuria, ultrastructural abnormalities in the glomerular basement membrane, renal failure, or 'end stage' kidneys. The presence of at least one affected parent for each affected offspring, the approximately equal male/female ratio and the apparent absence of 'generation-skipping', strongly supported an autosomal dominant mode of inheritance, assuming a fully penetrant single major gene locus. Further evidence was not compatible with either an autosomal recessive or X-linked inheritance pattern. This contrasts with the X-linked inheritance shown in Alport's-type human hereditary nephritis and hereditary glomerulopathy in the samoyeds. Hereditary nephritis in the bull terrier should be a useful model for non-Alport's-type human hereditary nephritis, which is also reported to have an autosomal dominant inheritance pattern.

PMID: 2356601 [PubMed - indexed for MEDLINE]

Aust Vet J. 1989 Jul;66(7):193-5.

Chronic renal disease in bull terriers.

Robinson WF, Shaw SE, Stanley B, Huxtable CR, Watson AD, Friend SE, Mitten R.

School of Veterinary Studies, Murdoch University, Western Australia.

Chronic renal failure was diagnosed in 15 Bull terrier dogs. The dogs ranged in age from one to 8 years. History and clinical findings typically included lethargy, anorexia, polyuria, polydipsia and weight loss. Affected dogs were azotaemic, had elevated serum phosphate and cholesterol, and proteinuria was apparent in all dogs tested (13/13). The concentration of urine was consistently in the nil to minimally concentrated range (specific gravities 1.011-1.017). In those dogs necropsied, both kidneys were approximately two-thirds normal size, tough in consistency, with a pale cortex and a finely nodular capsular surface. Histologically, there was marked nephron loss, diffuse interstitial fibrosis and focal dense radial fibrosis which was especially evident in the renal medulla. Tubular dilation was widespread with focal mineralisation of tubular epithelium and adjacent basement membranes. Glomeruli were often shrunken and segmentally fibrotic. Some Bowman's spaces were extremely dilated. Many less severely affected glomeruli had thickened basement membranes.

PMID: 2775060 [PubMed - indexed for MEDLINE]

N Z Vet J. 1989 Jun;37(2):79-82.

Familial progressive nephropathy in young Bull Terriers.

Jones BR, Gething MA, Badcoe LM, Pauli JV, Davies E.

Department of Veterinary Clinical Sciences, Massey University, Palmerston North.

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes. The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.

PMID: 16031526 [PubMed]

Tail Chasing:

J Am Vet Med Assoc. 1998 Apr 15;212(8):1252-7.

Description and development of compulsive tail chasing in terriers and response to clomipramine treatment.

Moon-Fanelli AA, Dodman NH.

Department of Clinical Sciences, School of Veterinary Medicine, Tufts University, North Grafton, MA 01536, USA.

Comment in:

J Am Vet Med Assoc. 1998 Jul 15;213(2):198-9.

OBJECTIVE: To identify factors associated with onset and continued elicitation of tail chasing in Bull Terriers and other terriers and to determine response to treatment with clomipramine hydrochloride, a serotonin-reuptake inhibitor. DESIGN: Prospective study. ANIMALS: 18 tail-chasing terriers (15 Bull Terriers, 1 Miniature Bull Terrier, 1 American Staffordshire Terrier, 1 Jack Russell Terrier). PROCEDURE: 5 dogs were evaluated for tail chasing by a veterinarian at the behavior clinic of the veterinary teaching hospital and 13 dogs were evaluated by the owner's local veterinarian, who confirmed the diagnosis and treated the dog. It was recommended that all dogs in the study be given clomipramine orally at a dosage of 1 to 2 mg/kg (0.5 to 0.9 mg/lb) of body weight, every 12 hours. RESULTS: Of the 18 dogs, 15 were treated with clomipramine within the recommended dosage range, and 3 dogs required treatment at a slightly higher dosage range to control tail chasing. After 1 to 12 weeks of treatment, 9 of 12 (75%) dogs were reported to have a 75% or greater improvement (reduction) in tail chasing. CLINICAL IMPLICATIONS: Findings of this study may aid in recognition and treatment of compulsive tail chasing. In conjunction with appropriate management changes, clomipramine administration appears to be an effective treatment for this otherwise refractory condition.

PMID: 9569164 [PubMed - indexed for MEDLINE]

J Am Vet Med Assoc. 1993 Mar 1;202(5):758-60.

Tail chasing in a bull terrier.

Dodman NH, Bronson R, Gliatto J.

Section of Anesthesia and Behavioral Pharmacology, School of Veterinary Medicine, Tufts University, North Grafton, MA 01536.

A Bull Terrier that was continuously chasing its tail was examined clinically, electroencephalographically, and by computed tomography of the head. The dog was also given test treatments with an anticonvulsant (diazepam) and a pure opioid antagonist (naloxone). The dog appeared to be hysterical and dissociated from its surroundings. Electroencephalography revealed a seizure pattern that was most marked over the temporal lobe, and computed tomography revealed mild hydrocephalus. Diazepam effectively controlled tail chasing, whereas naloxone did not. The dog was discharged on anticonvulsant therapy but subsequently had to be euthanatized when aggression developed. Results of examination and treatment have led the investigators to propose a hereditary mechanism for tail chasing, perhaps related to zinc malabsorption.

PMID: 8454509 [PubMed - indexed for MEDLINE]

(Lethal) skin related problems:

J Am Vet Med Assoc. 1986 Apr 15;188(8):833-9.

Lethal acrodermatitis in bull terriers.

Jezyk PF, Haskins ME, MacKay-Smith WE, Patterson DF.

A lethal syndrome characterized clinically by growth retardation, progressive acrodermatitis, chronic pyoderma and paronychia, diarrhea, pneumonia, and abnormal behavior was observed in 17 related Bull Terrier pups. Median survival time was 7 months. Laboratory evaluation revealed non-degenerative neutrophilia, consistently low activities of serum alkaline phosphatase and alanine transaminase, and frequently, hypercholesterolemia. Lymphocyte blastogenic responses were decreased and there was dysgammaglobulinemia in pups in which quantitative studies of immunoglobulins were made. The mean of plasma zinc concentrations in 5 affected pups was significantly lower than the mean of age- and breed-matched controls. Pathologic findings included parakeratosis, hyperkeratosis, and superficial bacterial infections of the skin. There was severe reduction of lymphocytes in T-lymphocyte areas of lymphoid tissue. Bronchopneumonia and dilatation of the cerebral ventricles were found in most affected pups. Family studies indicated that the syndrome is inherited as an autosomal recessive trait. In spite of its similarities to lethal trait A46 in Black Pied Danish cattle and acrodermatitis enteropathica in man, oral or parenteral treatment with zinc failed to ameliorate the clinical signs of the syndrome.

PMID: 3710872 [PubMed - indexed for MEDLINE]

Klik hier voor meer honden artikelen.

www.hondenwinkel.nl, Alles voor uw hond, online bestellen


Alles voor uw hond. Begin ook met geld besparen door online te bestellen.


  Rate this page

5 Stars. Average rating: 5 from 8 votes.

  If you have any comments you can submit them here

[ 2010-10-20 ] :: perro
evidence-based. good stuff!

Bull and Terrier Breeds, origins of Bull & Terrier breeds Bull and Terriers - Research English Bull Terrier (EBT) and influence in game dogs
Origins of Bulldog and Mastiff Breeds 1 Origins of Bulldog and Mastiff Breeds 2 Origins of Bulldog and Mastiff Breeds 3
Staffordshire Bull Terrier - Height and Weight Ratios Original and Revised Tosa Inu - Working Type


Top of Page
Bookmark and Share
Top of Page
Home
This site and all its content is © of and hosted by: By Spartan Law!