Myokymia and neuromyotonia in 37 Jack Russell terriers

The clinical and clinicopathological characteristics, treatment and outcome of vermicular muscle contractions (myokymia) and generalized muscle stiffness (neuromyotonia) in 37 Jack Russell terriers were evaluated retrospectively. Thirty dogs were affected by both disorders, whereas seven were presented with myokymia and never developed neuromyotonia. Clinical signs started at the mean age of 8 months. Except for signs of myokymia and neuromyotonia, clinical and neurological examination was normal in all dogs. Thirty dogs demonstrated typical signs of hereditary ataxia.Changes in serum chemistry included increased creatine kinase, aspartate aminotransferase and alanine aminotransferase concentrations. Electromyographic abnormalities, especially in muscles showing macroscopically visible myokymia, consisted of semirhythmic bursts of doublet, triplet, or multiplet discharges of a single motor unit. The amplitudes varied between 80 μV and 1 mV and occurred with an interburst frequency between 10 and 40 Hz and an intraburst frequency between 150 and 280 Hz.Most dogs were treated with a sodium channel blocker with variable results. Seven dogs died (most likely because of hyperthermia) or were euthanased during a neuromyotonic attack; 15 dogs were euthanased due to worsening of clinical signs, or lack of or no long-lasting effect of medication, and three were euthanased for unknown or unrelated reasons. Nine dogs were lost to follow-up and three were still alive 5–10.5 years after the start of clinical signs. In conclusion, young Jack Russell terriers with myokymia and neuromyotonia should undergo a complete blood and electrophysiological examination. Long-term prognosis is not favourable.     

Cerebellar cortical degeneration in adult American Staffordshire Terriers

Adult-onset cerebellar cortical degeneration recently has been reported in American Staffordshire Terriers. We describe the clinical and histopathologic features of this disease and examine its mode of inheritance in 63 affected dogs. The age at which neurologic deficits 1st were recognized varied from 18 months to 9 years, with the majority of dogs presented to veterinarians between 4 and 6 years of age. Time from onset of clinical signs to euthanasia varied from 6 months to 6.5 years, with the majority of affected dogs surviving from 2 to 4 years. Initial neurologic findings included stumbling, truncal sway, and ataxia exacerbated by lifting the head up and negotiating stairs. Signs progressed to obvious ataxia characterized by dysmetria, nystagmus, coarse intention tremor, variable loss of menace reaction, marked truncal sway, and falling with transient opisthotonus. With continued progression, dogs became unable to walk without falling repeatedly. Cerebellar atrophy was visible on magnetic resonance images and on gross pathology. Histopathologic findings included marked loss of Purkinje neurons with thinning of the molecular and granular layers and increased cellularity of the cerebellar nuclei. The closest common ancestor of the dogs was born in the 1950s and inheritance was most consistent with an autosomal recessive mode of transmission with a prevalence estimated at 1 in 400 dogs. This inherited disease is comparable to the group of diseases known as spinocerebellar ataxias in humans. Many spinocerebellar ataxias in humans are caused by nucleotide repeats, and this genetic aberration merits investigation as a potential cause of the disease in American Staffordshire Terriers.     

A Homozygous KCNJ10 Mutation in Jack Russell Terriers and Related Breeds with Spinocerebellar Ataxia with Myokymia,Seizures, or Both

Background

Juvenile‐onset spinocerebellar ataxia has been recognized in Jack Russell Terriers and related Russell group terriers (RGTs) for over 40 years. Ataxia occurs with varying combinations of myokymia, seizures, and other signs of neurologic disease. More than 1 form of the disease has been suspected.

Hypothesis/Objectives

The objective was to identify the mutation causing the spinocerebellar ataxia associated with myokymia, seizures, or both and distinguish the phenotype from other ataxias in the RGTs.

Animals

DNA samples from 16 RGTs with spinocerebellar ataxia beginning from 2 to 12 months of age, 640 control RGTs, and 383 dogs from 144 other breeds along with the medical records of affected dogs were studied.

Methods

This case‐control study compared the frequencies of a KCNJ10 allele in RGTs with spinocerebellar ataxia versus control RGTs. This allele was identified in a whole‐genome sequence of a single RGT with spinocerebellar ataxia and myokymia by comparison to whole‐genome sequences from 81 other canids that were normal or had other diseases.

Results

A missense mutation in the gene coding for the inwardly rectifying potassium channel Kir4.1 (KCNJ10:c.627C>G) was significantly (P < .001) associated with the disease. Dogs homozygous for the mutant allele all had spinocerebellar ataxia with varying combinations of myokymia and seizures.

Conclusions and Clinical Importance

Identification of the KCNJ10 mutation in dogs with spinocerebellar ataxia with myokymia, seizures, or both clarifies the multiple forms of ataxia seen in these breeds and provides a DNA test to identify carriers.     

Case Report Cutaneous vasculitis in five Jack Russell Terriers

Abstract A new, possibly breed associated, vasculitis of Jack Russell Terriers is described. Lesions include alopecia and focal crusted ulcers of the distal extremities and bony prominences. Histopathological lesions include single cell necrosis of the epithelium, pigmentary incontinence, leucocytoclastic vasculitis and ischaemic degeneration of hair follicles. Dermal oedema and an infiltrate of lymphocytes and/or macrophages are often seen. Clinically and histopathologically the disease most closely resembles dermatomyositis of Collies and Shetland sheepdogs but the obvious breed discrepancy makes systemic lupus erythematosus the most likely differential diagnosis. Dapsone and anti-inflammatory doses of prednisone have proved to be satisfactory treatments. Résumé— Une nouvelle dermatose à prédisposition raciale, de type vascularite est décrite chez des jack russel terriers. Les lésions cliniques incluent une alopécie, des ulcèrations focales et croûteuses des extrémités distales et des points de pression. Les lésions histolopathologiques montrent des nécroses isolées des kératinocytes, une incontinence pigmentaire, une vascularite leucocytoclasique et une dégénérescence ischémique des follicules pileux. Un oedème dermique et une infiltration lymphocytaire et/ou macrophagique sont également observés. Sur les plans clinique et histopathologique, cette maladie ressemble plus aux dermatomyosites du Colley et du Shetland, mais la discordance raciale évidente fait du lupus érythémateux systémique le diagnostic différentiel le plus vraisemblable. La dapsone et la prednisone à dose antiinflammatoire sont des traitements satisfaisants. [Parker, W.M., Foster, R.A. Cutaneous vasculitis in five Jack Russell Terriers (Vascularite cutanée chez 5 jack russel terriers). Veterinary Dermatology 1996; 7 : 109–115.] Resumen Se describe una vasculitis nueva, posiblemente asociada a la raza en el terrier Jack Russell. Las lesiones incluyen alopecia y ulceraciones costrosas en las extremidades distales y en prominencias óseas. Las lesiones histopatológicas incluyen necrosis celular individual del epitelio, incontinencia pigmentaria, vasculitis leucocitoclástica y degeneración isquémica de los foliculos pilosos. Con frecuencia se observa edema dérmico y una infiltración por linfocitos y/o macrófagos. Este cuadro se asemeja clinica e histopatológicamente a la dermatomiositis de los perros Collie y Shetland pero la distancia obvia entre estas razas hace que el diagnóstico diferencial más probable sca el de lupus eritematoso sistémico. Se consiguieron tratamientos satisfactorios con Dapsona y dosis antiinflamatorias de prednisona. [Parker, W.M., Foster, R.A. Cutaneous vasculitis in five Jack Russell Terriers (Vasculitis cutánea en cinco Terriers Jack Russell). Veterinary Dermatology 1996; 7 : 109–115.] Zusammenfassung— Es wird eine neue, möglicherweise rasseabhängige Vaskulitis bei Jack Russell Terriern beschrieben. Die Veränderungen bestehen in Alopezie, fokalen verkrusteten Geschwüren der distalen Extremitäten und Knochevorsprünge. Histopathologische Veränderungen bestehen in Einezelzellnekrose des Epithels, Pigmentinkontinenz, leukozytoklastischer Vaskulitis und ischämischer Degeneration der Haarfollikel. Dermales ödem und Lymphozyten- und/oder Makrophageninfiltrate werden häufig beobachtet. Klinisch und histopathologisch ähnelt die Erkrankung sehr der Dermatomyositis von Collie und Sheltie, aber die offensichtliche Rassendiskrepanz läßt den systemischen Lupus erythematosus als wahrscheinlichste Differentialdiagnose erscheinen. Dapson und entzündungshemmende Dosen von Prednison zeigten sich als ausreichende Behandlung. [Parker, W. M., Foster, R. A. Cutaneous vasculitis in five Jack Russell Terriers (Kutane Vaskulitis bei fünf Jack Russell Terriern). Veterinary Dermatology 1996; 7 : 109–115.]     

Clinical and histopathological features and prognosis of gastrointestinal adenocarcinomas in Jack Russell Terriers

There has been an increase in the number of Jack Russell Terriers (JRTs) diagnosed with adenomas and adenocarcinomas of the gastrointestinal tract in Japan. This study retrospectively investigated the clinical and histopathological features and prognosis of adenocarcinomas arising in the gastrointestinal tract in JRT dogs. Seven JRTs and 39 dogs of other breeds diagnosed with gastrointestinal adenocarcinoma were included in the study. The most common sites of gastrointestinal adenocarcinoma in JRTs were the pylorus and rectum. On histopathological examination, these adenocarcinomas showed a papillary or tubular growth pattern, and the lesions were confined within the mucosal epithelium and poorly invasive. Among all dogs with gastric adenocarcinoma, the median survival time (MST) for five of the JRTs could not be determined because more than half of the cases remained alive, while the MST for nine non-JRT dogs was 34 days. Among all dogs with adenocarcinoma in the large intestine, the MST for three of the JRTs could not be determined, while the MST for nine non-JRT dogs was 1,973 days. The difference in MST between JRT and non-JRT dogs with gastric adenocarcinoma was significant (P=0.0220). Since gastrointestinal adenocarcinomas in JRTs show distinct characteristics with respect to their clinical features, treatment course, and prognosis, a different surgical and medical treatment plan should be considered compared to the management of gastrointestinal adenocarcinomas in other dog breeds.     

Inheritance of cataracts and primary lens luxation in Jack Russell Terriers

OBJECTIVE: To characterize heritability and mode of inheritance of cataracts and primary lens luxation in Jack Russell Terriers. ANIMALS: 872 Jack Russell Terriers from which buccal epithelial cells were collected and phenotypes for cataracts and lens luxation were determined and an additional 1,898 Jack Russell Terriers without phenotypic information used to complete pedigree relationships and that were included in the analyses. PROCEDURES: Narrow-sense heritabilities and genetic correlation for cataracts and lens luxation were modeled by use of threshold analysis, whereas complex segregation analysis was used to characterize mode of inheritance. For the analyses, dogs < 6 years old, unless confirmed as having cataracts or lens luxation, were classified as an unknown phenotype. The possible involvement of an HSF4 mutation in cataracts was determined by DNA sequencing. RESULTS: Cataracts and primary lens luxation were highly heritable and genetically correlated, and neither was controlled by a single gene. Cataracts were not associated with an HSF4 mutation. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of the data indicated that concerted selection against both cataracts and primary lens luxation when choosing breeding animals can be used to improve ocular health in Jack Russell Terriers.     

Hereditary ataxia in the Jack Russell Terrier--clinical and genetic investigations

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.     

A KCNJ10 mutation previously identified in the Russell group of terriers also occurs in Smooth-Haired Fox Terriers with hereditary ataxia and in related breeds

Background

Hereditary ataxias with similar phenotypes were reported in the Smooth-Haired Fox Terrier, the Jack Russell Terrier and the Parson Russell Terrier. However, segregation analyses showed differing inheritance modes in these breeds. Recently, molecular genetic studies on the Russell group of terriers found independent mutations in KCNJ10 and CAPN1, each associated with a specific clinical subtype of inherited ataxia. The aim of this study was to clarify whether or not Smooth-Haired Fox Terriers with hereditary ataxia and dogs of other related breeds harbor either of the same mutations. A sub goal was to update the results of KCNJ10 genotyping in Russell group terriers.

Findings

Three Smooth-Haired Fox Terriers with hereditary ataxia and two Toy Fox Terriers with a similar phenotype were all homozygous for the KCNJ10 mutation. The same mutation was also found in a heterozygous state in clinically unaffected Tenterfield Terriers (n = 5) and, in agreement with previous studies, in Jack Russell Terriers, Parson Russell Terriers, and Russell Terriers.

Conclusions

A KCNJ10 mutation, previously associated with an autosomal recessive spinocerebellar ataxia in Jack Russell Terriers, Parson Russell Terriers, and Russell Terriers segregates in at least three more breeds descended from British hunting terriers. Ataxic members of two of these breeds, the Smooth-Haired Fox Terrier and the Toy Fox Terrier, were homozygous for the mutation, strengthening the likelihood that this genetic defect is indeed the causative mutation for the disease known as “hereditary ataxia” in Fox Terriers and “spinocerebellar ataxia with myokymia, seizures or both” in the Russell group of terriers.     

Footpad Hyperkeratosis in a Family of Dogues de Bordeaux

Abstract— Footpad hyperkeratosis is reported in a male Dogue de Bordeaux dog and six of his offspring. In each dog, the lesions were noted by the owners before six months of age. The hyperkeratosis can be improved but not resolved by regular footsoaks in propylene glycol, and secondary bacterial infection can be controlled with antibiotic therapy. This appears to be a new autosomal genodermatosis, but the exact mode of inheritance is unknown. Résumé— L'hyperkératose des coussinets plantaires chez un chien male de race Dogue de Bordeaux ainsi que chez six de ses chiots est rapportée. Dans chaque cas, les lésions ont été notées par le propriétaire avant l'âge de six mois. L'hyperkératose peut être améliorée mais non guéri par des bains de pieds réguliers dans du propylène glycol et l'infection bactérienne secondaire peut être controlée à l'aide d'une antibiothérapie orale. Ceci semble être une nouvelle génodermatose autosomique, toutefois le mode d'héridité exact n'est pas connu. Zusammenfassung— Es wird über eine Hyperkératose der Pfotenballen bei einem Bordeauxdoggenrüden und bei sechs seiner Nachkommen berichtet. Bei jedem Tier wurden die Veränderungen vor dem Alter von 6 Monaten vom Besitzer bemerkt. Die Hyperkératose kann durch regelmäßige Pfotenbäder mit Propylenglykol gebessert, nicht aber geheilt werden. Die sekundäre bakterielle Infektion kann durch antibiotische Therapie kontrolliert werden. Bei dem vorliegenden Fall scheint es sich um eine neue autosomale Génodermatose zu handeln, der genaue Erbgang ist jedoch unbekannt. Resumen En un dogo de Burdeos macho y 6 cachorros de su camada se reportó hiperkeratosis plantar. En cada caso, las lesiones fueron observadas por a el dueño antes de los seis meses de edad. Baños regulares con propilen glicol pueden controlar la hiperkeratosis, pero no curarla y la infección secundaria causada por bacteria, es susceptible at tratamiento con antibióticos. Aparentemente esto es debido a un nueva genodermatosis autosómica, pero el mode exacto de transmisión hereditaria es desconocido.     

Clinical, bronchoscopic, histopathologic, diagnostic imaging, and arterial oxygenation findings in West Highland White Terriers with idiopathic pulmonary fibrosis

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, interstitial lung disease primarily affecting West Highland White Terriers (WHWTs). Objective: To describe the clinicopathological and diagnostic imaging features in WHWTs with IPF. Animals: Twelve WHWTs with IPF and 14 healthy control WHWTs. Method: Prospective study. Clinical signs and findings of physical examination, blood and arterial blood gas analyses, radiography, high‐resolution computed tomography (HRCT), bronchoscopy and bronchoalveolar lavage (BAL) of IPF dogs were obtained and compared with controls. Histopathologic changes in IPF dogs were evaluated. Results: Mean partial pressure of oxygen was significantly lower in IPF (mean ± SD, 65.5 ± 15.4 mmHg) than in controls (99.1 ± 7.8 mmHg, P<.001). The alveolar‐arterial oxygen gradient was significantly higher in IPF (50.1 ± 17.3 mmHg) than in controls (17.5 ± 4.9 mmHg, P<.001). In HRCT, ground glass opacity (GGO) was detected in all IPF dogs, traction bronchiectasis in 4, and honeycombing in 1. Bronchoscopic airway changes were noted in all IPF dogs. On BAL fluid (BALF) cytology, the total cell count (TCC) was higher in IPF dogs, and the numbers but not the percentages of macrophages, neutrophils, and mast cells were increased. On histopathology, multifocal or diffuse interstitial fibrosis, type II pneumocyte hyperplasia, prominent intraalveolar macrophages, distortion of alveolar architecture, and emphysematous change were detected. Conclusion and Clinical Importance: IPF causes substantial hypoxemia. In HRCT, GGO is a consistent finding. IPF dogs have concurrent airway changes and an increase in BALF TCC.     

Progressive ataxia and seizures in a Cocker Spaniel: a new type of neurodegenerative disease with novel intra-neuronal inclusions

AIMS: To describe the histopathological lesions of a new canine disease characterised by progressive ataxia, head tremor and seizures, and to deduce the cause of the lesions.

METHODS: Formalin-fixed tissues were processed into paraffin wax and epoxy resin for light and transmission electron microscopy of variously stained tissue sections.

RESULTS: Significant lesions relevant to the disease were found only in the brain. They consisted of hypoplasia of the cerebellum and the presence of large pale inclusions in the perikaryon of neurons in the neocortex and in macrophages. The inclusion material was not compartmentalised and did not stain for carbohydrate, mucopolysaccharide or lipid. This material displaced nuclei to the periphery of the cells where they were seen as basophilic distorted crescent-shaped structures.

CONCLUSIONS: The inclusions were probably made of polymerised protein similar, though not identical, to those of Pick, Lewy and Collins bodies that characterise a variety of chronic neurodegenerative diseases of humans. A genetic basis to this disease was considered probable.     

Idiopathic Pyogranulomatous Inflammation and Leukocytoclastic Vasculitis of the Nasal Planum, Nostrils and Nasal Mucosa in Scottish Terriers in Denmark

Abstract— A unique, presumably hereditary pyogranulomatous and vasculitic disorder of the nasal planum, nostrils and nasal mucosa is described in five Scottish terriers. Clinical signs were first heralded by a bilateral nasal discharge at 3 to 4 weeks of age or a bilateral ulcerative and destructive process of the nasal planum, nostrils and nasal mucosa at 5 to 6 months of age. Histopathological findings included nodular-to-diffuse pyogranulomatous inflammation with concurrent leukocytoclastic vasculitis. Special stains were negative for microorganisms. Therapy was unsuccessful and all dogs were euthanized. Résumé— Un pyogranulome et une vasculite isolés planaum nasale, des narines et de la muqueuse nasale, probablement héréditaires, sont décrits chez 5 Scottish Terriers. Les premiers signes cliniques sont un jetage bilatéral à l'áge de 3–4 semaines ou une ulcération et une destruction bilatérale du planaum nasale, des narines et de la muqueuse nasale à 5–6 mois. Les lésions histologiques sont celles d'une inflammation nodulaire à pyogranulomateuse diffuse associée à une vasculite leucocyoclasique. Des colorations spécifiques n'ont permis de meure en évidence des microorganismes. Les traitements on été inefficaces et les animaux euthanasiés. Zusammenfassung— Bei fünf Scotchterriern wird eine einzigartige, wahrscheinlich erbliche, pyogranulomatöse und vaskulitische Veränderung des Nasenspiegels, der Nasenöffnungen und der Nasenschleimhaut beschrieben. Die klinischen Symptome wurden zuerst durch einen beidseitigen Nasenausfluß im Alter von 3 bias 4 Wochen oder durch beidseitige, ulzerative und destruktive Veränderungen des Nasenspiegels, der Nasenöffhungen und der Nasenschleimhaut im Alter von 5 bis 6 Monaten angekündigt. Die histopathologischen Befunde bestanden unter anderem in nodulärer bis diífuser pyogranulomatöser Entzündung mit gleichzeitiger leukozytoklastischer Vaskulitis. Spezialfärbungen auf Mikoorganismen verliefern negative. Die Therapie war erfolglos, alle Hunde wurden euthanasiert. Resumen Un único, presumiblente hereditario piogranulomatoso y vasculítico trastorno del piano nasal, ventanas y mucosa nasal es descrito en cinco Scottish Terriers. Los signos clínicos fueron anunicados primero por una descarga nasal bilateral entre las 3 y 4 semanas de edad o un proceso bilateral, ulcerativo y destructivo del piano nasal, ventanas y mucosa nasal entre, los 5 y 6 meses de edad. Los descubrimientos histopatológicos incluían inflammación piogranulomatosa de nodular a difusa con vasculitis leucocitoclástica concurrente. Manchas especiales eran negatives para microorganismos. La terapia no fue exitosa y se practicó la eutanasia a todos los perros.     

Cataracts in Labrador Retriever and Jack Russell Terrier From the United Kingdom: A Two-Year Retrospective Study

Cataracts are among the most common ocular diseases, and are a leading cause of vision loss in humans and dogs. Jack Russell Terriers (JRT) and Labrador Retrievers (LR) are among the most popular canine breeds in the United Kingdom, and also among the most affected by cataracts.This study aimed to analyze the clinical features and the surgical outcome of cataracts in JRT and LR in an ophthalmologic reference Veterinary Hospital in the United Kingdom. For that purpose, medical records from JRT and LR diagnosed with cataracts between January 2015 and December 2016 were retrospectively evaluated. Data related to identification, clinical history, preoperative features, and surgical outcomes were analyzed.Forty-four dogs (81 eyes), including 26 JRT and 18 LR, were enrolled in the study. Mean ages were 10.2 ± 3.2 years in JRT and 8.5 ± 3.7 years in LR. Twenty-eight (63.6%) were females and 16 (36.4%) were males. Most dogs (84.1%) presented with bilateral cataracts. Nuclear and cortical cataracts were the most prevalent type in both breeds (JRT: n?=?30, 61.2%; LR: n?=?16, 50.0%), although subcapsular cataracts were also frequent in LR (n?=?10, 31.3%). Significant differences in cataract location within the lens were detected between the two breeds (P?=?.002).Senile in JRT (n?=?7) and genetic in LR (n?=?7) were the most common etiologies. Concomitant ocular lesions were more frequent in dogs presented with cataracts in advanced stages, and included lens (n?=?18; JRT: n?=?15; LR: n?=?3) and retinal alterations (n?=?8; JRT: n?=?2; LR: n?=?6), and glaucoma (n?=?6; JRT: n?=?5; LR: n?=?1). Thirty-three animals (75.0%, 51 eyes) were submitted to phacoemulsification with intraocular lens placement. Of these, 28 eyes (54.9%; JRT: n?=?21; LR: n?=?7) were visual, 19 eyes (37.3%; JRT: n?=?11; LR: n?=?8) presented impaired vision and four eyes (7.8%; JRT: n?=?0; LR: n?=?4) were blind at last clinical record. Postoperative complications were detected in 11 eyes (21.6%), and were more frequent in dogs presented with cataracts in advanced stages.These results and the multifactorial nature of cataracts call for further studies to identify and characterize the variables in a broader assessment, including other breeds and influencing factors.     

Clinical and magnetic resonance imaging characteristics of quadrigeminal cysts in dogs

BACKGROUND: Quadrigeminal cysts (QC) are the most common intracranial intra-arachnoid cysts in dogs, primarily affecting small breeds. Clinical significance is controversial. HYPOTHESIS: Male, brachycephalic, small breed dogs are predisposed to QC, and objective measurement of parenchymal compression can distinguish clinically relevant QC from incidental findings. ANIMALS: A total of 4,100 client-owned dogs. METHODS: A retrospective study that recorded signalment, history, clinical signs, and magnetic resonance imaging features. The degree of brain compression was evaluated in the presence of relevant clinical signs. The percentage compression of cerebellum and forebrain was calculated by comparing the expected to the actual diameter and longitudinal dimension, respectively. RESULTS: QC were diagnosed in 28 dogs, of which 21 (75%) were small breed dogs. Fifteen dogs (54%) were brachycephalic. Eighteen dogs were male, and 10 were female. Cerebellar, occipital lobe, or compression in both areas occurred in 86% (24/28 dogs). Clinical signs included focal and generalized seizures in 5 dogs and cerebellar signs in 6 dogs. Mean occipital lobe compression was 17% (SD = 4) in clinically affected and 10% (SD = 3) in normal dogs (P = .006). Occipital lobe compression >14% was always associated with clinical signs. The mean cerebellar compression was 18%, but there was no association between compression and clinical signs. The animals were more likely to develop clinical signs if both areas were compressed (P = .04). CONCLUSIONS AND CLINICAL IMPORTANCE: Parenchymal compression by QC can be incidental, and other central nervous system diseases must be excluded when assessing the clinical significance of QC. However, occipital lobe compression over 14% is likely to cause clinical signs.     

Clinical significance of plasma mannose concentrations in healthy and diabetic dogs

Circulating levels of monosaccharides can act as a reflection of systemic glucose/ energy metabolism. Characteristic changes observed in these levels can be seen in patients with diabetes and other metabolic disorders. There have been a few reports describing the significance of mannose metabolism as an energy source under physiological and pathological conditions. However, the relationship between circulating levels of mannose and the pathophysiology of diabetes mellitus are unknown in dogs. This study examined circulating levels of mannose between healthy control and diabetic dogs and evaluated the clinical significance of mannose levels in dogs. Diabetic dogs demonstrated a higher circulating level of mannose in comparison to normal healthy control dogs. Plasma mannose was positively correlated with plasma glucose and fructosamine, respectively. Interestingly, plasma mannose levels were affected by plasma insulin levels. In the context of feeding and glucose tolerance tests, plasma mannose levels responded to changes in circulating insulin levels. Circulating plasma mannose levels decreased after feeding in both control and diabetic animals in spite of observed insulin level differences. However, when glucose tolerance tests were given, a positive correlation between mannose levels and insulin levels was observed. Therefore, plasma mannose levels obtained via glucose tolerance testing may be used as a new diagnostic method for evaluating insulin resistance or deficiency in diabetic dogs.