Mucopolysaccharidosis IIIA (Sanfilippo syndrome) in a New Zealand Huntaway dog with ataxia

Aim: To investigate the nature of a progressive ataxia in a New Zealand Huntaway dog.

Methods: The affected dog was examined clinically before being humanely killed and necropsied. Selected tissues were submitted to light and electron microscopy and to biochemical analyses.

Results: The histological lesions were interpreted as indicative of one of the forms of mucopolysaccharidosis type-III (dMPS-III), a lysosomal storage disease. Biochemically there was a deficiency of heparan sulphamidase. All the heparan sulphate chains had non-reducing-end glucosamine-N-sulphate residues.

Conclusion: The disease is dMPS-IIIA (Sanfilippo syndrome). An autosomal recessive mode of inheritance can be provisionally assumed from the nature of this disease in other species.     

Black-hair follicular dysplasia in a New Zealand Huntaway dog

CASE HISTORY: A 6-year-old intact male New Zealand Huntaway dog had slowly progressive alopecia that was first observed at 12 weeks of age.

CLINICAL FINDINGS: Patchy alopecia was confined to the black-haired areas of the body, and was most evident on the head and dorsum of the body; tan-haired areas of skin appeared normal. Histological examination of black-haired skin revealed distended melanocytes and large aggregates of melanin within, and surrounding, the hair follicles and the epidermis. Macrophages distended with melanin were also visible within the perifollicular and superficial dermis, and follicular lumina were often plugged by keratin that contained aggregates of melanin. The follicles were dysplastic and few hair shafts were visible emerging from follicular infundibula within the sections.

DIAGNOSIS: The clinical and histological findings were consistent with black-hair follicular dysplasia (BHFD).

CLINICAL RELEVANCE: This is the first report of BHFD in a dog in New Zealand, and is the first report in a Huntaway. The most significant effect of BHFD is a predisposition to follicular plugging and secondary bacterial skin infections. Due to the hereditary nature of the follicular dysplasias, breeding from affected dogs should be discouraged. Histological examination of the skin is required to differentiate between the different follicular dysplasias as well as differentiating between follicular dysplasia and follicular atrophy due to endocrinopathy.     

Hip dysplasia in the New Zealand Huntaway and Heading dog

AIMS: To conduct a practice-based survey to obtain, for the first time, data on hip dysplasia in the New Zealand working dog breeds of Huntaway and Heading Dogs. METHODS: A mailed request and personal approaches to farmer clients of Taihape and Waimarino Veterinary Services were used to recruit dog owners from the Taihape district in the North Island of New Zealand. Recruited dogs were radiographed under anaesthesia in a standard position with both hind limbs extended so that the femurs were parallel and rotated medially. The standard scoring system adopted by the New Zealand Veterinary Association (NZVA) Hip Dysplasia Scheme was used to score the hip radiographs of the dogs. RESULTS: Radiographs of the hips of 141 dogs (93 Huntaways; 48 Heading Dogs), were evaluated. The overall prevalence of hip dysplasia (defined as a combined score from both hips of 10) was 17.7%. Prevalences in Huntaways and Heading Dogs were 23.6% and 6.3%, respectively; in this sample of dogs, the odds ratio (and 95% confidence interval) for Huntaways having a score of 10 was 4.6 (1.316.0) that of Heading Dogs. The average scores were 10.8 for Huntaways and 5.9 for Heading Dogs. Huntaways were at the higher end of the breed average scores for dogs recorded in the NZVA Hip Dysplasia Scheme and Heading Dogs at the lower end. CONCLUSIONS: This preliminary study indicates that hip dysplasia may be a problem in the Huntaway breed. Investigation of the epidemiology of the condition in this breed is warranted and consideration should be given to removing high-risk Huntaways from the breeding pool.     

Progressive myelopathy and neuropathy in New Zealand Huntaway dogs

Aim: To investigate the nature and cause of a progressive ataxia in three 20-month-old Huntaway dogs that were litter mates.

Methods: Affected dogs were examined before they were humanely killed and submitted to necropsy. Selected formalin-fixed tissues were examined by light and electron microscopy.

Results: The lesions were those of axon and myelin degeneration within sensory, proprioceptive and motor tracts of the spinal cord and to a lesser degree some peripheral nerves.

Conclusion: A progressive myelopathy and neuropathy, tentatively described as a central-peripheral distal axonopathy, was present in all 3 dogs.The cause was not determined but was likely to be either genetic or nutritional.

Clinical relevance: In the early stages of this disease, careful examination maybe necessary to distinguish the signs of ataxia from orthopaedic disease such as hip dysplasia. Affected animals are unlikely to be of use as working dogs.     

Progressive myelopathy and neuropathy in New Zealand Huntaway dogs

AIM: To investigate the nature and cause of a progressive ataxia in three 20-month-old Huntaway dogs that were litter mates. METHODS: Affected dogs were examined before they were humanely killed and submitted to necropsy. Selected formalin-fixed tissues were examined by light and electron microscopy. RESULTS: The lesions were those of axon and myelin degeneration within sensory, proprioceptive and motor tracts of the spinal cord and to a lesser degree some peripheral nerves. CONCLUSION: A progressive myelopathy and neuropathy, tentatively described as a central-peripheral distal axonopathy, was present in all 3 dogs. The cause was not determined but was likely to be either genetic or nutritional. CLINICAL RELEVANCE: In the early stages of this disease, careful examination may be necessary to distinguish the signs of ataxia from orthopaedic disease such as hip dysplasia. Affected animals are unlikely to be of use as working dogs.     

Cerebrospinal fluid from a dog with hind limb ataxia

A 9-year-old spayed female German Shepherd dog with a history of orthopedic disease was presented to the North Carolina State University Veterinary Teaching Hospital for evaluation of recent, progressive, bilateral, hindlimb ataxia. Analysis of cisternal and lumbar cerebrospinal fluid (CSF) samples revealed normal total nucleated cell counts and a mild increase in protein concentration in the lumbar sample. In cytocentrifuged specimens of both CSF samples, aggregates of refractile, angular to irregular, pale blue to colorless, crystalline material were observed in the background. Some of the material appeared birefringent under polarized light. Differentials for the material included contrast agent, epidural anesthetics or other pharmacologic agents, or artifact introduced through sample processing, collection, or handling. Based on investigation of clinical and laboratory processes it was determined that tubes used to collect CSF in the hospital recently had been changed from additive-free glass tubes to silica-coated shatter-resistant plastic tubes (BD Vacutainer Plus serum tubes, silicone-coated, Becton Dickinson). A cytocentrifuged preparation of saline placed in a silica-coated tube contained crystalline material identical to that observed in the CSF samples; saline placed in an additive-free glass tube contained no material. In this case, we document the microscopic appearance of highly concentrated silica particles in cytocentrifuged preparations of CSF and underscore the importance of recognizing and identifying this artifact in cytologic preparations.     

A syndrome resembling feline dysautonomia (Key-Gaskell syndrome) in a dog.

Dysautonomia, or autonomic nervous system dysfunction, was diagnosed in a 1-year-old dog. Clinical signs of disease included diarrhea, vomiting, prolapse of nictitating membranes, and urinary incontinence. Bilateral keratoconjunctivitis sicca, xerostomia, and decreased anal sphincter tone were also observed. On the basis of response to atropine, results of intradermal histamine testing and gastric motility studies, and ocular response to parasympathomimetics and sympathomimetics (direct and indirect acting), autonomic nervous system function was determined to be abnormal. Treatment with metoclopramide hydrochloride and bethanechol chloride resulted in improved attitude, appetite, Schirmer tear test response, and decrease in frequency of vomiting within 24 hours. Bladder function and anal tone improved within 3 weeks.     

Serratospiculosis in a New Zealand Falcon (Falco novaeseelandiae)

CASE HISTORY: An adult New Zealand falcon was presented with metacarpal fractures in the left wing. CLINICAL FINDINGS: In addition to the fractures, radiographs revealed an area of opacity in the air sacs. A few days after hospitalisation and initiation of treatment of the fractures, the bird developed signs of respiratory disease; the area of opacity was found to have increased in size and density. Treatment with antibiotics and nebulisation was commenced; the bird initially responded but respiratory signs subsequently worsened and the bird died. At necropsy, air sacculitis and bronchopneumonia were associated with numerous nematodes in the air sacs, which were morphologically consistent with Serratospiculum guttatum. DIAGNOSIS: Serratospiculosis CLINICAL RELEVANCE: The discovery of this parasite and the associated disease for the first time in New Zealand indicates that it should be considered in the differential diagnosis of respiratory disease in falcons and possibly other raptors in New Zealand.     

Tuberculosis in a New Zealand (Hooker's) sea lion

Extract

Tuberculosis has been described in seven species of pinnipeds. Based on host preference, phenotype and genetic and antigenic testing, the causal bacterium has been classified as a distinct species, Mycobacterium pinnipedii, within the M. tuberculosis complex. An adult male New Zealand sea lion (Phocarctos hookeri) was found dead on the Otago coastline in mid 2005. Gross necropsy revealed multiple caseous foci throughout the lungs, subcutaneous and thoracic lymph nodes, and mesenteric lymph nodes. Histopathological examination showed granulomatous lesions containing numerous intra-lesional acid fast organisms. The organism was confirmed as being a member of the M. tuberculosis complex, based on restriction enzyme analysis. Spoligotyping is pending. This is the first confirmed case of mycobacterial disease in a New Zealand sea lion.     

Serratospiculosis in a New Zealand Falcon (Falco novaeseelandiae)

CASE HISTORY: An adult New Zealand falcon was presented with metacarpal fractures in the left wing.

CLINICAL FINDINGS: In addition to the fractures, radiographs revealed an area of opacity in the air sacs. A few days after hospitalisation and initiation of treatment of the fractures, the bird developed signs of respiratory disease; the area of opacity was found to have increased in size and density. Treatment with antibiotics and nebulisation was commenced; the bird initially responded but respiratory signs subsequently worsened and the bird died. At necropsy, air sacculitis and bronchopneumonia were associated with numerous nematodes in the air sacs, which were morphologically consistent with Serratospiculum guttatum.

DIAGNOSIS: Serratospiculosis

CLINICAL RELEVANCE: The discovery of this parasite and the associated disease for the first time in New Zealand indicates that it should be considered in the differential diagnosis of respiratory disease in falcons and possibly other raptors in New Zealand.     

Presumptive tremorgenic mycotoxicosis in a dog in New Zealand, after eating mouldy walnuts

CASE HISTORY: A 1-year-old, intact male Labrador-cross dog vomited after eating walnuts that had been on the ground for 5 months. The dog then developed tremors, ataxia, increased salivation, and hyperaesthesia. CLINICAL FINDINGS: The dog had marked generalised tremors, ataxia and a temperature of 39.9 degrees C. Both pupils were of normal size and normally responsive to light. Vomiting was induced, and walnut shell was visible in the vomitus. DIAGNOSIS: Due to the sudden onset of tremors, lack of exposure to other convulsive toxins, and the evidence of ingestion of walnuts, the provisional diagnosis was tremorgenic mycotoxicosis. The dog was treated symptomatically, and made a full recovery over 18 hours. Tremorgenic mycotoxins were detected within walnuts collected from the dog's environment. CLINICAL RELEVANCE: Fungi that produce tremorgenic mycotoxins are present in New Zealand. Intoxication should be suspected in dogs that suddenly develop muscle tremors, especially if there is a history of ingestion of mouldy food 2-3 hours prior to the development of tremors.     

First report of a mecA-positive multidrug-resistant Staphylococcus pseudintermedius isolated from a dog in New Zealand

CASE HISTORY: A 14-year-old neutered male Sealyham terrier was referred for assessment of a persistent pyoderma. It had experienced numerous episodes of dermatitis involving pododermatitis, pyoderma and otitis over the previous 6 years.

CLINICAL FINDINGS: Superficial, focally deep and mucocutaneous pyoderma were present, with yellow mucoid exudate on both nares and the lower lips crusted with haemopurulent exudate. Epidermal collarettes were present on the dorsal and lateral trunk. There were peri-anal crusts and mild erythema was present on the concave aspect of both pinnae.

MICROBIOLOGICAL FINDINGS: Culture and microbiological testing identified Staphylococcus pseudintermedius as the infecting organism. Kirby-Bauer disc susceptibility testing revealed the isolate was resistant to numerous antimicrobials including oxacillin. PCR testing of the isolate identified the presence of the mecA gene which confers resistance to β-lactam antimicrobials. Pulsed field gel electrophoresis typing suggested the isolate was not related to the methicillin-resistant S. pseudintermedius that had been reported to be associated with canine infections in Western Australia.

DIAGNOSIS: Superficial, deep and mucus membrane pyoderma associated with a multi-drug resistant S. pseudintermedius.

CLINICAL RELEVANCE: This is the first recorded case of canine pyoderma involving methicillin-resistant multidrug-resistant S. pseudintermedius in New Zealand. Treatment of such cases is difficult because the number of effective and available antimicrobials is limited. This finding should raise the awareness of the veterinary and medical professions to the presence of such organisms in New Zealand and stimulate a discussion about possible biosecurity barriers, treatment strategies and prevention of zoonotic and nosocomial infections.     

Myelodysplastic syndrome with sideroblastic differentiation in a dog

A dog with myelodysplastic syndrome had microcytic hypochromic anemia, with siderocytes, poikilocytosis, hypersegmented neutrophils and giant platelets in peripheral blood. In bone marrow, the erythroid series showed immaturity, asynchronous maturation and sideroblasts. Dysgranulopoiesis and dysthrombopoiesis also were present, and hemosiderin was increased. Serum iron concentration was high, and both iron deficiency and lead toxicity were excluded as the cause of dyscrasia. This case represents a unique variant of myelodysplastic syndrome, best described as sideroblastic myelodysplasia. We propose the terms dyserythropoiesis, sideroblastic dyserythropoiesis, dyserythropoiesis with excess blasts, myelodysplasia and sideroblastic myelodysplasia to describe and categorize myelodysplastic syndromes in dogs.     

Abdominal compartment syndrome in a dog with babesiosis

Objective: To describe a case of abdominal compartment syndrome in a dog with babesiosis. Case summary: A 9‐year‐old female Bull Terrier presented with complicated babesiosis. Additional findings including respiratory distress, abdominal distension, and a decrease in urine output associated with an elevated abdominal pressure (23.5–25 cmH₂O) led to a further diagnosis of abdominal compartment syndrome. This case report describes the clinical course of both conditions through resolution. New information provided: Abdominal compartment syndrome is not well described in the veterinary literature, but clinicians should be aware of this potential complication in critically ill patients. The pathophysiology and veterinary literature of abdominal compartment syndrome are reviewed.