Hypertrophic osteodystrophy preceding canine juvenile cellulitis in an Australian shepherd puppy

A 10-week-old intact female Australian shepherd dog was presented sternally recumbent, mildly pyrexic, and painful on long bone palpation of both forelimbs. Based on radiographs she was diagnosed with hypertrophic osteodystrophy. Analgesia was provided with intravenous, oral, and topical medications. Approximately 2 wk later she was presented for facial swelling, regional dermatitis, and lymphadenopathy. Canine juvenile cellulitis was diagnosed and successfully treated.     

Hypertrophic osteopathy associated with infective endocarditis in an adult boxer dog

A 20-month-old, entire male boxer dog was presented with lethargy and intermittent shifting limb lameness. Diagnostic tests revealed aortic valve vegetations suggestive of infective endocarditis causing severe aortic outflow obstruction, and hypertrophic osteopathy of all four limbs. The dog was treated symptomatically and euthanased four days later. The association of infective endocarditis and hypertrophic osteopathy has been poorly documented in the veterinary literature. The pathogenesis of hypertrophic osteopathy is unknown; however, four theories have been put forth to explain this disease: pulmonary shunting, vagal nerve stimulation, humoral substances produced by neoplastic cells and megakaryocyte/platelet clump hypothesis.     

Developmental orthopedic disease.

Developmental orthopedic diseases are a common cause of pain and lameness in young dogs. Most occur in large-breed dogs with rapid growth rates. This article reviews the signalment, etiology and pathogenesis, clinical signs, diagnosis, treatment, and prognosis for many of the common developmental orthopedic diseases, including hypertrophic osteodystrophy, panosteitis, osteochondrosis, Legg-Calve-Perthes disease, hip dysplasia, elbow dysplasia, and pes verus.     

Chronic hypertrophic gastritis in a dog: successful treatment by partial gastrectomy

A dog with listlessness, anorexia and iron-deficiency anaemia was found to have chronic hypertrophic gastritis. The animal returned to good health following partial gastrectomy, suggesting that the gastric lesion was the cause of the clinical signs. The cause of the gastric lesion was not determined.     

Metaphyseal osteopathy (hypertrophic osteodystrophy) in growing dogs. A clinical study

Based on the different investigations performed, the author finds that the diseases called skeletal scurvy, infantile scurvy, Jvfcller Barlow's disease, hypertrophic osteodystrophy and osteodystrophy II must be the same entity.
This study deals with twenty-six dogs suffering from this disease. Contrary to earlier reports, the prognosis is favourable. There were no significant differences in recovery between dogs intensively treated and those not treated. Relapses were rare, and only two dogs subsequently developed classical hypertrophies.
Based on these findings, and recognizing that the aetiology is still unknown, the author suggests the name metaphyseal osteopathy for this affection.     

Refractory shock,hypercoagulability, and multiorgan thrombosis associated with hypertrophic osteodystrophy in a dog

Objective

To describe the clinical findings and case progression in a dog presenting with severe systemic inflammatory response, refractory shock, progressive metabolic acidosis, and respiratory failure that was ultimately diagnosed with hypertrophic osteodystrophy (HOD).

Case Summary

A 4-month-old male intact Mastiff presented with a 24-hour history of lethargy and generalized ostealgia. On examination, the dog was recumbent, febrile, and tachycardic with pain on palpation of the abdomen, right femur, and mandible. Appendicular joint radiographs showed changes consistent with osteochondrosis and ulnar-retained cartilaginous cores, with no overt evidence of HOD. Initial treatment included IV fluid therapy, multimodal analgesia, and broad-spectrum antimicrobials. Vasopressor therapy was initiated following hemodynamic decompensation. Synovial fluid cytological analysis and culture revealed nonseptic suppurative inflammation and no bacterial growth, respectively. Blood and urine cultures also yielded no growth. Viscoelastic testing was consistent with hypercoagulability. The dog initially had a metabolic acidosis with appropriate respiratory compensation that progressed to a mixed metabolic and respiratory acidosis despite aggressive therapies that included antimicrobials, vasopressors, positive inotropes, and corticosteroids. Humane euthanasia was elected approximately 32 hours after admission. Necropsy yielded a diagnosis of HOD.

New or Unique Information Provided

This is the first report detailing the occurrence of refractory shock and hypercoagulability associated with HOD in a dog without evidence of another identified comorbidity. HOD should be considered in any young, large-breed dog with generalized ostealgia and signs of systemic illness, even in the absence of classic radiographic abnormalities. Further investigation of coagulation status in dogs with HOD and a secondary systemic inflammatory response is warranted.     

Scurvy as a cause of osteodystrophy

Two cases of hypertrophic osteodystrophy (HOD) showed the characteristic stigmata of scurvy. The effective treatment, for both patients, was ascorbic acid. The clinical and radiographic findings and a discussion of the possible causes of hypovitaminosis C are presented.     

Pre-operative fibrous osteodystrophy and severe,refractory, post-operative hypocalcemia following parathyroidectomy in a dog

A 13-year-old dog exhibited dramatic, radiographic osteopenia consistent with fibrous osteodystrophy secondary to primary hyperparathyroidism. Following parathyroidectomy, the dog developed severe, prolonged hypocalcemia, but was successfully treated and discharged 32 d after surgery. A variety of factors may have contributed to this dog’s hypocalcemia including hypoparathyroidism and hungry bone syndrome.     

Renal dysplasia in a Rhodesian ridgeback dog

A six-month-old Rhodesian ridgeback dog was presented for evaluation of facial swelling. Chronic renal failure was clinically diagnosed based on urinalysis, biochemical changes and ultrasonography. The facial swelling was due to fibrous osteodystrophy, which was evident on survey radiographs of the skull. On post mortem examination, chronic renal failure as a result of renal dysplasia was confirmed. This is the first reported case of renal dysplasia in this breed of dog.     

Renal osteodystrophy with facial hyperostosis and 'rubber jaw' in an adult dog

A nine-year-old male Sheltie dog was presented with bilaterally symmetrical maxilliary swelling, loose teeth and flexible mandibles. The condition was progressive over a period of two months. Biochemical and histopathological examinations supported a diagnosis of renal osteodystrophy with facial hyperostosis and 'rubber jaw'.     

Renal osteodystrophy with facial hyperostosis and ‘rubber jaw’ in an adult dog

A nine-year-old male Sheltie dog was presented with bilaterally symmetrical maxilliary swelling, loose teeth and flexible mandibles. The condition was progressive over a period of two months. Biochemical and histopathological examinations supported a diagnosis of renal osteodystrophy with facial hyperostosis and ‘rubber jaw’.     

Hypertrophic osteopathy in a dog with a chronic lung abscess

A 2-year-old dog was examined because of gradual lameness of all 4 limbs and weight loss. Hypertrophic osteopathy was diagnosed. Radiography revealed a mass in the caudal lobe of the right lung. At necropsy, the mass was determined to be a chronic abscess. Corynebacterium pyogenes was cultured from the lesion. Although hypertrophic osteopathy in dogs is commonly associated with a thoracic lesion, most often neoplastic, the chronic lung abscess in this dog might have been formed as a result of a paralaryngeal abscess that was treated 3 months before the onset of the lameness.     

Treatment of renal nephroblastoma in an adult dog

An 8-year-old Labrador retriever was diagnosed with a unilateral malignant nephroblastoma and hypertrophic osteopathy. The histopathologically malignant tumor was confined to the renal capsule, but the sarcomatous component was anaplastic, resulting in its classification as a Stage I tumor with unfavorable histopathology. The dog was treated with unilateral nephrectomy, vincristine, and doxorubicin. This dog has remained disease free for >25 months. Reported treatments of renal nephroblastoma in the dog have not described disease-free intervals of >8 months.     

Focal cystic hypertrophic gastropathy in a dog

A 6-year-old female dog had a 3-day history of postprandial vomiting of undigested food. Plain and contrast radiography revealed a large mass on the greater curvature of the stomach. On exploratory gastrotomy, the mass was found to consist of hypertrophic rugae resembling cerebral gyri and sulci. The histopathologic findings were similar to those for hypertrophic gastropathy in man and the dog.     

Nutrition in relation to skeletal growth deformities

The pathophysiology of alimentary hyperparathyroidism and its pathological fractures and growth deformities are described. Renal hyperparathyroidism with hyperostotic osteodystrophy in young animals and isostotic osteodystrophy in old animals is briefly mentioned. Hypercalcitoninism caused by excessive prolonged calcium intake in growing dogs will go together with disturbances in skeletal remodelling and disturbed enchrondral ossification, leading to such entities as canine wobbler syndrome, enostosis, osteochrondrosis dissecans, and radius curvus syndrome. Dogs, who are dependent upon dietary vitamin D sources, can develop rickets with skeletal growth deformities when a diet deficient in vitamin D is fed under controlled conditions. Growth plates and mineralisation grade normalised when commercial dog food was given. As a sole therapy normalisation of the diet will not be sufficient in all skeletal growth deformities as described above. Prevention by feeding diets with optimal contents will be of benefit to veterinarians and their patients.     

Idiopathic hypertrophic pachymeningitis in six dogs: MRI, CSF and histological findings, treatment and outcome

Idiopathic hypertrophic pachymeningitis has been described in humans as a rare, chronic progressive non-specific inflammatory and fibrotic disease of the dura mater. This is a case series of six canine cases of presumptive or confirmed intracranial idiopathic hypertrophic pachymeningitis. These dogs were included in this retrospective study, based on magnetic resonance imaging findings. All presented with pachymeningeal thickening and enhancement without involvement of the leptomeninges on magnetic resonance imaging and no underlying cause identified on cerebrospinal fluid analysis, complete blood count, serum biochemistry and infectious disease titres. Histopathological examination was available in one case. Response to immunomodulatory treatment (corticosteroids and cytosine arabinoside) was achieved in five cases. Idiopathic hypertrophic pachymeningitis should be considered as a possible differential diagnosis for dogs with pachymeningeal thickening on magnetic resonance imaging and no identified underlying cause. The prognosis appears to be fair to poor.     

The role of the dog in the epidemiology of neosporosis in cattle

Neospora caninum is an intracellular protozoan parasite that was discovered in a dog in 1988. Since then, N. caninum has been demonstrated in a variety of animal species and it has been recognized as an important cause of abortion in cattle. An infection with N. caninum can be maintained in cattle herds for several generations by transplacental transmission from cow to calf. Recently, it was demonstrated that dogs can act as definitive hosts of N. caninum and therefore may be a source of infection for other species by shedding oocysts. Further evidence of a role of the dog in spreading the infection to cattle has been derived from epidemiological studies. The present state of knowledge is reviewed in this paper.     

Hypertrophic osteopathy associated with renal pelvis transitional cell carcinoma in a dog

A 6-year-old male, Belgian shepherd dog was presented with lethargy, oliguria, hematuria, and reluctance to move. The dog developed hypertrophic osteopathy secondary to renal pelvis transitional cell carcinoma. A nephrectomy was performed and after a year, the dog was completely asymptomatic, and no evidence of metastatic disease was present.     

Acute pancreatitis in two dogs given azathioprine and prednisone

Acute pancreatitis was diagnosed in 2 dogs given azathioprine and prednisone. Prednisone and azathioprine had been given as immunosuppressive therapy for pemphigus foliaceus in dog 1 and for polymyositis in dog 2. Azathioprine was discontinued in both dogs. In dog 1, prednisone was reinstituted on day 6 of hospitalization. Prednisone was continued throughout the period of hospitalization in dog 2. Both dogs recovered without complication. Glucocorticoid therapy has been associated with the development of pancreatitis. In human beings, a common side effect of azathioprine is the development of drug-induced pancreatitis. Definitive identification of azathioprine as the cause of pancreatitis in these dogs was not possible; the owners refused to permit retreatment with the drug. Therefore, the synergistic action between these 2 drugs could not be ruled out as the cause of pancreatitis.     

An osteodystrophy apparently caused by vitamin D deficiency in growing pigs

An osteodystrophy with features of both rickets and fibrous osteodystrophy was diagnosed in growing pigs housed indoors and fed on a diet deficient in vitamin D. Affected pigs were severely lame and preferred to remain recumbent. At necropsy, the long bones had reduced breaking strength and in one five-month-old pig the articular surfaces of both proximal humeri were indented due to collapse of subchondral bone. Microscopic changes in the bones included prominent osteoclastic activity in the proximal metaphyses, variable myelofibrosis, trabecular microfractures, and focal thickening of the hypertrophic zone in some growth plates. Treatment consisted of an injection of Vitamin D3, addition of dicalcium phosphate to the diet for 18 days and long-term supplementation of the diet with fat-soluble vitamins. This is the first report of an osteodystrophic disease in pigs in New Zealand.