Clinical and pathological observations in English cocker spaniels with primary metabolic vitamin E deficiency and retinal pigment epithelial dystrophy

Fifteen English cocker spaniels with confirmed vitamin E deficiency were examined physically, ophthalmologically and neurologically. Eleven of them had clinical signs of neurological dysfunction which included ataxia, proprioceptive deficits, abnormal spinal reflexes and muscle weakness. In the two dogs examined histopathologically there was central neuronal fibre degeneration with prominent neuroaxonal dystrophy, particularly within the sensory relay nuclei of the brainstem, and one of the dogs had severe intestinal lipofuscinosis.     

Acute peritonitis secondary to traumatic breeding in the bitch

Objective: To discuss 2 cases of acute peritonitis caused by traumatic breeding in the bitch. Series summary: Two bitches presented with acute abdominal pain, clinical signs, and laboratory abnormalities compatible with peritonitis. Both bitches were in estrus and had been observed copulating with male dogs prior to the onset of clinical signs. Diagnostic testing revealed bacterial peritonitis in both dogs, and intracellular and extracellular spermatozoa in ascites from 1 of the dogs. Surgical exploration revealed rupture of the uterine body and generalized peritonitis in both animals. Both bitches recovered following surgical and medical treatment. New or unique information provided: This is the first reported series of cases of peritonitis secondary to traumatic breeding. These cases introduce a unique presentation for peritonitis and acute abdominal distress. Peritonitis because of traumatic seeding of the abdominal cavity with bacteria from the urogenital tract, with or without seminoperitoneum, should be considered for bitches presenting with appropriate history, signalment, and clinical signs.     

Dysautonomia in dogs: 65 cases (1993-2000)

OBJECTIVE: To determine signalment, history, clinical findings, results of autonomic function testing and other antemortem diagnostic tests, and pathologic findings in dogs with dysautonomia. DESIGN: Retrospective study. ANIMALS: 65 dogs with dysautonomia. PROCEDURE: Case records of 68 dogs with a diagnosis of dysautonomia were reviewed; inclusion criteria included histologic confirmation of dysautonomia or clinical signs and results of pharmacologic testing consistent with dysautonomia. RESULTS: 65 dogs fulfilled all criteria for dysautonomia. Dogs from rural environments were overrepresented, and cases of dysautonomia were reported for every month, although the highest number of cases was reported in February and March. Vomiting was the most common clinical sign, followed by diarrhea, signs of anorexia and depression, weight loss, and dysuria. The most common physical examination finding was decreased or absent anal tone, followed by absent pupillary light reflexes and elevated nictitating membrane. Results of pharmacologic testing were consistent with dysautonomia, although no single test was 100% sensitive. Histologic lesions consistent with dysautonomia were found in the autonomic ganglia, brainstem nuclei, and ventral horns of the spinal cord. CONCLUSIONS AND CLINICAL RELEVANCE: Dysautonomia is an endemic disease in Kansas, and a high index of suspicion of the disease can be made by combining clinical signs, physical examination findings, and results of pharmacologic testing.     

Five cases of canine dysautonomia in England (2004 to 2006)

Canine dysautonomia was diagnosed definitively in five dogs by histopathology. All dogs were seen between June 2004 and July 2006 and originated from south-east England; four dogs originated from an urban area and one from a rural area. Of the urban dogs, one had recently visited Scotland and one had visited a kennel in a rural area nearby. Acute-onset but progressive vomiting, diarrhoea, depression and inappetence were the most common presenting clinical signs. Reduced or absent anal tone, dysuria, absence of pupillary light reflexes with intact vision, mydriasis, decreased corneal sensitivity and nictitating membrane protrusion were among the most frequent neurological findings. Abnormalities in pharmacological autonomic and physiological function testing (including orthostatic hypotension in two dogs) and diagnostic imaging studies were detected in some of the animals. All dogs failed to respond adequately to treatment, and given the poor prognosis, they were eventually euthanased. Histopathology identified marked chromatolysis of ganglion cell bodies. This case series emphasises that dysautonomia should be considered when a dog is presented in the UK with acute- or subacute-onset gastrointestinal signs and compatible physical and neurological abnormalities.     

Two cases of severe iron-deficiency anaemia due to inflammatory bowel disease in the dog

Two dogs were referred for investigation of lethargy and anaemia. Preliminary examinations by the referring veterinary surgeons had revealed severe anaemia, which was poorly regenerative. In one case, the anaemia was microcytic and, in the other, it was hypochromic. These findings were suggestive of chronic blood loss anaemia. Neither dog had external signs of gastrointestinal disease, although one had vomited on a single occasion during the two weeks preceding referral. Although both dogs were producing grossly normal faeces, further investigations detected faecal occult blood. Multiple full thickness gastrointestinal biopsies were taken at laparotomy. These showed segmental eosinophilic enteritis of the duodenum and proximal jejunum in one case, and marked chronic lymphocytic gastritis in the other. Both cases illustrate the fact that severe systemic disease can result from gastrointestinal pathology in the absence of clinical signs of gastrointestinal disease.     

Retinopathy associated with ivermectin toxicosis in two dogs

CASE DESCRIPTION: 2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange. CLINICAL FINDINGS: On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs. TREATMENT AND OUTCOME: Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring. CLINICAL RELEVANCE: To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.     

The influence of age on patellar reflex response in the dog

The patellar tendon reflex is a clinical parameter commonly used to assess neurological status. Factors such as quadriceps muscle fiber composition, femur length, and patient age have been reported to influence total and fractionated reflex times in human beings. The purpose of this blinded, cross-sectional study was to examine the effect of age on the patellar reflex in the dog. Eighty-six dogs without evidence of neurological impairment or orthopedic disease of the stifle (eg, patellar luxation or cranial cruciate ligament rupture) were assigned to 1 of 2 groups on the basis of age: group 1, <10 years old (n = 72); or group 2, > or =10 years old (n = 14). Patellar reflexes were elicited in both pelvic limbs by a reflex hammer while the dog was in lateral recumbency. The reflex was scored as present or absent by a blinded individual. Two dogs in group I had reflexes absent in both limbs, 3 dogs in group 2 had reflexes absent in both limbs, and 1 dog in group 2 lacked a response in 1 limb. The proportion of dogs with absent patellar reflexes in group 2 (4 of 14, 95% CI, 8-58%) was significantly higher than the proportion of dogs with absent patellar reflexes in group 1 (2 of 72, 95% CI, 0-10%) (P < .006). Furthermore, dogs lacking at least 1 patellar reflex were older than those having both reflexes present (P = .04). Weight was not related to the presence of both reflexes (P = .49). These findings suggest that neurologically normal dogs may have an age-dependent decline in patellar reflex magnitude or a prolongation of total reflex time (TRT).     

Rocky Mountain spotted fever in dogs and its differentiation from canine ehrlichiosis

Rocky Mountain spotted fever (RMSF) or ehrlichiosis was diagnosed in dogs on the basis of specific immunofluorescent testing for each disease. Comparisons between clinical and laboratory findings were made between the 2 diseases. The incidence of RMSF tended to be more seasonal and it affected younger dogs. Purebred dogs appeared to be more susceptible to both diseases. In general, RMSF had a more rapid and severe course of clinical illness than did ehrlichiosis, but acute ehrlichiosis was difficult to differentiate from RMSF. Both diseases were characterized by fever, depression, lymphadenopathy, and signs of neurologic dysfunction; petechial hemorrhages or other signs of hemorrhagic diathesis were evident only in a small proportion of cases. Anemia, leukopenia, and thrombocytopenia were more common in dogs with ehrlichiosis, whereas those with RMSF more often had leukocytosis and thrombocytopenia. Hypoalbuminemia was found in dogs with both diseases, but those with ehrlichiosis usually had concurrent hyperglobulinemia. High serum alkaline phosphatase activity and serum cholesterol concentration, and low serum calcium concentration were more common in dogs with RMSF than with ehrlichiosis. Rising serum titers or positive direct immunofluorescence for Rickettsia rickettsii in skin biopsy specimens were used to confirm RMSF, whereas a single serum titer for Ehrlichia canis enabled detection of ehrlichiosis. In the absence of neurologic deficits and when dogs were treated with tetracycline, dogs with RMSF made a more rapid and consistent recovery than did dogs with ehrlichiosis.     

Idiopathic facial paralysis in the dog

Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.     

Extradural spinal juxtafacet (synovial) cysts in three dogs

Three dogs were presented for investigation of spinal disease and were diagnosed with extradural spinal juxtafacet cysts of synovial origin. Two dogs that were presented with clinical signs consistent with pain in the lumbosacral region associated with bilateral hindlimb paresis were diagnosed using magnetic resonance imaging. Both cysts were solitary and associated with the L6-7 dorsal articulations; both the dogs had a transitional vertebra in the lumbosacral region. A third dog that was presented with progressive paraparesis localised to T3-L3 spinal cord segments and compression of the spinal cord at T13-L1 was diagnosed using myelography. A solitary multiloculated cyst was found at surgery. Decompressive surgery resulted in resolution of the clinical signs in all three dogs. Immunohistological findings indicated that one to two layers of vimentin-positive cells consistent with synovial origin lined the cysts.     

Malignant mesothelioma in urban dogs

Clinical and postmortem materials from six dogs with a diagnosis of malignant mesothelioma were studied retrospectively. The dogs were urban pets with clinical signs of malignant effusions. Two mesotheliomas were pleural, one pericardial, and one peritoneal. Both pleura and pericardium were involved in one dog, and the pleura and peritoneum in another. On gross examination at necropsy, diffuse granular or velvety plaques covering mesothelial surfaces were found in all dogs; firm discrete pleural nodules also were present in two dogs. Neither distant metastases nor areas of deep lung invasion were found. The tumors varied histologically, but the most common type was epithelial with a papillary pattern. Ultrastructurally, the neoplastic cells had prominent surface microvilli, numerous desmosomes, and tonofilaments. Lung tissue from these dogs and from control dogs was evaluated for the presence of ferruginous bodies. Asbestos bodies were found in three of five dogs with mesotheliomas but rarely were found in control dogs. As a group, the mesothelioma cases had significantly more asbestos bodies and total ferruginous bodies than controls. The clinical and morphologic appearance of canine mesothelioma is similar to human mesothelioma and also may be associated with exposure to airborne fibers.     

Anosmia associated with canine distemper

The sense of smell in dogs infected with canine distemper virus (CDV) was examined by use of EEG olfactometry, behavioral olfactometry, and electro-olfactography. Infection with CDV was confirmed by a direct immunofluorescence technique in 8 active cases and was suggested by clinical history compatible with canine distemper 10 to 26 weeks earlier in 6 cases. Pathologic alterations of the olfactory mucosa in 3 clinically affected dogs was examined by light microscopy. Infection with CDV was found to be associated with anosmia and lack of recorded responses on electro-olfactogram in 8 of 8 dogs with clinical signs of acute distemper from naturally acquired infections. Anosmia was found in 5 of 6 dogs that had recovered from acute distemper 10 to 26 weeks earlier. The sixth dog had hyposmia, with abnormalities on the electro-olfactogram. Histologic examination was not performed on the 6 dogs that had recovered. Histologic lesions observed at necropsy in 3 dogs that had had clinical signs of acute distemper were those of subacute purulent rhinitis and atrophy of the olfactory epithelium. Altered olfactory function could be explained by mucopurulent exudate blocking odors from olfactory receptors in the acutely affected dogs, but alteration of olfactory function in the dogs that had recovered without clinical evidence of rhinitis could not be explained.     

Familial progressive nephropathy in young Bull Terriers

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.     

Collie eye anomaly in the rough collie in Norway

The results of eye examinations of 741 rough collies for collie eye anomaly (CEA) are described. Of the examined dogs, 40-8 per cent had CEA, including, in most cases, chorioretinal dysplasia (CRD). 7-7 per cent had coloboma of the optic disc while 3–5 per cent had complications of CEA, either retinal detachment or intraocular bleeding. There was no sex difference nor was the frequency of the disease influenced by coat colour. After estimating the total frequencies of the different manifestations of the disease, the dogs were divided into two groups according to the age at first examination. In the group of dogs examined between seven weeks and three months old, 48-9 per cent had CEA, compared to a frequency of 25-6 per cent in the group of dogs examined after three months of age. All the puppies with coloboma also showed signs of CRD, while among the older dogs 11 of the 66 CEA cases reported showed signs of coloboma without CRD. Twenty-two dogs which had been examined as puppies and given the diagnosis CEA with minor chorioretinal changes were re-examined at an older age. Of these dogs, 15 had ophthalmoscopi-cally normal fundi at re-examination while seven were unchanged from the first examination.     

Acute idiopathic polyneuropathy in the dog

From among a large group of dogs with acute tetraparesis, we identified 10 dogs with a distinct peripheral nerve disorder. Prior to the onset of signs, all of the dogs had been healthy, and none was known to have been exposed to a neurotoxin or raccoon bite. Weakness, with hypoactive or absent segmental reflexes, became progressively worse for 1 to 21 days. Results of electromyography and nerve conduction studies invariably were compatible with a diagnosis of polyneuropathy that predominantly affected proximal nerve segments. Appearance of nerve biopsy specimens and the short time course for functional recovery suggested a demyelinative component to the disorder. The extent of recovery was variable but often rapid and complete in dogs that did not succumb to complications in the early period. Corticosteroid therapy did not demonstrably influence the outcome. This acute idiopathic polyneuropathy in the dog shares many clinical and pathologic features with idiopathic polyradiculoneuritis (Coonhound paralysis).     

Familial progressive nephropathy in young Bull Terriers

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.     

Medical management of congenital portosystemic shunts in 27 dogs—a retrospective study

Case records of 27 dogs with medically managed congenital portosystemic shunts were reviewed. Fourteen were followed up by telephone questionnaires to the owners. Age, breed, sex, clinical signs and blood results were similar to previous studies. Weight and quality of life were stable or improved on treatment in all cases. Total serum protein concentration and alanine aminotransferase and alkaline phosphatase activities fell significantly during treatment. Fourteen dogs were euthanased, four were lost to follow-up and nine remained alive. Mean survival time for the dogs euthanased was 9.9 months. Mean follow-up period for the dogs still alive was 56.9 months and all had survived more than 36 months from diagnosis. Surviving dogs with intrahepatic shunts had a significantly shorter follow-up period than dogs with extrahepatic shunts. Two prognostic indicators were identified, age at initial signs and blood urea concentration on presentation, both correlating with survival time. It was demonstrated that a significant proportion of dogs with portosystemic shunts managed medically have a good prognosis.     

Inherited copper toxicosis in the Bedlington terrier: a report of two clinical cases

The clinical signs, laboratory findings and pathological changes are described in two cases of inherited copper toxicosis in the Bedlington terrier. The first case presented with acute signs of depression, vomiting, anorexia, weight loss and jaundice while the second case followed a more chronic course with less severe clinical signs which included weight loss and ascites. Both dogs had elevated circulating levels of alanine aminotransferase (ALT), however other haematological and biochemical parameters, while reflecting liver involvement, varied between the two cases. Chemical analysis of the liver revealed elevated copper levels in both cases (951·7 and 1093·4 μg/g wet weight respectively; normal less than 150 μg/g). These levels, however, are less than some affected but asymptomatic Bedlington terriers. Pathologically the first case had micronodular cirrhosis, while the second had focal hepatitis with fibrosis. Both dogs showed vacuolation of the white matter in the cerebrum, cerebellum, midbrain and medulla. Attention is drawn to the similarities and differences between copper toxicosis in the Bedlington terrier and Wilson's disease in man.     

A Retrospective Study of Cavernous Sinus Syndrome in 4 Dogs and 8 Cats

Cavernous sinus syndrome (CSS) is characterized by deficits in more than one of the cranial nerves (CN) that traverse the cavernous sinus at the base of the cranial vault: CN III (oculomotor), IV (trochlear), VI (abducens), and the first two branches of CN V (trigeminal). Records from 4 dogs and 8 cats with CSS diagnosed over a 14-year period were reviewed. The most common clinical signs were ophthalmoparesis or ophthalmoplegia, mydriasis with no direct or consensual pupillary light reflexes, ptosis, decreased corneal sensation, and decreased retractor oculi reflex. All cats had initial signs referable to a left CSS lesion (one had bilateral CSS), whereas in all dogs the lesions were localized to the right cavernous sinus. Median ages at diagnosis were 9 and 10 years of age for dogs and cats, respectively. Cerebel lomedullary cisternae cerebrospinal fluid analysis in 6 animals was useful as a sensitivebut nonspecific diagnostic test of an intracranial inflammatory or neoplastic lesion. Magnetic resonance imaging scans provided a more definitive diagnostic test in all dogs, revealing a contrast-enhancing mass on T1 weighted scans in the region of the cavernous sinus. A definitive pathological diagnosis was obtained in 2 dogs: a primary intracranial neoplasm and a metastatic intracranial neoplasm. A definitive diagnosis was obtained in 6 cats: metastatic neoplasm (n =1), primary intracranial neoplasm (n = I), primary intracranial infectious disease (n = 2). and associated systemic infectious disease (n = 2). The prognosis associated with CSS in dogs and cats was considered guarded to poor. J Vet Intern Med 1996_;10:65–71. Copyright © 1996 by the American College of Veterinary Internal Medicine .     

Comparison of Immunoperoxidase Plaque Staining and Neutralizing Tests for Canine Distemper Virus

The use of immunoperoxidase plaque staining (IP) in the antibody test for canine distemper virus (CDV) and its diagnostic value were investigated. Antibody titres by the IP test and neutralizing test (NT) against CDV were compared in 114 specific pathogen-free (SPF) dogs, including 84 CDV-vaccinated and 30 unimmunized dogs. All of the unimmunized dogs, which had negative NT titres, also showed negative IP titres, and all of the CDV-vaccinated dogs, which had positive NT titres, showed positive IP titres. Furthermore, the IP titres showed similar changes with time after vaccination to the NT titres in five CDV-vaccinated SPF dogs. These findings indicate that the IP test has similar specificity to the NT.Next, the IP and NT titres were compared in 190 clinically suspected cases of canine distemper (CD), including 107 dogs with neurological signs and 83 dogs without neurological signs, and also in 50 clinically healthy dogs. Among the suspected cases of CD, of 46 dogs with neurological signs and 29 dogs without neurological signs, and which had negative NT titres, 33 (72%) and 19 (66%), respectively, showed positive IP titres. Many suspected cases of CD showed a high IP titre despite a low NT titre. In contrast, among healthy dogs, none of 9 NT-negative dogs showed positive IP titres.The difference in the IP and NT titres (log₁₀ [reciprocal of IP titre] – log₁₀ [reciprocal of NT titre]) was measured to investigate the agreement between IP test and NT. The differences were 1.488±0.867, 1.245±0.833, 0.595±0.351 and 0.594±0.372, respectively, in the suspected cases of CD with neurological signs, the suspected cases of CD without neurological signs, the healthy dogs and the SPF dogs. The differences in the suspected cases of CD were significantly high compared to those for the SPF dogs (p<0.001).Furthermore, in 8 dogs diagnosed as cases of CD from their paired sera, whose initial sera showed a markedly low NT titre compared to the IP titre, 5 dogs without neurological signs developed neurological signs later.These findings suggest that the IP test can detect CD during its early phases and in dogs with low antibody levels, undetectable by NT, and so would be useful for serological diagnosis.