Clinical and molecular analysis of GM2 gangliosidosis in two apparent littermate kittens of the Japanese domestic cat

This case report documents clinical and molecular findings in two littermate kittens of the Japanese domestic cat with GM2 gangliosidosis variant 0. Analysis included detailed physical, magnetic resonance imaging, biochemical, pathological and genetic examinations. At first, these littermate kittens showed typical cerebellar signs at approximately 2 months of age. About 2 months later, they progressively showed other neurological signs and subsequently died at about 7 months of age. Magnetic resonance imaging just before the death showed an enlarged ventricular system, T1 hyperintensity in the internal capsule, and T2 hyperintensity in the white matter of the whole brain. Histological findings suggested a type of lysosomal storage disease. Biochemical studies demonstrated that the kittens were affected with GM2 gangliosidosis variant 0, and a DNA assay finally demonstrated that these animals were homozygous for the mutation, which the authors had identified in a different family of the Japanese domestic cat. The findings in the present cases provide useful information about GM2 gangliosidosis variant 0 in Japanese domestic cats.     

Inherited hyperchylomicro-naemia in the cat: Lipoprotein lipase function and gene structure

Hyperchylomicronaemia was identified in a four-week-old Siamese kitten with lethargy, in-appetence, hindlimb ataxia and profound anaemia. The kitten was euthanased and at necropsy a thrombus was found occluding the caudal aorta. Two littermates later presented with lethargy, inappetence and hypertriglyceri-daemia which resolved after being weaned on to a low fat diet. A similar condition was subsequently diagnosed in a kitten born to the same sire but a different queen. The expression of hyperchylomicronaemia in two related litters was suggestive of an inherited, familial defect in the function of lipoprotein lipase (LPL). The activity of this enzyme was reduced in all three parents, the two recovered cases and two related, but apparently unaffected kittens, compared with a control group of unrelated cats belonging to the breeder. This reduction in activity was not attributable to defective activation of LPL by its serum cofactor apolipoprotein C-II or the presence in plasma of a factor that inhibited LPL. The gene that codes for LPL was examined by restriction fragment length polymorphism analysis using a human LPL cDNA probe. The results showed that the cat has a similar, but not identical, LPL gene to man. However, there were no differences in the restriction fragment patterns obtained from affected, unaffected and control animals.     

Reversible pulmonary hypertension associated with lungworm infection in a young cat

Two ten-week-old kittens presented with dyspnea. Two weeks later dyspnea had worsened and both kittens had developed a heart murmur. One kitten died and necropsy showed severe granulomatous pneumonia and moderate bronchi(oli)tis and peribronchi(oli)tis caused by Aelurostrongylus abstrusus. The results from echocardiography, thoracic radiography and the other kitten's fecal examination were interpreted as severe parasitic pneumonia caused by A. abstrusus infection with pulmonary hypertension. Repeated administration of milbemycine-oxime and praziquantel resulted in cessation of larvae shedding and resolution of clinical, radiographic and echocardiographic signs of bronchopneumonia and pulmonary hypertension.     

Rapidly progressive diffuse retinal degeneration in a kitten

Advanced diffuse bilateral retinal degeneration was identified in a 13-week old female domestic short-haired kitten. The animal was in good physical health but had steady deterioration in vision over a period of a month. Clinical signs were mydriasis, tapetal hyper-reflectivity, marked loss of retinal vasculature and almost total blindness. Histological examination of the retina showed degeneration of the photoreceptor and outer nuclear layers. The clinical and pathological features are similar to those described in inherited retinal degeneration in Persian kittens.     

Late onset of cerebellar abiotrophy in a Siamese cat

A late onset of cerebellar degeneration was diagnosed in a one-and-a-half-year-old Siamese cat. The animal had been presented with mild ataxia involving all four limbs. Over the following two years, the signs gradually progressed to severe incoordination, a frequent tendency to fall and a head tremor. The neurological signs were consistent with a diffuse cerebellar lesion and the cat was euthanased. Profound and diffuse Purkinje cell loss was found on histopathological examination, but no aetiological agent was detected.     

Late onset and rapid progression of cerebellar abiotrophy in a domestic shorthair cat

A two-year-old male domestic shorthair cat was seen because of sudden onset of incoordination and tremors that had rapidly worsened over five days. Neurological examination revealed severe cerebellar ataxia, intention tremors and bilaterally decreased menace response. Blood work evaluation included a complete cell blood count (CBC), serum biochemistry profile, urinalysis, faecal flotation, cerebrospinal fluid (CSF) analysis and retroviral testing. Except for testing positive for feline immunodeficiency virus (FIV) antibodies, all other results were within the normal range. The patient was euthanased two days later because of progression of clinical signs, and a necropsy was performed. Histologically, lesions were limited to the cerebellum and consistent with cerebellar abiotrophy. No secondary diseases that could explain the rapid development of clinical signs were found. It was considered unlikely that cerebellar degeneration was related to FIV positivity, as virus invasion of the central nervous system (CNS) is mainly limited to the cerebral cortex. This case report is the first to describe late onset and rapid progression cerebellar abiotrophy in a cat.     

Transmission of feline immunodeficiency virus from infected queens to kittens.

This study demonstrates the transmission of feline immunodeficiency virus (FIV) from infected queens to kittens in two separate litters. Queen 1 was infected by intravenous administration of FIV at 22 days prior to parturition. Two out of three kittens from the litter were found to be viremic at 10 weeks of age as detected by culture isolation and polymerase chain reaction detection of FIV DNA in peripheral blood mononuclear leukocytes. The third kitten remained aviremic through 40 weeks of age. Queen 2 was infected by subcutaneous administration of FIV 2 days prior to parturition. This litter also had two out of three kittens infected with FIV; however, viremia was not detected in one of the kittens until 21 weeks of age. Culture isolation was found to be superior to polymerase chain reaction for the early detection of FIV, and viremia was found to precede seroconversion by up to 4 weeks. Although all infected kittens have remained healthy, depressed CD4:CD8 lymphocyte ratios suggest that clinical disease may develop. This study suggests that FIV infection in cats may be a useful model system for the study of HIV transmission from mothers to infants.     

Diabetes mellitus and bilateral cataracts in a kitten

An 18-week-old male domestic long-hair kitten was presented with a history of polyuria and polydipsia for several weeks. The general condition was unremarkable, but the kitten was considerably smaller than expected for the age and showed cataracts in both eyes. Serum glucose concentrations were persistently elevated and based on clinical findings and an elevated serum fructosamine concentration, a diagnosis of diabetes mellitus was established. Diabetes mellitus is not commonly diagnosed in young kittens, nor are cataracts recognised as a frequent feature of this disease in cats. The cataracts progressed in spite of the insulin therapy and the kitten was euthanised 10 weeks after referral. Histopathological examination of the pancreas revealed few and small islets of Langerhans compared to the examination of pancreas from a healthy kitten of the same age. Histopathological changes in the eyes included cataracts affecting both cortex and nucleus.     

Effects of a single dose of an intranasal feline herpesvirus 1, calicivirus, and panleukopenia vaccine on clinical signs and virus shedding after challenge with virulent feline herpesvirus 1

The objective of this study was to determine whether intranasal administration of a commercially available FVRCP vaccine to kittens lessened clinical signs and feline herpesvirus 1 (FHV-1) viral shedding when compared to unvaccinated control kittens after FHV-1 challenge. Three groups of 10 unvaccinated kittens were administered one dose of vaccine 6 days (group 1), 4 days (group 2), or 2 days (group 3) before challenge, respectively. One group was maintained as unvaccinated controls (group 4). FHV-1 challenge was then induced and the kittens were observed for 14 days. When the grouped vaccinated kitten results (groups 1-3) were compared to group 4 results, clinical scores following challenge were significantly lower (P<0.05) and significantly lower body temperatures (P<0.05) were detected on days 0, 5 and 9 post-challenge. When evaluated by individual group, group 1 and group 2 kittens had significantly lower clinical scores (P<0.05) than group 4 kittens post-challenge. In addition, FHV-1 shedding was lower in group 1 kittens when compared to group 4 kittens on day 6 after challenge (P<0.05). Administration of this vaccine within several days prior to exposure lessened clinical signs of disease and FHV-1 shedding compared to unvaccinated kittens.     

Effect of vaccination on parvovirus antigen testing in kittens

OBJECTIVE: To determine the frequency and duration of feline panleukopenia virus (FPV) vaccine-induced interference with fecal parvovirus diagnostic testing in cats. DESIGN: Prospective controlled study. ANIMALS: Sixty-four 8- to 10-week-old specific-pathogen-free kittens. PROCEDURES: Kittens were inoculated once with 1 of 8 commercial multivalent vaccines containing modified-live virus (MLV) or inactivated FPV by the SC or intranasal routes. Feces were tested for parvovirus antigen immediately prior to vaccination, then daily for 14 days with 3 tests designed for detection of canine parvovirus. Serum anti-FPV antibody titers were determined by use of hemagglutination inhibition prior to vaccination and 14 days later. RESULTS: All fecal parvovirus test results were negative prior to vaccination. After vaccination, 1 kitten had positive test results with test 1, 4 kittens had positive results with test 2, and 13 kittens had positive results with test 3. Only 1 kitten had positive results with all 3 tests, and only 2 of those tests were subjectively considered to have strongly positive results. At 14 days after vaccination, 31% of kittens receiving inactivated vaccines had protective FPV titers, whereas 85% of kittens receiving MLV vaccines had protective titers. CONCLUSIONS AND CLINICAL RELEVANCE: Animal shelter veterinarians should select fecal tests for parvovirus detection that have high sensitivity for FPV and low frequency of vaccine-related test interference. Positive parvovirus test results should be interpreted in light of clinical signs, vaccination history, and results of confirmatory testing. Despite the possibility of test interference, the benefit provided by universal MLV FPV vaccination of cats in high-risk environments such as shelters outweighs the impact on diagnostic test accuracy.     

Aplastic anemia in two kittens following a prescription error

A medication error resulted in two kittens being treated with azathioprine (12 and 12.5 mg/kg) instead of azithromycin for 2 weeks. On clinical examination, the kittens were febrile, weak, and had oronasal hemorrhage. Complete blood cell counts indicated severe bone marrow suppression. Treatment consisted of multiple transfusions, antibiotics, and granulocyte colony-stimulating factor. One of the kittens responded to therapy and had a complete recovery. The other kitten was treated for 40 days with no clinical response before dying. Both kittens also contracted Mycoplasma hemofelis infection from a contaminated blood transfusion.     

Kitten mortality in the United Kingdom: a retrospective analysis of 274 histopathological examinations (1986 to 2000)

The postmortem findings in 274 kittens were reviewed. The kittens were grouped by age at death: perinatal (< one day), neonatal (one to 14 days), preweaning (15 to 34 days) and postweaning (35 to 112 days); 203 (74 per cent) of the kittens were postweaning and 38 (14 per cent) were preweaning. Infectious disease was identified in 55 per cent of the kittens, and 71 per cent of the infectious disease was viral and detected significantly more frequently in rescue shelter kittens than in kittens from private homes. Twenty-five per cent of all kitten mortality was due to feline parvovirus (FPV). During the neonatal and preweaning periods, the main viral infections were feline herpesvirus and calicivirus. Feline infectious peritonitis caused the death of 17 kittens in the postweaning period. The rescue shelter kittens were significantly younger than the kittens from private homes (median survival 49 and 56 days) and were more likely to have FPV. The non-pedigree kittens were significantly younger than the pedigree kittens (42 v 56 days), and the pedigree kittens were significantly less likely to originate from rescue shelters. There was no significant difference between the age distribution of the male and female kittens. No diagnosis could be found in 33 per cent of the kittens, and this failure was correlated significantly with the submission of tissue samples as opposed to the whole carcase.     

Computed tomography diagnosis of eight dogs with brain infarction

Objective Medical records of eight dogs presenting with acute onset of neurological signs and a diagnosis of brain infarction as determined by computed tomography (CT) imaging were reviewed. Design Retrospective single-centre case review Results Ischaemic infarction in the territory of the rostral cerebellar artery was identified in three spaniel-breed dogs. All cerebellar infarcts were non-haemorrhagic. Telencephalic infarcts were identified in five dogs, in the territories of the middle cerebral artery (2/5) and rostral cerebral artery (3/5). One of these dogs had an ischaemic infarction, but all other infarctions appeared haemorrhagic. All dogs were geriatric (≥8 years old), with concurrent medical conditions identified in six dogs. One dog was euthanased after diagnosis because of the severity of its neurological signs and one dog was euthanased as a result of associated renal disease 2 months after diagnosis. Six dogs were alive at least 1 year after diagnosis. Conclusions CT is useful in the diagnosis of cerebrovascular accident in dogs, which can present as a spectrum of images with early changes in attenuation and subtle mass effects detected after infarction. CT is particularly sensitive for detecting haemorrhagic infarction, but under-represent ischaemic and lacunar infarctions when compared with MRI.     

Presentation,clinical pathological and post‐mortem findings in three related Scottish terriers with ligneous membranitis

Ligneous conjunctivitis and gingivitis were diagnosed in three related Scottish terrier dogs presented for investigation of severe conjunctivitis and respiratory signs. Hypoplasminogenaemia was confirmed in one of the three affected dogs. Supportive treatment was not effective, and the dogs died or were euthanased because of the disease. Post‐mortem analysis of two of the dogs revealed multiple abnormalities including severe proliferative fibrinous lesions affecting the conjunctiva, gingiva, trachea, larynx and epicardium and multiple fibrous adhesions throughout the thoracic and abdominal cavities. One dog had internal hydrocephalus and lacked a cerebellar vermis. Ligneous membranitis was confirmed on histopathology. This is a rare condition in dogs but an important differential diagnosis for severe conjunctivitis and gingivitis.     

Intramyocardial arterial narrowing in dogs with subaortic stenosis

Earlier studies have described intramyocardial arterial narrowing based on hyperplasia and hypertrophy of the vessel wall in dogs with subaortic stenosis (SAS). In theory, such changes might increase the risk of sudden death, as they seem to do in heart disease in other species. This retrospective pathological study describes and quantifies intramyocardial arterial narrowing in 44 dogs with naturally occurring SAS and in eight control dogs. The majority of the dogs with SAS died suddenly (n=27); nine had died or been euthanased with signs of heart failure and eight were euthanased without clinical signs. Dogs with SAS had significantly narrower intramyocardial arteries (P<0.001) and more myocardial fibrosis (P<0.001) than control dogs. Male dogs and those with more severe hypertrophy had more vessel narrowing (P=0.02 and P=0.02, respectively), whereas dogs with dilated hearts had slightly less pronounced arterial thickening (P=0.01). Arterial narrowing was not related to age, but fibrosis increased with age (P=0.047). Dogs that died suddenly did not have a greater number of arterial changes than other dogs with SAS. This study suggests that most dogs with SAS have intramyocardial arterial narrowing and that the risk of dying suddenly is not significantly related to the overall degree of vessel obliteration.     

Vitamin D-dependent rickets type II in a cat

A cat with clinical signs Indicating rickets was diagnosed as having a defect of vitamin D receptors. Clinical signs had been seen from four months of age. Treatment with calcium supplementation and various forms of vitamin D did not alter plasma calcium levels or reverse skeletal lesions of lateral antebrachial bowing, lumbar spinal lordosis and costochondral beading. Analgesics were effective for relieving skeletal pain during the bone growth phase and were withdrawn when the animal reached skeletal maturity. Therapy for hip osteoarthritis was given from five years of age until the cat was euthanased at nine years of age as a result of refractory hip pain.     

Pathogenesis studies with Australian bat lyssavirus in grey-headed flying foxes (Pteropus poliocephalus)

OBJECTIVE: To examine the susceptibility of the grey-headed flying fox (Pteropus poliocephalus) to Australian bat lyssavirus (ABL), and to provide preliminary observations on the pathogenesis of the disease in flying foxes. PROCEDURE: Ten flying foxes were inoculated intramuscularly with ABL, and four with a bat-associated rabies virus. Inoculated animals were observed daily, and clinical samples collected every 9 to 14 days. Animals with abnormal clinical signs were euthanased, and samples collected for histological, serological, virological and immunohistological examinations. At 3 months post inoculation (PI), all survivors were euthanased, and each submitted to a similar examination. RESULTS: Three ABL-inoculated flying foxes, and two rabies-inoculated animals developed abnormal clinical signs between 15 and 24 days PI. All three ABL-inoculated animals had histological lesions consistent with a lyssavirus infection, and lyssaviral antigen was identified in the central nervous system (CNS) of each. Virus was isolated from the brain of two affected animals. Of the rabies-inoculated flying foxes, both had histological lesions and viral antigen in the CNS. Virus was recovered from the brain of only one. None of the five affected flying foxes developed anti-lyssavirus antibodies, but, by 3 months PI, five of the seven ABL-inoculated survivors, and one of the two rabies virus-inoculated survivors, had seroconverted. The dynamics of the immune responses were quite variable. CONCLUSIONS: The response of flying foxes to ABL, administered by a peripheral route of inoculation, was similar to that of bats inoculated peripherally with bat-derived rabies viruses.     

Pathogenesis of feline gastric chlamydial infection

Studies were conducted to determine whether the gastric chlamydiae that have been observed recently in cats are of pathologic significance. Chlamydiae were isolated in mouse L cell cultures from the homogenized pooled gastric mucosa of 3 cats that had been identified, by histopathologic examination, to have gastric chlamydiosis. Ten specific-pathogen-free kittens were exposed by aerosol and oral inoculation to the harvested feline gastric chlamydiae cell-culture media. In general, the clinical signs and lesions were conjunctivitis, rhinitis, and mild gastritis. The clinical signs and lesions were most severe in 2 chlamydia-infected kittens that had received methylprednisolone acetate (50 mg/kg of body weight). Chlamydiae were demonstrated in epithelial cells of conjunctival and nasal smears in 10 of 10 infected kittens from postexposure days 7 through 35. In addition, chlamydiae were isolated in L cell cultures from a variety of antemortem and postmortem specimens from infected kittens. The present study provided evidence that feline gastric chlamydiae, under appropriate conditions, were capable of inducing, in cats, clinical signs and lesions similar to those induced by the feline pneumonitis agent.     

Feline neonatal isoerythrolysis in two litters

The clinical, pathological and serological findings for feline neonatal isoerythrolysis (FNI) in two litters are described. In each litter one of four kittens died shortly after birth, two showed varying degrees of depression, jaundice and haemoglobinuria and one remained healthy (clinically unaffected). Three of the kittens with jaundice died and the necropsy findings included variable degrees of erythrophagocytosis in the spleen and liver and many casts containing haemoglobin in the tubules and collecting ducts of the kidney. Blood typing and haemocompatibility testing were performed on the surviving kittens, queens and sires. Both queens and the healthy kittens were Type B while both sires and the surviving affected kitten were Type A. In both litters the queens sera haemolysed the sires erythrocytes but did not affect the erythrocytes of the healthy kittens. The erythrocytes of the surviving affected kitten were haemolysed by the serum of its queen. The pathogenesis and treatment of FNI are discussed.     

Magnetic resonance imaging in two dogs with central nervous system disease

Accurate localization of the lesions in two dogs with progressive neurological disease was demonstrated with magnetic resonance imaging (MRI). The first dog had unilateral cerebellar signs with associated paradoxical vestibular symptoms. The CSF tap and clinical localization suggested a right-sided cerebellar tumour and this was confirmed with MRI scanning. The second dog had predominantly asymmetrical fore-brain signs with circling, personality changes, seizures and contralateral proprioceptive deficits. CSF analysis suggested an inflammatory or neoplastic condition. MRI showed a diffuse oedematous lesion of the left cerebral hemisphere which corresponded exactly with the lesions seen at necropsy. The advantages of MRI over CT scans are discussed.