Bilateral hippocampal malformation and concurrent granulomatous meningoencephalitis in a dog with refractory epilepsy.

A 5-year-old dog was referred with a history of anorexia and apathy for 3 weeks and acute status epilepticus. Ten weeks later the animal was humanely destroyed due to refractory epilepsy despite anti-epileptic medical treatment. Microscopical examination of the brain revealed bilateral malformation of the dentate gyrus with abnormal gyration. Cornu ammonis segments comprised of sparse pyramidal cells accompanied by marked gliosis. Additionally, there was severe generalized disseminated granulomatous meningoencephalitis, mainly localized to the white matter of the cerebral hemispheres. This is the first description of bilateral hippocampal malformation in a dog.

Suspected limbic encephalitis and seizure in cats associated with voltage-gated potassium channel (VGKC) complex antibody.

BACKGROUND: Treatment-resistant complex partial seizures (CPS) with orofacial involvement recently were reported in cats in association with hippocampal pathology. The features had some similarity to those described in humans with limbic encephalitis and voltage-gated potassium channel (VGKC) complex antibody. HYPOTHESIS/OBJECTIVES: The purpose of this pilot study was to evaluate cats with CPS and orofacial involvement for the presence of VGKC-complex antibody. ANIMALS: Client-owned cats with acute orofacial CPS and control cats were investigated. METHODS: Prospective study. Serum was collected from 14 cats in the acute stage of the disease and compared with 19 controls. VGKC-complex antibodies were determined by routine immunoprecipitation and by binding to leucine-rich glioma inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2), the 2 main targets of VGKC-complex antibodies in humans. RESULTS: Five of the 14 affected cats, but none of the 19 controls, had VGKC-complex antibody concentrations above the cut-off concentration (>100 pmol/L) based on control samples and similar to those found in humans. Antibodies in 4 cats were directed against LGI1, and none were directed against CASPR2. Follow-up sera were available for 5 cats in remission and all antibody concentrations were within the reference range. CONCLUSION AND CLINICAL IMPORTANCE: Our study suggests that an autoimmune limbic encephalitis exists in cats and that VGKC-complex/LGI1 antibodies may play a role in this disorder, as they are thought to in humans.

Species, developmental stage and infection with microbial pathogens of engorged ticks removed from dogs and questing ticks.

Research into tick-borne diseases implies vector sampling and the detection and identification of microbial pathogens. Ticks were collected simultaneously from dogs that had been exposed to tick bites and by flagging the ground in the area in which the dogs had been exposed. In total, 200 ticks were sampled, of which 104 came from dogs and 96 were collected by flagging. These ticks were subsequently examined for DNA of Borrelia burgdorferi sensu lato, Anaplasma phagocytophilum, Rickettsia spp. and Babesia canis. A mixed sample of adult ticks and nymphs of Ixodes ricinus (Ixodida: Ixodidae) and Haemaphysalis concinna (Ixodida: Ixodidae) was obtained by flagging. Female I. ricinus and adult Dermacentor reticulatus (Ixodida: Ixodidae) ticks dominated the engorged ticks removed from dogs. Rickettsia spp. were detected in 17.0% of the examined ticks, A. phagocytophilum in 3.5%, B. canis in 1.5%, and B. burgdorferi s.l. in 16.0%. Ticks with multiple infections were found only among the flagging sample. The ticks removed from the dogs included 22 infected ticks, whereas the flagging sample included 44 infected ticks. The results showed that the method for collecting ticks influences the species composition of the sample and enables the detection of a different pattern of pathogens. Sampling strategies should be taken into consideration when interpreting studies on tick-borne pathogens.

In-clinic laboratory diagnosis of canine babesiosis (Babesia canis canis) for veterinary practitioners in Central Europe.

OBJECTIVE: Haematological changes in dogs and climatic conditions favourable for the vector may assist in the quick in-house diagnosis of canine babesiosis. MATERIAL AND METHODS: Blood samples from 358 dogs suspected to have canine babesiosis were evaluated. The diagnosis was confirmed in 113 dogs by detection of Babesia canis by microscopic examination of a stained blood smear using the concentration line technique. RESULTS: Thrombocytopenia was present in all 113 dogs. Red blood cell count, packed cell volume and haemoglobin values were below the reference range in 62.8%, 61.1% and 46.0% of affected dogs, respectively. An increased reticulocyte count was apparent in five Babesia canis -positive dogs. Leukopenia, lymphopenia, neutropenia and monocytosis were present in 54.9%, 47.8%, 30.4% and 6.5% of the dogs, respectively. Evaluating haematological parameters by CART-analysis revealed a predictive model (accuracy= 93.5%) for canine babesiosis, when using the leucocyte, thrombocyte, and reticulocyte count. Climatic conditions present at the most probable time of Babesia canis- infection accounted for biseasonal occurrence. Changes of climatic factors during the year influence the vector activity and in conclusion should highlight babesiosis in the ranking of differentials for veterinarians. CONCLUSION: The results demonstrate that a tentative diagnosis of canine babesiosis can be made based on typical haematological changes. The results recorded match well with the seasonality of the tick vector and were confirmed here by the month of sample submission.

Phylogenetic analysis of Austrian canine distemper virus strains from clinical samples from dogs and wild carnivores.

Austrian field cases of canine distemper (14 dogs, one badger [Meles meles] and one stone marten [Martes foina]) from 2002 to 2007 were investigated and the case histories were summarised briefly. Phylogenetic analysis of fusion (F) and haemagglutinin (H) gene sequences revealed different canine distemper virus (CDV) lineages circulating in Austria. The majority of CDV strains detected from 2002 to 2004 were well embedded in the European lineage. One Austrian canine sample detected in 2003, with a high similarity to Hungarian sequences from 2005 to 2006, could be assigned to the Arctic group (phocine distemper virus type 2-like). The two canine sequences from 2007 formed a clearly distinct group flanked by sequences detected previously in China and the USA on an intermediate position between the European wildlife and the Asia-1 cluster. The Austrian wildlife strains (2006 and 2007) could be assigned to the European wildlife group and were most closely related to, yet clearly different from, the 2007 canine samples. To elucidate the epidemiological role of Austrian wildlife in the transmission of the disease to dogs and vice versa, H protein residues related to receptor and host specificity (residues 530 and 549) were analysed. All samples showed the amino acids expected for their host of origin, with the exception of a canine sequence from 2007, which had an intermediate position between wildlife and canine viral strains. In the period investigated, canine strains circulating in Austria could be assigned to four different lineages reflecting both a high diversity and probably different origins of virus introduction to Austria in different years.

Spongy degeneration with cerebellar ataxia in Malinois puppies: a hereditary autosomal recessive disorder?

BACKGROUND: There is a high incidence of hereditary degenerative diseases of the central nervous system in purebred dogs. HYPOTHESIS: Cerebellar ataxia in Malinois puppies, caused by degenerative changes that predominate in cerebellar nuclei and the granular cell layer, is a hereditary disorder that is distinct from cerebellar cortical abiotrophies. ANIMALS: Thirteen Malinois puppies with cerebellar ataxia. METHODS: Retrospective study. Records of Malinois puppies with spongy degeneration of the cerebellar nuclei were analyzed including clinical signs, histopathological changes, and pedigree data. RESULTS: Signs of cerebellar dysfunction were observed in puppies of both sexes from 5 different litters (1995-2009) of phenotypically normal parents. Clinical signs started before the age of 2 months and resulted in euthanasia of all puppies by the age of 13 weeks. Histopathology disclosed marked bilateral spongy degeneration of the cerebellar nuclei and vacuoles in the granular cell layer and foliate white matter of the cerebellum. In some puppies, discrete vacuoles in gray and white matter were present in other parts of the brain. Furthermore, spheroids and dilated myelin sheaths were observed. Pedigree data and segregation frequency support an autosomal recessive hereditary disorder. CONCLUSIONS AND CLINICAL IMPORTANCE: Malinois suffer from a hereditary spongiform degeneration that predominates in the cerebellum and causes an early onset of clinical signs with unfavorable prognosis. Future efforts should increase awareness among veterinarians and breeders and aim to identify underlying metabolic mechanisms and the affected genes.

Generalized encephalitozoonosis in a young kitten with cerebellar hypoplasia.

In recent years opportunistic infections due to microsporidial organisms have become increasingly important in immunocompromised people. Infected animals could serve as reservoirs of such infections. A case of generalized encephalitozoonosis in a young kitten is reported. Diagnosis was established by histopathological, immunohistochemical and molecular biological investigations demonstrating characteristic lesions and DNA of Encephalitozoon cuniculi in formalin-fixed and paraffin wax-embedded tissue sections. Infections due to E. cuniculi are not common in cats, but a potential role of domestic cats in transmission of the infectious agent cannot be excluded.

Ticks and haemoparasites of dogs from Praia, Cape Verde.

In February 2008 an epidemiological field study on arthropod-borne infections in dogs was carried out in Praia, the capital city of Cape Verde. For this purpose 130 dogs were included in the study. Of these, 94.6% were infested with ticks. Altogether, 1293 ticks of the genus Rhipicephalus (in all evaluated cases R. sanguineus) were collected. Examination for haemotropic parasites was performed via polymerase chain reaction (PCR). Lymph node fine-needle aspirates were screened by PCR for Leishmania infantum infections in 20 dogs with enlarged lymph nodes. Our investigation revealed two species of protozoa (Babesia canis vogeli and Hepatozoon canis) and two species of rickettsiae (Anaplasma platys and Ehrlichia canis). In 101 dogs (77.7%) DNA of one or more pathogens was detected. The PCR examination for H. canis was positive in 83 dogs (63.8%), for E. canis in 34 dogs (26.2%), for A. platys in 10 dogs (7.7%) and for B. canis in five dogs (3.8%), whereas neither B. gibsoni nor L. infantum DNA could be detected. Of the infected dogs, 71.3% had a monoinfection, 27.7% had infections with two pathogens and 1.0% with three pathogens. B. canis, H. canis, E. canis, A. platys and their vector tick R. sanguineus are endemic to Cape Verde and can be present in dogs in high prevalences. These results outline the risk of importing tropical canine diseases when Capeverdian stray dogs are taken to Europe.

Myotonic dystrophy in two European grey wolves (Canis lupus).

Two related European Grey wolves (Canis lupus) with the history of muscle stiffness beginning at 2 weeks of age were examined in this study. Muscle tone and muscle mass were increased in both animals. Muscle stiffness was worsened by stress so that the animals fell into lateral recumbency. Blood chemistry revealed mildly increased serum creatine kinase activity. Abnormal potentials typical of myotonic discharges were recorded by electromyography. Cataract, first-degree atrioventricular (AV) block and inhomogeneous myocardial texture by ultrasound suggested extramuscular involvement. Myopathology demonstrated dystrophic signs in the muscle biopsy specimen. The presumptive diagnosis based on the in vivo findings was myotonic dystrophy. Immunochemistry of the striated muscles revealed focal absence of dystrophin 1 and beta-dystroglycan in both cases. Cardiac and ophthalmologic involvement suggested a disorder very similar to a human form of myotonic dystrophy. This is the first description of myotonic dystrophy in wolves.

Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury.

Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).

Gliomatosis cerebri in a dog.

Gliomatosis cerebri is a rare tumourous disease of the central nervous system consisting of glial cells characterized by diffuse widespread infiltration and preservation of preformed brain structures. This report describes a case of gliomatosis cerebri in a 9-year-old, male, flat-coated retriever dog with central nervous symptoms. Magnetic resonance imaging of the brain demonstrated ill-defined hyperintense zones of paramedian white matter within the right cerebral hemisphere, brainstem and cerebellum. Histological examination showed a proliferation of tumour cells in the brain structures mentioned. Glial fibrillary acidic protein-immunohistochemistry revealed a lot of fibres positively stained. Based on these findings, the alteration was diagnosed as gliomatosis cerebri.

Occurrence of the ear-mite Raillietia auris in cattle in Austria.

We describe here the first documented case in Austria of the cattle ear mite Raillietia auris in a four-year-old dairy cow. The cow was mildly depressed, and keratoconjunctivitis was diagnosed in both eyes with Horner's syndrome in the left eye. The animal showed a mild head tilt to the left and a generalized ataxia with a tendency to move to the right side, which became exacerbated if the animal was blind-folded. Head pressing to the right side, dysphagia and a dropped jaw were also observed. Numerous rather mobile ear mites were observed at necropsy in the basal part of the left ear canal. The clinical significance of the cattle ear mite is uncertain and the clinical signs could have been caused by listerial encephalitis, which was also confirmed histologically in this case.

Pipecolic acid concentrations in brain tissue of nutritionally pyridoxine-deficient rats.

Elevated concentrations of pipecolic acid have been reported in plasma and CSF of patients with pyridoxine-dependent epilepsy, but its molecular background is unclear. To investigate any further association of pyridoxine and pipecolic acid metabolism, we have performed an animal trial and have measured the concentration of pipecolic acid in brain tissue of rats with nutritional pyridoxine deficiency and in control littermates. Concentrations of pyridoxal phosphate were significantly reduced in brain tissue of pyridoxine-deficient rats (p < 0.001), while concentrations of pipecolic acid were not significantly different from the normally nourished control group (p = 0.3). These data indicate that a direct association of pyridoxine and pipecolic acid metabolism is unlikely. We therefore assume that the characteristic elevation of pipecolic acid in pyridoxine-dependent epilepsy could rather be a secondary phenomenon with the primary defect of pyridoxine-dependent epilepsy being located outside the pipecolic acid pathway.

Tick-borne encephalitis virus as a possible cause of optic neuritis in a dog.

A 3-year-old spayed female Siberian Husky was presented due to acute vision loss. Examination revealed bilateral optic neuritis and lymphocytic meningoencephalitis. The serum (1:800) and cerebrospinal fluid (CSF; 1:200) immunoglobulin (Ig)G titers for tick-borne encephalitis virus (TBEV) were elevated as were the serum IgG titer for Anaplasma phagocytophilum (1:640) and serum IgM titer for Toxoplasma gondii (1:20). Intracytoplasmic inclusion bodies such as ehrlichial or anaplasmal morulae were not observed in the CSF or blood smear. The dog was treated with methylprednisone and doxycycline. The left eye regained vision; the right eye remained blind. Anti-inflammatory therapy was stopped on day 18 after diagnosis. Four days later the dog showed evidence of hyperesthesia in the cervical region. Analysis of CSF showed no abnormalities and CSF IgG titers for TBEV and A. phagocytophilum were negative. Funduscopic evidence of active papillitis was absent on day 22 in the left eye and on day 86 in the right eye. On day 243, the dog was presented again with lethargy, ataxia, disorientation and temporary head tilt. The IgG titer for TBEV was again elevated in the CSF (1:800) and in serum (1:400). After interpretation of all findings, we assume that meningoencephalitis and optic neuritis in this patient was caused by TBEV and associated immune-mediated inflammation. In endemic areas, TBEV should be considered as cause of optic neuritis in dogs.