A case of diffuse leptomeningeal oligodendrogliomatosis affecting the brain and spinal cord of a dog is presented. A 7.5‐year old, male neutered Staffordshire bull terrier presented for evaluation of a chronic history of tetraparesis and seizures, with a multifocal neuroanatomical localization was determined. Extra‐axial intradural lesions with an atypical presentation of a dural tail sign were seen on MRI. Histologically, the lesions were consistent with leptomeningeal oligodendrogliomatosis. To the authors’ knowledge, a dural tail sign has not previously been reported as an MRI characteristic of diffuse leptomeningeal oligodendrogliomatosis in dogs.

Choroid plexus tumors (CPT) are intraventricular neoplasms accounting for 10% of all primary central nervous system tumors in dogs. They are frequently classified according to the human WHO classification into choroid plexus papilloma (CPP, grade I), atypical CPP (aCPP, grade II), and choroid plexus carcinoma (CPC, grade III). Histological features observed in canine CPT such as increased vascular density (IVD) and glomeruloid microvascular proliferation (GMVP) are not part of the WHO classification. This multi-centric study aimed to investigate tumor-associated vascular hyperplasia in dogs by determining the prevalence of GMVP and IVD in 52 canine CPT and their association with tumor grade. In addition, the expression of angiogenic factors was assessed by immunohistochemistry in 25 tumors to investigate the pathogenesis of tumor-associated vascular hyperplasia. Based on the classical histological hallmarks, this study of 52 CPT identified 22 (42%) CPP (grade I) and 30 of (58%) CPC (grade III). GMVP was more prevalent in CPC (13/30; 43%) than CPP (1/22; 4%), whereas IVD occurred to a similar extent in CPP and CPC. Desmoplasia was more common in CPC (19/30; 63%) than CPP (2/22; 9%), and similarly, the proliferative index (PI) of neoplastic epithelium was significantly higher in CPC (5.14%) than CPP (0.94%). The majority of CPT expressed platelet-derived growth factor (PDGF), PDGFRα, PDGFRβ, and vascular endothelial growth factor (VEGF) irrespective of tumor grade or tumor-associated vascular hyperplasia. These results suggest that tumor-associated GMVP, desmoplasia, and PI may serve as histological indicators of malignancy in CPT.

A 10 year-old castrated male Domestic Short-hair cat with a history of chronic bilateral keratitis was referred for assessment of a red, elevated mass involving the left cornea. The rapid growth of the mass, over a month period in combination with pronounced vascularization and invasion of the corneal surface suggested an aggressive inflammatory or neoplastic process. Following keratectomy, the lesion was diagnosed histopathologically as a hemangiosarcoma. The tumor recurred locally within 3 weeks and enucleation was performed. Histopathologic examination of the globe confirmed the diagnosis and did not reveal infiltration of the limbus and conjunctiva. No signs of local recurrence or metastatic disease have been observed 18 months following enucleation. To the authors' knowledge this is the first case of primary corneal hemangiosarcoma described in the feline species.

An 11-year-old male, neutered European cat was presented for anisocoria due to pupillary dilation in the right eye. Ophthalmic findings were restricted to this eye and consisted of a raised, darkly pigmented, retrolental mass associated with retinal detachment. Ultrasonography identified the mass lesion protruding into the vitreous cavity from the posterior pole of the eyeball and confirmed the detachment of the retina. A tentative diagnosis of an intraocular tumor was made. Radiographic evaluation and retromandibular lymph node cytology did not reveal evidence of distant metastasis. Orbital exenteration of the affected eye was performed and the tumor was diagnosed as a choroidal melanocytic tumor with no criteria of malignancy (melanocytoma). The cat died 5 months later from renal lymphoma, and necropsy did not detect metastasis of the melanocytic tumor. To our knowledge this is the first reported case of feline choroidal melanocytoma.

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Bovine spongiform encephalopathy (BSE) is caused by different prion strains that are discriminated by the molecular characteristics of the pathological prion protein. In 2011, Switzerland reported two presumptive cases of BSE in cattle with a prion protein phenotype different from previously described strains, and it was unclear whether these findings were related to a transmissible disease and have implications on animal and public health. In this study, brain tissues of these cases were inoculated into transgenic mice expressing the bovine prion protein (BoPrP-Tg110) and into cattle. Clinical and pathological investigations as well as molecular testing did not provide evidence for the presence of BSE in the Swiss cases after two passages in BoPrP-Tg110 mice and a challenge period of 3.5 years in cattle. This lack of disease transmission suggests that the Swiss 2011 cases were not affected by a prion disease and were unrelated to the feed-born BSE epidemic.

Background Listeria monocytogenes (Lm) is a bacterial pathogen of major concern for humans and ruminants due to its neuroinvasive potential and its ability to cause deadly encephalitis (neurolisteriosis). On one hand, polymorphonuclear neutrophils (PMN) are key players in the defense against Lm, but on the other hand intracerebral infiltration with PMN is associated with significant neural tissue damage. Lm-PMN interactions in neurolisteriosis are poorly investigated, and factors inducing PMN chemotaxis to infectious foci containing Lm in the central nervous system (CNS) remain unidentified. Methods In this study, we assessed bovine PMN chemotaxis towards Lm and supernatants of infected endogenous brain cell populations in ex vivo chemotaxis assays, to identify chemotactic stimuli for PMN chemotaxis towards Lm in the brain. In addition, microglial secretion of IL-8 was assessed both ex vivo and in situ. Results Our data show that neither Lm cell wall components nor intact bacteria elicit chemotaxis of bovine PMN ex vivo. Moreover, astrocytes and neural cells fail to induce bovine PMN chemotaxis upon infection. In contrast, supernatant from Lm infected microglia readily induced chemotaxis of bovine PMN. Microglial expression and secretion of IL-8 was identified during early Lm infection in vitro and in situ, although IL-8 blocking with a specific antibody could not abrogate PMN chemotaxis towards Lm infected microglial supernatant. Conclusions These data provide evidence that host-derived rather than bacterial factors trigger PMN chemotaxis to bacterial foci in the CNS, that microglia have a primary role as initiators of bovine PMN chemotaxis into the brain during neurolisteriosis and that blockade of these factors could be a therapeutic target to limit intrathecal PMN chemotaxis and PMN associated damage in neurolisteriosis.