Suppurative meningoencephalitis and perineuritis caused by Streptococcus gallolyticus in a Japanese Black calf

A 179-day-old calf, which was weak and stunted, showed neurological signs and was euthanized. Postmortem examination revealed extensive and severe cloudy area in the meninges, and pleural pneumonia. Gram-positive cocci were isolated from systemic organs. Biochemical and 16S rRNA gene sequence analyses identified the isolate as Streptococcus gallolyticus, and its subspecies was suggested to be gallolyticus (SGG). The isolate was classified as a novel sequence type (ST115) by the multilocus sequence typing scheme for SGG and showed susceptibility to penicillin, ampicillin, amoxicillin, florfenicol, sulfamethoxazole-trimethoprim, and chloramphenicol. Histopathologically, suppurative meningoencephalitis and perineuritis were detected. As SGG has been isolated solely from a cow with mastitis in Japan, this is the first SGG infection in a calf with suppurative meningoencephalitis and perineuritis in this country.     

A study of experimental autoimmune encephalomyelitis in dogs as a disease model for canine necrotizing encephalitis

In the present study, the use of dogs with experimental autoimmune encephalomyelitis (EAE) as a disease model for necrotizing encephalitis (NE) was assessed. Twelve healthy dogs were included in this study. Canine forebrain tissues (8 g), including white and grey matter, were homogenized with 4 mL of phosphate-buffered saline for 5 min in an ice bath. The suspension was emulsified with the same volume of Freund''s complete adjuvant containing 1 mg/mL of killed Mycobacterium tuberculosis H37Ra. Under sedation, each dog was injected subcutaneously with canine brain homogenate at four sites: two in the inguinal and two in the axillary regions. A second injection (booster) was administered to all the dogs using the same procedure 7 days after the first injection. Clinical assessment, magnetic resonance imaging, cerebrospinal fluid analyses, necropsies, and histopathological and immunohistochemical examinations were performed for the dogs with EAE. Out of the 12 animals, seven (58%) developed clinically manifest EAE at various times after immunization. Characteristics of canine EAE models were very similar to canine NE, suggesting that canine EAE can be a disease model for NE in dogs.     

Nasopharyngeal cryptococcosis

Naturally occurring cryptococcosis in five cats, a dog and a koala is described. Involvement of the nasopharynx was documented in all patients, and nasopharyngeal mass lesions accounted for the major presenting complaints in four. Signs referable to nasopharyngeal disease included snoring, stertor, inspiratory dyspnoea and aerophagia. Diagnoses were made by caudal rhinoscopy using a retroverted flexible endoscope, vigorous orthograde flushing with saline, or at necropsy. Concurrent cryptococcal rhinitis was present in all cases, although involvement appeared limited to the caudal nasal cavity in most cases. Typical signs of nasal cavity disease, such as sneezing and nasal discharge, were often absent. Treatment of nasopharyngeal cryptococcosis should include physical dislodgement or debulking of lesion(s) to provide immediate alleviation of upper airway obstruction, followed by systemic antifungal therapy to eliminate residual infection from the nasal cavity. Infections caused by Cryptococcus neoformans var gattii accounted for a disproportionately large number of these cases.     

Amoebic meningoencephalitis caused by Balamuthia mandrillaris in an orang utan

Objective
To describe a case of meningoencephalitis caused by Balamuthia mandrillaris in an orang utan.
Design
A pathological case report.
Animal
A 20 years old male orang utan (Pongo pygmaeus).
Procedure
The disease process was investigated by clinical pathology, necropsy, histopathology and immunofluorescence labelling.
Results
The orang utan developed sudden onset of depression, lethargy, inappetence and apparent head pain. The condition was considered to be related to a 2 year history of upper and lower respiratory disease, and the animal was placed on antibiotics after extensive testing. By the seventh day the animal had become ataxic and disoriented and a brain abscess was suspected. He died on the ninth day of illness. At necropsy, and subsequent sectioning, the brain showed multiple circular, soft, white to grey brown areas of varying size, the largest being in the left temporal (3.5 cm diameter) and right occipital (2.5 cm diameter) regions of the cerebrum. Histological examination of these regions revealed many amoebic trophozoites and occasional cysts associated with areas of haemorrhage and inflammatory necrosis. The trophozoites were packed in perivascular spaces and their nuclei often contained two or more prominent nucleoli. Immunofluorescent labelling of histological sections suggested that the agent was B mandrillaris.
Clinical implications
This report provides further evidence that B mandrillaris , a free living amoeba, can act as a pathogen in animals as well as people, and cause fatal meningoencephalitis. Along with Naegleria and Acanthamoeba spp, B mandrillaris should be considered amongst the causes of acute onset meningoencephalitis in animals.     

UNIQUE TOPOGRAPHIC DISTRIBUTION OF GREYHOUND NONSUPPURATIVE MENINGOENCEPHALITIS

Greyhound nonsuppurative meningoencephalitis is an idiopathic breed‐associated fatal meningoencephalitis with lesions usually occurring within the rostral cerebrum. This disorder can only be confirmed by postmortem examination, with a diagnosis based upon the unique topography of inflammatory lesions. Our purpose was to describe the magnetic resonance (MR) imaging features of this disease. Four Greyhounds with confirmed Greyhound nonsuppurative meningoencephalitis were evaluated by MR imaging. Lesions predominantly affected the olfactory lobes and bulbs, frontal, and frontotemporal cortical gray matter, and caudate nuclei bilaterally. Fluid attenuation inversion recovery (FLAIR) and T2 weighted spin‐echo (T2W) sequences were most useful to assess the nature, severity, extension, and topographic pattern of lesions. Lesions were predominantly T2‐hyperintense and T1‐isointense with minimal or absent contrast enhancement.     

Clinical signs, imaging features, neuropathology, and outcome in cats and dogs with central nervous system cryptococcosis from California

Background: Cryptococcus spp. is a fungal pathogen with a predilection for the central nervous system (CNS). Objectives: To compare the clinical, advanced imaging, and neuropathologic findings in dogs and cats with CNS cryptococcosis, and to evaluate outcome of treatment in these animals. Animals: Twenty‐six cats and 21 dogs with CNS cryptococcosis. Methods: Medical records were reviewed for clinical findings and results of CNS imaging. Archived cerebrospinal fluid and CNS tissue specimens were reviewed for pathology. Findings in cats were compared with those in dogs and the effects of variables on survival were determined by survival curve analysis. Results: When present, pain was localized to the cervical region in dogs and was generalized or localized to the thoracolumbar spine or pelvic limbs in cats. Magnetic resonance imaging (MRI) findings were variable but correlated with CNS histopathological findings of meningitis, meningitis with gelatinous pseudocyst formation, and granulomatous mass lesions. Peripherally enhancing brain lesions were seen only in cats. Histopathologically, the inflammatory response was milder in cats compared with dogs. Remissions of ≥1 year occurred in 32% of treated animals. Altered mentation was associated with negative outcome. Glucocorticoid use after diagnosis was associated with improved survival in the first 10 days. Conclusions and Clinical Importance: Lesions seen on MRI reflected neuropathological findings and were similar to those reported in human patients. The immune response to infection may differ between cats and dogs, or relate to the infecting cryptococcal species. Long‐term (>6 month median survival time) survival may be possible in animals surviving ≥4 days after diagnosis.     

Fatal equine meningoencephalitis in the United Kingdom caused by the panagrolaimid nematode Halicephalobus gingivalis: case report and review of the literature

A fatal case of eosinophilic and granulomatous meningoencephalitis caused by the free-living panagrolaimid nematode Halicephalobus gingivalis is reported in a 10-year-old Welsh gelding in the United Kingdom. Clinical examination first revealed behavioural abnormalities which rapidly progressed to severe ataxia, reduced mentation status and cranial nerve signs. Despite symptomatic treatment no amelioration of neurological signs was achieved and the horse was subjected to euthanasia. A complete post mortem examination revealed eosinophilic and granulomatous meningoencephalitis mainly affecting the cerebellum and brain stem with intralesional adult nematodes, larvae and eggs. There was also eosinophilic meningitis of the cervical spinal cord. The intralesional nematodes were morphologically consistent with the panagrolaimid nematode H. gingivalis. Although infection by this facultative neurotropic parasite is extremely rare, it needs to be considered in the differential diagnosis of central nervous signs in horses and, in particular, other equine helminthic infection of the central nervous system. This fatal case is unusual since lesions were locally very extensive and the nematodes did not colonise haematogenously to other organs as seen often in equine halicephalobosis. As the taxonomy of H. gingivalis has changed and some recent reports in the literature still refer to this species as Micronema deletrix or Halicephalobus deletrix, we here provide a short update of the species and some insights on the order Tylenchida, which contains free-living nematodes with parasitic tendencies.     

POSITRON EMISSION TOMOGRAPHY FEATURES OF CANINE NECROTIZING MENINGOENCEPHALITIS

A Yorkshire terrier and a Chihuahua were referred for acute onset, generalized tonic‐clonic seizures and were suspected to have meningoencephalitis based on magnetic resonance (MR) imaging findings. Brain lesions appeared hyperintense with T2‐weighted imaging and hypointense with T1‐weighted imaging, and were characteristic of necrotizing meningoencephalitis. Both dogs were diagnosed with necrotizing meningoencephalitis based on pathologic findings. Fluorine‐18 fluorodeoxyglucose positron emission tomography (FDG‐PET) was performed on both animals before euthanasia with the permission of the owner. In FDG‐PET images, these lesions seen in MR images were characterized by multifocal or diffuse hypometabolism. Our FDG‐PET results provided evidence of glucose hypometabolism in areas of necrosis and cavitation associated with necrotizing meningoencephalitis. FDG‐PET has the potential to provide valuable diagnostic information in dogs with suspected necrotizing encephalitis.