Utility of 5-aminolaevulinic acid fluorescence-guided endoscopic biopsy for malignant mesothelioma in a cat and dog.

Malignant mesothelioma (MM) is uncommon in cats and dogs and can be challenging to diagnose. Adequate tissue sampling is required for superior diagnostic accuracy. Protoporphyrin IX, a metabolite of 5-aminolaevulinic acid (5-ALA), is a photosensitiser for photodynamic diagnosis (PDD). To the best of our knowledge, no study has reported the use of 5-ALA-PDD to detect MM in veterinary medicine. The present study describes the use of 5-ALA-PDD for MM diagnosis in a cat and dog, as well as the effectiveness of intracavitary chemotherapy. We evaluated the use of PDD with 5-ALA hydrochloride (5-ALA-PDD) in two cases of MM. A 12-year-old cat presented with a 1-month history of respiratory distress, and a 9-year-old dog presented with a 3-month history of mild abdominal distention. We endoscopically biopsied lesions in both the cases using 5-ALA-PDD. Histopathological examination revealed mesothelioma, and immunohistochemical staining was positive for calretinin. Both patients were treated with carboplatin. The cat died of respiratory failure. Although, the dog's condition improved 21 days after the first chemotherapeutic drug administration, the dog died on day 684 owing to cardiac-related issues. 5-ALA-PDD is thus, safe and feasible for the diagnosis of MM in veterinary medicine.

Photodynamic detection of a canine glioblastoma using 5-aminolevulinic acid.

Photodynamic detection using 5-aminolevulinic acid has been used to identify the surgical margins during resection of human primary brain tumours. Although there are some reports on its use in malignant tumours in veterinary medicine, it has never been used for primary brain tumours. Here we describe a canine glioblastoma that was detected at autopsy with protoporphyrin IX fluorescence induced by orally administered 5-aminolevulinic acid. The fluorescence was strongest towards the centre of the lesion and was absent in normal brain tissue. Moreover, the fluorescence findings were consistent with MRI and histopathological findings. Our findings suggest that photodynamic detection using 5-aminolevulinic acid might be useful for intraoperative fluorescence-guided resection of malignant gliomas in dogs.

Pathogenesis of Renal Lesions in Chickens After Experimental Infection With 9a5b Newcastle Disease Virus Mutant Isolate.

In this study, we investigated the pathogenesis of Newcastle disease virus (NDV) in the chicken kidney. Twenty-six 32-day-old specific pathogen-free chickens were intranasally inoculated with the 9a5b NDV mutant isolate. Kidney tissue samples, collected at 6 and 12 hours postinoculation (hpi) and 1, 2, 3, 5, and 10 days postinoculation (dpi), were analyzed by histopathology, immunohistochemistry (IHC), reverse transcription polymerase chain reaction (RT-PCR), and virus titration. Histopathologically, tubulointerstitial nephritis was detected in the renal cortex and predominantly in the medulla. Nephrotropism of 9a5b NDV was confirmed by IHC, RT-PCR, and virus isolation. Massive degenerative changes and infiltration of CD3-immunopositive cells accompanied replication of the 9a5b NDV isolate in chicken kidneys. In conclusion, pathological changes that were caused by NDV in chicken kidneys were similar to those caused by avian influenza virus, infectious bronchitis virus, and avian nephritis virus, and this highlights the importance of including NDV in the differential diagnosis of kidney disease in chickens.

Pathogenesis of Pancreatitis in Chickens after Experimental Infection with 9a5b Newcastle Disease Virus Mutant Isolate.

The aim of this study was to investigate the effect of Newcastle disease virus (NDV) on the chicken pancreas. A virulent 9a5b mutant NDV isolate was inoculated intranasally into 32-day-old specific pathogen-free white Leghorn chickens. The pancreas was examined grossly and fixed for histopathological, immunohistochemical and electron microscopical investigations. Inflammatory changes were observed in the peripancreatic tissue at the early stage of infection (12 h post infection) and became more prevalent towards the end of the experiment. Multifocal areas of necrotizing inflammation were detected in the exocrine portion of the pancreas by 5 days post infection (dpi) and became more severe at 10 dpi. The endocrine islets were generally preserved, but slight degenerative changes were observed at 10 dpi. Immunohistochemically, NDV-nucleoprotein (NDV-NP) signals were detected in the peripancreatic tissues (associated with macrophages and other lymphoid cells) by 1 dpi. In the exocrine portion of the pancreas, NDV-NP signals were detected at 5 dpi and increased in intensity and distribution by 10 dpi. NDV particles were confirmed in the cytoplasm of exocrine acinar cells by transmission electron microscopy. CD3-positive cells were observed in the peripancreatic tissues earlier than in the pancreatic tissue. Moreover, in comparison with control chickens, insulin immunoexpression was unchanged, except on the last day of the experiment, when it was slightly reduced. The 9a5b NDV infection induced an inflammatory reaction and viral replication in the peripancreatic tissues earlier than in the pancreatic tissue. Furthermore, necrosis affected mainly the exocrine portion of the pancreas, while the endocrine portion was generally unaffected.

Neurogenic cardiomyopathy in rabbits with experimentally induced rabies.

Cardiomyopathies have been rarely described in rabbits. Here we report myocardial necrosis of the ventricular wall in rabbits with experimentally induced rabies. Myocardial lesions were found only in rabbits with brain lesions, and the severity of the cardiac lesions was proportional to that of the brain lesions. Neither the frequency nor the cumulative dose of anesthesia was related to the incidence or the severity of the myocardial lesions. The myocardial lesions were characterized by degeneration and/or necrosis of myocardial cells and were accompanied by contraction band necrosis, interstitial fibrosis, and infiltration of inflammatory cells. The brain lesions due to rabies virus infection were most prominent in the cerebral cortex, thalamus, hypothalamus, brainstem, and medulla. Rabies virus antigen was not found in the hearts of any rabbits. Based on these findings, the myocardial lesions were classified as neurogenic cardiomyopathy.

Temporary regression of locally invasive polypoid rhinosinusitis in a dog after photodynamic therapy.

A 5-year-old male cross-breed dog with chronic rhinosinusitis was presented. Computed tomography (CT) revealed opacities consistent with soft tissue or fluid in the left nasal cavity and frontal sinus. A diagnosis of chronic rhinosinusitis with myxomatous polyps was based on the histology of biopsy samples, so prednisolone treatment was administered for 1 month. Although the clinical signs slightly improved, no changes were observed on the CT images. At 8 months after the initial presentation, the dog was treated with antivascular photodynamic therapy (PDT) using benzoporphyrin derivative monoacid ring A and, 11 days later, CT revealed remarkably decreased soft tissue opacity; the facial swelling and sneezing also resolved. Three additional sessions of PDT were performed at 114, 210, and 303 days after the first PDT because of recurrence of clinical signs. The disease was well controlled for approximately 10 months by antivascular PDT.

Hepatic myelolipoma and amyloidosis with osseous metaplasia in a swan goose (Anser cygnoides).

An adult swan goose (Anser cygnoides) kept in a zoological garden had gross hepatic enlargement with extensive ill-defined white foci. Microscopically, the hepatic lesions were composed of a mixture of adipocytes and myeloid cells. The goose was also affected with systemic amyloidosis and there were areas of osseous metaplasia associated with deposition of amyloid within the liver.

The vagus nerve is one route of transneural invasion for intranasally inoculated influenza a virus in mice.

Intranasally inoculated neurotropic influenza viruses in mice infect not only the respiratory tract but also the central nervous system (CNS), mainly the brain stem. Previous studies suggested that the route of invasion of virus into the CNS was via the peripheral nervous system, especially the vagus nerve. To evaluate the transvagal transmission of the virus, we intranasally inoculated unilaterally vagectomized mice with a virulent influenza virus (strain 24a5b) and examined the distribution of the viral protein and genome by immunohistochemistry and in situ hybridization over time. An asymmetric distribution of viral antigens was observed between vagal (nodose) ganglia: viral antigen was detected in the vagal ganglion of the vagectomized side 2 days later than in the vagal ganglion of the intact side. The virus was apparently transported from the respiratory mucosa to the CNS directly and decussately via the vagus nerve and centrifugally to the vagal ganglion of the vagectomized side. The results of this study, thus, demonstrate that neurotropic influenza virus travels to the CNS mainly via the vagus nerve.

Persistence of viral RNA segments in the central nervous system of mice after recovery from acute influenza A virus infection.

One-hundred thirty-seven BALB/c mice were intranasally inoculated with neurotropic avian influenza A virus (H5N3). Thirty-nine of these mice died within 16 days post-inoculation (PID) and 98 of the mice recovered from the infection. To investigate whether viral antigens and genomes persist in the central nervous system (CNS) of recovered mice, immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) methods were performed. Histopathologically, mild interstitial pneumonia and non-suppurative encephalomyelitis restricted to the basal part of the frontal lobe of the cerebrum, brain stem and thoracic spinal cord were observed in BALB/c mice until 40 PID. Small amounts of viral antigens were detected in the brain and spinal cord and some viral RNA segments (NA, NP, M, PA, HA, NS, PB1) were intermittently detected in the CNS until 48 PID. Immunosuppression of these mice by dexamethazone (DEX) treatment did not increase the frequency of detection of the lesions, viral antigens or genomes. These findings suggest that viral genomes of neurovirulent influenza virus persist with restricted transcriptive activity in the CNS of the mice even after clinical recovery from the infection.