Renal epitheliotropism of feline morbillivirus in two cats

The association of feline morbillivirus (FeMV) with kidney disease in cats is controversial. Two cats with a history of severe hematuria had eosinophilic inclusion-like bodies in the renal tubular epithelial cells, without any inflammatory cellular reaction. Ultrastructurally, aggregations of electron-dense viral-like particles were found where the inclusion-like bodies were located. Immunohistochemistry (IHC) using antibodies against FeMV matrix protein labeled these inclusion-like bodies, and also labeled the cytoplasm of tracheal and bronchiolar epithelial cells, and lymphocytes and macrophages in spleen and mesenteric lymph node. Using double IHC, FeMV antigen was detected in astroglia and oligodendroglia but not in microglia. Phylogenetic characterization of the fusion and hemagglutinin gene sequences revealed FeMV-1A genotypes in both cats. These findings indicated an active viral infection with FeMV. We propose that FeMV is a renal epitheliotropic virus and also localizes in various other tissues.

Alteration in Oxidative Stress Biomarkers and Cytoarchitecture of Hepatic Tissues in Freshwater Fish Clarias batrachus (Linn.) under Sub lethal Butachlor Stress: Spectrophotometric and TEM Study

<p>The present study addresses the deleterious impact of sub lethal exposure of butachlor 2-chloro-N-(2-6-diphenyl) acetamide on hepatic cells of air breathing fish <em>Clarias batrachus</em> (Linn.) based on light and transmission electron microscopy and estimation of oxidative stress biomarker enzymes <em>viz.</em> reduced glutathione and lipidperoxidase. Fishes were exposed to 1.0µl/L butachlor for 5, 10 and 15 days respectively. After schedule exposure, blood sample were collected and extracted serum were analyzed for quantitative estimation of serum reduced glutathione and lipid peroxidase activity by spectrophotometer. The liver tissues were processed for light and electron microscope. Light photomicrographs of hepatic cells reveal dose related abnormalities which increases with the duration of exposure. Major changes attributed to the hepatic cell were parenchyma degeneration, necrosis along with fibrosis, widening of sinusoids, vacuolation, and infiltration of eosinophilic inclusion, karyolysis, pyknosis and perivenular congestion. Transmission electron microscopy of hepatic cells also revealed degenerated hepatic parenchyma, accumulation of lipid and electron dense material, degenerated mitochondria, nuclear shrinkage and enlarged lysosomes engulfing cytoplasmic particles in contrast to control fish. On prolonged exposure, the most frequent pathological modifications were mitochondrial swelling with regression of cristae and giant lysosome with myelinated phospholipid membrane pointing towards phospholipidosis. The activities of all the marker enzymes showed high fluctuation indicating significant imbalance in comparison to control. The study highlights the oxidative stress caused by butachlor correlated with histopathological anomalies of hepatic cells. It can be used as sensitive index for assessing the magnitude of oxidative damage and physiological dysfunction of experimental fish under laboratory condition.</p>

Histopathological findings of infections caused by canine distemper virus, Trypanosoma cruzi, and other parasites in two free-ranging White-nosed Coatis Nasua narica (Carnivora: Procyonidae) from Costa Rica

Canine distemper virus (CDV) causes systemic infections and immunosuppression in carnivores, which subsequently makes animals highly susceptible to opportunistic infections. Although Trypanosoma cruzi infects procyonids, chagasic myocarditis in Coatis has not been reported in Central America. The aim of this study was to report the histopathological findings caused by canine distemper virus, T. cruzi, and other parasites in two free-ranging White-nosed Coatis Nasua narica found dead in a national park on the Pacific coast of Costa Rica. Heart, lung, tongue, liver, brain and spleen samples were subjected to macroscopic and microscopic examination. A mononuclear meningoencephalitis associated with intra-nuclear eosinophilic inclusion bodies consistent with canine distemper virus was observed in nervous tissue. Myocarditis and associated nests of amastigotes of T. cruzi were observed during microscopic examination in cardiac tissue, and in muscle from the tongue of both animals. Molecular analysis confirmed T. cruzi in formalin-fixed paraffin embedded cardiac tissues. The myocardial damage caused by the opportunistic infection due to T. cruzi in these individuals could be the result of a severe compromised immunological status associated to the CDV infection, and subsequent opportunistic polyparasitism described herein. To the authors knowledge this is the first report of chagasic myocarditis in free-ranging coatis from Central America.

Myocarditis caused by naturally acquired canine distemper virus infection in 4 dogs

Canine distemper virus (CDV) has long been recognized as a cause of myocarditis; however, cases of myocarditis caused by naturally acquired CDV infection have been reported only rarely in dogs. We describe here our retrospective study of naturally acquired systemic CDV infection in 4 dogs, 4–7 wk old, that had myocarditis, with myocardial necrosis and fibrosis. One of the 4 dogs had intracytoplasmic eosinophilic inclusion bodies in cardiomyocytes. Other lesions included bronchointerstitial pneumonia (4 of 4), necrotizing hepatitis (2 of 4), splenic lymphoid necrosis (2 of 4), encephalitis (1 of 3; brain was not submitted in 1 case), and necrotizing gastroenteritis (1 of 4). The presence of CDV in the heart was confirmed by immunohistochemistry in all 4 dogs.

Molecular evidence for vaccine-induced canine distemper virus and canine adenovirus 2 coinfection in a fennec fox

A 61-d-old fennec fox ( Vulpes zerda), 11 d after receiving a multivalent, modified-live virus vaccine containing canine distemper virus (CDV), canine adenovirus 2 (CAdV-2), parainfluenza virus, parvovirus, and canine coronavirus, developed oculonasal discharge, and subsequently convulsions, and hemoptysis, and died. Microscopic changes in the cerebrum were evident, including neuronal degeneration and necrosis; intracytoplasmic eosinophilic inclusion bodies were observed in astrocytes. CDV was detected in the brain tissue by immunohistochemistry. Pulmonary lesions of multifocal necrotizing bronchopneumonia had Cowdry type A intranuclear inclusions in the bronchial epithelial cells. Electron microscopy revealed crystalline arrays of adenovirus-like particles within the intranuclear inclusions. Additionally, the hemagglutinin gene of CDV and the CAdV-2 DNA polymerase gene were detected in the fennec fox; sequence analysis showed 100% identity with those of the vaccine strain viruses. To our knowledge, vaccine-induced CDV and CAdV-2 coinfections using molecular analysis have not been reported previously. Therefore, vaccine strains should be considered prior to CDV vaccination in nondomestic carnivores.

Outbreak of Encephalitis Caused by Human Herpesvirus Type 1 (HSV-1) in NonHuman Captive Primates in São Paulo, SP, Brazil

Human herpesvirus type 1 (HSV-1), a Alphaherpesvirinae, has a broad range of cross-species infectivity with considerable variation in expression and disease severity among different hosts. Infection in humans, results in mild disease characterized by mucocutaneous lesions. In some species of nonhuman primates, however, the infection can be lethal. Transmission occurs through food contaminated by humans with labial herpes, offered to monkeys, constituting an important anthropozoonosis. In this study, we describe the occurrence of two outbreaks of encephalitis caused by HSV-1, occurring in the State of São Paulo, Brazil. The first outbreak affected a Brown howler monkey and three marmosets. The Brown howler monkey had tongue ulcers and enteritis and the marmosets were found dead without presenting clinical symptomatology. The second outbreak affected ten marmosets that were found dead suddenly in the enclosure without presenting symptoms or clinical signs. Organ fragments were processed for transmission electron microscopy, histopathology and inoculation in cell culture techniques. Ballooning degeneration, foci of monolymphocytic inflammatory reaction, corpuscle of eosinophilic inclusion, monolymphocytic meningitis and desquamative monolymphocytic enterocolitis, were the main lesions observed by histopathology. By the negative staining technique, enveloped and non-enveloped, herpesvirus particles were found, measuring 120-200 nm in diameter in all samples of organ fragments. The presence of aggregates formed by antigenantibody complex, characterized the positive result obtained in the immunoelectron microscopy technique for HSV-1. Using the immunocytochemistry technique, the antigen-antibody interaction was strongly enhanced by the colloidal gold particles over the herpesvirus, confirming the presence of HSV-1. Intranuclear incomplete particles measuring 80-100 nm in diameter and complete or enveloped scattered in the cytoplasm, were visualized in ultrathin sections of liver and cell culture measuring 140 nm of diameter. Immature particles budding from cell membranes were also observed. In viral isolation in VERO cells, typical cytopathic effect was observed in brain samples.

Outbreaks of myxomatosis in Egyptian domestic rabbit farms

<p class="Default">Myxomatosis is an endemic infectious, severe and often fatal disease of rabbit caused by myxoma virus. In the present study, myxomatosis outbreaks were reported in 7 domestic rabbit farms in Egypt. Rabbits showed oedema of the eyelids, facial oedema and blepharoconjunctivitis. The morbidity and lethality rates were 18-100% and 20-80%, respectively. The myxomatosis diagnosis was based on histopathology, virus isolation on rabbit kidney cell line (RK-13), polymerase chain reaction (PCR) and sequence analysis. Histopathological examination revealed the presence of epidermal hyperplasia, dermal necrosis and intracytoplasmic eosinophilic inclusion bodies. The virus was isolated on RK-13 cells and induced cytopathic effect. Using PCR, a band of 471 base pair corresponding to the M071L gene was amplified from extracted DNA. Sequence alignment of four out of the 7 isolates revealed that these isolates were 98-99% identical to European and Australian rabbit myxoma reference viruses. In conclusion, rabbit myxomatosis outbreaks and virus isolation procedures are reported herein for the first time in Egypt. Preventive policies against disease circulation should be adopted by the national authorities.</p>

Outbreak of Bovine Herpetic Meningoencephalomyelitis in Southern Brazil

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells. Inflammation was also seen in a milder degree in the spinal cord, characterized by infiltrate of lymphocytes at grey matter, mainly around vessels. A herpesvirus which induced typical cytopathic effect in cell cultures was recovered from tissues. The isolated virus was typed as BoHV-5 by nucleotide sequencing analysis of the gC coding region.Discussion: The diagnosis of meningoencephalomyelitis associated to BoHV-5 was based on epidemiological, clinical, macroscopical, histological, virological and genomic findings. In the outbreak here reported, the disease occurred in young animals, with low morbidity but high lethality rates. Clinical signs on this case were consistent with previous reports on the literature. Bovines affected by BoHV-5 may display no gross lesions within the CNS; however, inflammatory and degenerative changes are frequently seen, characterized by malacia, leptomeningeal vessels hyperemia, edema and hemorrhages. Histologically, non-suppurative necrotizing meningoencephalitis is seen, with perivascular inflammatory infiltrates and, occasionally, intranuclear eosinophilic inclusion bodies in astrocytes and neurons. Similar but milder lesions were seen in the spinal cords of two of the necropsied calves, a feature which has only been previously associated to BoHV-1 infections. The identification of the implicated agent was accomplished by virus isolation in cell cultures followed by genome typing. Specific treatments for this condition are not currently available, and the number of animals that recover from clinically apparent disease is extremely low. Preventive measures are based on serological testing of herds, and segregation or elimination of seropositive calves. To avoid progression of the disease in seropositive animals, control efforts must be directed to avoid stressful conditions. Vaccination with BoHV-1 and BoHV-5 vaccines is expected to confer protection to clinical disease.

Lewy and his inclusion bodies: Discovery and rejection

ABSTRACT Fritz Jacob Heinrich Lewy described the pathology of Paralysis agitans [Parkinson disease] and was the first to identify eosinophilic inclusion bodies in neurons of certain brain nuclei, later known as Lewy bodies, the pathological signature of the Lewy body diseases. In 1912, he published his seminal study, followed soon after by an update paper, and 10 years later, in 1923, by his voluminous book, where he exhaustively described the subject. The publication provided extensive information on the pathology of Paralysis agitans, and the entirely novel finding of eosinophilic inclusion bodies, which would become widely recognized and debated in the future. His discovery was acknowledged by important researchers who even named the structure after him. However, after his last publication on the issue, inexplicably, he never mentioned his histopathological discovery again. Despite several hypotheses, the reasons that led him to neglect (reject) the structure which he so preeminently described have remained elusive.