Subcutaneous cysticercosis due to Taenia crassiceps (Cestoda: Taeniidae) in an imported steppe lemming in Japan.

This study describes a subcutaneous proliferative cysticercosis in a pet steppe lemming, Lagurus lagurus (Rodentia: Cricetidae), bred and imported from Czech Republic into Japan. Numerous metacestodes were collected from the subcutaneous cystic lesion of the left medial thigh. Four surgical removals were coupled with anthelmintic treatment but ended with recurrence. Based on morphological features and mitochondrial DNA sequences, the metacestodes were identified as the larval stage of Taenia crassiceps (Zeder, 1800). This is the first case of infection with larval T. crassiceps in rodents of the genus Lagurus, and becomes the third case of the parasite detected from imported animals in Japan. Related public health concerns are discussed.

African pygmy hedgehog adenovirus: Virus replication, virus-induced cytopathogenesis and activation of mitogen-activated protein kinase signaling pathways in infected MDCK cells.

We examined several aspects of African hedgehog adenovirus (AhAdv-1) that was isolated from an African pygmy hedgehog, including: replication kinetics of, virus-induced cytopathic effect (CPE), activation status of mitogen-activated protein kinase (MAPK) signaling pathways, and possible roles of these signaling pathways in virus replication and virus-induced CPE in MDCK cells. AhAdv-1 efficiently replicated and induced CPE in infected cells and caused accumulation of cleaved caspase-3 at 24 h post-infection (p.i.), suggesting apoptosis induction. Analysis of several intracellular signal transduction pathways, which are involved in apoptosis, showed activation of p38 MAPK, Akt and ERK1/2 pathways at 3 h p.i., and upregulation of phosphorylated SAPK/JNK at 24 h p.i. Although p38 MAPK inhibitor and SAPK/JNK inhibitor suppressed activation of the respective pathways in infected cells, they did not inhibit virus-induced CPE. Treatment of infected cells with inhibitor of the Akt pathway, the p38 pathway, the SAPK/JNK pathway or the ERK pathway revealed that inhibitors of p38 pathway inhibited viral replication by real-time PCR and TCID50 assay in infected MDCK cells, suggesting that AhAdv-1 uses p38 pathway for multiplication in infected cells.

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.

Complete Genome Sequence of an Adenovirus-1 Isolate from an African Pygmy Hedgehog (Atelerix albiventris) Exhibiting Respiratory Symptoms in Japan.

This study reports the complete genome sequence of an African pygmy hedgehog adenovirus-1 isolate from an African pygmy hedgehog which displayed respiratory symptoms that included nasal discharge, sniffling, coughing, and respiratory distress. The viral genome is 31,764 bp long and shows four deletion sites compared to that of skunk adenovirus-1.

Epidemic nodular facial myxomatous dermatitis in juvenile Cranwell's horned frogs Ceratophrys cranwelli.

In 2017, approximately 40 out of 100 captive Cranwell's horned frogs Ceratophrys cranwelli from several facilities in Japan exhibited protruding facial lesions. Histopathological examination was performed on 6 specimens with such lesions randomly selected from 2 facilities. Lesions consisted of scattered stellate to spindle-shaped cells without atypia in an abundant myxoid matrix and occasional lymphocytic infiltrates. Maxillary bone was resorbed. No etiological organisms were detected using light microscopy or metagenomic analysis of the lesions. Macroscopic and histological assessments indicate that the lesions are associated with nodular facial myxomatous dermatitis, which has never been reported in amphibians.

Morphological and molecular characterization of Cystoisospora sp. from Asian small-clawed otters Aonyx cinereus.

In this study, we provide the first description of Cystoisospora infection in Asian small-clawed otters (Aonyx cinereus). In July 2017, three juvenile otters recently imported from the Republic of Indonesia showed severe diarrhea and were diagnosed with coccidial infection; two of them eventually died. Fecal examination revealed the presence of numerous oocysts. Sporulated oocysts showed typical Cystoisospora features, measuring 24.6 ±â€¯1.6 (22.0-27.0) × 21.8 ±â€¯1.4 (19.0-25.0) µm, with an oocyst length/width ratio of 1.1 ±â€¯0.1 (1.0-1.3). Each sporocyst contained four sporozoites in a head-to-tail arrangement. The Stieda body was absent, and the sporocyst residuum was present. These morphological characteristics differentiated this species from the other valid Cystoisospora species described from mustelids. Molecular analysis was conducted at two loci: the nuclear 18S ribosomal RNA and mitochondrial cytochrome c oxidase subunit I genes. The 18S sequence showed high similarity with canine Cystoisispora ohioensis (1-bp difference, 1422/1423 [99.9%]). At the cytochrome c oxidase subunit I gene locus, the sequence from otters was identical to that of feline Cystoisospora rivolta (847/847 [100%]). Phylogenetic analyses using concatenated data demonstrated that Cystoisospora sp. from otters and C. rivolta grouped together in the same Cystoisospora clade. Based on these data, we concluded that Cystoisospora sp. detected from otters appeared to be highly similar to C. rivolta.

First report of fatal disseminated microsporidiosis in two inland bearded dragons Pogona vitticeps in Japan.

Introduction.Encephalitozoon pogonae is a newly described pathogen belonging to the phylum Microsporidia. In Austria and the USA, this species has been isolated from fatal and disseminated cases of captive-bred inland bearded dragons. Here, we report the case of fatal disseminated microsporidiosis caused by E. pogonae in two bearded dragons in Japan. Case Presentation. The two lizards from different private households in Tokyo, Japan, had been brought to an animal hospital for examination. In both cases, the animal presented with a history of weight loss for several weeks. There were no improvements in clinical symptoms and the lizards deteriorated and finally died. Histopathological examination demonstrated necrotizing granulomatous inflammation attributed to disseminated microsporidian infection. Nucleotide sequencing of the nuclear ribosomal internal transcribed spacer region identified the microsporidian as E. pogonae with sequence identity of 100 %. Conclusion. We report the first case, to our knowledge, of disseminated microsporidiosis caused by E. pogonae in inland bearded dragons in Japan. Although it is difficult to diagnose prenatally since the signs are nonspecific, the disease should be considered in the differential diagnosis of chronic infections that do not respond to antibiotics.

Ranavirus in an outbreak of dermatophilosis in captive inland bearded dragons (Pogona vitticeps).

BACKGROUND: Various pathogens cause skin diseases in lizards. An outbreak of skin disease occurred in a population of 100 inland bearded dragons at a breeding facility in Japan; 50 developed skin lesions and 15 mortalities were reported. HYPOTHESIS/OBJECTIVES: To identify the pathogens responsible for the skin lesions and to determine the cause of death. ANIMALS: Eight specimens (three dead, two euthanized, three living) were randomly selected from a group of inland bearded dragons with skin lesions consisting of multifocal superficial dermatitis. METHODS: Biopsy samples were taken from skin lesions and healthy skin of the live specimens. Postmortem examinations were performed on the dead and euthanized specimens. Skin samples were processed for microbiological culture, 16S ribosomal DNA (rDNA) sequencing for bacteria, ranavirus major capsid protein (MCP) gene sequencing and histopathological examination. Histopathological examinations were also performed on postmortem tissue samples. RESULTS: Both Austwickia chelonae and ranavirus (DNA) were detected in the skin lesions. Pathological examination revealed no significant visceral lesions caused by A. chelonae or ranavirus infection in dead specimens. CONCLUSIONS AND CLINICAL IMPORTANCE: To the best of the authors' knowledge this is the first report of dermatophilosis due to A. chelonae infection in lizards and the first description of a concurrent infection with a ranavirus. The combined infection associated with the skin lesions may have been the primary cause of death. Co-infection with a ranavirus should be considered as a possible factor in cases of reptilian dermatophilosis.