Hepatitis B virus (HBV) is a human pathogen of global concern, while a high diversity of viruses related to HBV have been discovered in other animals during the last decade. Recently, the novel mammalian hepadnavirus, tentatively named domestic cat hepadnavirus (DCH), was detected in an immunocompromised cat. Herein, a collection of 209 cat sera and 15 hepato-diseased cats were screened for DCH using PCR, resulting in 12.4% and 20% positivity in the tested sera and necropsied cats, respectively. Among the DCH-positive sera, a significantly high level of co-detection with retroviral infection was found, with the highest proportion being co-detection with feline immunodeficiency virus (FIV). Full-length genome characterization of DCH revealed the genetic diversity between the nine Thai DCH sequences obtained, and that they phylogenetically formed three distinct monophyletic clades. A putative DCH recombinant strain was found, suggesting a possible role of recombination in DCH evolution. Additionally, quantitative PCR was used to determine the viral copy number in various organs of the DCH-moribund cats, while the pathological findings were compared to the viral localization in hepatocytes, adjacent to areas of hepatic fibrosis, by immunohistochemical (IHC) and western blot analysis. In addition to the liver, positive-DCH immunoreactivity was found in various other organs, including kidneys, lung, heart, intestine, brain, and lymph nodes, providing evidence of systemic infection. Ultrastructure of infected cells revealed electron-dense particles in the nucleus and cytoplasm of hepatocytes, bronchial epithelial cells, and fibroblasts. We propose the intracellular development mechanism of this virus. Although the definitive roles of pathogenicity of DCH remains undetermined, a contributory role of the virus associated with systemic diseases is possible.

Feline bocavirus-1 (FBoV-1) was identified in cats from different households with hemorrhagic enteritis during outbreaks of an unusual clinical presentation of feline panleukopenia virus (FPLV) in Thailand. Use of polymerase chain reaction revealed the presence of the FBoV-1 DNA in several tissues, suggesting hematogenous viremia, with the viral nucleic acid, detected by in situ hybridization (ISH), was localized in intestinal cells and vascular endothelium of intestinal mucosa and serosa, and in necrosis areas primarily in various lymph nodes while FPLV-immunohistochemical analysis revealed viral localization only in cryptal cells, neurons, and limited to leukocytes in the mesenteric lymph node. Full-length coding genome analysis of the Thai FBoV-1 strains isolated from moribund cats revealed three distinct strains with a high between-strain genetic diversity, while genetic recombination in one of the three FBoV-1 strains within the NS1 gene. This is the first report identifying natural genetic recombination of the FBoV-1 and describing the pathology and viral tropism of FBoV-1 infection in cats. Although the role of FBoV-1 associated with systemic infection of these cats remained undetermined, a contributory role of enteric infection of FBoV-1 is possible. Synergistic effects of dual infection with FPLV and FBoV-1 are hypothesized, suggesting more likely severe clinical presentations.

Background Cutaneous mastocytosis (CM) is a rare disease of dogs characterized by rash, pruritus and proliferation of mast cells in the skin. Oral H1 antihistamines are recommended as the treatment to control pruritus. Hypothesis/Objective To describe the effective treatment of pruritus associated with CM with lokivetmab in one dog. Animal A 4‐year‐old, spayed female cross‐bred dog presented with severely pruritic, erythematous to pigmented macules and papules involving the ventral abdomen, interdigital skin, perivulval area and both pinnae; the pruritus had been unresponsive to treatment with antihistamines, prednisone and ciclosporin. Methods and materials Complete blood count and serum biochemistry, abdominal ultrasound, blood smear and skin cytological evaluation, PCR, histopathological and immunohistochemical examination of skin biopsies. Results Skin cytological evaluation revealed high numbers of uniform, heavily granulated mast cells; histopathological findings showed focal dermal proliferations of well‐differentiated, uniform mast cells consistent with a low‐grade mast cell tumour (MCT). Clinical staging revealed that the disease was confined to the skin. Mutations of c‐kit exon 8 and 11 were not detected. Treatment was initiated with anti‐canine‐interleukin (IL)‐31 monoclonal antibody lokivetmab; antihistamines were continued. The dog's pruritus resolved within seven days and was maintained in remission over 15 months with once monthly lokivetmab injections; the skin lesions improved but did not resolve. Conclusion and clinical importance Lokivetmab treatment was effective in resolving and maintaining pruritus remission in this dog with widespread cutaneous mast cell disease. Whether CM in dogs represent a separate entity that should be distinguished from a low‐grade MCT requires further investigation.

No abstract

Melioidosis is caused by Burkholderia pseudomallei and is an important zoonotic infectious disease causing high mortality from fulminant septicaemia in humans and a wide variety of animal species. The incidence of fatal melioidosis in zoo animals has been significant in many Thai zoos. A total number of 32 cases were evaluated throughout the Thai zoo animal populations. The highest prevalence of disease has been reported from the north-eastern region followed by the zoos in the southern part of the country, approximately 47% and 38%, respectively, while the other zoos reported sporadic infections. Herbivores and non-human primates were the most commonly affected animals with incidences of 59% and 28%, respectively. This appears to be a seasonal correlation with the highest incidence of melioidosis in zoo animals reported in the rainy season (44%) or subdivided monthly in June (19%) followed by September and November (16% and 12%, respectively). The route of infection and the incubation period still remain unclear. This retrospective study examined the clinical presentation in various zoo species, pathological findings and epidemiological data as well as conducting an in depth literature review.

Carnivore protoparvovirus-1 (CPPV-1), a viral species containing feline panleukopenia virus (FPV) and canine parvovirus (CPV) variants, are widely spread among domestic and wild carnivores causing systemic fatal diseases. Wild fishing cats (Prionailurus viverrinus), a globally vulnerable species, have been found dead. Postmortem examination of the carcasses revealed lesions in intestine, spleen and kidney. CPPV-1 antigen identification in these tissues, using polymerase chain reaction (PCR) and immunohistochemistry (IHC), supported the infection by the virus. PCR- and IHC-positivity in kidney tissues revealed atypical localization of the virus while in situ hybridization (ISH) and transmission electron microscopy (TEM) with the pop-off technique confirmed the first description of viral localization in kidneys. Complete genome characterization and deduced amino acid analysis of the obtained CPPV-1 from the fishing cats revealed FPV as a causative agent. The detected FPV sequences showed amino acid mutations at I566M and M569R in the capsid protein. Phylogenetic and evolutionary analyses of complete coding genome sequences revealed that the fishing cat CPPV-1 genomes are genetically clustered to the FPV genomes isolated from domestic cats in Thailand. Since the 1970s, these genomes have also been shown to share a genetic evolution with Chinese FPV strains. This study is the first evidence of CPPV-1 infection in fishing cats and it is the first to show its localization in the kidneys. These findings support the multi-host range of this parvovirus and suggest fatal CPPV-1 infections may result in other vulnerable wild carnivores.

No abstract

Japanese encephalitis virus (JEV) is a viral pathogen belonging to the Flavivirus genus, Flaviviridae family. JEV was first described in humans with encephalitis in Japan during the 19th century (Webster, 1938). Since then, it has been detected in humans in large area of Asia, especially eastern and southern Asian countries (Jeffries & Walker, 2015). Mosquitoes, primarily Culex sp, serve as the vector to transmit the virus into birds with spillover to a wide range of vertebrates as susceptible hosts including humans, and domestic and wild animals, that results in disease (Xiao-Xia et al., 2014;Mansfield et al., 2017). JEV infection in animals includes livestock species (i.e. pigs, horses, cattle and sheep), domestic animals (cats and dogs), reptiles and amphibians (Oliveira et al., 2017). While infected pigs and cattle are considered as the amplifying host due to prolonged viremia, other domesticated animals and wildlife species are classed as the dead-end hosts which display a range of clinical severity. Although the infection in the dead-end animal hosts is