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Background: Cutaneous infections are important diseases in captive and free‐ranging pinnipeds and are associated with various causative agents. Some special agents, such as fungi, morbillivirus and mycobacteria, can cause cutaneous specific granulomatous inflammation. Objectives: To identity the cause of chronic dermatitis in a spotted seal in an aquarium. Methods: Herein, we analyze the clinical history and cutaneous samples of the spotted seal through differential diagnosis (histopathology, microorganism culture, special histochemical staining methods, PCR), and antibiotic susceptibility test. Results: This is a rare pyogranulomatous dermatitis case caused by E. faecalis in a captive adult male spotted seal (Phoca largha) in an aquarium. Conclusions: We provide a meaningful approach to the diagnosis and treatment of bacterial dermatitis in pinnipeds. [ABSTRACT FROM AUTHOR]

Sarcoptic mange, a disease caused by the burrowing mite Sarcoptes scabiei, is globally endemic and an emerging threat to wildlife. Although many studies have shown that wildlife diseases play key roles in biodiversity conservation, knowledge about sarcoptic mange is still insufficient. In this study, we aim to improve the understanding of the impacts of sarcoptic mange on wildlife populations, the mechanisms involved in its eco‐epidemiology and the associated risks to public and ecosystem health by investigating mass death events in gorals and serows in the Qinling Mountains. We conducted interviews with practitioners and local people in the central Qinling Mountains. From the same locations, we collected 24 cutaneous samples from various animals and surveillance data from infrared cameras. Pathological, parasitological and microbiological examinations of the samples were performed. Mite‐induced cutaneous lesions, mites and eggs were observed in samples from dead gorals and one dead serow but not in other species. Molecular analysis confirmed the mites to be S. scabiei and shared the same cox 1 genotype. The data obtained from the interviews and infrared cameras indicated that the death of wildlife was related to sarcoptic mange infection and that there had been a decrease in the goral population since the outbreak of the disease. We confirmed that sarcoptic mange was the major cause of the mass death events and may have spread from the western to eastern Qinling Mountains. Based on our findings, we propose several protection strategies to help preserve biodiversity in the Qinling Mountains. [ABSTRACT FROM AUTHOR]

Infection with H5N6 highly pathogenic avian influenza virus caused high mortality in chickens, while ducks often appear to be asymptomatic. But, some recent H5Nx subtype viruses could cause high mortality in ducks. The variation between different species and the mechanisms by which some H5Nx viruses cause death in ducks requires investigation to identify the key processes in influenza susceptibility and pathogenesis. Here, we characterized two representative H5N6 viruses, A/ Pavo cristatus /Jiangxi/JA1/2016 (JA1) and A/ Anas crecca /shanghai/SH1/2016 (SH1), and compared their pathogenicity and expression profiles of immune-related genes in chickens and ducks to identify the elements of the host immune-related response that were involved in disease lethality. Results suggested that H5N6 HPAIVs had higher pathogenic and inflammatory effect in chickens than in ducks. Importantly, the TNF-α, IL-6, IFN-γ and iNOS levels were significantly higher in the lung of SH1 infected chickens compared to those of ducks. And we found higher systemic levels of IL-6 induced by JA1 in chickens than in ducks. In addition, our experiments demonstrated that JA1 was associated with greater pathogenicity in ducks were accompanied by the excessive expression of iNOS in the brain. These results are helpful to understand the relationship between the pathogenicity of H5N6 AIVs and inflammatory responses to them in chickens and ducks. [ABSTRACT FROM AUTHOR]

Hepatitis E virus (HEV) infection has been associated with extrahepatic manifestations, particularly neurological disorders. Although it has been reported that HEV infection induced hepatocyte apoptosis associated with mitochondria injury, activation of mitochondrial apoptotic pathway in the central nervous system during HEV infection was not clearly understood. In this study, the induction of mitochondrial apoptosis-associated proteins and pro-inflammatory cytokines were detected in HEV infected Mongolian gerbil model and primary human brain microvascular endothelial cells (HBMVECs). Mitochondrial exhibited fragments with loss of cristae and matrix in HEV infected brain tissue by transmission electron microscope (TEM). In vitro studies showed that expression of NADPH oxidase 4 (NOX4) was significantly increased in HEV infected HBMVECs (p < 0.05), while ATP5A1 was significantly decreased (p < 0.01). Expressions of pro-apoptotic proteins were further evaluated. Bax was significantly increased in both HEV infected brain tissues and HBMVECs (p < 0.01). In vivo studies showed that caspase-9 and caspase-3 were activated after HEV inoculation (p < 0.01), associated with PCNA overexpression as response to apoptosis. Cytokines were measured to evaluate tissue inflammatory levels. Results showed that the release of TNFα and IL-1β were significantly increased after HEV infection (p < 0.01), which might be attributed to microglia activation characterized by high level of IBA1 expression (p < 0.01). Taken together, these data support that HEV infection induces high levels of pro-inflammatory cytokines, associated with mitochondria-mediated apoptosis. The results provide new insight into mechanisms of extra-hepatic injury of HEV infection, especially in the central nervous system. [ABSTRACT FROM AUTHOR]

Extrahepatic injury, particularly neurologic dysfunctions such as Guillain-Barré syndrome, neurologic amyotrophy, and encephalitis/meningoencephalitis/myositis were associated with HEV infection, which was supported by both clinical and laboratory studies. Thus, it is crucial to figure out how the virus invades into the central nervous system (CNS). In this study, CNS lesions were determined in rabbits and Mongolian gerbils inoculated with genotype 4 HEV. Junctional proteins were detected in HEV infected primary human brain microvascular cells (HBMVCs). Viral encephalitis associated perivascular cuffs of lymphocytes and microglial nodules were observed in HEV infected rabbits. Both positive- and negative-strand of HEV RNA was detected in brain and spinal cord in rabbits intraperitoneally infected with HEV at 28 dpi (days postinoculation), but not in rabbits gavaged with HEV. HEV ORF2 protein was further examined in both brain and spinal cord sections of infected rabbits, with positive signals located mainly in neural cells and perivascular areas. Ultrastructural study showed thickened and reduplicated basement membranes of capillary endothelium in HEV RNA positive brain tissues. In vitro study showed loss of tight junction proteins including Claudin5, Occludin, and ZO-1 (zonula occludens-1) in HBMVCs inoculated with HEV for 48 h. These findings indicated that disruption of the blood-brain barrier (BBB) might be potential mechanisms of HEV invasion into the CNS. It provides new insights to further study HEV associated neurologic disorders and will be helpful for seeking potential therapeutics for HEV infection in the future. [ABSTRACT FROM AUTHOR]

Increasing evidence demonstrates that hepatitis E virus (HEV) can be transmitted across species. According to previous reports, swine HEV has two genotypes, genotype 3 and 4, and both can infect humans by the fecal-oral route. Thus, it is crucial for the control of HEV zoonotic transmission to evaluate the dynamics of viral shedding and distribution in different tissues during cross-species infection by HEV. In this study, rabbits were infected with genotype 4 swine HEV by the intraperitoneal route. The results showed that HEV RNA not only shed in the feces but also in the saliva of some rabbits during infection with swine HEV. Viremia appeared late after infection, and anti-HEV IgG was not obvious until the appearance of high viremia levels. After the rabbits were euthanized, a histopathological examination showed that the livers developed overt hepatitis accompanied by an elevation of alanine aminotransferase (ALT) and aspartate transaminase (AST). Furthermore, HEV RNA was detected in various tissues, especially in the salivary glands and tonsils. Subsequently, negative-stranded HEV RNA was practiced in tissues with positive HEV RNA, which demonstrated that HEV replicated in the tissues. Next, we harvested additional tissues from the liver, salivary gland, tonsil, spleen, thymus gland, lymph node and intestine, which are known as replication sites of swine HEV. Additionally, we also observed the HEV antigen distributed in the organs above through immunohistochemical staining. These results demonstrate that rabbits could be used as an animal model for researching cross-species infection of genotype 4 HEV. It is also noteworthy that HEV can shed in the saliva and presents the risk of droplet transmission. These new data provide valuable information for understanding cross-species infection by HEV. [ABSTRACT FROM AUTHOR]

This study involved a death which occurred in four Himalayan griffons housed in Beijing zoo, China. Based on pathogen identification and the pathological changes observed, we did characterize the fungi and Hepatitis E virus (HEV) in four dead Himalayan griffons. Pathological changes were severe. Membranous-like material was observed on the surface of the internal organs. Spleen was necrotic. Focal lymphocyte infiltration in the liver and many sunflower-like fungi nodules were evident in the tissues, especially in the kidney. PCR was used to identify the pathogen. Based on the 18SrRNA genomic sequence of known fungi, the results confirmed that all four dead Himalayan griffons were infected with Aspergillus. At the same time the detection of HEV also showed positive results. To the best of our knowledge, this work appears to be the first report of concurrent presence of Aspergillosis and Hepatitis E virus in rare avian species. [ABSTRACT FROM AUTHOR]

Rabbit hepatitis E virus (HEV) is a novel genotype of HEV, and is considered to pose a risk of zoonotic transmission. Research into the systemic distribution of rabbit HEV in rabbits during different periods of infection has rarely been reported. To better understand this virus, we infected rabbits with second-passage rabbit HEV via an intraperitoneal route. After inoculation, the infection showed two types, temporary and constant infection. The detection of HEV RNA in the feces varied with time, and serum antigen correlated with fecal HEV RNA. Viremia only appeared 72 days after inoculation. The rabbits remained antibody negative throughout the experimental period. When HEV was localized, several organs besides the liver were HEV RNA positive. Tissue antigen was observed immunohistochemically in the different cells of various organs, especially in parts of the small intestine and the characteristic rabbit gut-associated lymphoid tissue. These data provide valuable information for future research into the pathogenesis of HEV. [ABSTRACT FROM AUTHOR]

The male reproductive toxicity of melamine (MA) has been recognized in recent years excepted for its renal toxicity. Our previous in vivo studies revealed that the damages of Sertoli cell barrier played a critical role in MA-induced testicular toxicity in mice. Herein, we performed an in vitro study to comprehensively evaluate the toxicity of MA on Sertoli cell by examining the influences of MA on the viability, morphology, mortality and intercellular junctions of mouse TM4 Sertoli cells (TM4 cells). The results showed that MA suppressed cell viability, induced obvious ultrastructural changes and cell apoptosis in concentration-dependent manner. Moreover, MA down-regulated the expressions of junction-associated proteins including occludin, N-cadherin, and vimentin, suggesting that MA disrupted the integrity of Sertoli cell barrier. Thus, these results indicated that Sertoli cell might be an important cellular target for MA-induced male reproductive toxicity. [ABSTRACT FROM AUTHOR]

Hepatitis E virus (HEV) infection can induce infertility and miscarriage in pregnant women and infect neonates through vertical transmission. However, the mechanism of infertility and vertical transmission remains unclear. In the present study, we evaluated the replication of HEV in the ovary and structural and molecular changes induced by HEV after intraperitoneal injection of HEV in rabbits. Positive- and negative-strand HEV RNA was detected in the ovaries at 28 and 49 days post-infection. Positive HEV open reading frames 2 and 3 signals were observed in the ovaries by immunohistochemistry staining. Histopathological changes of ovarian tissues were observed, including scattered cell necrosis and lymphocyte infiltration. The ratio of normal follicles decreased, whereas the ratio of atresia follicles increased in the HEV RNA-positive ovaries compared to the control group by counting the number of follicles at all levels. In addition, TUNEL results showed that apoptosis in follicle cells and oocytes was promoted by HEV infection. These results suggest that the ovary is one of the replication sites of HEV and that the expression of HEV RNA and antigen in ovarian tissue caused structural and molecular changes that promoted germ cell apoptosis. HEV can infect and replicate in the ovum at different stages, which is a novel mechanism for HEV vertical transmission., Competing Interests: CONFLICTS OF INTEREST None.

Background: Human Cytomegalovirus (HCMV) infections can be found throughout the body, especially in epithelial tissue. Animal model was established by inoculation of HCMV (strain AD-169) or coinoculation with Hepatitis E virus (HEV) into the ligated sacculus rotundus and vermiform appendix in living rabbits. The specimens were collected from animals sacrificed 1 and a half hours after infection., Results: The virus was found to be capable of reproducing in these specimens through RT-PCR and Western-blot. Severe inflammation damage was found in HCMV-infected tissue. The viral protein could be detected in high amounts in the mucosal epithelium and lamina propria by immunohistochemistry and immunofluorescense. Moreover, there are strong positive signals in lymphocytes, macrophages, and lymphoid follicles. Quantitative statistics indicate that lymphocytes among epithlium cells increased significantly in viral infection groups., Conclusions: The results showed that HCMV or HEV + HCMV can efficiently infect in rabbits by vivo ligated intestine loop inoculation. The present study successfully developed an infective model in vivo rabbit ligated intestinal Loop for HCMV pathogenesis study. This rabbit model can be helpful for understanding modulation of the gut immune system with HCMV infection.

Background: Hemoglobin is a rich source of biological peptides. As a byproduct and even wastewater of poultry-slaughtering facilities, chicken blood is one of the most abundant source of hemoglobin., Results: In this study, the chicken hemoglobin antimicrobial peptides (CHAP) were isolated and the antimicrobial and bactericidal activities were tested by the agarose diffusion assay, minimum inhibitory concentration (MIC) analysis, minimal bactericidal concentration (MBC) analysis, and time-dependent inhibitory and bactericidal assays. The results demonstrated that CHAP had potent and rapid antimicrobial activity against 19 bacterial strains, including 9 multidrug-resistant bacterial strains. Bacterial biofilm and NaCl permeability assays, transmission electron microscopy (TEM) and scanning electron microscopy (SEM) were further performed to detect the mechanism of its antimicrobial effect. Additionally, CHAP showed low hemolytic activity, embryo toxicity, and high stability in different temperatures and animal plasma., Conclusion: CHAP may have great potential for expanding production and development value in animal medication, the breeding industry and environment protection.