Objective To establish and analyze a mouse model of Staphylococcus aureus?induced arthritis ( Staphy?lococcus aureus septic arthritis, SA) , and provide an animal model for arthritis mechanism research and drug development. Methods Mice were immunosuppressed with cyclophosphamide, then intravenously inoculated with Staphylococcus au?reus. The gross characteristics of the joints were observed, the arthritis indexes were analyzed, and the pathological scores of the model mice were evaluated. Results From the first day after bacterial inoculation, the mouse joints were swollen. Pathological examination revealed lesions varying from mild and disarranged joint synovial hyperplasia to synovial thickening and intra?articular invasion, and increased neutrophil infiltration. Conclusions A mouse model of Staphylococcus aureus?induced arthritis is successfully established in this study. This model can be developed in a relatively short time, can not only simulate the clinical symptoms and signs and disease progression of human arthritis, but also to a certain extent reflects the etiology, infection and immunological mechanisms of human arthritis.

Objective To establish a mouse model of systemic C. albicans infection by oral inoculation of the pathogen and observe the proliferation and distribution of C. albicans in vivo tissues. Methods Male ICR mice(n=46) were used as the experiment group(n=40) and blank group (n=6). Cotton swabs with C. albicans were used to infect the mice (7 × 106 CFU/mL), and the blank group with saline. The mice of the experiment group were randomly divided into two groups:model group A for clinical assessment (n=20) and model group B for tissue fungal burden detection (n=20). Clinical score, survival and autopsy were carried out among the model group A. Five mice were randomly killed from the model group B at 3 d, 5 d and7 d after infection, respectively ( blank group killed 2 mice each time) . Microbial load tablet method was used to detect the tissue fungal burdens in different tissues, meanwhile samples of tongue, esophagus, stomach, liver, kidney, lung of infected mice were taken for pathological examination. Results White spot appeared on the surface of tongue since 3 d postinfection and increased with time and finally caused death. The mortality reached over 50% at 5 d. C. albicans was not only detected from the tongue (87?5%), stomach (87?5%), liver (54?5%), kidney (50?5%), lung (20%) and heart (4%), but also was microscopically seen mycelia proliferation in the tongue, stomach, liver, and kidney , yet not seen in the control group, showing that C. albicans caused disseminated systemic infection through mucosal infection in mice. Conclusions C. albicans can induce opportunistic systemic infection by breakthrough the mucosal immune barrier, so as to increase the infection to death.

Objective Establishing the drug?resistant Candida albicans disseminative infected mice model for new drug screening. Methods The disseminative infected mouse model was generated by intravenously injecting a clinical Drug?resistant Candida albicans strain ( CaR) to immunosuppressive ICR mice. The features of model was evaluated by clinical symptom, survival condition, fungal burden in tissue, histopathology, cytokines assay and medication. Results After infected with CaR (0 day), the death of mice started at the first day, though, compared to clinical drug sensitive strain ( CaS) infected group, the difference of mortality rate in 16?day observation period was not significant in two groups (CaR, 90?7%;CaS, 86?2%, P =0?158), mice in CaR group died faster than those in CaS group at the early stage;On the fourth day of infection, Candida albicans could be detected in the different tissues, and we found fungal burden in kidney and brain was a significant difference. The typical granuloma caused by fungal infection was the main histopathological feature observed in the kidney, brain and heart. Cytokines in renal tissue were detected by flow cytometry, The changes of IL?1α,IL?6,TNF?αand IFN?γin kidney were significant. Compared with CaS group, IL?1 and IFN?γ were significantly higher and TNF?αdecreased significantly in CaR group. The mice of groups CaR and CaS were treated with 10 mg/kg fluconazole, the mortality rates were 83?3% and 37?5%, which have a significant difference. Conclusions In this study, we successfully established a drug?resistant Candida albicans disseminative infected mice model which is potential tool for the development of new anti?infectious agent.

Objective To investigate the natural infection of Theiler's murine encephalomyelitis virus (TMEV) in mice,and to survey the distribution of virus in tissues and the changes of serum antibody in the experimentally TMEV-infected mice.Methods Enzyme linked immunosorbent assay (ELISA) and fluorescence quantitative RT-PCR (qRT-PCR) assay were used to detect the antibody and nucleic acid of TMEV in clinical samples.These samples included SPF mice collected from Guangdong area in 2010-2015,mice obtained from a non-barrier laboratory rodent colony,and wild Rattus norvegicus live-trapped around the non-barrier laboratory rodent colony.36 ICR mice were intracerebrally inoculated with TMEV BeAn strain.The clinical signs of the animals were observed daily post-inoculation.Three mice were euthanatized at day 0,3,7,10,17,21,31,39 and 46 post-inoculation (dpi),respectively.Tissue and serum samples were collected for TMEV detection.Results The TMEV antibody and nucleic acid positive rates of SPF mice collected from Guangdong area in 2010-2015 were 5.29％ (n=2834) and 27.27％ (n=457),respectively.The TMEV antibody and nucleic acid positive rates of the mice obtained from a non-barrier laboratory rodent colony were 71.95％ (n=82) and 53.66％ (n=82),respectively.The TMEV nucleic acid positive rate of wild Rattus norvegicus was 25.93％ (n=27).In the TMEV positive mice,only two mice showed obvious clinical symptoms.The cecal contents,feces and brain samples were the best candidates for qRT-PCR assay.The viral nucleic acid could be detected in the brain,heart,liver,lung and stomach of ICR mice at 3 dpi,but no viral nucleic acid was detected in the spleen,kidney,and cecum.The viruses in liver,heart,lungs and stomach were completely cleared at 10 dpi,and the viruses persisted in the brain throughout the experiment.The TMEV antibody could be detected at 7 dpi,and then the antibody positive rate reached 100％ at 17 dpi.The antibody level increased gradually and maintained up to 46 days.ICR mice showed latent infection after TMEV inoculation,with no obvious symptoms and eye pathological changes.Conclusions The experimental mice and wild Rattus norvegicus in Guangdong area are both infected with TMEV,and the infection rate is high.The mice inoculated with TMEV BeAn strain show latent infection.The TMEV antibody produced in mice can be detected at 7 dpi and persisted until the end of the experiment.The viruses are found in the liver,heart,lung and stomach for a short time,but are persisted in the brain for a long time.There is a good consistency of TMEV detection between qRT-PCR and ELISA.The qRT-PCR assay can be used as a powerful complement method for the national standard of laboratory animals.