Infectious diseases and antimicrobial resistance (AMR) has become pressing concerns in China. We aimed to comprehensively investigate the burden of them. Data on infectious diseases and AMR were collected by the Global Antimicrobial Resistance Burden study 2019. Multinomial network meta-regression, logistic regression, and ensemble Spatiotemporal Gaussian process regression were used to fit the number and rate in DisMod-MR 2.1 modelling framework. We reported the number and rates of the disease burdens of 12 infectious syndromes by age and sex; described the burden caused by 43 pathogens; estimated the AMR burden of 22 bacteria and bacteria–antibiotics combinations. There were an estimated 1.3 million (95% uncertainty intervals, UI 0.8–1.9) infection-related deaths, accounting for 12.1% of the total deaths in China 2019. Males were 1.5 times more affected than females. Bloodstream infections (BSIs) were most lethal infectious syndrome, associating with 521,392 deaths (286,307–870,583), followed by lower respiratory infections (373,175), and peritoneal and intra-abdominal infections (152,087). These five leading pathogens were S aureus, A baumannii, E coli, S pneumoniae, and E spp., which were associated with 41.2% (502,658/1,218,693) of all infection-related deaths. The pathogens of different infectious syndromes exhibited significant heterogeneity. In 2019, more than 600 thousand deaths were associated with AMR, including 145 thousand deaths attributable to AMR. The top 3 AMR attributable to death were carbapenems-resistance A baumannii (18,143), methicillin-resistance S aureus (16,933) and third-generation cephalosporins-resistance E coli (8032). Infectious diseases and bacterial antimicrobial resistance were serious threat to public health in China, related to 1.3 million and more than 600 thousand deaths per-year, respectively. Antimicrobial stewardship was urgent. This work was supported by 10.13039/501100001809 National Natural Science Foundation of China (82270626); China Mega-Project for Infectious Diseases (2017ZX10203202, 2013ZX10002005); the Project of Beijing Science and Technology Committee (Z191100007619037).

Since December 2019, COVID-19 has spread to almost every corner of the world. In theory, tocilizumab and favipiravir are considered to be reliable drugs for the treatment of COVID-19 with elevated IL-6. We aimed to assess the efficacy and safety of tocilizumab combined with favipiravir in patients with COVID-19. This was a multicenter trial in adults with COVID-19. Patients were randomly assigned (3:1:1) to a 14-day combination of favipiravir combined with tocilizumab (combination group), favipiravir, and tocilizumab. The primary outcome was the cumulative lung lesion remission rate (lung CT examination indicated absorption of lung inflammation). Between Feb 2 and March 15, 2020, 26 patients were recruited; 14 were randomly assigned to the combination group, 7 were assigned to the favipiravir group and 5 were assigned to the tocilizumab group. The cumulative lung lesion remission rate at day 14 was significantly higher in combination group as compared with favipiravir group (P = 0.019, HR 2.66 95 % CI [1.08–6.53]). And there was also a significant difference between tocilizumab and favipivavir (P = 0.034, HR 3.16, 95 % CI 0.62–16.10). In addition, there was no significant difference between the combination group and the tocilizumab group (P = 0.575, HR 1.28 95 %CI 0.39–4.23). Furthermore, combined therapy can also significantly relieve clinical symptoms and help blood routine to return to normal. No serious adverse events were reported. Tocilizumab combined with or without favipiravir can effectively improve the pulmonary inflammation of COVID-19 patients and inhibit the deterioration of the disease.

Since December 2019, coronavirus disease (COVID‐19) has rapidly swept the world. So far, more than 30 million people have been infected and nearly one million have died. Although the world is still in the stage of COVID‐19 pandemic, the treatment of new cases and critically ill patients is the focus of the current work. However, COVID‐19 patients lead to pulmonary fibrosis, such a serious threat to the prognosis of complications were also worthy of our attention. First of all, we proposed the possible mechanism of pulmonary fibrosis caused by SARS‐CoV‐2, based on the published data of COVID‐19 ((i) Direct evidence: pulmonary fibrosis was found in autopsy and pulmonary puncture pathology. (ii) Indirect evidence: increased levels of fibrosis‐related cytokines[transforming growth factor [TGF]‐ β, tumor necrosis factor [TNF]‐ α, interleukin [IL]‐6, etc] in peripheral blood of severe patients.) What is more, we summarized the role of three fibrosis‐related signaling pathways (TGF‐ β signal pathway, WNT signal pathway and YAP/TAZ signal pathway) in pulmonary fibrosis. Finally, we suggested the therapeutic value of two drugs (pirfenidone and nintedanib) for idiopathic pulmonary fibrosis in COVID‐19‐induced pulmonary fibrosis.

Pneumocystis jirovecii pneumonia (PJP) and pulmonary cytomegalovirus (CMV) infection are common opportunistic infections among immunocompromised patients. However, few studies have evaluated their co-infection, especially among non-HIV patients. Therefore, we aimed to evaluate the outcomes and prognostic factors among non-HIV patients with PJP according to their CMV infection status. This retrospective study evaluated non-HIV patients who were diagnosed with PJP between January 2009 and January2016.The patients were classified and compared according to their pulmonary CMV infection status (positive infection: bronchoalveolar lavage fluid [BALF] CMV DNA loads of >500copies/mL). Among 70 non-HIV patients with PJP, we identified 38 patients (54.3%) with pulmonary CMV infection. There was no significant difference in the mortality rates for the two groups (p = 0.15). Pulmonary CMV infection was significantly more common among patients who were receiving glucocorticoids and immunosuppressants, compared to corticosteroids only (p = 0.02). Pulmonary CMV infection was also significantly associated with severe dyspnea, a lower PaO2/FiO2, and the presence of centrilobular nodules (p = 0.008). Higher CMV DNA loads in the BALF were positively associated with mortality (p = 0.012). Combined therapy using corticosteroids and other immunosuppressants may be a risk factor for pulmonary CMV co-infection among patients with PJP. In addition, CMV pneumonia should be considered when centrilobular nodules and/or severe hypoxemia are observed in non-HIV patients with PJP. Furthermore, antiviral treatment should be promptly initiated for patients with a high CMV DNA load in BALF, based on their poor prognosis.