Gastrointestinal involvement of COVID-19 and potential faecal transmission of SARS-CoV-2.

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was found initially in Wuhan, China in early December 2019. The pandemic has spread to 216 countries and regions, infecting more than 23310 000 people and causing over 800 000 deaths globally by Aug. 24, 2020, according to World Health Organization (https://www.who.int/emergencies/diseases/ novel-coronavirus-2019). Fever, cough, and dyspnea are the three common symptoms of the condition, whereas the conventional transmission route for SARS-CoV-2 is through droplets entering the respiratory tract. To date, infection control measures for COVID-19 have been focusing on the involvement of the respiratory system. However, ignoring potential faecal transmission and the gastrointestinal involvement of SARS-CoV-2 may result in mistakes in attempts to control the pandemic.

Surveillance study of the prevalence, species distribution, antifungal susceptibility, risk factors and mortality of invasive candidiasis in a tertiary teaching hospital in Southwest China.

BACKGROUND: Invasive candidiasis (IC) is the most common invasive fungal infection. The epidemiology of IC in hospitalized patients has been widely investigated in many metropolitan cities; however, little information from medium and small cities is known. METHODS: A 5-year retrospective study was carried out to analyze the prevalence, species distribution, antifungal susceptibility, risk factors and mortality of inpatients with invasive Candida infection in a regional tertiary teaching hospital in Southwest China. RESULTS: A total of 243 inpatients with invasive Candida infection during the five-year study period were identified, with a mean annual incidence of 0.41 cases per 1000 admissions and a 30-day mortality rate of 12.3%. The species distributions of Candida albicans, Candida glabrata, Candida tropicalis, Candida krusei, Candida parapsilosis and other Candida species was 45.3, 30.0, 15.2, 4.9, 2.1 and 2.5%, respectively. The total resistance rates of fluconazole (FCA), itraconazole (ITR) and voriconazole (VRC) were 18.6, 23.1 and 18.5%, respectively. Respiratory dysfunction, pulmonary infection, cardiovascular disease, chronic/acute renal failure, mechanical ventilation, abdominal surgery, intensive care in adults, septic shock and IC due to C. albicans were associated with 30-day mortality (P < 0.05) according to the univariate analyses. Respiratory dysfunction [odds ratio (OR), 9.80; 95% confidence interval (CI), 3.24-29.63; P < 0.001] and IC due to C. albicans (OR, 3.35; 95% CI, 1.13-9.92; P = 0.029) were the independent predictors of 30-day mortality. CONCLUSIONS: This report shows that the incidence and mortality rates are lower and that the resistance rates to azoles are higher in medium and small cities than in large cities and that the species distributions and risk factors in medium and small cities are different from those in large cities in China. It is necessary to conduct epidemiological surveillance in medium and small cities to provide reference data for the surveillance of inpatients with IC infections.

Mechanisms of carbapenem resistance in cephalosporin-susceptible Pseudomonas aeruginosa in China.

Twenty-nine Pseudomonas aeruginosa isolates, which are resistant to carbapenems but susceptible to ceftazidime or/and cefepime, were recovered from our hospital from July 2011 to October 2011. The results of Western blotting showed that the OprD was reduced or lost. None of the 29 clinical isolates produced carbapenemases, extended-spectrum ß-lactamases, or Ambler class C ß-lactamases enzymes by the modified 3-dimensional test. The sequencing of oprD for these isolates showed that there are multiple point mutations, large fragment substitutions, deletions, and insertions. It showed that the expression of oprD decreased while mexA and mexX increased by real-time reverse transcriptase-PCR. These results suggested that the loss of OprD and overexpression of mexXY-OprM and mexAB-OprM are associated with carbapenem resistance in cephalosporin-susceptible Pseudomonas aeruginosa.