Résumé
@#Abstract: To report a case of Aspergillus salwaensis-induced spinal infection and its laboratory detection. The inflammatory granulation and necrotic tissue samples of a patient with spinal infection were collected from, the Affiliated Hospital of Chengde Medical College on June 17, 2020 for direct smear microscopy and culture, and the isolated strain was identified by microscopy by smear staining, matrix-assisted laser desorption ionization-time-of-flight mass spectrometry (MALDI-TOF-MS), molecular identification and in vitro antifungal susceptibility test. The patient was 62 years old female and presented with recurrent chest and back pain with no obvious cause. The initial diagnosis was spinal infection, after 7 days of treatment with levofloxacin, the effect was not good. Surgery was then performed remove the lesion via posterior thoracic debridement, and fungal hypha was observed under microscope in tissue specimens. The isolated strains had no typical structure, MALDI-TOF-MS was used for identification for many times, but there was no identification result. After 7 days of fluconazole treatment, the patient's condition improved, and her chest and back pain were alleviated compared to before surgery. The patient was discharged and followed up in the outpatient department, the fungus was later identified as Aspergillus salwaensis by sequence analysis of the internal transcribed spacer (ITS) gene sequencing, and the patient's antifungal medication was changed to voriconazole after with the attending physician. The patient consciously recovered well with no pain in the operative area and normal spinal activity at 1 year follow-up. The possibility of spinal fungal infection should be considered in patients with back pain without a clear cause and poor response to routine antibiotic treatment. Direct smear report of microscopic results are very important for guiding clinical antibiotic selection for rare filament fungi with atypical colony and microscopic morphology and unsuccessful MALDI-TOF-MS identification, molecular biological methods such as ITS sequence analysis can be helpful for early identification of the fungal species, improving identification speed.
Résumé
@# Objective To investigate the drug resistance of Enterobacter cloacae isolated from blood samples in 75 member units of the Bacterial Drug Resistance Monitoring Network in Hebei, 2016- 2021, so as to provide a basis for rational drug use in clinic. Methods WHONET 5.6 software was used to retrospectively analyze drug susceptibility of Enterobacter cloacae isolated from 32 secondary hospitals and 43 tertiary hospitals. SPSS19.0 software was used for statistical analysis. Results After removing the duplicate strains, 1 225 strains of E. cloacae were isolated from blood samples of 75 hospitals during 6 years, including 157 strains from secondary hospitals and 1 068 strains from tertiary hospitals. In this study, the resistance of Enterobacter cloacae to 16 kinds of antibiotics was analyzed. The drug resistance rates to cefuroxime (52.4%-67.8%), piperacillin (27.4%-31.2%), ceftazidime (27.8%-35.5%), ceftriaxone (29.5%-45.0%), aztreonam (22.2%-32.3%), cotrimoxazole (21.6%-28.7%) were higher; the resistance rates to amikacin and tobramycin were lower than 15.0%. The resistance rates to imipenem and meropenem were 3.6%-12.3% and 5.1%-11.4%, respectively. The resistance rate to ciprofloxacin in tertiary hospitals was 22.4%, and the resistance rate to cotrimoxazole was 23.9%. Except for these two antimicrobials, the resistance rates to other antimicrobial drugs in tertiary hospitals were higher than that in secondary hospitals. A total of 121 carbapenem-resistant Enterobacter cloacae strains were detected in the past 6 years, with an increasing detection rate (χ2trend=6.305, P=0.012). Conclusions Enterobacter cloacae has great differences in antimicrobial resistance to different antibiotics, and is sensitive to carbapenems. The drug resistance in tertiary hospitals is generally higher than that in secondary hospitals. Drug resistance monitoring and drug resistance mechanism research should be strengthened to better guide clinical drug use and curb the rise of drug resistance.