Linezolid-Induced Pure Red Cell Aplasia: A Case Report.

Linezolid (LZD) has been widely used for treating the infections of multidrug-resistant gram-positive organisms. As we know, anemias induced by Linezolid (LZD) are common. However, LZD-induced pure red cell aplasia (PRCA) is very rare. In this paper, we report on a 68-year-old woman with intravascular stent infection who developed PRCA after treatment with LZD. The patient presented to our hospital with a 6-month history of fever after stent implantation for aneurysms in both lower limbs. Bone culture grew methicillin-resistant Staphylococcus hemolyticus (MRSH). She received LZD after developing adverse reactions to initial antibiotics. Although her infective symptoms were improved by LZD, progressive thrombocytopenia was observed 23 days after LZD therapy. Her platelets declined to 66*109/L and hemoglobin level was 10.1 g/dL. Thrombocytopenia recovered 12 days after cessation of LZD. LZD was administered again due to recovered fever. 57 days after LZD administration, her hemoglobin level was 4.1 g/dL and reticulocytes were 0.2%. Bone marrow smear revealed active granulocyte proliferation and markedly decreased erythropoiesis with vacuolar degeneration. 12 days after cessation of LZD, her hemoglobin and reticulocyte levels rose to 9.6 g/dL and 5.1%, respectively. LZD was used for the third time as fever and inflammatory markers progressively increased, but Hb was reduced to 6.7g/dL 15 days after LZD therapy. 12 days after cessation of LZD, the hemoglobin level rose to 11.9 g/dL. In summary, we suggest complete blood count and reticulocyte count should be monitored to detect bone marrow suppression during long-term LZD therapy, especially in patients aged over 58 and/or with pre-existing anemia, chronic infections, and renal insufficiency.

Clinical and Microbiological Characteristics of a Community-Acquired Carbapenem-Resistant Escherichia coli ST410 Isolate Harbouring blaNDM-5-Encoding IncX3-Type Plasmid From Blood.

Objectives: The aim of this research was to investigate the clinical and microbiological characteristics of a case of community-acquired carbapenem-resistant Escherichia coli isolated from a patient with a bloodstream infection in China. Methods: Escherichia coli Huamei202001 was recovered from the first blood culture from a patient hospitalised in China. An antimicrobial susceptibility test was performed, and the genome was sequenced on an Illumina HiSeq X 10 platform with a 150-bp paired-end approach. The generated sequence reads were assembled using Unicycler, and the whole genome sequence data were analysed using bioinformatics tools. Moreover, the patient and her main family members obtained a faecal sample screening test for CRE, the positive strain was further isolated and the identification and antimicrobial susceptibility testing was performed. Results: Escherichia coli Huamei202001 belonged to sequence type 410. In addition, a blaNDM-5-encoding IncX3-type plasmid was responsible for the spreading of carbapenem resistance. Only the patient was detected as having a positive faecal sample screening test for CRE. Strain Fec01 was identified as E. coli, and the antibiotic susceptibility profile was the same as that of E. coli Huamei202001. Conclusions: Escherichia coli Huamei202001 is defined as community-acquired carbapenem-resistant Enterobacteriaceae. The clone ST410 that harbours the blaNDM-5-encoding IncX3-type plasmid is causing new high-risk clones globally. Thus, infection control measures should be strengthened to curb the dissemination of IncX3.

Extracellular electron transfer of Enterobacter cloacae SgZ-5T via bi-mediators for the biorecovery of palladium as nanorods.

In nature, microbes use extracellular electron transfer (EET) to recover noble metals. Most attention has been paid to the biorecovery process occurring intracellularly and on the cell surface. In this work, we report that Pd nanorods could be biosynthesized by Enterobacter cloacae SgZ-5T in the extracellular space. This bacterium possesses both a direct EET pathway through membrane redox systems and an indirect EET pathway via the self-secreted electron carrier hydroquinone (HQ). When exposed to Pd(II), the bacteria adjusted their metabolic pathway and membrane-bound proteins to secrete riboflavin (RF). However, no HQ was detected in the supernatant in presence of Pd(II). No significant change was observed through metabolomic analysis regarding the abundance of HQ in presence of Pd(II) compared to Pd(II)-free supernatant. Similar results were also obtained through transcriptomic analysis of YqjG gene encoding glutathionyl-HQ reductase synthase. X-ray photoelectron spectroscopic evidence indicated that HQ may adsorb to the surface of Pd nanorods. Moreover, the gene encoding RF synthase (ribE) was up-regulated in the present of Pd(II), suggesting that this bioreduction process induced RF synthase, which had been shown in previous results. The UV-vis spectroscopy data demonstrated that the Pd(II) reduction rate was enhanced by 5%, 5.5% and 30% by the addition of 3.33 µM HQ, 3.33 µM RF and the both, respectively. All these results revealed that the bi-mediators secreted by bacteria were beneficial for biorecovery of Pd. This work is of significance for understanding metal biorecovery processes and natural biogeochemical processes.