First report of polymyxin B activity in Klebsiella pneumoniae biofilm

2019 ◽  
Vol 31 (3) ◽  
pp. 127-131 ◽  
Author(s):  
Karina Marjorie Silva Herrera ◽  
Fernanda Kelen da Silva ◽  
Michael Eder de Oliveira ◽  
Magna Cristina de Paiva ◽  
Adriana Cristina Soares ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Polymyxin B ◽  
First Report

Emergence and Recovery of Ceftazidime-avibactam Resistance in blaKPC-33-Harboring Klebsiella pneumoniae Sequence Type 11 Isolates in China

2020 ◽  
Vol 71 (Supplement_4) ◽  
pp. S436-S439
Author(s):  
Qingyu Shi ◽  
Dandan Yin ◽  
Renru Han ◽  
Yan Guo ◽  
Yonggui Zheng ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Infection Control ◽  
Polymyxin B ◽  
Sequence Type ◽  
First Report ◽  
Clinical Strains

Abstract This is the first report of ceftazidime–avibactam resistance caused by the blaKPC-33 mutation through the D179Y variant during the treatment of blaKPC-2-positive Klebsiella pneumoniae-related infections in China. The blaKPC-33-containing K. pneumoniae was susceptible to meropenem–vaborbactam, cefepime–zidebactam, tigecycline, and polymyxin B. The blaKPC-33 gene was located on a 77 551-bp transformable plasmid harboring qnrS1 and blaLAP-2. Detecting blaKPC-33-positive K. pneumoniae clinical strains is important for infection control.

scholarly journals Comparison of Polymyxin B, Tigecycline, Cefepime, and Meropenem MICs for KPC-Producing Klebsiella pneumoniae by Broth Microdilution, Vitek 2, and Etest

2013 ◽  
Vol 51 (7) ◽  
pp. 2472-2472
Author(s):  
A. Lat ◽  
S. A. Clock ◽  
F. Wu ◽  
S. Whittier ◽  
P. Della-Latta ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Polymyxin B ◽  
Broth Microdilution ◽  
Vitek 2

Disease Severity Is an Independent Risk Factor of Mortality and Outcomes in Critically Ill Patients With Carbapenem-resistant Klebsiella Pneumoniae Bloodstream Infections: a 5-year Retrospective Analysis

2021 ◽  
Author(s):  
Yuzhen Qiu ◽  
Wen Xu ◽  
Yunqi Dai ◽  
Ruoming Tan ◽  
Jialin Liu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Septic Shock ◽  
Klebsiella Pneumoniae ◽  
Critically Ill Patients ◽  
Bloodstream Infections ◽  
Polymyxin B ◽  
Mortality Rates ◽  
Carbapenem Resistant ◽  
All Cause Mortality ◽  
Independent Risk Factors

Abstract Background: Carbapenem-resistant Klebsiella pneumoniae bloodstream infections (CRKP-BSIs) are associated with high morbidity and mortality rates, especially in critically ill patients. Comprehensive mortality risk analyses and therapeutic assessment in real-world practice are beneficial to guide individual treatment.Methods: We retrospectively analyzed 87 patients with CRKP-BSIs (between July 2016 and June 2020) to identify the independent risk factors for 28-day all-cause mortality. The therapeutic efficacies of tigecycline-and polymyxin B-based therapies were analyzed.Results: The 28-day all-cause mortality and in-hospital mortality rates were 52.87% and 67.82%, respectively, arising predominantly from intra-abdominal (56.32%) and respiratory tract infections (21.84%). A multivariate analysis showed that 28-day all-cause mortality was independently associated with the patient’s APACHE II score (p = 0.002) and presence of septic shock at BSI onset (p = 0.006). All-cause mortality was not significantly different between patients receiving tigecycline- or polymyxin B-based therapy (55.81% vs. 53.85%, p = 0.873), and between subgroups mortality rates were also similar. Conclusions: Critical illness indicators (APACHE II scores and presence of septic shock at BSI onset) were independent risk factors for 28-day all-cause mortality. There was no significant difference between tigecycline- and polymyxin B-based therapy outcomes. Prompt and appropriate infection control should be implemented to prevent CRKP infections.

Phenotypic detection of Klebsiella pneumoniae carbapenemase among burns patients: First report from Iran

Burns ◽  
2013 ◽  
Vol 39 (1) ◽  
pp. 174-176 ◽  
Author(s):  
Abdolaziz Rastegar Lari ◽  
Leila Azimi ◽  
Mohammad Rahbar ◽  
Fatemeh Fallah ◽  
Reza Alaghehbandan
Keyword(s):  
Klebsiella Pneumoniae ◽  
First Report ◽  
Klebsiella Pneumoniae Carbapenemase

scholarly journals Polymyxin B and fosfomycin thwart KPC-producing Klebsiella pneumoniae in the hollow-fibre infection model

2018 ◽  
Vol 52 (1) ◽  
pp. 114-118 ◽  
Author(s):  
Zackery P. Bulman ◽  
Miao Zhao ◽  
Michael J. Satlin ◽  
Liang Chen ◽  
Barry N. Kreiswirth ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Polymyxin B ◽  
Hollow Fibre ◽  
Infection Model

scholarly journals Lipidomic Analysis of the Outer Membrane Vesicles from Paired Polymyxin-Susceptible and -Resistant Klebsiella pneumoniae Clinical Isolates

2018 ◽  
Vol 19 (8) ◽  
pp. 2356 ◽  
Author(s):  
Raad Jasim ◽  
Mei-Ling Han ◽  
Yan Zhu ◽  
Xiaohan Hu ◽  
Maytham Hussein ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Outer Membrane ◽  
Membrane Vesicles ◽  
Average Diameter ◽  
Polymyxin B ◽  
Outer Membrane Vesicles ◽  
Resistant Isolate ◽  
Average Particle ◽  
Lipid Species ◽  
The Impact

Gram-negative bacteria produce outer membrane vesicles (OMVs) as delivery vehicles for nefarious bacterial cargo such as virulence factors, which are antibiotic resistance determinants. This study aimed to investigate the impact of polymyxin B treatment on the OMV lipidome from paired polymyxin-susceptible and -resistant Klebsiella pneumoniae isolates. K. pneumoniae ATCC 700721 was employed as a reference strain in addition to two clinical strains, K. pneumoniae FADDI-KP069 and K. pneumoniae BM3. Polymyxin B treatment of the polymyxin-susceptible strains resulted in a marked reduction in the glycerophospholipid, fatty acid, lysoglycerophosphate and sphingolipid content of their OMVs. Conversely, the polymyxin-resistant strains expressed OMVs richer in all of these lipid species, both intrinsically and increasingly under polymyxin treatment. The average diameter of the OMVs derived from the K. pneumoniae ATCC 700721 polymyxin-susceptible isolate, measured by dynamic light scattering measurements, was ~90.6 nm, whereas the average diameter of the OMVs isolated from the paired polymyxin-resistant isolate was ~141 nm. Polymyxin B treatment (2 mg/L) of the K. pneumoniae ATCC 700721 cells resulted in the production of OMVs with a larger average particle size in both the susceptible (average diameter ~124 nm) and resistant (average diameter ~154 nm) strains. In light of the above, we hypothesize that outer membrane remodelling associated with polymyxin resistance in K. pneumoniae may involve fortifying the membrane structure with increased glycerophospholipids, fatty acids, lysoglycerophosphates and sphingolipids. Putatively, these changes serve to make the outer membrane and OMVs more impervious to polymyxin attack.

Case of acute onset ataxia caused by Klebsiella pneumoniae sepsis with the appearance of anti-GD1b antibody

2021 ◽  
Vol 14 (8) ◽  
pp. e242396
Author(s):  
Shigeo Yamada ◽  
Takashi Umeya
Keyword(s):  
Klebsiella Pneumoniae ◽  
Polymyxin B ◽  
Endotoxin Shock ◽  
Acute Onset ◽  
Serum Samples ◽  
Igg Antibody ◽  
Fisher Syndrome ◽  
Truncal Ataxia ◽  
Genetic Features ◽  
Suppurative Cholangitis

Various disorders can cause acute onset ataxia including those that have toxic/metabolic, traumatic, neoplastic, vascular, demyelinating/dysmyelinating, infectious, postinfectious and genetic features. We present a case of postseptic acute ataxia. A 72-year-old woman was diagnosed with septic shock secondary to acute obstructive suppurative cholangitis. A blood sample for bacterial culture was positive for Klebsiella pneumoniae. Thus, we initiated antibiotics and intravenous immunoglobulin therapies to control the infection. We later added extracorporeal endotoxin removal with a polymyxin B immobilised fibre cartridge for endotoxin shock. The patient’s condition improved soon after endotoxin removal. Mildly slurred and explosive speech with limb and truncal ataxia, which improved gradually, developed shortly afterwards. Serum samples obtained on day 15 after admission were positive for anti-GD1b IgG antibody. The clinical course of monophasic illness with good recovery, neurological findings and the appearance of anti-GD1b antibody suggest that this case is a variant of Miller-Fisher syndrome.

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