Klebsiella Pneumoniae
Recently Published Documents





Cureus ◽  
2022 ◽  
Sneha Adidam ◽  
Lorenzo Leys ◽  
Siham Mahgoub

Medicine ◽  
2022 ◽  
Vol 101 (2) ◽  
pp. e28415
Jingru Zhao ◽  
Tiantian Huo ◽  
Xintong Luo ◽  
Fan Lu ◽  
Shuo Hui ◽  

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261588
Laura J. Rose ◽  
Hollis Houston ◽  
Marla Martinez-Smith ◽  
Amanda K. Lyons ◽  
Carrie Whitworth ◽  

Results from sampling healthcare surfaces for pathogens are difficult to interpret without understanding the factors that influence pathogen detection. We investigated the recovery of four healthcare-associated pathogens from three common surface materials, and how a body fluid simulant (artificial test soil, ATS), deposition method, and contamination levels influence the percent of organisms recovered (%R). Known quantities of carbapenemase-producing KPC+ Klebsiella pneumoniae (KPC), Acinetobacter baumannii, vancomycin-resistant Enterococcus faecalis, and Clostridioides difficile spores (CD) were suspended in Butterfield’s buffer or ATS, deposited on 323cm2 steel, plastic, and laminate surfaces, allowed to dry 1h, then sampled with a cellulose sponge wipe. Bacteria were eluted, cultured, CFU counted and %R determined relative to the inoculum. The %R varied by organism, from <1% (KPC) to almost 60% (CD) and was more dependent upon the organism’s characteristics and presence of ATS than on surface type. KPC persistence as determined by culture also declined by >1 log10 within the 60 min drying time. For all organisms, the %R was significantly greater if suspended in ATS than if suspended in Butterfield’s buffer (p<0.05), and for most organisms the %R was not significantly different when sampled from any of the three surfaces. Organisms deposited in multiple droplets were recovered at equal or higher %R than if spread evenly on the surface. This work assists in interpreting data collected while investigating a healthcare infection outbreak or while conducting infection intervention studies.

2022 ◽  
Vol 5 (1) ◽  
Qingqing Fang ◽  
Yu Feng ◽  
Alan McNally ◽  
Zhiyong Zong

AbstractCarbapenem-resistant Klebsiella pneumoniae (CRKP) has emerged as a severe global health challenge. We isolate and characterize two previously unidentified lytic phages, P24 and P39, with large burst sizes active against ST11 KL64, a major CRKP lineage. P24 and P39 represent species of the genera Przondovirus (Studiervirinae subfamily) and Webervirus (Drexlerviridae family), respectively. P24 and P39 together restrain CRKP growth to nearly 8 h. Phage-resistant mutants exhibit reduced capsule production and decreased virulence. Modifications in mshA and wcaJ encoding capsule polysaccharide synthesis mediate P24 resistance whilst mutations in epsJ encoding exopolysaccharide synthesis cause P39 resistance. We test P24 alone and together with P39 for decolonizing CRKP using mouse intestinal colonization models. Bacterial load shed decrease significantly in mice treated with P24 and P39. In conclusion, we report the characterization of two previously unidentified lytic phages against CRKP, revealing phage resistance mechanisms and demonstrating the potential of lytic phages for intestinal decolonization.

Antibiotics ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 92
Ângela Novais ◽  
Rita Veiga Ferraz ◽  
Mariana Viana ◽  
Paula Martins da Costa ◽  
Luísa Peixe

The changing epidemiology of carbapenem-resistant Klebsiella pneumoniae in Southern European countries is challenging for infection control, and it is critical to identify and track new genetic entities (genes, carbapenemases, clones) quickly and with high precision. We aimed to characterize the strain responsible for the first recognized outbreak by an NDM-1-producing K. pneumoniae in Portugal, and to elucidate its diffusion in an international context. NDM-1-producing multidrug-resistant K. pneumoniae isolates from hospitalized patients (2018–2019) were characterized using FTIR spectroscopy, molecular typing, whole-genome sequencing, and comparative genomics with available K. pneumoniae ST11 KL105 genomes. FT-IR spectroscopy allowed the rapid (ca. 4 h after incubation) identification of the outbreak strains as ST11 KL105, supporting outbreak control. Epidemiological information supports a community source but without linkage to endemic regions of NDM-1 producers. Whole-genome comparison with previous DHA-1-producing ST11 KL105 strains revealed the presence of different plasmid types and antibiotic resistance traits, suggesting the entry of a new strain. In fact, this ST11 KL105 clade has successfully disseminated in Europe with variable beta-lactamases, but essentially as ESBL or DHA-1 producers. We expand the distribution map of NDM-1-producing K. pneumoniae in Europe, at the expense of a successfully established ST11 KL105 K. pneumoniae clade circulating with variable plasmid backgrounds and beta-lactamases. Our work further supports the use of FT-IR as an asset to support quick infection control.

2022 ◽  
Vol 8 (1) ◽  
Carla Rodrigues ◽  
Siddhi Desai ◽  
Virginie Passet ◽  
Devarshi Gajjar ◽  
Sylvain Brisse

The rapid emergence of multidrug-resistant Klebsiella pneumoniae is being driven largely by the spread of specific clonal groups (CGs). Of these, CG147 includes 7-gene multilocus sequence typing (MLST) sequence types (STs) ST147, ST273 and ST392. CG147 has caused nosocomial outbreaks across the world, but its global population dynamics remain unknown. Here, we report a pandrug-resistant ST147 clinical isolate from India (strain DJ) and define the evolution and global emergence of CG147. Antimicrobial-susceptibility testing following European Committee on Antimicrobial Susceptibility Testing (EUCAST) guidelines and genome sequencing (Illumina and Oxford Nanopore Technologies, Unicycler assembly) were performed on strain DJ. Additionally, we collated 217 publicly available CG147 genomes [National Center for Biotechnology Information (NCBI), May 2019]. CG147 evolution was inferred within a temporal phylogenetic framework (beast) based on a recombination-free sequence alignment (Roary/Gubbins). Comparative genomic analyses focused on resistance and virulence genes and other genetic elements (BIGSdb, Kleborate, PlasmidFinder, phaster, ICEfinder and CRISPRCasFinder). Strain DJ had a pandrug-resistance phenotype. Its genome comprised the chromosome, seven plasmids and one linear phage-plasmid. Four carbapenemase genes were detected: bla NDM-5 and two copies of bla OXA-181 in the chromosome, and a second copy of bla NDM-5 on an 84 kb IncFII plasmid. CG147 genomes carried a mean of 13 acquired resistance genes or mutations; 63 % carried a carbapenemase gene and 83 % harboured bla CTX-M. All CG147 genomes presented GyrA and ParC mutations and a common subtype I-E CRISPR-Cas system. ST392 and ST273 emerged in 2005 and 1995, respectively. ST147, the most represented phylogenetic branch, was itself divided into two main clades with distinct capsular loci: KL64 (74 %, DJ included, emerged in 1994 and disseminated worldwide, with carbapenemases varying among world regions) and KL10 (20 %, emerged in 2002, predominantly found in Asian countries, associated with carbapenemases NDM and OXA-48-like). Furthermore, subclades within ST147-KL64 differed at the yersiniabactin locus, OmpK35/K36 mutations, plasmid replicons and prophages. The absence of IncF plasmids in some subclades was associated with a possible activity of a CRISPR-Cas system. K. pneumoniae CG147 comprises pandrug-resistant or extensively resistant isolates, and carries multiple and diverse resistance genes and mobile genetic elements, including chromosomal bla NDM-5. Its emergence is being driven by the spread of several phylogenetic clades marked by their own genomic features and specific temporo–spatial dynamics. These findings highlight the need for precision surveillance strategies to limit the spread of particularly concerning CG147 subsets.

Eve A. Maunders ◽  
Katherine Ganio ◽  
Andrew J. Hayes ◽  
Stephanie L. Neville ◽  
Mark R. Davies ◽  

Klebsiella pneumoniae is a leading cause of healthcare-associated infections, including pneumonia, urinary tract infections, and sepsis. Treatment of K. pneumoniae infections is becoming increasingly challenging due to high levels of antibiotic resistance and the rising prevalence of carbapenem-resistant, extended-spectrum β-lactamases producing strains.

2022 ◽  
Vol 509 (1) ◽  
Phạm Thị Hồng Phương ◽  
Đặng Quốc Tuấn

Mục tiêu: Đánh giá kết quả điều trị viêm phổi và nhiễm khuẩn huyết do Klebsiella.pneumoniae sử dụng amikacin có giám sát nồng độ trong máu và mô tả độc tính trên thận. Đối tượng và phương pháp nghiên cứu: Nghiên cứu lâm sàng can thiệp trên bệnh nhân nhiễm khuẩn huyết hoặc viêm phổi do K.pneumoniae  tại khoa Hồi sức tích cực. Liều amikacin là 30 mg/kg cân nặng hiệu chỉnh (ABW). Mục tiêu giám sát nồng độ thuốc trong máu (TDM) là Cpeak : 45 – 60 mg/L, Cpeak/MIC: 8-10, Ctrough< 2mg/L. Chúng tôi ghi nhận đáp ứng lâm sàng và sự phát triển tổn thương thận cấp. Kết quả: 42 bệnh nhân được nhận vào nghiên cứu, có tuổi trung bình 56,1 ± 19. Nam giới chiếm 76,2%. Điểm APACHE II 16, điểm SOFA ngày vào khoa 8[4,5], điểm Chalson 1[2]. Tỉ lệ sốc nhiễm khuẩn tại thời điểm dùng amikacin 35,7%. Bệnh nhân thở máy chiếm 85,7%. Viêm phổi chiếm 83,3%. MIC của K.pneumoniae với amikacin 4[2-5], tỉ lệ MIC≤8 là 92,9%. Tỉ lệ  bệnh nhân đáp ứng lâm sàng hoàn toàn là 57,1%. Tỉ lệ đáp ứng lâm sàng hoàn toàn ngày thứ 5 tăng hơn ngày thứ 3, ngày thứ 7 tăng hơn ngày thứ 5 (p<0,05). Nhóm đáp ứng lâm sàng hoàn toàn và nhóm không đáp ứng lâm sàng hoàn toàn có sự khác biệt về điểm APACHE II, điểm SOFA ngày vào khoa, điểm SOFA lúc bắt đầu điều trị, Hct lúc bắt đầu điều trị và tỉ lệ thở máy (p<0,05), không có sự khác biệt về Cpeak/MIC và MIC (p>0,05). Trong những bệnh nhân Ctrough<2mg/L tỉ lệ xuất hiện tổn thương thận là 38,1% và 87,5% ở giai đoạn nguy cơ. Thời gian xuất hiện tổn thương thận là 6,1±3,6 ngày. Kết luận: Tỉ lệ đáp ứng lâm sàng hoàn toàn khi điều trị viêm phổi, nhiễm khuẩn huyết do K.pneumoniae sử dụng amikacin liều 30 mg/kg ABW là 57,1%. Bệnh nhân có điểm APACHE II cao, SOFA lúc vào khoa cao, SOFA lúc bắt đầu điều trị cao và bệnh nhân thở máy có đáp ứng lâm sàng kém hơn. Tỉ lệ tổn thương thận cấp ở các bệnh nhân nghiên cứu là 38,1%.

Sign in / Sign up

Export Citation Format

Share Document