scholarly journals Genomic Insights into a Complete Deletion of the mgrB Locus in Colistin-Resistant Klebsiella pneumoniae ST2268 Isolated from a Human Infection

2021 ◽  
Author(s):  
Yunjia Song ◽  
Jinge Yang ◽  
Yingjiao Ju ◽  
Dejun Liu ◽  
Yang Wang ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Human Infection ◽  
Complete Deletion

scholarly journals Complete Deletion of theramRGene in anIn Vitro-Selected Mutant of Klebsiella pneumoniae Overexpressing the AcrAB Efflux Pump

2012 ◽  
Vol 57 (1) ◽  
pp. 672-673 ◽  
Author(s):  
Suzanne Bialek-Davenet ◽  
Véronique Leflon-Guibout ◽  
Olivier Tran Minh ◽  
Estelle Marcon ◽  
Richard Moreau ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Efflux Pump ◽  
Acrab Efflux Pump ◽  
Complete Deletion

scholarly journals Animal Model To Study Klebsiella pneumoniae Gastrointestinal Colonization and Host-to-Host Transmission

2020 ◽  
Vol 88 (11) ◽  
Author(s):  
Taylor M. Young ◽  
Andrew S. Bray ◽  
Ravinder K. Nagpal ◽  
David L. Caudell ◽  
Hariom Yadav ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Close Contact ◽  
Epidemiological Studies ◽  
Multidrug Resistant ◽  
Transmission Efficiency ◽  
Oral Route ◽  
Human Infection ◽  
Gi Tract ◽  
Content Type ◽  
Immunocompetent Mice

ABSTRACT An important yet poorly understood facet of the life cycle of a successful pathogen is host-to-host transmission. Hospital-acquired infections (HAI) resulting from the transmission of drug-resistant pathogens affect hundreds of millions of patients worldwide. Klebsiella pneumoniae, a Gram-negative bacterium, is notorious for causing HAI, with many of these infections difficult to treat, as K. pneumoniae has become multidrug resistant. Epidemiological studies suggest that K. pneumoniae host-to-host transmission requires close contact and generally occurs through the fecal-oral route. Here, we describe a murine model that can be utilized to study mucosal (oropharynx and gastrointestinal [GI]) colonization, shedding within feces, and transmission of K. pneumoniae through the fecal-oral route. Using an oral route of inoculation, and fecal shedding as a marker for GI colonization, we showed that K. pneumoniae can asymptomatically colonize the GI tract in immunocompetent mice and modifies the host GI microbiota. Colonization density within the GI tract and levels of shedding in the feces differed among the clinical isolates tested. A hypervirulent K. pneumoniae isolate was able to translocate from the GI tract and cause hepatic infection that mimicked the route of human infection. Expression of the capsule was required for colonization and, in turn, robust shedding. Furthermore, K. pneumoniae carrier mice were able to transmit to uninfected cohabitating mice. Lastly, treatment with antibiotics led to changes in the host microbiota and development of a transient supershedder phenotype, which enhanced transmission efficiency. Thus, this model can be used to determine the contribution of host and bacterial factors toward K. pneumoniae dissemination.

scholarly journals An Animal Model to Study Klebsiella pneumoniae Gastro-Intestinal Colonization and Host-to-Host Transmission

2020 ◽  
Author(s):  
Taylor M. Young ◽  
Andrew S. Bray ◽  
Ravinder K. Nagpal ◽  
David L. Caudell ◽  
Hariom Yadav ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Close Contact ◽  
Epidemiological Studies ◽  
Transmission Efficiency ◽  
Oral Route ◽  
Human Infection ◽  
Drug Resistant ◽  
Gi Tract ◽  
Fecal Shedding ◽  
Immunocompetent Mice

AbstractAn important yet poorly understood facet in the life cycle of a successful pathogen is the host-to-host transmission. Hospital-acquired infections (HAI) resulting from the transmission of drug-resistant pathogens affect hundreds of millions of patients worldwide. Klebsiella pneumoniae (Kpn), a gram-negative bacterium, is notorious for causing HAI, with many of these infections difficult to treat as Kpn has become multi-drug resistant. Epidemiological studies suggest that Kpn host-to-host transmission requires close contact and generally occurs through the fecal-oral route. Herein, we describe a murine model that can be utilized to study mucosal (oropharynx and gastrointestinal [GI]) colonization, shedding within feces, and transmission of Kpn through the fecal-oral route. Using an oral route of inoculation, and fecal shedding as a marker for GI colonization, we show that Kpn can asymptomatically colonize the GI tract of immunocompetent mice, and modifies the host GI microbiota. Colonization density within the GI tract and levels of shedding in the feces differed among the clinical isolates tested. A hypervirulent Kpn isolate was able to translocate from the GI tract and cause hepatic infection that mimicked the route of human infection. Expression of the capsule was required for colonization and, in turn, robust shedding. Furthermore, Kpn carrier mice were able to transmit to uninfected cohabitating mice. Lastly, treatment with antibiotics led to changes in the host microbiota and development of a transient super-shedder phenotype, which enhanced transmission efficiency. Thus, this model can be used to determine the contribution of host and bacterial factors towards Kpn dissemination.

scholarly journals A plasmid locus associated with Klebsiella clinical infections encodes a microbiome-dependent gut fitness factor

2020 ◽  
Author(s):  
Jay Vornhagen ◽  
Christine M. Bassis ◽  
Srividya Ramakrishnan ◽  
Robert Hein ◽  
Sophia Mason ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Gut Microbiota ◽  
Virulence Genes ◽  
Physiological Function ◽  
Human Infection ◽  
Diverse Group ◽  
Toxic Compound ◽  
Fitness Advantage ◽  
Gut Colonization ◽  
Indigenous Microbiota

Introductory paragraphGut colonization by the pathogen Klebsiella pneumoniae (Kp) is consistently associated with subsequent Kp disease1-5, and patients are predominantly infected with their colonizing strain1,2. However, colonizing strains likely vary in their potential to cause infection. We previously identified the plasmid-encoded tellurium resistance (ter) operon as highly associated with infection when compared to asymptomatic colonization in hospitalized patients1. The ter operon bestows resistance to the toxic compound tellurite oxide (TeO3−2), but this is unlikely to be its physiological function, as tellurium and TeO3−2 are exceedingly rare. Here we show that terC is necessary and terZABCDEF is sufficient for phenotypic TeO3−2 resistance. Next, we demonstrate that ter is encoded on a diverse group of plasmids without known plasmid-encoded virulence genes, suggesting an independent role in infection. Finally, our studies indicate that ter is a gut fitness factor, and its fitness advantage is conferred only when specific gut microbiota constituents are present. Collectively, these data reveal the Kp ter operon that is highly associated with human infection likely acts early in pathogenesis as a horizontally-transferrable fitness factor promoting robust gut colonization in the presence of the indigenous microbiota.

scholarly journals Deciphering the complete deletion of the mgrB locus in an unusual colistin-resistant Klebsiella pneumoniae isolate colonising the gut of a traveller returning from India

2018 ◽  
Vol 51 (3) ◽  
pp. 529-531 ◽  
Author(s):  
Odette J. Bernasconi ◽  
Valentina Donà ◽  
João Pires ◽  
Esther Kuenzli ◽  
Christoph Hatz ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Complete Deletion

scholarly journals Genome sequence analysis of a hypermucoviscous/hypervirulent and MDR CTX-M-15/K19/ST29 Klebsiella pneumoniae isolated from human infection

2017 ◽  
Vol 75 (9) ◽  
Author(s):  
Quézia Moura ◽  
Fernanda Esposito ◽  
Miriam R Fernandes ◽  
Maria Espinoza-Muñoz ◽  
Tiago A Souza ◽  
...  
Keyword(s):  
Sequence Analysis ◽  
Klebsiella Pneumoniae ◽  
Genome Sequence ◽  
Human Infection ◽  
Genome Sequence Analysis

Human infection with Dirofilaria

1978 ◽  
Vol 114 (4) ◽  
pp. 593-594 ◽  
Author(s):  
H. M. Payan
Keyword(s):  
Human Infection

Combination of Antibiotic Treatment with the Thrombin Inhibitor Recombinant Hirudin for the Therapy of Experimental Klebsiella pneumoniae Sepsis

1994 ◽  
Vol 71 (06) ◽  
pp. 768-772 ◽  
Author(s):  
Gerhard Dickneite ◽  
Jörg Czech
Keyword(s):  
Septic Shock ◽  
Klebsiella Pneumoniae ◽  
Organ Failure ◽  
Therapeutic Effect ◽  
Disseminated Intravascular Coagulation ◽  
Post Infection ◽  
Thrombin Inhibitor ◽  
Bolus Administration ◽  
Bacterial Burden ◽  
Recombinant Hirudin

SummaryRats which were infected with the gramnegative pathogen Klebsiella pneumoniae develop disseminated intravascular coagulation (DIC), multi-organ failure (MOF) and finally die in a septic shock. We investigated the therapeutic effect of antibiotic (tobramycin) treatment combined with the infusion of the highly specific thrombin inhibitor rec. hirudin. Although administration of 2 mg/kg tobramycin alone leads to a decrease of the bacterial burden, DIC could not be prevented. Infusion of rec. hirudin (0.25 mg/kg x h) for 4 h (start of treatment 1 h post infection), in addition to a bolus administration of tobramycin, led to an amelioration of DIC parameters as fibrinogen, thrombin-antithrombin complex (TAT) and platelets. Serum transaminase levels (GOT, GPT) as a marker of MOF were significantly improved by rec. hirudin, the T50 value increased from 17 h in the tobramycin group to 42 h in the tobramycin + rec. hirudin giuup, muilality rates were 90% or 60%, respectively. Combination of heparin (10011/kg x h) and tobramycin was not effective on survival.

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