scholarly journals A Rapidly Fatal Infection With Haemophilus influenzae Serotype E Harboring blaROB-1: The Dilemma of Safe De-escalation in the Setting of Potential Extended-Spectrum β-Lactamase Production

2018 ◽  
Vol 5 (12) ◽  
Author(s):  
John Hanna ◽  
Yetunde Ogunsesan ◽  
Erik Snesrud ◽  
Rosslyn Maybank ◽  
Ana Ong ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Fatal Infection ◽  
Extended Spectrum

scholarly journals Haemophilus influenzae bla ROB-1 Mutations in Hypermutagenic ΔampC Escherichia coli Conferring Resistance to Cefotaxime and β-Lactamase Inhibitors and Increased Susceptibility to Cefaclor

2003 ◽  
Vol 47 (8) ◽  
pp. 2551-2557 ◽  
Author(s):  
Juan-Carlos Galán ◽  
María-Isabel Morosini ◽  
María-Rosario Baquero ◽  
Milagro Reig ◽  
Fernando Baquero
Keyword(s):  
Escherichia Coli ◽  
Haemophilus Influenzae ◽  
Molecular Forms ◽  
Extended Spectrum ◽  
Selective Agents ◽  
Amoxicillin Clavulanate ◽  
Double Amino Acid ◽  
Cloned Gene ◽  
Selective Process ◽  
Increased Susceptibility

ABSTRACT The clinical use of cefaclor has been shown to enrich Haemophilus influenzae populations harboring cefaclor-hydrolyzing ROB-1 β-lactamase. Such a selective process may lead to the increased use of extended-spectrum cephalosporins or β-lactams plus β-lactamase inhibitors and, eventually, resistance to these agents, which has not previously been observed in H. influenzae. In order to establish which bla ROB-1 mutations, if any, could confer resistance to extended-spectrum cephalosporins and/or to β-lactamase inhibitors, a plasmid harboring bla ROB-1 was transformed into hypermutagenic strain Escherichia coli GB20 (ΔampC mutS::Tn10), and this construct was used in place of H. influenzae bla ROB-1. Strain GB20 with the cloned gene was submitted to serial passages in tubes containing broth with increasing concentrations of selected β-lactams (cefotaxime or amoxicillin-clavulanate). Different mutations in the bla ROB-1 gene were obtained during the passages in the presence of the different concentrations of the selective agents. Mutants resistant to extended-spectrum cephalosporins harbored either the Leu169→Ser169 or the Arg164→Trp164 substitution or the double amino acid change Arg164→Trp164 and Ala237→Thr237. ROB-1 mutants that were resistant to β-lactams plus β-lactamase inhibitors and that harbored the Arg244→Cys244 or the Ser130→Gly130 replacement were also obtained. The cefaclor-hydrolyzing efficiencies of the ROB-1 variants were strongly decreased in all mutants, suggesting that if bla ROB-1 mutants were selected by cefaclor, this drug would prevent the further evolution of this β-lactamase toward molecular forms able to resist extended-spectrum cephalosporins or β-lactamase inhibitors.

scholarly journals Emergence of clonally related multidrug resistant Haemophilus influenzae with penicillin-binding protein 3-mediated resistance to extended-spectrum cephalosporins, Norway, 2006 to 2013

2014 ◽  
Vol 19 (49) ◽  
Author(s):  
D Skaare ◽  
I L Anthonisen ◽  
G Kahlmeter ◽  
E Matuschek ◽  
O B Natås ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Binding Protein ◽  
Empiric Therapy ◽  
Multidrug Resistant ◽  
Beta Lactamase ◽  
Penicillin Binding Protein ◽  
Beta Lactam ◽  
Blood Isolate ◽  
Extended Spectrum ◽  
High Level

Resistance to cephalosporins in Haemophilus influenzae is usually caused by characteristic alterations in penicillin-binding protein 3 (PBP3), encoded by the ftsI gene. Resistance to extended-spectrum cephalosporins is associated with high-level PBP3-mediated resistance (high-rPBP3), defined by the second stage S385T substitution in addition to a first stage substitution (R517H or N526K). The third stage L389F substitution is present in some high-rPBP3 strains. High-rPBP3 H. influenzae are considered rare outside Japan and Korea. In this study, 30 high-rPBP3 isolates from Norway, collected between 2006 and 2013, were examined by serotyping, multilocus sequence typing (MLST), ftsI sequencing, detection of beta-lactamase genes and minimum inhibitory concentration (MIC) determination. MICs were interpreted according to clinical breakpoints from the European Committee on Antimicrobial Susceptibility Testing (EUCAST). Respiratory isolates predominated (proportion: 24/30). The 30 isolates included one serotype f isolate, while the remaining 29 lacked polysaccharide capsule genes. Resistance to extended-spectrum cephalosporins (cefixime, 29 isolates/30 isolates; cefepime, 28/30; cefotaxime, 26 /30; ceftaroline, 26/30; ceftriaxone, 14/30), beta-lactamase production (11/30) and co-resistance to non-beta-lactams (trimethoprim-sulfamethoxazole, 13/30; tetracycline, 4/30; chloramphenicol, 4/30; ciprofloxacin, 3/30) was frequent. The N526K substitution in PBP3 was present in 23 of 30 isolates; these included a blood isolate which represents the first invasive S385T?+?N526K isolate reported from Europe. The L389F substitution, present in 16 of 30 isolates, coincided with higher beta-lactam MICs. Non-susceptibility to meropenem was frequent in S385T?+?L389F?+?N526K isolates (8/12). All 11 beta-lactamase positive isolates were TEM-1. Five clonal groups of two to 10 isolates with identical MLST-ftsI allelic profiles were observed, including the first reported high-rPBP3 clone with TEM-1 beta-lactamase and co-resistance to ciprofloxacin, tetracycline, chloramphenicol and trimethoprim-sulfamethoxazole. Prior to this study, no multidrug resistant high-rPBP3 H. influenzae had been reported in Norway. Intensified surveillance of antimicrobial resistance is needed to guide empiric therapy.

scholarly journals Disc diffusion-based screening tests for extended-spectrum β-lactamases in Haemophilus influenzae

2005 ◽  
Vol 55 (4) ◽  
pp. 570-573 ◽  
Author(s):  
Stephen G. Tristram ◽  
Bülent Bozdogan ◽  
Peter C. Appelbaum
Keyword(s):  
Haemophilus Influenzae ◽  
Screening Tests ◽  
Disc Diffusion ◽  
Extended Spectrum

scholarly journals Multicenter Surveillance of Antimicrobial Resistance of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis in Taiwan during the 1998–1999 Respiratory Season

2000 ◽  
Vol 44 (5) ◽  
pp. 1342-1345 ◽  
Author(s):  
Po-Ren Hsueh ◽  
Yung-Ching Liu ◽  
Jainn-Ming Shyr ◽  
Tsu-Lan Wu ◽  
Jing-Jou Yan ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Antimicrobial Resistance ◽  
Haemophilus Influenzae ◽  
Moraxella Catarrhalis ◽  
Surveillance Study ◽  
Extended Spectrum

ABSTRACT A susceptibility surveillance study of 276 isolates ofStreptococcus pneumoniae, 301 of Haemophilus influenzae, and 110 of Moraxella catarrhalis was carried out from November 1998 to May 1999 in Taiwan. High rates of nonsusceptibility to penicillin (76%), extended-spectrum cephalosporins (56%), azithromycin (94%), clarithromycin (95%), and trimethoprim-sulfamethoxazole (TMP-SMX) (65%) for S. pneumoniae isolates and high rates of nonsusceptibility to amoxicillin (58%) and TMP-SMX (52%) for H. influenzaeisolates were found. Higher percentages of S. pneumoniaeisolates nonsusceptible to aminopenicillins, extended-spectrum cephalosporins, macrolides, and TMP-SMX were observed among penicillin-intermediate and -resistant isolates. All quinolones tested were active in vitro against these three organisms.

Ultrastructural studies on the interaction of haemophilus influenzae with human endothelial cells in vitro

1990 ◽  
Vol 48 (3) ◽  
pp. 636-637
Author(s):  
D.J.P. Ferguson ◽  
M. Virji ◽  
H. Kayhty ◽  
E.R. Moxon
Keyword(s):  
Endothelial Cells ◽  
Haemophilus Influenzae ◽  
Intercellular Junctions ◽  
Blood Stream ◽  
Ultrastructural Studies ◽  
Endothelial Barriers ◽  
Serotype B ◽  
Meningitis In Children ◽  
Respiratory Epithelial

Haemophilus influenzae is a human pathogen which causes meningitis in children. Systemic H. influenzae infection is largely confined to encapsulated serotype b organisms and is a major cause of meningitis in the U.K. and elsewhere. However, the pathogenesis of the disease is still poorly understood. Studies in the infant rat model, in which intranasal challenge results in bacteraemia, have shown that H. influenzae enters submucosal tissues and disseminates to the blood stream within minutes. The rapidity of these events suggests that H. influenzae penetrates both respiratory epithelial and endothelial barriers with great efficiency. It is not known whether the bacteria penetrate via the intercellular junctions, are translocated within the cells or carried across the cellular barrier in 'trojan horse' fashion within phagocytes. In the present studies, we have challenged cultured human umbilical cord_vein endothelial cells (HUVECs) with both capsulated (b+) and capsule-deficient (b-) isogenic variants of one strain of H. influenzae in order to investigate the interaction between the bacteria and HUVEC and the effect of the capsule.

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