Colistin‐Tobramycin Combinations Are Superior to Monotherapy Concerning the Killing of Biofilm<i>Pseudomonas aeruginosa</i>

Herrmann, Gloria; Yang, Liang; Wu, Hong; Song, Zhijun; Wang, Hengzhuang; Høiby, Niels; Ulrich, Martina; Molin, Søren; Riethmüller, Joachim; Döring, Gerd

doi:10.1086/656788

Cited by 199 publications

(152 citation statements)

References 36 publications

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“…The molecular mechanisms responsible for resistance are a mixture of conventional resistance mechanisms, which also protect planktonic growing bacteria and the specific properties of biofilms that increase the tolerance of the bacteria against antibiotics [3]. The conventional resistance mechanisms to betalactam antibiotics and colistin have been most thoroughly studied in P. aeruginosa biofilms where the resistance mechanisms are induced when the biofilm is exposed to these two classes of antibiotics [3,26]. The response of the biofilm is the production of increased amounts of chromosomal beta-lactamase which degrade beta-lactam antibiotics [3], or the production of a modified lipopolysaccharide, which makes the bacteria resistant to colistin [3,27].…”

Section: The Occurrence and Architecture Of Bacterial Biofilmsmentioning

confidence: 99%

“…It would therefore be desirable to use QSIs without conventional growth-inhibiting or bactericidal activity, and accordingly is now a focus of current research [56]. Examples of such naturally occurring QSI are found in ginseng [26] and garlic extracts, and can sensitize otherwise resistant P. aeruginosa biofilms to antibiotic therapy and to PMN activity. The consequence of these QSIs is, more or less, eradication of the biofilm via antibiotic therapy and PMN activity, which dominates the inflammatory response in CF patients ( Figure 6) [64][65].…”

Section: Quorum Sensing Inhibitors (Qsi)mentioning

confidence: 99%

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The clinical impact of bacterial biofilms

Høiby¹,

Ciofu²,

Johansen³

et al. 2011

Int J Oral Sci

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735

536

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Bacteria survive in nature by forming biofilms on surfaces and probably most, if not all, bacteria (and fungi) are capable of forming biofilms. A biofilm is a structured consortium of bacteria embedded in a self-produced polymer matrix consisting of polysaccharide, protein and extracellular DNA. Bacterial biofilms are resistant to antibiotics, disinfectant chemicals and to phagocytosis and other components of the innate and adaptive inflammatory defense system of the body. It is known, for example, that persistence of staphylococcal infections related to foreign bodies is due to biofilm formation. Likewise, chronic Pseudomonas aeruginosa lung infections in cystic fibrosis patients are caused by biofilm growing mucoid strains. Gradients of nutrients and oxygen exist from the top to the bottom of biofilms and the bacterial cells located in nutrient poor areas have decreased metabolic activity and increased doubling times. These more or less dormant cells are therefore responsible for some of the tolerance to antibiotics. Biofilm growth is associated with an increased level of mutations. Bacteria in biofilms communicate by means of molecules, which activates certain genes responsible for production of virulence factors and, to some extent, biofilm structure. This phenomenon is called quorum sensing and depends upon the concentration of the quorum sensing molecules in a certain niche, which depends on the number of the bacteria. Biofilms can be prevented by antibiotic prophylaxis or early aggressive antibiotic therapy and they can be treated by chronic suppressive antibiotic therapy. Promising strategies may include the use of compounds which can dissolve the biofilm matrix and quorum sensing inhibitors, which increases biofilm susceptibility to antibiotics and phagocytosis.

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Section: The Occurrence and Architecture Of Bacterial Biofilmsmentioning

confidence: 99%

Section: Quorum Sensing Inhibitors (Qsi)mentioning

confidence: 99%

The clinical impact of bacterial biofilms

Høiby¹,

Ciofu²,

Johansen³

et al. 2011

Int J Oral Sci

Self Cite

735

536

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“…Ингаляционные ан тибиотики не используются в качестве монотерапии без системных препаратов, т. к. степень их адсорб ции в кровь низка (2-4 %) и недостаточна для лече ния сопутствующих НП инфекций. Частота побоч ных эффектов (нефро и нейротоксичность) при применении ингаляционных антибиотиков невысо ка [7,[12][13][14][15][16][17][18].…”

Section: заметки из практикиunclassified

An Experience of Administration of Inhaled Tobramycin in Severe Nosocomial Pneumonia

Половников¹,

Kuzovlev²,

Ильичев³

2011

Pulʹmonologiâ (Mosk.)

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“…At the moment, due to the 100% susceptibility to colistin, we use this antimicrobial as the last line of defence. The combined use of colistintobramycin inhalation in animal and in vitro studies has been shown to be superior to monotherapy since its use significantly decreased bacterial burden [11].…”

Section: Discussionmentioning

confidence: 99%

Antimicrobial susceptibility of Pseudomonas aeruginosa before and after initiation of inhaled tobramycin in Bulgaria

Petrova

Miteva

Lazova

et al. 2016

J Infect Dev Ctries

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Introduction: In aim to achieve better infection control and possible eradication of the pathogens involved in chronic infections of patients with cystic fibrosis (CF) scientists have developed a new way to administer antimicrobials -inhalation. The first and so far the only available inhalable antimicrobial in Bulgaria is inhaled tobramycin (TOBI), introduced in 2009.We aimed to evaluate the antimicrobial susceptibility of Pseudomonas aeruginosa isolates from cystic fibrosis (CF) patients before and after initiation of TOBI in the regular treatment regimen. Methodology: We have determined the minimal inhibitory concentration (MIC) of 17 antimicrobials by the E-test (LIOFILCHEM) in sputa samples of 118 CF patients for the period of 2005-2014. The results were interpreted according to the annual Clinical and Laboratory Standards Institute guidelines. Results: In the sputa of 70 patients a total of 102 P. aeruginosa isolates were found. Sixty-eight out of 102 (66.7%) were susceptible to all studied antimicrobials. We divided the isolates in two chronological groups: those collected before the introduction of TOBI as a regular treatment in 2009 and those collected after 2009. A significant reduction (p < 0,001-0,02) in susceptibility for the strains after 2009 was noted towards piperacillin (100% vs 50%), ceftazidime (100% / 77.3%), cefepime (97.9% / 68.2%), amikacin (100% / 63.6%), gentamicin (95.7% / 40.9%), tobramycin (93.6% / 59.1%) and ciprofloxacin (93.6% / 45.5%). Conclusion: The introduction of inhaled tobramycin as a regular therapy for CF patients in Bulgaria lead to a significant change in antimicrobial susceptibility of CF P. aeruginosa.

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Colistin‐Tobramycin Combinations Are Superior to Monotherapy Concerning the Killing of BiofilmPseudomonas aeruginosa

Abstract: Colistin-tobramycin combinations are more efficient than respective single antibiotics for killing P. aeruginosa in biofilms in vitro, and they significantly reduced P. aeruginosa cell counts in a rat lung infection model and in patients with cystic fibrosis.

Cited by 199 publications

References 36 publications

The clinical impact of bacterial biofilms

The clinical impact of bacterial biofilms

An Experience of Administration of Inhaled Tobramycin in Severe Nosocomial Pneumonia

Antimicrobial susceptibility of Pseudomonas aeruginosa before and after initiation of inhaled tobramycin in Bulgaria

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