In vitro activities of meropenem, PD 127391, PD 131628, ceftazidime, chloramphenicol, co-trimoxazole, and ciprofloxacin against Pseudomonas cepacia

Lewin, C. S.; Doherty, C.; Govan, John R. W.

doi:10.1128/aac.37.1.123

Cited by 58 publications

(49 citation statements)

References 23 publications

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“…The specific mechanisms by which B. cepacia is able to subvert host defense mechanisms, invade deeper tissues of the lung, and ultimately become blood-borne are poorly understood. Compounding this lack of knowledge is the inherent resistance of B. cepacia to multiple antibiotics, which has made treatment of B. cepacia infections especially difficult (14,21). Once a CF patient is colonized with B. cepacia, the organism is rarely eradicated.…”

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confidence: 99%

Invasion and Intracellular Survival of Burkholderia cepacia

2000

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Burkholderia cepacia has emerged as an important pulmonary pathogen in immunocompromised patients and in patients with cystic fibrosis (CF). Little is known about the virulence factors and pathogenesis of B. cepacia, although the persistent and sometimes invasive infections caused by B. cepacia suggest that the organism possesses mechanisms for both cellular invasion and evasion of the host immune response. In this study, cultured human cells were used to analyze the invasion and intracellular survival of B. cepacia J2315, a highly transmissible clinical isolate responsible for morbidity and mortality in CF patients. Quantitative invasion and intracellular growth assays demonstrated that B. cepacia J2315 was able to enter, survive, and replicate intracellularly in U937-derived macrophages and A549 pulmonary epithelial cells. Transmission electron microscopy of infected macrophages confirmed the presence of intracellular B. cepacia and showed that intracellular bacteria were contained within membrane-bound vacuoles. An environmental isolate of B. cepacia, strain J2540, was also examined for its ability to invade and survive intracellularly in cultured human cells. J2540 entered cultured macrophages with an invasion frequency similar to that of the clinical strain, but it was less invasive than the clinical strain in epithelial cells. In marked contrast to the clinical strain, the environmental isolate was unable to survive or replicate intracellularly in either cultured macrophages or epithelial cells. Invasion and intracellular survival may play important roles in the ability of virulent strains of B. cepacia to evade the host immune response and cause persistent infections in CF patients.

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confidence: 99%

Invasion and Intracellular Survival of Burkholderia cepacia

2000

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“…In the late 1980s, surveillance studies in the UK indicated a maximum prevalence of 7% [39,50-521; however, in some CF centres this later increased to approach the prevalence of 40% described in contemporary North American studies [53]. The three major issues concerning B. cepacia can be summarised as follows: 1, the clinical risk of rapid and fatal pulmonary decline, even in patients with previously mild disease; 2, patient-topatient spread of epidemic strains within and between regional CF centres and between centres in the UK and North America; and 3, the innate multiresistance of most B. cepacia isolates to available antibioticswhich deprives patients of effective antimicrobial therapy [46,54]--combined with the failure to reduce the bacterial population in sputum and a relatively poor clinical response even when the colonising strain exhibits in-vitro susceptibility.…”

Section: B Cepacia and Cystic Fibrosismentioning

confidence: 99%

Burkholderia cepacia: medical, taxonomic and ecological issues

Govan

Hughes

Vandamme

1996

Journal of Medical Microbiology

300

275

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“…In up to 20% of patients, Bcc colonization may be associated with rapid pulmonary deterioration, leading to death by an invasive infection termed "cepacia syndrome" (2,3,9). It is difficult to eliminate infections caused by Bcc bacteria because of their high levels of innate resistance to both antibiotics (10) and biocides (11) and their ability to form biofilms (12). Furthermore, Bcc bacteria can spread between people (13)(14)(15) and can survive in respiratory droplets on surfaces (16).…”

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confidence: 99%

Burkholderia cepacia Complex Phage-Antibiotic Synergy (PAS): Antibiotics Stimulate Lytic Phage Activity

Kamal

Dennis

2015

Appl Environ Microbiol

177

195

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The Burkholderia cepacia complex (Bcc) is a group of at least 18 species of Gram-negative opportunistic pathogens that can cause chronic lung infection in cystic fibrosis (CF) patients. Bcc organisms possess high levels of innate antimicrobial resistance, and alternative therapeutic strategies are urgently needed. One proposed alternative treatment is phage therapy, the therapeutic application of bacterial viruses (or bacteriophages). Recently, some phages have been observed to form larger plaques in the presence of sublethal concentrations of certain antibiotics; this effect has been termed phage-antibiotic synergy (PAS). Those reports suggest that some antibiotics stimulate increased production of phages under certain conditions. The aim of this study is to examine PAS in phages that infect Burkholderia cenocepacia strains C6433 and K56-2. Bcc phages KS12 and KS14 were tested for PAS, using 6 antibiotics representing 4 different drug classes. Of the antibiotics tested, the most pronounced effects were observed for meropenem, ciprofloxacin, and tetracycline. When grown with subinhibitory concentrations of these three antibiotics, cells developed a chain-like arrangement, an elongated morphology, and a clustered arrangement, respectively. When treated with progressively higher antibiotic concentrations, both the sizes of plaques and phage titers increased, up to a maximum. B. cenocepacia K56-2-infected Galleria mellonella larvae treated with phage KS12 and low-dose meropenem demonstrated increased survival over controls treated with KS12 or antibiotic alone. These results suggest that antibiotics can be combined with phages to stimulate increased phage production and/or activity and thus improve the efficacy of bacterial killing.

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In vitro activities of meropenem, PD 127391, PD 131628, ceftazidime, chloramphenicol, co-trimoxazole, and ciprofloxacin against Pseudomonas cepacia

Cited by 58 publications

References 23 publications

Invasion and Intracellular Survival of Burkholderia cepacia

Invasion and Intracellular Survival of Burkholderia cepacia

Burkholderia cepacia: medical, taxonomic and ecological issues

Burkholderia cepacia Complex Phage-Antibiotic Synergy (PAS): Antibiotics Stimulate Lytic Phage Activity

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