Parapharyngeal abscess from Pseudomonas aeruginosa infection in an HIV positive patient.
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In order to elucidate any changes in imipenem-resistant Pseudomonas aeruginosa (IRPA) infections in Japan, we examined 511 P. aeruginosa stains isolated from our surgical ward between 1987 and 2001. These isolates were subjected to susceptibility testing against various antipseudomonal agents including imipenem, meropenem, ceftazidime, gentamicin and ciprofloxacin. They were serotyped with the slide agglutination test and genotyped using pulsed-field gel electrophoresis (PFGE). The annual incidences of IRPA infections were particularly high in the early 1990s. Epidemiological investigations revealed that these outbreaks were due to dissemination of hospital-acquired IRPA isolates. Intensive use of imipenem promoted the selection of highly resistant strains. Further study of resistance mechanisms revealed that none of the 110 IRPA strains were metallo-beta-lactamase (MBL) producers. Polymerase chain reaction (PCR) analysis using bla(IMP) specific primers confirmed that no IMP-1 type MBL gene-positive strains were detected from our ward. Susceptibilities of those IRPA strains against other antipseudomonal agents showed relatively low levels, suggesting that imipenem resistance was mainly due to impermeability of the OprD porin. In conclusion, hospital-acquired outbreaks of IRPA were recently reduced by guidelines for, and surveillance of, appropriate use of antimicrobial agents. When the rate of IRPA isolation increases, serotyping should be performed initially and PFGE is required to confirm outbreaks. A computer-assisted genotyping technique is available to perform epidemiological studies of IRPA isolates.
The purpose of this study was to investigate the effect of the corticosteroid, fluticasone propionate (FP), on Pseudomonas aeruginosa infection of the respiratory mucosa of an organ culture model in vitro. Organ cultures infected with P. aeruginosa had significantly (p< or =0.05) elevated levels of mucosal damage and significantly (p< or =0.05) less ciliated cells compared to controls. Preincubation of tissue with FP (10(-6) or 10(-5) but not 10(-7) M) prior to P. aeruginosa infection significantly (p< or =0.05) reduced the bacterially induced mucosal damage in a concentration-dependent manner. FP (10(-5) M) also significantly (p< or =0.05) prevented loss of ciliated cells. FP did not alter the density of bacteria adherent to the different mucosal features of the organ cultures, but did reduce total bacterial numbers due to the reduced amount of damaged tissue, which is a preferred site of P. aeruginosa adherence. It has previously been shown that the long-acting beta2-agonist salmeterol (4 x 10(-7)M) also reduces the mucosal damage caused by P. aeruginosa infection, probably via elevation of intracellular cyclic adenosine monophosphate concentrations. Preincubation of tissue with both 10(-7)M FP and 10(-7)M salmeterol, concentrations at which they did not by themselves influence the effect of P. aeruginosa infection, significantly (p< or =0.05) reduced P. aeruginosa-induced loss of cilia. However, there was no additional benefit from adding 4 x 10(-7)M salmeterol to 10(-6)M FP. In conclusion fluticasone propionate reduced mucosal damage caused by P. aeruginosa infection in vitro and preserved ciliated cells. There was a synergistic action with salmeterol in the preservation of ciliated cells.
Due to the extensive drug resistance of Pseudomonas aeruginosa (P. aeruginosa), it is still a great clinical challenge. The clustered regularly interspaced short palindromic repeats and associated proteins (CRISPR-Cas) system has become a promising strategy against this pathogen. This review critically evaluates the multifaceted applications of CRISPR-Cas technology in P. aeruginosa, including its role in antimicrobial resistance, diagnostics, genome editing, and emerging therapeutic and vaccine strategies. In addition to conducting a comprehensive analysis of various studies, we also compared the performance and limitations of various CRISPR platforms, and discussed the main technologies and transformation obstacles in this field. Finally, we look forward to the direction of applying these experimental tools to clinical research in the future.
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BACKGROUND: Data from the Belgian Cystic Fibrosis Registry consistently show that in one of the seven reference centres, the prevalence of Pseudomonas aeruginosa is half that observed at the national level. OBJECTIVES: To report the characteristics of non-transplanted patients in this clinic at the end of 2003, with special focus on paediatric patients. To describe and discuss our policy of inhaled antibiotic therapy. FINDINGS: The prevalence of P. aeruginosa among 116 patients is 20.7%. The chronic colonization rate is 19.8% but only 2.8% in patients aged under 18 (n=72). Serologic data strongly support these results. Most paediatric patients (95%) are prescribed inhaled antibiotics, at least on an intermittent basis but the mean number of days of intravenous antibiotic treatment is four times lower than in other CF children in Belgium. 70% of children have an FEV1> or =90% predicted. DISCUSSION: We have reported a distinctly low rate of chronic colonization by P. aeruginosa in a cohort of CF children and suspect that a strategy of early, often < > use of inhaled antibiotics, progressively implemented for over 15 years has substantially contributed to these results. Given the major impact of chronic P. aeruginosa colonization on prognosis in CF, it is suggested that a large prospective study of this approach is warranted.
In this report we describe the historical, clinical, histopathological and microbiological features, as well as treatments and clinical outcome, of pyoderma where Pseudomonas aeruginosa alone was isolated on bacterial culture from lesional skin. Twenty dogs were included in this retrospective study. Seven dogs without prior history of systemic or skin disease presented with acute deep pseudomonal pyoderma characterized by a sudden onset of dorsal truncal pain. Skin lesions in these dogs consisted of erythematous papules, haemorrhagic bullae, ulcers and haemorrhagic crusts confined to the dorsum. An excellent clinical response was achieved with 3-4 weeks of treatment with oral fluoroquinolones. Thirteen dogs with a more gradual onset of skin lesions associated with pseudomonal pyoderma had a history of prior skin, ear or systemic disease and had previously been treated with antibiotics and/or immunomodulatory drugs. Skin lesions in these dogs were variable and similar to those described for superficial and deep staphylococcal pyoderma. In this group, one dog was euthanized prior to commencement of treatment, two dogs were lost to follow up, and 9 had resolution of lesions following treatment with topical silver sulfadiazine (one dog), fluoroquinolones (six dogs) or cephalexin (two dogs) administered orally for 3 to 12 weeks. Rod-shaped bacteria were not always detected on cytology. Histopathology of dogs with deep pseudomonal pyoderma was characterized by severe perforating suppurative folliculitis and furunculosis.
Twenty-one patients with cystic fibrosis and chronic Pseudomonas lung infection were treated at random with ceftazidime, 150 mg/kg/day, or with piperacillin, 300 mg/kg/day, and tobramycin, 10 and more mg/kg/day for 14 days. On admission and at discharge, body weight, erythrocyte sedimentation rate, white blood cell count, and differential were determined. Pulmonary function analysis and chest X-rays were also obtained on both occasions as was sputum bacteriology. After hospitalization, the patients were followed in the outpatient department for 14-26 months. Both treatments were associated with significant improvement in most of the parameters that were studied, but neither treatment was superior.
In an attempt to determine the actual relevance of Pseudomonas aeruginosa as a target of empiric antimicrobial first-line therapy in febrile cancer patients, 44 reports of clinical trials on antimicrobial treatment regimens and 53 reports on the epidemiology of microbiologically documented infections in cancer patients were reviewed. The incidence of infections due to Pseudomonas aeruginosa was 1-2.5% among all patients presenting with first fever during neutropenia, and 5-12% among patients with microbiologically documented infections. The proportion of Pseudomonas aeruginosa infections among cases of gram-negative bacteremia has not generally declined during the past 2 decades. There were marked local and regional differences regarding the incidence of documented Pseudomonas aeruginosa infections. No clear differences between neutropenic and non-neutropenic cancer patients, between patients with solid tumors and those with hematologic malignancies, or between inpatients and outpatients presenting with fever and neutropenia were detected with respect to the likelihood of Pseudomonas aeruginosa involvement. The mortality rate in patients with Pseudomonas aeruginosa bacteremia, particularly with polymicrobial bacteremia or bacteremic pneumonia with Pseudomonas aeruginosa involvement, is considerably high. The beneficial impact on mortality of an empiric antimicrobial treatment regimen with high antipseudomonal activity has not yet been demonstrated unequivocally. Additional factors such as the quality of intensive care management, effective second-line antimicrobial regimens, local resistance patterns, and patient-related cofactors are very likely to influence the outcome of Pseudomonas aeruginosa infections in cancer patients.
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