ABSTRACT
BACKGROUND: Endoscopes represent the medical devices most commonly linked to health care-associated outbreaks and pseudo-outbreaks. Most of the recent outbreaks and pseudo-outbreaks have resulted from contaminated automated endoscope reprocessors (AER) or the use of damaged or malfunctioning bronchoscopes or contaminated equipment. OBJECTIVES: We investigated a pseudo-outbreak of Pseudomonas putida and Stenotrophomonas maltophilia recovered from bronchial washing (BW) specimens obtained during bronchoscopy in a bronchoscopy unit. METHODS: Samples were obtained from environmental surfaces in the endoscopy suite, bronchoscopes, and bronchoscopic dispensable material, and specimens of cleaning solutions, cleaning brushes, the AER, and the ultrasound system were sent for bacterial culture. Medical records were reviewed to identify possible infections after a bronchoscopy. RESULTS: P. putida and S. maltophilia were isolated from BW samples of 39 patients. The bronchoscopy models Olympus BF-1T160 and BF-160 were contaminated. Both bronchoscopes and other contaminated material (cleaning brushes, diluted cleaning solutions, and the sink) were isolated, but new cases continued to appear. The AER was recently installed, and new connections were used for the water lines and new tubes were connected to the AER. Initially, specimens were obtained from the external circuits and the internal walls of the AER. Finally, cultures were made from the filters on the water lines, and growth of P. putida and S. maltophilia was found. The investigation revealed that the BW specimens were contaminated because sterile saline was injected by means of the biopsy port of the bronchoscope and was recovered through the same channel by means of the proximal suction port. No patients developed clinical signs or symptoms of infection, but the positive cultures did lead to treatment of 21 patients. CONCLUSIONS: We described a pseudo-outbreak related to a contaminated bronchoscope because of inadequate installation of the AER for used new water lines and because the new tubes were connected to the AER. The antibacterial filters of the AER used tap water, and this may have contained low levels of microorganisms. No serious clinical complications derived from this pseudo-outbreak.
Subject(s)
Bronchoalveolar Lavage Fluid/microbiology , Bronchoscopes/microbiology , Cross Infection/epidemiology , Disease Outbreaks , Equipment Contamination , Gram-Negative Bacterial Infections/epidemiology , Pseudomonas Infections/epidemiology , Aged , Bronchoscopy , Cross Infection/diagnosis , Diagnostic Errors , Female , Gram-Negative Bacterial Infections/diagnosis , Humans , Male , Middle Aged , Pseudomonas Infections/diagnosis , Pseudomonas putida/isolation & purification , Spain/epidemiology , Stenotrophomonas maltophilia/isolation & purificationABSTRACT
Introducción: La hipertensión arterial pulmonar (HAP) es una enfermedad en la que se implican, entre otras, la vía del óxido nítrico (NO). Se ha descrito un polimorfismo en el gen de la sintasa inducible del NO (NOS2) que consiste en la repetición del pentanucleótido CCTTT dando lugar a menor producción de NO. El objetivo del estudio fue conocer si este polimorfismo incrementa la susceptibilidad para desarrollar HAP. Métodos: Se compararon 64 pacientes diagnosticados de HAP grupos I y IV y 50 controles sanos. Mediante PCR se genotiparon las muestras de ADN para este polimorfismo. Se comparó la distribución en ambos grupos y se correlacionó con parámetros clínicos, hemodinámicos y respuesta terapéutica. Resultados: Se observó una distribución significativamente diferente en el número de repeticiones entre pacientes y controles (p < 0,0001). Agrupando las muestras en formas cortas (ambos alelos con menos de 12 repeticiones) y largas (≥ 12 repeticiones) se observó que los primeros tenían un riesgo casi 4 veces superior de desarrollar HAP (odds ratio: 3,83; IC 95%: 1,19-12,32; p = 0,024). No hubo diferencias entre los tipos más frecuentes de HAP ni en la respuesta terapéutica o supervivencia. No existió correlación entre parámetros hemodinámicos y el número de repeticiones en los pacientes, solo débil correlación con la presión arterial pulmonar sistólica. Conclusiones: Existen diferencias significativas en la distribución del polimorfismo CCTTT del gen NOS2 entre pacientes con HAP y población sana. Una menor repetición del pentanucleótido CCTTT en el gen de la NOS2 podría incrementar el riesgo de desarrollar HAP
Introduction: One of the pathways involved in pulmonary arterial hypertension (PAH) is the nitric oxide (NO) pathway. A polymorphism in the inducible NO synthase (NOS2) gene has been described, consisting of the CCTTT pentanucleotide repeat, which causes a reduction in NO production. The aim of this study was to determine if this polymorphism increases susceptibility to developing PAH. Methods: Sixty-four patients with a diagnosis of PAH groups I and IV and 50 healthy controls were compared. DNA genotyping of the samples for this polymorphism was performed using PCR. The distribution between both groups was compared and correlated with clinical and hemodynamic parameters and therapeutic response. Results: A significantly different distribution was observed in the number of repeats between patients and controls (P < 0.0001). When the samples were categorized by short forms (both alleles with less than 12 repeats) and long forms (≥12 repeats), it was observed that the former had an almost 4-fold risk of developing PAH (odds ratio: 3.83; 95% CI: 1.19-12.32, P = 0.024). There were no differences between the most common types of PAH, either in therapeutic response or survival. There was no correlation between hemodynamic parameters and the number of repeats in the patients, and only a weak correlation with systolic PAH. Conclusions: There are significant differences in the distribution of the NOS2 promotor CCTTT polymorphism between patients with PAH and the healthy population. A minor CCTTT pentanucleotide repeat in the NOS2 gene may increase the risk of developing PAH
Subject(s)
Humans , Hypertension, Pulmonary/physiopathology , Nitric Oxide Synthase/pharmacokinetics , Biomarkers/analysis , Risk Factors , Polymorphism, Genetic , Genetic Markers , Genetic Predisposition to Disease , Case-Control StudiesABSTRACT
INTRODUCTION: One of the pathways involved in pulmonary arterial hypertension (PAH) is the nitric oxide (NO) pathway. A polymorphism in the inducible NO synthase (NOS2) gene has been described, consisting of the CCTTT pentanucleotide repeat, which causes a reduction in NO production. The aim of this study was to determine if this polymorphism increases susceptibility to developing PAH. METHODS: Sixty four patients with a diagnosis of PAH groupsi and iv and 50 healthy controls were compared. DNA genotyping of the samples for this polymorphism was performed using PCR. The distribution between both groups was compared and correlated with clinical and haemodynamic parameters and therapeutic response. RESULTS: A significantly different distribution was observed in the number of repeats between patients and controls (P<.0001). When the samples were categorised by short forms (both alleles with less than 12repeats) and long forms (≥12 repeats), it was observed that the former had an almost 4-fold risk of developing PAH (odds ratio: 3.83; 95%CI: 1.19-12.32, P=.024). There were no differences between the most common types of PAH, either in therapeutic response or survival. There was no correlation between haemodynamic parameters and the number of repeats in the patients, and only a weak correlation with systolic PAH. CONCLUSIONS: There are significant differences in the distribution of the NOS2 promotor CCTTT polymorphism between patients with PAH and the healthy population. A minor CCTTT pentanucleotide repeat in the NOS2 gene may increase the risk of developing PAH.
