Нозокомиальные инфекции, вызванные Pseudomonas aeruginosa, в онкологической клинике

The purpose of the study was to evaluate the frequency of isolation of multi-resistant Pseudomonas aeruginosa and identify the mechanisms of resistance to carbapenems.Material and methods. We analyzed 866 strains of Pseudomonos aeruginosaisolated from clinical samples from cancer patients in the period 2014–2016. the level of resistance to piperacillin/tazobactam, ceftazidime, cefepime, imipenem, meropenem, ciprofloxacin, amikacin in dynamics was determined. carbapenem-resistant (car-R) strains were examined for the presence of enzymes.Results. Between 2014 and 2016, the number of strains resistant to piperacillin/tazobactam was 20.1–12.9 %, to ceftazidime – 33.0–32.9 %, to cefepime – 25.6–32.9 %, ciprofloxacin – 36.8–43.8 %, amikacin – 23.8–24.9 %. No statistically significant differences were found (p>0.05). However, an increase in the number of car-R strains from 31.7 to 43.8 % was observed (p<0.05). of 7 strains of P. aeruginosainvestigated for the presence of acquired carbapenemases, the production of metal-beta-lactamase of group Vimwas detected in 2 strains, and class acarbapenemases of the gEs-5 group in one strain.Conclusion. P. aeruginosaresistance to all antibiotic groups did not exceed 50 % and remained almost unchanged for 3 years, with the exception of the increase in car-R strains. three out of 7 (42.9 %) carbapenem-resistant strains were genetically stable.Цель исследования – оценить частоту выделения мультирезистентных Pseudomonas aeruginosaи выявить механизмы резистентности к карбапенемам.Материал и методы. Проанализировано 866 штаммов синегнойных палочек, выделенных из патологических материалов от онкологических больных в 2014–16 гг. Определен уровень резистентности к пиперациллину/тазобактаму, цефтазидиму, цефепи-му, имипенему, меропенему, ципрофлоксацину, амикацину в динамике. Резистентные к карбапенемам (car-R) штаммы исследовали на наличие ферментов.Результаты. Число штаммов, резистентных к пиперациллину/тазобактаму в период 2014–2016 гг., составляло 20,1 % и 12,9 %, цефтазидиму – 33,0–32,9 %, цефепиму – 25,6–32,9 %, ципрофлоксацину – 36,8–43,8 %, амикацину – 23,8–24,9 %. Разница во всех случаях недостоверна (p>0,05). В то же время наблюдалось увеличение числа car-R штаммов с 31,7 до 43,8 % (p<0,05). Анализ 7 штаммов в отношении приобретенных карбапенемаз выявил продукцию металло-бета-лактамаз группы Vimу 2 штаммов, gEs-5 – у 1 штамма.Заключение. Резистентность P. aeruginosaко всем группам антибиотиков не превышала 50 % и практически не изменялась в течение 3 лет, за исключением нарастания car-R штаммов. Из 7 (42,9 %) изученных карбапенем-резистентных штаммов 3 были устойчивы генетически

Nosocomial infections causedby Pseudomonas aeruginosa in cancer clinics

The purpose of the study was to evaluate the frequency of isolation of multi-resistant Pseudomonas aeruginosa and identify the mechanisms of resistance to carbapenems.Material and methods. We analyzed 866 strains of Pseudomonos aeruginosaisolated from clinical samples from cancer patients in the period 2014–2016. the level of resistance to piperacillin/tazobactam, ceftazidime, cefepime, imipenem, meropenem, ciprofloxacin, amikacin in dynamics was determined. carbapenem-resistant (car-R) strains were examined for the presence of enzymes.Results. Between 2014 and 2016, the number of strains resistant to piperacillin/tazobactam was 20.1–12.9 %, to ceftazidime – 33.0–32.9 %, to cefepime – 25.6–32.9 %, ciprofloxacin – 36.8–43.8 %, amikacin – 23.8–24.9 %. No statistically significant differences were found (p>0.05). However, an increase in the number of car-R strains from 31.7 to 43.8 % was observed (p<0.05). of 7 strains of P. aeruginosainvestigated for the presence of acquired carbapenemases, the production of metal-beta-lactamase of group Vimwas detected in 2 strains, and class acarbapenemases of the gEs-5 group in one strain.Conclusion. P. aeruginosaresistance to all antibiotic groups did not exceed 50 % and remained almost unchanged for 3 years, with the exception of the increase in car-R strains. three out of 7 (42.9 %) carbapenem-resistant strains were genetically stable