Infection prevention in practice · 2026
Containing a PER-1-producing Pseudomonas aeruginosa outbreak linked to sink contamination in an intensive care unit.
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Araújo Pírez L, Papa-Ezdra R, Outeda M, Guzmán R, Hernández N, Méndez G, Gadea P, Moreira M, Inchausti A, Burghi G, Seija V, Vignoli R, Albornoz Da Silva H
Аннотация
BACKGROUND: Healthcare-associated infections in intensive care units (ICUs) are associated with reservoirs such as sinks and drainage systems that sustain biofilms and disseminate Gram-negative bacteria. Between July 2021 and November 2022, an increase in PER-1-producing Pseudomonas aeruginosa (PaePER) was detected in the ICU of a university hospital in Uruguay.
AIM: The objective was to describe the clinical epidemiology, confirm the environmental source and assess the impact of control measures.
METHODS: An outbreak investigation was conducted. Cases were ICU patients with at least one PaePER-positive sample; all other ICU patients were considered exposed. Data collection included clinical and laboratory surveillance, observation of healthcare processes and targeted environmental sampling of seven sinks. Isolates were identified by Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS); antimicrobial susceptibility was assessed using VITEK2 (bioMérieux), E-test and disk diffusion; extended-spectrum β-lactamase production was evaluated by double-disk synergy and bla PER-1 was confirmed by polymerase chain reaction. Clonal relatedness was assessed by pulsed-field gel electrophoresis (PFGE). Control measures included discontinuation of patient room sink use, relocation of medication preparation, renewal of drainage systems and scheduled decontamination with a solution of 15% acetic acid.
FINDINGS: Among 1221 exposed patients, 31 were affected (attack rate: 2.8%): 25 infections and six colonisation episodes. Eighty-three clinical isolates were recovered, mainly from respiratory and blood samples. Isolates showed high resistance to ceftazidime, cefepime, ceftazidime/avibactam, ceftolozane/tazobactam and amikacin, with preserved susceptibility to carbapenems and cefiderocol. PaePER was recovered from four of seven sinks. PFGE confirmed a single ST309 clone.
CONCLUSION: Sinks and drainage systems acted as the source of a PaePER outbreak. Targeted interventions rapidly interrupted transmission.
AIM: The objective was to describe the clinical epidemiology, confirm the environmental source and assess the impact of control measures.
METHODS: An outbreak investigation was conducted. Cases were ICU patients with at least one PaePER-positive sample; all other ICU patients were considered exposed. Data collection included clinical and laboratory surveillance, observation of healthcare processes and targeted environmental sampling of seven sinks. Isolates were identified by Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS); antimicrobial susceptibility was assessed using VITEK2 (bioMérieux), E-test and disk diffusion; extended-spectrum β-lactamase production was evaluated by double-disk synergy and bla PER-1 was confirmed by polymerase chain reaction. Clonal relatedness was assessed by pulsed-field gel electrophoresis (PFGE). Control measures included discontinuation of patient room sink use, relocation of medication preparation, renewal of drainage systems and scheduled decontamination with a solution of 15% acetic acid.
FINDINGS: Among 1221 exposed patients, 31 were affected (attack rate: 2.8%): 25 infections and six colonisation episodes. Eighty-three clinical isolates were recovered, mainly from respiratory and blood samples. Isolates showed high resistance to ceftazidime, cefepime, ceftazidime/avibactam, ceftolozane/tazobactam and amikacin, with preserved susceptibility to carbapenems and cefiderocol. PaePER was recovered from four of seven sinks. PFGE confirmed a single ST309 clone.
CONCLUSION: Sinks and drainage systems acted as the source of a PaePER outbreak. Targeted interventions rapidly interrupted transmission.