Acinetobacter baumannii has the capability of long-term survival and can persistently inhabit most inanimate surfaces in hospital, including the air, medical equipment system and sickrooms occupied by patients with Acinetobacter baumannii infection or colonization. It has been reported that sputum aspirator, respirator, air conditioning, mechanical ventilation equipment could be contaminated by Acinetobacter baumannii and function as risk factors for facilitating dissemination [11–13]. In our study, 16 strains of XDR Acinetobacter baumannii ST369 were isolated and characterized from the clinical samples in the tertiary care teaching hospital. Among them, 4 strains were isolated from the patients hospitalized in EICU, and others were isolated from the environment, such as air, computer mouse, ambulance and mechanical ventilator. Recently, some studies demonstrated that tapwater contaminated by Acinetobacter baumannii was the important transmission route [10]. Therefore, these results suggested that we should thoroughly disinfect environment contaminated by Acinetobacter baumannii once this pathogen was observed in hospital.
Acinetobacter baumannii is an important causal agent for nosocomial infection [14]. In the present study, infection caused by blaOXA−23−like harboring Acinetobacter baumannii also occurred in EICU in our hospital. The therapeutic effect of carbapenems is getting worse with the emergence and increasing spread of blaOXA−type-producing Acinetobacter baumannii. The majority of hospital outbreaks reported in the recent years were caused by carbapenem-resistant Acinetobacter baumannii [15–17]. In this study, 16 antibiotics were used to perform the susceptibility testing, but all strains were only susceptible to tigecycline and polymyxin B, which indicated that maybe the early fair use of tigecycline and polymyxin B therapy was a good option. Further study showed that all strains had an intrinsic blaOXA−51−like gene and the acquired blaOXA−23−like carbapenemase gene. The blaOXA−23−like gene was widespread, and, it is the most common carbapenemase gene in Acinetobacter baumannii in China [18]. Although hydrolytic efficiencies of enzymes produced by Acinetobacter baumannii carrying blaOXA−23−like gene are relatively low and the resistant to carbapenem antibiotics are not 100%, the various insertion sequences (ISs) located in the upstream of the blaOXA carbapenemase genes, including ISAba1, ISAba2 and ISAba4, provide promoters for blaOXA carbapenemase genes and facilitate their expressions [19, 20]. In our study, ISAba1 gene was found upstream of blaOXA−23−like gene, which govern the expression of the blaOXA−23−like gene and mediate resistance to carbapenems. Yokoyama et al reported 16S rRNA methylase could result in the resistance to aminoglycosides [21], only ant(3’’)-I aminoglycoside resistance gene and armA 16S rRNA methylase gene were seen in all strains of the present study, which were mainly responsible for the aminoglycoside resistance.
To prevent and control infections, disinfectants are frequently used in hospitals. But the excessive use of disinfectants can lead to a wide distribution of disinfectant resistance genes. Many disinfectant resistance genes have been confirmed in MDR bacteria, such as qacA/B, qacC, qacD, qacE, qacE△1, qacH, and qacJ genes [22, 23]. Among them, qacE△1 evolved from qacE, and it is the deletion form of qacE gene. It was found that qacE△1 existed in all strains in our study, but not other disinfectant resistance genes. More recently, a total of 51 carbapenem-resistant strains collected between 2014 and 2015 were used to detect the frequency of qac-resistant genes, and result showed that the qacE△1 gene was detected in 96.07% with the highest detection rate [15]. These data indicated that the reduced susceptibility to compound disinfectant of quaternary ammonium salt, such as benzalkonium chloride and chlorhexidine, in carbapenem-resistant Acinetobacter baumannii. Therefore, scientific and effective disinfectants should be considered. The hospital in our study is a referral hospital, a large number of patients are transferred from outpatient clinics to our hospital for care. Therefore, we were unable to identify the index case for this infection. However, infection control measures were immediately implemented, mainly including the isolation of infected patients, environmental disinfection, antimicrobial stewardship, and the improvement of the hand hygiene compliance of medical staffs. Since then, we consecutively monitored the clinical samples from patients, medical personnel and equipment in EICU for two months without detection of the Acinetobacter baumannii isolate.
Currently, many STs were involved in the outbreak of Acinetobacter baumannii, such as Acinetobacter baumannii ST208 was a predominant prevalence clone in Sichuan and Zhejiang provinces of China [24]. ST219 infection was observed in a hospital in Japan [10]. The clonal spread of ST417 occurred in one hospital in Mexico, and some novel STs, such as ST758, ST762 and ST777 were also reported [5]. More recently, some researches revealed that Acinetobacter baumannii ST369 was implicated in the outbreak occurred in hospitals of China and Korean, but it was not the dominant ST [5, 25, 26]. However, ST369 was identified and responsible for this infection in our hospital according to MLST analysis. To our knowledge, this is the first report about infection of Acinetobacter baumannii only caused by ST369. It was unclear whether the virulence of Acinetobacter baumannii ST369 was increasing, but given that it can cause small-scale infection or outbreak in the hospital, we should raise awareness to strengthen epidemiological surveillance and infection control measures to prevent spread.