The aim of this study was to investigate the susceptibility profiles to disinfectants and antimicrobial agents of 283 non-repetitive Acinetobacter clinical isolates obtained in 97 Japanese hospitals in March 2002.
Susceptibility profiles of the above isolates to four disinfectants, six antimicrobial agents and two dyes were investigated. MICs were measured by the agar dilution method recommended by the CLSI (formerly NCCLS). MBC measurements and time-kill assays were performed using a slightly modified quantitative suspension test based on the European Standard EN 1040.
No evident resistance to disinfectants was seen among the 283 strains of Acinetobacter spp. isolated in 2002, but the MIC(90)s of chlorhexidine gluconate, benzalkonium chloride and alkyldiaminoethylglycine hydrochloride were 50, 50 and 400 mg/L, respectively. Interestingly, the MICs of alkyldiaminoethylglycine hydrochloride and benzethonium chloride for four and three clinical isolates, respectively, reached 800 mg/L (approximately half the in-use concentration). The MBCs for the 28 disinfectant reduced susceptibility (DRS) isolates, for which the MICs of at least one of the four disinfectants tested were higher than the MIC(90), were comparable to those for susceptible isolates, in general; however, significant differences (P < 0.01) were observed between disinfectant-susceptible and DRS isolates in the time-kill assays of chlorhexidine gluconate, benzalkonium chloride and benzethonium chloride. Furthermore, DRS isolates tended to demonstrate multiresistance profiles to ceftazidime, ciprofloxacin and amikacin (P < 0.05).
Since several Acinetobacter clinical isolates have developed augmented resistance to multiple antimicrobials and disinfectants, it is worth checking the susceptibility to disinfectants if multidrug-resistant Acinetobacter spp. are recurrently isolated clinically.
"We adjusted the growth medium at three different pHs: 5, 9 and 6.7. The 5 and 9 pHs were chosen to represent mean pH values of the disinfectants most commonly used at a hospital setting (Doidge et al., 2010; Kawamura-Sato et al., 2010; Koburger et al., 2010; Weber et al., 2010). However, the pH 6.7 represents the mean pH value of the lung compartment (Effros and Chinard, 1969), and was chosen since lung infections and pneumonia are the most common infections caused by A. baumannii (Dijkshoorn et al., 2007; Qiu et al., 2009). "
[Show abstract][Hide abstract] ABSTRACT: Acinetobacter baumannii is one of the most significant threats to global public health. This threat is compounded by the fact that A. baumannii is rapidly becoming resistant to all relevant antimicrobials. Identifying key microbial factors through which A. baumannii resists hostile host environment is paramount to the development of novel antimicrobials targeting infections caused by this emerging pathogen. An attractive target could be a molecule that plays a role in the pathogenesis and stress response of A. baumannii. Accordingly, the universal stress protein A (UspA) was chosen to be fully investigated in this study. A platform of A. baumannii constructs, expressing various levels of the uspA gene ranging from zero to thirteen folds of wild-type level, and a recombinant E. coli strain, were employed to investigate the role of UspA in vitro stress and in vivo pathogenesis. The UspA protein plays a significant role in protecting A. baumannii from H2O2, low pH, and the respiratory toxin 2,4-DNP. A. baumannii UspA protein plays an essential role in two of the deadliest types of infection caused by A. baumannii; pneumonia and sepsis. This distinguishes A. baumannii UspA from its closely related homolog, the Staphylococcus aureus Usp2, as well as from the less similar Burkholderia glumae Usps. Heterologous and overexpression experiments suggest that UspA mediates its role via an indirect mechanism. Our study highlights the role of UspA as an important contributor to the A. baumannii stress and virulence machineries, and polishes it as a plausible target for new therapeutics.
International Journal of Medical Microbiology 11/2014; 305(1). DOI:10.1016/j.ijmm.2014.11.008 · 3.61 Impact Factor
"Moreover, A. baumannii causes community-acquired infections, predominately in Asia and tropic Australia (Falagas et al., 2007). A. baumannii infection is facilitated through biofilm formation on indwelling medical devices and other hospital surfaces and the ability to withstand desiccation and disinfection (Vidal et al., 1996; Wendt et al., 1997; Neely, 2000; Tomaras et al., 2003; Kawamura-Sato et al., 2010; Pour et al., 2011). In addition to the wide repertoire of diseases caused by A. baumannii, this organism has acquired antibiotic resistance at alarming rates. "
[Show abstract][Hide abstract] ABSTRACT: Acinetobacter baumannii is a significant contributor to intensive care unit (ICU) mortality causing numerous types of infection in this susceptible ICU population, most notably ventilator-associated pneumonia. The substantial disease burden attributed to A. baumannii and the rapid acquisition of antibiotic resistance make this bacterium a serious health care threat. A. baumannii is equipped to tolerate the hostile host environment through modification of its metabolism and nutritional needs. Among these adaptations is the evolution of mechanisms to acquire nutrient metals that are sequestered by the host as a defense against infection. Although all bacteria require nutrient metals, there is diversity in the particular metal needs among species and within varying tissue types and bacterial lifecycles. A. baumannii is well-equipped with the metal homeostatic systems required for the colonization of a diverse array of tissues. Specifically, iron and zinc homeostasis is important for A. baumannii interactions with biotic surfaces and for growth within vertebrates. This review discusses what is currently known regarding the interaction of A. baumannii with vertebrate cells with a particular emphasis on the contributions of metal homeostasis systems. Overall, published research supports the utility of exploiting these systems as targets for the development of much-needed antimicrobials against this emerging infectious threat.
Frontiers in Cellular and Infection Microbiology 12/2013; 3:95. DOI:10.3389/fcimb.2013.00095 · 3.72 Impact Factor
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