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Acinetobacter are aerobic, non-motile, gram negative bacteria that are ubiquitous in the environment and have been identified in drinking water, sewage water, groundwater, dental lines, rivers, soil, human skin, vegetables and fruits, ponds and swamps ( Baumann P 1968; Warskow and Juni 1972; Bifulco et al. 1989; Tall et al. 1995; Barbeau et al. 1996; Ford TE 1999; Fournier and Richet 2006). Although Acinetobacter are not generally considered pathogenic, the A. baumannii - A. calcoaceticus complex is increasingly associated with nosocomial infections in compromised patients. There have been 128 Acinetobacter clinical outbreaks between 1977 and 2006 ( Fournier and Richet 2006; Seifert and Wisplinghoff 2008). Among the clinically relevant strains, A. baumannii, gen. sp3, and gen.sp13TU, are the most predominant isolates ( Wroblewska et al. 2004; Dijkshoorn et al. 2007). Acinetobacter have been associated with respiratory infections, wound infections, bacteremia, secondary meningitis, and urinary infections ( Bergogne-Berezin and Towner 1996; Wroblewska et al. 2004; Keum et al. 2006; Seifert and Wisplinghoff 2008). In immuno-compromised patients mortality rates can be as high as 64% ( Seifert and Wisplinghoff 2008). One of the reasons for this high mortality rate is the difficulty clearing Acinetobacter infections, as 10-33% of Acinetobacter strains isolated in hospital settings are multi-drug resistant ( Takahashi et al. 2000; Ecker et al. 2006; Coelho et al. 2006; Rodriguez-Baño et al. 2006; Fournier and Richet 2006; Turton et al. 2006a; Turton et al. 2006b; Dijkshoorn et al. 2007; Towner KJ 2008; Seifert and Wisplinghoff 2008). Multi-drug resistant A. baumannii has become a critical pathogen in wounded U.S. soldiers returning from Iraq and Afghanistan ( Dijkshoorn et al. 2007). Another reason for the difficult elimination of Acinetobacter spp. might be their ability of biofilm formation, which might also contribute to greater resistance to disinfection in the hospital setting ( Vidal et al. 1996; Tomaras et al. 2003; Shakeri et al. 2007; Loehfelm et al. 2008). Water supplies might be an important mode of hospital contamination as Acinetobacter is often part of the profile of waterborne heterotrophic bacteria ( Stewart and Rochelle 2006). While Acinetobacter do not typically pose a concern for the general public, these bacteria are emerging pathogens in the hospital setting, and therefore warrant concern in drinking water treatment standards.
Acinetobacter spp. are ubiquitous in environmental and treated waters, and have been found in sewage water, groundwater, surface water, and drinking water ( Baumann P 1968; Warskow and Juni 1972; Bifulco et al. 1989; Stewart and Rochelle 2006). Acinetobacter strains have been isolated in 97% of natural surface waters in numbers up to 100 cells/ml ( WHO 2006). In distributed water 5-92% of samples tested positive, and may constitute between 1-5.5% of heterotrophic plate count (HPC) flora in drinking water samples ( WHO 2006).
Examples of detection:
Acinetobacter spp. have been reported to have similar disinfection susceptibilities to other heterotrophic bacteria ( WHO 2006; Stewart and Rochelle 2006). Increased resistance to chlorine, chloramine and chlorine dioxide have been indicated in Acinetobacter cell aggregates ( Stewart and Rochelle 2006). There is evidence that A. calcoaceticus causes aggregation, and therefore may promote the formation of mixed-species biofilms ( Malik et al. 2003; Simões et al. 2008). In general, biofilms in the distribution system are much more resistant to disinfection than planktonic cells, and Acinetobacter have been found in drinking water distribution system biofilms ( Ford TE 1999; Simões et al. 2007b). An A. calcoaceticus strain isolated from drinking water was shown to form biofilms on stainless steel, copper, polypropylene, polyethylene and silicone ( Simões et al. 2007a). The promotion of biofilm formation by Acinetobacter may also be significant in harboring frank pathogens in the drinking water distribution system.
Selected studies on susceptibility to disinfection are summarized in the following:
Despite their ubiquitous presence in water, little information is available on the survival of Acinetobacter in water. Generally, Acinetobacter is resistant to desiccation, can grow on a broad spectrum of substrates, and form biofilms ( Dijkshoorn et al. 2007). Acinetobacter spp. were reported to survive for up to 6 days on dry filter paper ( Bergogne-Berezin and Towner 1996). Furthermore, A. baumannii was shown to survive for approximately 27 days on a dry glass cover slip ( Jawad et al. 1998a). Acinetobacter have also been shown capable of long term survival on hospital equipment including tap water faucets, ventilators, and bedside urinals, beds, and pillows ( Villegas and Hartstein 2003). Survival in the drinking water distribution system might be enhanced by the ability of Acinetobacter to form biofilms (section on susceptibility to disinfection).
The infectious dose of Acinetobacter spp. in humans is unknown, but these bacteria are generally considered low virulence. However, Acinetobacter are increasingly being associated with hospital-acquired infections. A. baumannii has a 50% lethal dose of 106-108 cells when inoculated intraperitoneally in neutropenic mice ( Bergogne-Berezin and Towner 1996). Results from Eveillard et al. 2010 show that virulence can vary greatly between strains of A. baumannii. Some factors that are associated with virulent strains of Acinetobacter include the presence of a capsule, adhesion to human epithelial cells, production of lipid degrading enzymes, the presence of lipid A and the production of the outer membrane protein OmpA ( Bergogne-Berezin and Towner 1996; Stewart and Rochelle 2006; Gaddy et al. 2009).
Molecular methods specifically for the detection of Acinetobacter in drinking water systems are non-existent. The majority of molecular methods available are used to distinguish and track epidemic outbreaks of the Acinetobacter calcoaceticus - Acinetobacer baumanni complex in clinical settings. These techniques include: pulsed-field gel electrophoresis (PFGE) ( Seifert et al. 2005), Ribotyping ( Gerner-Smidt P 1992; Seifert and Gerner-Smidt 1995), AFLP( Dijkshoorn et al. 1996), amplified ribosomal DNA restriction analysis (ARDRA) and restriction fragment length polymorphism (RFLP) ( Jawad et al. 1998b), tRNA spacer fingerprinting ( Wiedmann-al-Ahmad et al. 1994; Ehrenstein et al. 1996), 16S-23S spacer fingerprinting ( Chang et al. 2005), repetitive extragenic palindromic sequence-based PCR (REP-PCR) ( Snelling et al. 1996). An excellent summary of these techniques is provided in the recent book Acinetobacter Molecular Biology ( Dijkshoorn and Nemec 2008; Seifert and Wisplinghoff 2008).
Some of the following molecular methods developed may be adaptable for application to drinking water monitoring:
The following pictures are part of the Public Health Image Library (PHIL) from the Centers for Disease Control and Prevention (CDC). The photos are in the public domain and thus free of copyright restrictions. We would like to express our appreciation for providing these images.
This SEM depicts a number of clusters of aerobic Gram-negative, non-motile Acinetobacter baumannii bacteria under a relatively low magnification of 1,546x.
Photo ID: 10096
Content provider(s): Centers for Disease Control and Prevention/ Janice Haney Carr
This SEM depicts a highly magnified cluster of Gram-negative, non-motile Acinetobacter baumannii bacteria; Mag - 27600x.
Photo ID: 10095
Content provider(s): Centers for Disease Control and Prevention/ Matthew J. Arduino
This SEM depicts a highly magnified triad of Gram-negative, non-motile Acinetobacter baumannii bacteria; Mag - 24730x.
Photo ID: 6499
Content provider(s): Centers for Disease Control and Prevention/ Matthew J. Arduino, DRPH; Janice Carr; Jana Swenson
Links to useful external sites can be found in the following:
Centers for Disease Control and Prevention
Johns Hopkins Medicine
|Last Updated on Tuesday, 20 September 2011 13:30|