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Press Release: Bioquell invests for future growth
Automated filling and capping systems Ten steps to preventing infection in hospitals... Award by the NHS Purchasing and Supply Agency to BIOQUELL DoH & PASA Publish report on Success of BIOQUELL System in Showcase Hospital Programme BIOQUELL assist with clean up BIOQUELL Launch new Clarus L2 HPV Generator Briefing on the outbreak of Swine Influenza Virus BIOQUELL takes top prize at the Department of Health HCAI Technology Innovation Summit BBC News Films 'New Weapons Against Hospital Bugs' at Lewisham Hospital Department of Health Press Release Robot set to tackle killer hospital bugs BIOQUELL moves to newly renovated production facility Infection Control & Hospital Epidemiology Article - Impact of Hydrogen Peroxide Vapor Room Decontamination on Clostridium difficile... BIOQUELL technology showcased in seven NHS hospitals Best foot forward for cleaner hospitals East Sussex Hospitals NHS Trust Commence Deployment of RBDS Proactive Team Gloucestershire Hospitals NHS Foundation Trust are the first UK hospital to deploy a BIOQUELL Proactive team. "Hydrogen Peroxide Vapor can control Nosocomial MRSA Outbreak" - Clinical Infectious Diseases Article Rapid Review Panel upgrades BIOQUELL technology to Level One Status Department of Health Post BIOQUELL Case Studies as "Best Practice" on website Award of Joint Material Decontamination System (US military) sub-contract Deep Cleaning Service from BIOQUELL Category III decontamination service launched |
Acinetobacter baumannii Name: Acinetobacter baumannii Also known as: A. baumannii, A. calcoaceticus¡Vbaumannii complex Industry of interest: Healthcare Classification: Bacterium Microbiology: Acinetobacter sp. is an oxidase-negative, non-fermentative, Gram-negative rod, which commonly occurs in soil and can be an opportunist pathogen in man. The taxonomy of Acinetobacter is complex because considerable heterogeneity exists within the genus but the predominant species of medical importance are from the A. calcoaceticus¡Vbaumannii complex, which contains four distinct species including A. baumannii (Gerner-Smidt 1992). Acinetobacter spp. have progressively acquired resistance to many antibiotics. Consequently the carbapenems have become the therapy of choice for serious Acinetobacter sp. infection (Coelho et al. 2004;Henwood et al. 2002). Carbapenem-resistance has recently emerged in resistant strains, meaning that old antibiotics with reduced efficacy and increased side effects, such as colistin, have to be used to treat serious Acinetobacer sp. infection (Coelho et al. 2004). Carbapenen resistance can be conferred by several beta-lactam-dependant mechanisms including class D carbapenemases such as OXA-23 and -24 and class B carbapenemases such as IMP and VIM (Coelho et al. 2004;Livermore 2002;Walther-Rasmussen and Hoiby 2006). Beta-lactam-independent mechanisms are less commonly reported, possibility partially due to technical difficulties associated with identifying beta-lactam-independent carbapenem-resistance (Coelho et al. 2004). Importance: Acinetobacter spp. are rarely implicated as a cause of disease in healthy individuals. For this reason, Acinetobacter sp. isolated from clinical specimens was largely ignored until the 1970s when diseases caused by Acinetobacter spp. became increasing recognised (Joly-Guillou 2005). A. baumannii is the key species clinically. The diseases caused by A. baumannii are relatively low-grade compared to other nosocomial pathogens, such as MRSA, and are largely restricted to severely ill patients in critical care environments. In these environments, A. baumannii can cause pneumonia, tracheobronchitis, bloodstream infections, urinary tract infections, cathether-related infections and rarely wound infections (Joly-Guillou 2005). In tropical climates Acinetobacter sp. can cause severe community-acquired pneumonia (Houang et al. 2001). Although the infections caused by A. baumannii are typically low-grade, due to the severely ill nature of the patient affected, crude mortality is high typically ranging from 20-60% and attributable mortality is approximately 10-20%, though these mortality figures are hotly debated (Joly-Guillou 2005). Global prevalence: Acinetobacter spp. were responsible for 6.9% of pneumonias, 2.4% of bloodstream infections, 2.1% of surgical site infections and 1.6% of urinary tract infections in intensive care units across the USA in 2003 (2004). The prevalence of Acinetobacter spp. infections in on the increase. In the UK, the number of cases of Acinetobacter spp. bacteraemia increased by 6% to 1087 in 2003 compared to 2002 (Health Protection Agency 2004). Equally concerning is the greater than 300% increase in reports of multidrug-resistant (MDR) Acinetobacter sp. bacteraemia from 7 to 22 in the UK in 2003 compared to 2002 (Health Protection Agency 2004). In the USA, the proportion of Acinetobacter ICU pneumonia increased from 4% in 1986 to 7% in 2003 (Gaynes and Edwards 2005). Carbapenem resistance is also increasing in the USA, with the rate of resistance increasing from 1.8% in 1996 to 7.3% in 2002 and a further 6.2% showing intermediate resistance by 2002 (Coelho et al. 2004). There has been a recent increase in the number of reports of MDR-Acinetobacter sp. outbreaks from around the world (Afzal-Shah and Livermore 1998). Clonal outbreaks of MDR-Acinetobacter have been reported from, for example, the UK (Turton et al. 2004), other European countries (van et al. 2004) and the USA (Landman et al. 2002) (figure 1). Figure 1: Countries that have reported hospital outbreaks of carbapenem-resistant Acinetobacter highlighted in red, adapted from (Seifert 2005)
Treatment and control methods: Similarities exist between the epidemiology and transmission of Acinetobacter sp. and MRSA despite important differences in microbiology and disease severity (Joly-Guillou 2005). Both micro-organisms can be skin commensals and cause asymptomatic colonisation and both have the ability to survive and persist on environmental surfaces. Therefore, control measures for of Acinetobacter sp. are similar to those used to control MRSA, except that the at-risk patient group for Acinetobacter spp. is confined largely to those patients on critical care. For this reason, screening for Acinetobacter spp. colonisation is usually only conducted in critical care settings. Therefore, hand-hygiene, prompt identification and isolation of infected or colonised patients and stringent environmental hygiene are necessary for the effective control of Acinetobacter spp. (Boyce and Pittet 2002) Many studies have demonstrated the importance of the environmental reservoir for the successful control of Acinetobacter sp., especially during epidemics (Catalano et al. 1999;Denton et al. 2004;Getchell-White et al. 1989). One recent study from a team in Leeds demonstrated that there was statistically significant correlation between A. baumannii infection rates and A. baumannii environmental contamination over a 14-month period on a neurosurgical ICU (Denton et al. 2004). The same study demonstrated that failure to maintain low levels of environmental contamination resulted in increases in patient acquisition of A. baumannii, suggesting that the contamination is the cause rather than the effect of the acquisition of A. baumannii infection or colonisation. Outbreaks of Acinetobacter are reported commonly and are notoriously difficult to control. This has been attributed to the persistence of the outbreak strain on environmental surfaces resulting in continuation of the outbreak from an environmental reservoir (Aygun et al. 2002;Das et al. 2002). Front-line antibiotic therapy for Acinetobacter spp. infections are the carbapenems. If the strain is resistant to carbapenems, colistin and other older, less effective antibiotics are often the only alternative (Motaouakkil et al. 2006). Environmental survival: Acinetobacter spp. are routinely cultured from environmental surfaces in hospitals, especially during outbreaks. Acinetobacter sp. has been cultured from bed-rails, blood-pressure cuffs and many other items of furniture (2005;Bureau-Chalot et al. 2004;Catalano et al. 1999;Denton et al. 2004). Clinically significant species of Acinetobacter sp. are capable of long-term survival when dried onto environmental surfaces. Several studies have found that A. baumannii can survive dried onto surfaces at ambient temperature and relative humidity for many months (Getchell-White et al. 1989;Wagenvoort and Joosten 2002). Other studies have shown that Gram-negative rods such as Acinetobacter spp. can be transferred from contaminated surfaces to the hands of healthcare workers, hence representing a risk for indirect transmission (Bhalla et al. 2004). Role of BIOQUELL: Environmental hygiene is critical for the control of Acinetobacter spp., especially during epidemics, and Acinetobacter sp. persists despite terminal cleaning (Denton et al. 2004). BIOQUELL¡¦s technology has been applied in several hospitals for the eradication of Acinetobacter sp. environmental contamination and subsequent cessation of epidemics. For example, one French teaching hospital experienced an outbreak of MDR-Acinetobacter contamination in an Intensive Care Unit (ICU). Extensive bio-burden, including the Acinetobacter sp. outbreak strain, was discovered in the unit. BIOQUELL's Room Bio-Decontamination Service (RBDS) was used to bio-decontaminate the unit. No Acinetobacter sp. was recovered from the environment and no further patient acquisition occurred following the process. RBDS has been re-deployed twice by the same hospital to combat a similar problem in another ICU. Similar deployments have occurred in several large London ICUs. There is therefore evidence suggesting that RBDS combined with stringent infection control measures can be applied to control epidemics of Acinetobacter sp. in critical care units. Further research is required to investigate whether RBDS can be applied to reduce the levels of endemic Acineotbacter sp. infection. References (2004) National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, issued October 2004. Am. J Infect Control 32, 470-485. Joly-Guillou,M.L. (2005) Clinical impact and pathogenicity of Acinetobacter. Clin Microbiol Infect 11, 868-873. 
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