Acinetobacter baumannii

Biology

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).
 

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Symptoms/Effects

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).

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Informations techniques

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

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Afzal-Shah,M. and Livermore,D.M. (1998) Worldwide emergence of carbapenem-resistant Acinetobacter spp. J Antimicrob. Chemother. 41, 576-577.

Aygun,G., Demirkiran,O., Utku,T., Mete,B., Urkmez,S., Yilmaz,M., Yasar,H., Dikmen,Y. and Ozturk,R. (2002) Environmental contamination during a carbapenem-resistant Acinetobacter baumannii outbreak in an intensive care unit. J Hosp. Infect 52, 259-262.

Bhalla,A., Pultz,N.J., Gries,D.M., Ray,A.J., Eckstein,E.C., Aron,D.C. and Donskey,C.J. (2004) Acquisition of nosocomial pathogens on hands after contact with environmental surfaces near hospitalized patients. Infect Control Hosp. Epidemiol. 25, 164-167.

Boyce,J.M. and Pittet,D. (2002) Guideline for Hand Hygiene in Health-Care Settings: recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force. Infect Control Hosp. Epidemiol. 23, S3-40.

Bureau-Chalot,F., Drieux,L., Pierrat-Solans,C., Forte,D., de,C.C. and Bajolet,O. (2004) Blood pressure cuffs as potential reservoirs of extended-spectrum beta-lactamase VEB-1-producing isolates of Acinetobacter baumannii. J Hosp. Infect 58, 91-92.

Catalano,M., Quelle,L.S., Jeric,P.E., Di,M.A. and Maimone,S.M. (1999) Survival of Acinetobacter baumannii on bed rails during an outbreak and during sporadic cases. J Hosp. Infect 42, 27-35.

Coelho,J., Woodford,N., Turton,J. and Livermore,D.M. (2004) Multiresistant acinetobacter in the UK: how big a threat? J Hosp. Infect 58, 167-169.

Das,I., Lambert,P., Hill,D., Noy,M., Bion,J. and Elliott,T. (2002) Carbapenem-resistant Acinetobacter and role of curtains in an outbreak in intensive care units. J Hosp. Infect 50, 110-114.

Denton,M., Wilcox,M.H., Parnell,P., Green,D., Keer,V., Hawkey,P.M., Evans,I. and Murphy,P. (2004) Role of environmental cleaning in controlling an outbreak of Acinetobacter baumannii on a neurosurgical intensive care unit. J Hosp. Infect 56, 106-110.

Gaynes,R. and Edwards,J.R. (2005) Overview of nosocomial infections caused by gram-negative bacilli. Clin Infect Dis 41, 848-854.

Gerner-Smidt,P. (1992) Ribotyping of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex. J Clin Microbiol. 30, 2680-2685.

Getchell-White,S.I., Donowitz,L.G. and Groschel,D.H. (1989) The inanimate environment of an intensive care unit as a potential source of nosocomial bacteria: evidence for long survival of Acinetobacter calcoaceticus. Infect Control Hosp. Epidemiol. 10, 402-407.

Health Protection Agency (2004) Acinetobacter spp bacteraemia, England, Wales and Northern Ireland. CDR Weekly 14, 1-5.

Henwood,C.J., Gatward,T., Warner,M., James,D., Stockdale,M.W., Spence,R.P., Towner,K.J., Livermore,D.M. and Woodford,N. (2002) Antibiotic resistance among clinical isolates of Acinetobacter in the UK, and in vitro evaluation of tigecycline (GAR-936). J Antimicrob. Chemother. 49, 479-487.

Houang,E.T., Chu,Y.W., Leung,C.M., Chu,K.Y., Berlau,J., Ng,K.C. and Cheng,A.F. (2001) Epidemiology and infection control implications of Acinetobacter spp. in Hong Kong. J Clin Microbiol 39, 228-234.

Joly-Guillou,M.L. (2005) Clinical impact and pathogenicity of Acinetobacter. Clin Microbiol Infect 11, 868-873.

Landman,D., Quale,J.M., Mayorga,D., Adedeji,A., Vangala,K., Ravishankar,J., Flores,C. and Brooks,S. (2002) Citywide clonal outbreak of multiresistant Acinetobacter baumannii and Pseudomonas aeruginosa in Brooklyn, NY: the preantibiotic era has returned. Arch Intern Med 162, 1515-1520.

Livermore,D.M. (2002) The impact of carbapenemases on antimicrobial development and therapy. Curr. Opin. Investig. Drugs 3, 218-224.

Motaouakkil,S., Charra,B., Hachimi,A., Nejmi,H., Benslama,A., Elmdaghri,N., Belabbes,H. and Benbachir,M. (2006) Colistin and rifampicin in the treatment of nosocomial infections from multiresistant Acinetobacter baumannii. J Infect.

Seifert,H. (2005) Acinetobacter - What is the global epidemiology? Interscience Conference for Antimicrobial Agents and Chemotherapy, Washington DC.

Turton,J.F., Kaufmann,M.E., Warner,M., Coelho,J., Dijkshoorn,L., van der,R.T. and Pitt,T.L. (2004) A prevalent, multiresistant clone of Acinetobacter baumannii in Southeast England. J Hosp. Infect 58, 170-179.

van,D.H., Dijkshoorn,L., van der,R.T., Bakker,N., Paauw,A., van den,B.P., Verhoef,J. and Brisse,S. (2004) Identification of a new geographically widespread multiresistant Acinetobacter baumannii clone from European hospitals. Res. Microbiol 155, 105-112.

Wagenvoort,J.H. and Joosten,E.J. (2002) An outbreak Acinetobacter baumannii that mimics MRSA in its environmental longevity. J Hosp. Infect 52, 226-227.

Walther-Rasmussen,J. and Hoiby,N. (2006) OXA-type carbapenemases. Journal of Antimicrobial Chemotherapy 57, 373-383.
 

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