Acinetobacter

Acinetobacter (a-sin-EE-toe-bak-ter) is a genus of Gram-negative bacteria belonging to the wider class of Gammaproteobacteria. Acinetobacter species are not motile and oxidase-negative, and occur in pairs under magnification.

They are important soil organisms, where they contribute to the mineralization of, for example, aromatic compounds. Acinetobacter species are a key source of infection in debilitated patients in the hospital, in particular the species Acinetobacter baumannii.

Etymology

Acinetobacter is a compound word from scientific Greek [α + κίνητο + βακτηρ(ία)], meaning 'nonmotile rod'. The first element acineto- is a somewhat baroque rendering of the Greek morpheme ακίνητο-; the more common transliteration in English is akineto-, as in akinetic. Identification of Acinetobacter species is complicated by lack of standard identification techniques. Initially, identification was based on phenotypic characteristics such as growth temperature, colony morphology, growth medium, carbon sources, gelatin hydrolysis, glucose fermentation, among others. This method allowed identification of A. calcoaceticus–A. baumannii complex by the formation of smooth, rounded, mucoid colonies at 37°C. But closely related species could not be differentiated and individual species like A. baumannii and Acinetobacter genomic species 3 could not be positively identified phenotypically.

Description

Species of the genus Acinetobacter are strictly aerobic, nonfermentative, Gram-negative bacilli. They show preponderantly a coccobacillary morphology on nonselective agar. Rods predominate in fluid media, especially during early growth.

The morphology of Acinetobacter species can be quite variable in Gram-stained human clinical specimens, and cannot be used to differentiate Acinetobacter from other common causes of infection.

Most strains of Acinetobacter, except some of the A. lwoffii strain, grow well on MacConkey agar (without salt). Although officially classified as not lactose-fermenting, they are often partially lactose-fermenting when grown on MacConkey agar. They are oxidase-negative, nonmotile, and usually nitrate-negative.

Bacteria of the genus Acinetobacter are known to form intracellular inclusions of polyhydroxyalkanoates under certain environmental conditions (e.g. lack of elements such as phosphorus, nitrogen, or oxygen combined with an excessive supply of carbon sources).

Taxonomy

The genus Acinetobacter comprises 27 validly named and 11 unnamed (genomic) species.[1]

However, because routine identification in the clinical microbiology laboratory is not (yet) possible, they are divided and grouped into three main complexes:

With the upcoming of new method in taxonomy such as 16S rDNA sequencing, MALDI, and whole genome sequencing, the identification is clearer for the Acinetobacter genus.

Identification

Different species of bacteria in this genus can be identified using fluorescence-lactose-denitrification to find the amount of acid produced by metabolism of glucose. The other reliable identification test at genus level is chromosomal DNA transformation assay. In this assay, a naturally competent tryptophan auxotrophic mutant of Acinetobacter baylyi (BD4 trpE27) is transformed with the total DNA of a putative Acinetobacter isolate and the transformation mixture is plated on a brain heart infusion agar. The growth is then harvested after incubation for 24 h at 30 °C, plating on an Acinetobacter minimal agar (AMA), and incubating at 30 °C for 108 h. Growth on the AMA indicates a positive transformation assay and confirms the isolate as a member of the genus Acinetobacter. E. coli HB101 and A. calcoaceticus MTCC1921T can be used as the negative and positive controls, respectively.[2]

Some of the molecular methods used in species identification are repetitive extragenic palindromic sequence-based PCR, ribotyping, pulsed field gel electrophoresis (PFGE), random amplified polymorphic DNA, amplified fragment length polymorphism (AFLP), restriction and sequence analysis of tRNA and 16S-23S rRNA gene spacers and amplified 16S ribosomal DNA restriction analysis (ARDRA) [1]. PFGE, AFLP and ARDRA are validated common methods in use today because of their discriminative ability [2,3]. However, most recent methods include multilocus sequence typing and multilocus PCR and electrospray ionization mass spectrometry, which are based on amplification of highly conserved housekeeping genes and can be used to study the genetic relatedness between different isolates.[3]

Habitat

Acinetobacter species are widely distributed in nature, and commonly occur in soil. They can survive on moist and dry surfaces, including in a hospital environment. Some strains have been isolated from foodstuffs. In drinking water, they have been shown to aggregate bacteria that otherwise do not form aggregates.

Pathology

In healthy individuals, Acinetobacter colonies on the skin correlate with low incidence of allergies;[4] Acinetobacter is thought to be allergy-protective.[5]

A. baumannii is the second most commonly isolated nonfermenting bacterium in humans.

In immunocompromised individuals, several Acinetobacter species can cause life-threatening infections. Such species also exhibit a relatively broad degree of antibiotic resistance.

Acinetobacter is frequently isolated in nosocomial infections, and is especially prevalent in intensive care units, where both sporadic cases and epidemic and endemic occurrences are common. A. baumannii is a frequent cause of nosocomial pneumonia, especially of 'late-onset' ventilator-associated pneumonia. It can cause various other infections, including skin and wound infections, bacteremia, and meningitis, but A. lwoffi is mostly responsible for the latter. A. baumannii can survive on the human skin or dry surfaces for weeks.

Epidemiologic evidence indicates Acinetobacter biofilms play a role in infectious diseases such as periodontitis, bloodstream infections, and urinary tract infections, because of the bacteria's ability to colonize indwelling medical devices (such as catheters). Antibiotic resistance markers are often plasmid-borne, and plasmids present in Acinetobacter strains can be transferred to other pathogenic bacteria by horizontal gene transfer. The ability of Acinetobacter species to adhere to surfaces, to form biofilms, and to display antibiotic resistance and gene transfer motivates research into the factors responsible for their spread.[6]

Since the start of the Iraq War, more than 700 U.S. soldiers have been infected with A. baumannii. Four civilians undergoing treatment for serious illnesses at Walter Reed Army Medical Center in Washington, D.C., contracted A. baumannii infections and died. At Landstuhl Regional Medical Center, a U.S. military hospital in Germany, another civilian under treatment, a 63-year-old German woman contracted the same strain of A. baumannii infecting troops in the facility and also died. These infections appear to have been hospital-acquired. Based on genotyping of A. baumannii cultured from patients prior to the start of the Iraq War, the soldiers likely contracted the infections while hospitalized for treatment in Europe. The ability of the pathogen to cause infection is determined by the production of virulence factors. These factors enable the pathogen to reach and colonize the site of infection, obtain nutrients from the host, evade or fight the host immune response, cause damage to the host cells and spread throughout the host – as well as from one host to another. Virulence determinants have been described as multifactorial and multidimensional involving efficient regulation of the various factors with respect to time as well as the site of secretion.[7]

Clinical significance

A. baumannii is an important pathogen implicated in a number of hospital-acquired infections such as bacteremia, urinary tract infections (UTIs), secondary meningitis, infective endocarditis, and wound and burn infections.[8] However, it has gained notoriety because of its involvement with ventilator-associated nosocomial pneumonia. Its clinical significance is further enhanced by its capacity to develop resistance determinants against the array of all the available antibiotics. Reports indicate that it possesses resistance against broad-spectrum cephalosporins, b-lactam agents, aminoglycosides and quinolones. Resistance to carbapenems is also being increasingly reported.[9]

A. baumannii infections are found to be concentrated in the ICU with elderly and immune-compromised patients serving as major victims. Infections may also prove to be fatal depending on the site of infection and level of the patient’s immunosuppression with general mortality rates ranging from 20% to 60%.[10]

With the advent of invasive procedures, artificial ventilation and resuscitation techniques, an increase in the incidence of nosocomial pneumonia caused by A. baumannii has been reported particularly among patients admitted to the ICU ward. Risk factors include long-term intubation and tracheal or lung aspiration. In most cases of ventilator-associated pneumonia (VAP), the equipment used for artificial ventilation such as endotracheal tubes or bronchoscopes serve as an exogenous source and result in the colonization of the lower respiratory tract by A. baumannii. A. baumannii has also been found to be the major reason for ICU-acquired bacteremia with mortality rates ranging from 32% to 52%, only slightly less than those for P. aeruginosa and Candida sp. blood infections.

Further, the prognosis for patients with bacteremic nosocomial pneumonia appears to be worse than that for patients with nonbacteraemic nosocomial pneumonia. UTIs caused by A. baumannii appear to be associated with continuous catheterization as well as antibiotic therapy. A. baumannii has also been reported to infect skin and soft tissue in traumatic injuries and post-surgical wounds. Findings indicate that A. baumannii commonly super-infects burns and may result in complications owing to difficulty in treatment and eradication. Though less common, there is also evidence linking this bacterium to meningitis, most often following invasive surgery, and in very rare cases, to community-acquired primary meningitis wherein the majority of the victims were children.[11] Case reports also link A. baumannii to endocarditis, keratitis, peritonitis and very rarely fatal neonatal sepsis.[12]

Treatment

Acinetobacter species are innately resistant to many classes of antibiotics, including penicillin, chloramphenicol, and often aminoglycosides. Resistance to fluoroquinolones has been reported during therapy, which has also resulted in increased resistance to other drug classes mediated through active drug efflux. A dramatic increase in antibiotic resistance in Acinetobacter strains has been reported by the CDC, and the carbapenems are recognised as the gold-standard and treatment of last resort.[13] Acinetobacter species are unusual in that they are sensitive to sulbactam; sulbactam is most commonly used to inhibit bacterial beta-lactamase, but this is an example of the antibacterial property of sulbactam itself.[14]

In November, 2004, the CDC reported an increasing number of A. baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated.[15] Most of these were multidrug-resistant. Among one set of isolates from Walter Reed Army Medical Center, 13 (35%) were susceptible to imipenem only, and two (4%) were resistant to all drugs tested. One antimicrobial agent, colistin (polymyxin E), has been used to treat infections with multidrug-resistant A. baumannii; however, antimicrobial susceptibility testing for colistin was not performed on isolates described in this report. Because A. baumannii can survive on dry surfaces for up to 20 days, they pose a high risk of spread and contamination in hospitals, potentially putting immunocompromised and other patients at risk for drug-resistant infections that are often fatal and, in general, expensive to treat.

Reports suggest this bacterium is susceptible to phage therapy.[16]

Gene-silencing antisense oligomers in a form called peptide-conjugated phosphorodiamidate morpholino oligomers have also been reported to inhibit growth in tests carried out in animals infected with antibiotic-resistant A. baumanii.[17][18]

Aseptic Technique

The frequency of nosocomial infections in British hospitals prompted the National Health Service (NHS) to research the effectiveness of anions for air purification, finding that repeated airborne acinetobacter infections in a ward were eliminated by the installation of a negative air ioniser—the infection rate fell to zero.[19]

Natural transformation

Bacterial transformation involves the transfer of DNA from a donor to a recipient bacterium through the intervening liquid medium. Recipient bacteria must first enter a special physiological state termed competence to receive donor DNA. A. calcoaceticus is induced to become competent for natural transformation by dilution of a stationary culture into fresh nutrient medium.[20] Competence is gradually lost during prolonged exponential growth and for a period after entrance into the stationary state. The DNA taken up may be used to repair DNA damage or as a means to exchange genetic information by horizontal gene transfer.[20] Natural transformation in A. calcoaceticus may protect against exposure to DNA-damaging conditions in the natural environment of these bacteria, as appears to be the case for other bacterial species capable of transformation.[21]

References

  1. ↑ Visca P, Seifert H, Towner KJ (December 2011). "Acinetobacter infection--an emerging threat to human health". IUBMB Life 63 (12): 1048–54. doi:10.1002/iub.534. PMID 22006724.
  2. ↑ Rokhbakhsh-Zamin, F.; Sachdev, D.P.; Kazemi-Pour, N.; Engineer, A.; Zinjarde, S.S.; Dhakephalkar, P.K.; Chopade, B.A. (2012). "Characterization of plant growth promoting traits of Acinetobacter species isolated from rhizosphere of Pennisetum glaucum". J Microbiol Biotechnol 21 (6): 556–566.
  3. ↑ Antibiotic resistance is a major risk factor for epidemic behavior of Acinetobacter baumannii. Infect Control Hosp Epidemiol 2001; 22:284–288.
  4. ↑ Hanski, I.; Von Hertzen, L.; Fyhrquist, N.; Koskinen, K.; Torppa, K.; Laatikainen, T.; Karisola, P.; Auvinen, P.; Paulin, L.; Makela, M. J.; Vartiainen, E.; Kosunen, T. U.; Alenius, H.; Haahtela, T. (2012). "Environmental biodiversity, human microbiota, and allergy are interrelated". Proceedings of the National Academy of Sciences 109 (21): 8334. doi:10.1073/pnas.1205624109.
  5. ↑ Debarry, J.; Hanuszkiewicz, A.; Stein, K.; Holst, O.; Heine, H. (2009). "The allergy-protective properties of Acinetobacter lwoffii F78 are imparted by its lipopolysaccharide". Allergy 65 (6): 690–697. doi:10.1111/j.1398-9995.2009.02253.x. PMID 19909295.
  6. ↑ Antunes, LC; Imperi, F; Carattoli, A; Visca, P (2011). "Deciphering the Multifactorial Nature of Acinetobacter baumannii Pathogenicity". PLOS ONE 6 (8): e22674. doi:10.1371/journal.pone.0022674.
  7. ↑ Wilson, J; Schurr, M; LeBlanc, C; Ramamurthy, R; Buchanan, K; Nickerson, C (2002). "Mechanisms of bacterial pathogenicity". Postgrad Med J 78: 216–224. doi:10.1136/pmj.78.918.216.
  8. ↑ Dent Lemuel L, Marshall DR, Pratap S, Hulette RB. Multidrug resistant Acinetobacter baumannii: a descriptive study in a city hospital" BMC Infect Dis 2010; 10:196.
  9. ↑ Hu, Q; Hu, Z; Li, J; Tian, B; Xu, H; Li, J (2006). "Detection of OXA-type carbapenemases and integrons among carbapenem-resistant Acinetobactor baumannii in a Teaching Hospital in China. J Basic Microbiol 2011; 51:467–472.Pierre Edouard F, Richet H. The epidemiology and control of Acinetobacter baumannii in healthcare facilities". Clin Infect Dis 42: 692–699.
  10. ↑ Falagas, ME; Koletsi, PK; Bliziotis, IA (2006). "The diversity of definitions of multidrug-resistant (MDR) and pandrug-resistant (PDR)Acinetobacter baumannii and Pseudomonas aeruginosa". J Med Microbiol 55: 1619–1629. doi:10.1099/jmm.0.46747-0.
  11. ↑ Siegman-Igra, Y; Bar-Yosef, S; Gorea, A; Avram, J (1993). "Nosocomial Acinetobacter meningitis secondary to invasive procedures: report of 25 cases and review". Clin Infect Dis 17: 843–849. doi:10.1093/clinids/17.5.843.
  12. ↑ Falagas, ME; Karveli, EA; Kelesidis, I; Kelesidis, T (2007). "Community acquired Acinetobacter infections". Eur J Clin Microbiol Infect Dis 26: 857–868. doi:10.1007/s10096-007-0365-6.
  13. ↑ Rahal J (2006). "Novel antibiotic combinations against infections with almost completely resistant Pseudomonas aeruginosa and Acinetobacter species". Clin Infect Dis. 43 Suppl 2: S95–9. doi:10.1086/504486. PMID 16894522.
  14. ↑ Wood GC, Hanes SD, Croce MA, Fabian TC, Bougher BA. (2002). "Comparison of ampicillin-sulbactam and imipenem-cilastin for the treatment of Acinetobacter ventilator-associated pneumonia". Clin Infect Dis 34 (11): 1425–30. doi:10.1086/340055. PMID 12015687.
  15. ↑ Centers for Disease Control and Prevention (CDC) (2004). "Acinetobacter baumannii infections among patients at military medical facilities treating injured U.S. service members, 2002-2004". MMWR Morb Mortal Wkly Rep 53 (45): 1063–6. PMID 15549020.
  16. ↑ Matsuzaki S, Rashel M, Uchiyama J et al. (October 2005). "Bacteriophage therapy: a revitalized therapy against bacterial infectious diseases". J. Infect. Chemother. 11 (5): 211–9. doi:10.1007/s10156-005-0408-9. PMID 16258815.
  17. ↑ Geller BL, Marshall-Batty K, Schnell FJ et al. (October 2013). "Gene-Silencing Antisense Oligomers Inhibit Acinetobacter Growth In Vitro and In Vivo. J. Infect. Diseases,".
  18. ↑ "Beyond antibiotics: PPMOs offer new approach to bacterial infection". 2013-10-15. Retrieved October 15, 2013.
  19. ↑ "Air ionizers wipe out hospital infections". The New Scientist. Retrieved 2006-08-30.
  20. ↑ 20.0 20.1 Palmen R, Vosman B, Buijsman P, Breek CK, Hellingwerf KJ (February 1993). "Physiological characterization of natural transformation in Acinetobacter calcoaceticus". J. Gen. Microbiol. 139 (2): 295–305. doi:10.1099/00221287-139-2-295. PMID 8436948.
  21. ↑ Michod RE, Bernstein H, Nedelcu AM (May 2008). "Adaptive value of sex in microbial pathogens". Infect. Genet. Evol. 8 (3): 267–85. doi:10.1016/j.meegid.2008.01.002. PMID 18295550.http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf

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