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Comparative Genomics of Multidrug Resistance in Acinetobacter baumannii

Posted by PLOS_Genetics on 20 Feb 2008 at 11:08 GMT

Originally submitted as a Reader Response by Lenie Dijkshoorn ( on 2 August 2006 (additional authors: Mario Vaneechoutte, Harald Seifert, and Alexandr Nemec):

The landmark paper by Fournier et al. in the January 2006 issue of PLoS Genetics [1] provides new insights into the molecular basis of antibiotic resistance of Acinetobacter baumannii. Unfortunately, there were some common misconceptions involving the genus Acinetobacter in the report we would like to clarify.

First, the assumption [1] that A. baumannii is common in water and soil dates from the old literature [2], when the genus Acinetobacter had not yet been split up into species, and it therefore only applies to unspecified Acinetobacter strains. A. baumannii was first described in 1986, and to date, the genus comprises more than 30 named and unnamed genomic species [3]. Accurate phenotypic identification of these species is cumbersome or impossible. Identification by 16S rDNA sequencing is also problematic since different species exhibit high similarity values. Restriction digestion of the amplified 16S rDNA (ARDRA) and AFLP analysis are the only well-validated genotypic identification methods [4,5] for Acinetobacter species, but these are not widely used. It is of note that the soil organism Acinetobacter calcoaceticus, and the three clinically important species A. baumannii, unnamed genomic species 3, and 13TU cannot be reliably differentiated from each other phenotypically and are therefore sometimes referred to as a group - the A. calcoaceticus-A. baumannii (ACB) complex [6]. Thus, in most reports, Acinetobacter species names have to be interpreted with caution, and strains have to be referred to as Acinetobacter spp. or as belonging to the ACB complex if not identified by methods permitting identification according to the current taxonomy. To date, there is little information on the occurrence of A. baumannii in the natural environment. Although A. baumannii is an important nosocomial pathogen, it is not a common member of the normal human microflora [7,8], it is rarely if at all found in soil and water, and its natural reservoir remains to be determined.

A second comment on the paper [1] relates to the statement that A. baumannii was susceptible to most antibiotics in the 1970s. Since A. baumannii was not described before 1986, this statement cannot be made unless supported by studies testing susceptibilities of historic, well-identified strains, which to our knowledge have not yet been performed.

Third, the information on the genes identified by sequencing as listed in Table 3 [1] contains a few inaccuracies. APH(3')-Ia aminoglycoside-phosphotransferase encoded by aphA1 inactivates kanamycin but not, as stated [1], amikacin. Furthermore, the assertion that aphA1 and aac6' have not previously been described in Acinetobacter species is not correct. The aphA1 gene is one of the most prevalent aminoglyside-resistance genes in A. baumannii and many variants of the aac(6')-I genes have been identified among Acinetobacter spp. [9,10].

1. Fournier PE, et al. (2006) PLoS Genet. 2: DOI:10.1371/journal.pgen.0020007
2. P Baumann (1968). J Bacteriol 96:39-42
3. Nemec A, et al. (2003) Int J Syst Evol Microbiol. 53:1563-1567
4. Dijkshoorn L, et al. (1998) Syst Appl Microbiol 21:33-39
5. Nemec A, et al. (2001) Int J Syst Evol Microbiol. 51:1891-1899
6. Gerner-Smidt P, et al. (1991) J Clin Microbiol 29:277-282
7. Seifert H, et al. (1997) J Clin Microbiol 35:2819-2825
8. Dijkshoorn L, et al. (2005) Clin Microbiol Infect 11:329-332
9. Shaw KJ, et al. (1993) Microbiol Rev 57: 138-163
10. Nemec A, et al. (2004) J Med Microbiol 53: 1233-1240