Clonality and resistance features of Acinetobacter baumannii isolates: Comparison of ICU and burn-ward isolates

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Letter to the Editor

Clonality and resistance features of Acinetobacter baumannii isolates: Comparison of ICU and burnward isolates Dear Sir, Acinetobacter baumannii has been perpetually evolving to either acquire or upregulate antibiotic resistance and thus has attained the reputation for being one of the most troublesome pathogens in health care settings, particularly in immunosuppressed patients and those admitted to intensive care units (ICU) and burn wards [1]. The organism’s propensity toward multidrug resistance and its extensive or pan-drug resistance has halted all possibilities of development of empirical treatments. In this era of therapeutic limitations, the present study attempted to assess the activity of ceftazidime, cefotaxime, imipenem, ciprofloxacin, ofloxacin, and tetracycline against 75 isolates of A. baumannii obtained from ICU (n=47) and burn-ward (n=28) patients using the agar dilution method. In addition, the susceptibilities of the isolates toward gentamicin, amikacin, kanamycin, tobramycin, rifampicin, colistin, and tigecycline were determined using E-test strips (Liofilchem, Italy). The expression level of AdeABC efflux pump and the presence of aacA4, aacC1, aacC2, aadA1, aadB, aphA1, and aphA6 was assessed at a molecular level [2,3]. Clonal relatedness of the isolates was determined using trilocus sequence typing (3-LST) [4]. Antimicrobial susceptibility testing disclosed that all A. baumannii isolates in both groups (ICU and burn wards) were multidrug resistant. With the exception of one isolate from ICU, which showed susceptibility toward imipenem (MIC=2 mg/ml), tetracycline (MIC=8 mg/ml), and ciprofloxacin (MIC=1 mg/ml), all other isolates showed nonsusceptibility to ceftazidime (MIC50 >128 mg/ml), cefotaxime (MIC50 >256 mg/ ml), ofloxacine (MIC50 >32 mg/ml), imipenem (MIC50 >32 mg/ ml), tetracycline (MIC50 >64 mg/ml), and ciprofloxacin (MIC50 >64 mg/ml). Among the ICU isolates, tobramycin was the most active aminoglycoside, with a resistance rate of 59.5%, whereas kanamycin showed the least activity, with MIC50 of >256 mg/ml and resistance rate of 91.4%. Amikacin

resistance was recorded in 74.4% of the isolates, which was higher than that recorded for gentamicin (72.3%). However, the MIC50 of amikacin was calculated as 96 mg/ml, whereas that of gentamicin was 256 mg/ml. In the burn-ward isolates, resistance to tobramycin, kanamycin, amikacin, and gentamicin was recorded as 67.8%, 100%, 92.8%, and 71.4%, respectively (all with MIC50 >256 mg/ml). All the isolates in both the groups were susceptible to colistin (MIC50 =1 mg/ml) and tigecycline (MIC50 of 0.19 and 0.5 mg/ml in the ICU and burn-ward isolates, respectively). Similar observation was noted for rifampicin, with all isolates being susceptible, with the exception of three isolates from ICU (MICs of 4–8 mg/ml). The frequency of aphA6, aadB, aacC1, and aacA4 in A. baumannii was more in the burn-ward isolates than in the ICU isolates: 85.7% vs. 53.1%, 64.2% vs. 25.5%, 71.4% vs. 40.4%, and 35.7% vs. 25.5%, respectively. In contrast, the frequency of aadA1, aphA1, and aacC2 in the ICU isolates was more than that in the burn-ward isolates: 29.7% vs. 21.4%, 23.4% vs. 3.5%, and 10.6% vs. 3.5%, respectively. These differences were statistically significant in the case of aacC1, aphA6, aadB, and aphA1 (p<0.05). Real-time experiments showed the overexpression of adeB in 51% of the ICU isolates and 42.8% of the burn-ward isolates. Clonal typing of the isolates with 3-LST revealed that 48.9% of the ICU isolates and 46.4% of the burn-ward isolates belonged to international clone (IC) II and I, respectively (Table 1). When the clones were compared, enhanced expression of adeB was evident among IC II in ICU and IC I in the burn-ward isolates. In addition, the MIC50 of all the tested antibiotics were lower in IC I, particularly those from ICU, in comparison to other clones. Overall, the results showed the dominant presence of different clones of A. baumannii in ICU compared to burn wards, which in return influenced the phenotypic and genotypic features of A. baumannii in these wards.

Please cite this article in press as: A. Hasani, et al., Clonality and resistance features of Acinetobacter baumannii isolates: Comparison of ICU and burn-ward isolates, Burns (2017), http://dx.doi.org/10.1016/j.burns.2016.12.002

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<1:3 >1:2

<1:3

1 0.5

aphA6, aadB

0.5 0.5

aacC1, aadB, aphA6

>1:1 1 0.5

aacC1, aphA6

0.5 0.5

aphA6, aacC1, aacA4

>1:2

<1:2

<1:6 >1:7

<1:3 0.5 0.5

aphA6, aadB, aacC1

0.5 0.12

aphA6, aacC1, aadB

>1:0

>1:4

<1:4

<1:7 >1:14 aphA6, aacC1, aphA1, aadB 0.5 0.19

aadA1, aphA6, aacA4 0.38 0.19

[1] Peleg AY, Seifert H, Paterson DL. Acinetobacter baumannii: emergence of a successful pathogen. Clin Microbiol Rev 2008;21:538–82. [2] Noppe-Leclercq I, Wallet F, Haentjens S, Courcol R, Simonet M. PCR detection of aminoglycoside resistance genes: a rapid molecular typing method for Acinetobacter baumannii. Res Microbiol 1999;150:317–22. [3] Peleg AY, Adams J, Paterson DL. Tigecycline efflux as a mechanism for nonsusceptibility in Acinetobacter baumannii. Antimicrob Agents Chemother 2007;51:2065–9. [4] Turton J, Gabriel S, Valderrey C, Kaufmann M, Pitt T. Use of sequence-based typing and multiplex PCR to identify clonal lineages of outbreak strains of Acinetobacter baumannii. Clin Microbiol Infect 2007;13:807–15.

Alka Hasania,b Vajihe Sheikhalizadeha,b,* a Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

2

2

0.5

2

1

2

1

1

1

1

1.5 1 256 256 256 256 256 256 256 ND (n = 5)

256

1 256 256 256 256 256 256 256 IC III (n =7)

256

1 128 128 256 256 256 256 256 IC II (n = 3)

256

0.75 256 2 256 256 24 256 4

Department of Medical Microbiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Mohammad Ahangarzadeh Rezaee Department of Medical Microbiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran Hamid Reza Goli Department of Medical Microbiology and Virology, Mazandaran University of Medical Sciences, Sari, Iran

Akbar Hasani Department of Clinical Biochemistry and Laboratory Sciences, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran * Corresponding author at: Immunology Research Center and Department of Medical Microbiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Fax: +98 411 3364661. E-mail address: [email protected] (V. Sheikhalizadeh). Available online xxx http://dx.doi.org/10.1016/j.burns.2016.12.002 © 2016 Elsevier Ltd and ISBI. All rights reserved.

Burn (n =28)

256 256 256 256 256 ND (n = 7)

256 256 256 256 256 IC III (n =4)

256 256 256 256 256 IC II (n = 23)

256 48 12 3 IC I (n = 13)

16

IC I (n = 13)

256

1 256 256

256

2

6

2 1 1 128 256

256

1

2 1.5 2 1 128 256

256

2

2 1 1 256

2

0.5

1

2

b

ICU (n =47)

MIC50 MIC90 MIC50 MIC90 MIC50 MIC90 MIC50 MIC90 MIC50 MIC90 MIC50 MIC90 MIC50 MIC90

TIG RIF COL TOB KN AMK GEN IC (No.) Source ward

Table 1 – AME profile, MIC, and expression level of adeB among different clones of ICU and burn ward A. baumannii.

Predominant AMEs

>1:6

<1:7

Expression level of adeB

REFERENCES

Please cite this article in press as: A. Hasani, et al., Clonality and resistance features of Acinetobacter baumannii isolates: Comparison of ICU and burn-ward isolates, Burns (2017), http://dx.doi.org/10.1016/j.burns.2016.12.002