Contribution of the AbaI/AbaR Quorum Sensing System to Resistance and Virulence of Acinetobacter baumannii Clinical Strains

Figures & data

Table 1 Distribution of abaI and abaR Genes in 80 Clinical Isolates of A. baumannii

Genes	Positive Numbers	Positive Rates (n=80)
abaI^+	67	83.75%
abaR^+	63	78.75%
abaI^+ abaR^+	61	76.25%
abaI^+ abaR^−	6	7.5%
abaI^− abaR^+	2	2.5%
abaI^− abaR^−	11	13.75%

Table 2 Antibiotic Susceptibility of A. baumannii Clinical Isolates

Antimicrobial Agent	Resistant n (%)	Intermediate n (%)	Susceptible n (%)
Piperacillin	61 (76.25)	8 (10)	11 (13.75)
Ampicillin	73 (91.25)	4 (5)	3 (3.75)
Ampicillin-sulbactam	51 (63.75)	5 (6.25)	24 (30)
Piperacillin-tazobactam	55 (68.75)	7 (8.75)	18 (22.5)
Ticarcillin-clavulanic acid	56 (70)	3 (3.75)	21 (26.25)
Ceftazidime	57 (71.25)	3 (3.75)	20 (25)
Cefepime	58 (72.5)	1 (1.25)	21 (26.25)
Cefotaxime	60 (75)	13 (16.25)	7 (8.75)
Ceftriaxone	57 (71.25)	15 (18.75)	7 (8.75)
Imipenem	54 (67.5)	0 (0)	26 (32.5)
Meropenem	52 (65)	2 (2.5)	26 (32.5)
Gentamicin	49 (61.25)	1 (1.25)	30 (37.5)
Tobramycin	45 (56.25)	2 (2.5)	33 (41.25)
Amikacin	42 (52.5)	2 (2.5)	36 (45)
Minocycline	9 (11.25)	8 (10)	63 (78.75)
Ciprofloxacin	54 (67.5)	0 (0)	26 (32.5)
Levofloxacin	41 (51.25)	8 (10)	31 (38.75)
Polymyxin B	0 (0)	0 (0)	80 (100)

Figure 1 Correlation between drug resistance and carrier status of QS genes, (A) abaI and (B) abaR genes in clinical A. baumannii isolates.

Table 3 Characteristics of Five Clinical Isolates with Apparent Surface Motility

Strains	IC	Drug Sensitivity	AHLs	abaI Gene	abaR Gene	Biofilm	Motility Diameter (mm)*
A37	II	MDR	+	+	+	+++	58 ± 2.48
A38	II	MDR	+	+	+	++	39.51 ± 2.32
A41	II	MDR	+	+	+	+	71.18 ± 2.63
A76	5	MDR	+	+	+	+	30.98 ±11.20
A79	4	MDR	+	+	+	++	37.57 ± 5.93

Note: *values are mean ± S.D. (standard deviation).

Abbreviations: IC, international clone; MDR, multiple drug resistant; AHLs, N-acyl-homoserine lactones.

Figure 2 Surface-related motility of A. baumannii clinical isolates. ATCC17978 was used as a positive control to show surface motility. Five clinical strains A41, A37, A38, A79, and A76 showed apparent surface motility; A5 was used as a representative clinical strain without motility. DH5α was used as a negative control.

Figure 3 Correlation of invasiveness into A549 cells with carrier status of QS genes, (A) abaI and (B) abaR, and with (C) AHLs production in clinical A. baumannii isolates.*Means statistically significant and p <0.05; **Means statistically significant and p <0.01.

Figure 4 Kaplan–Meier survival curves of G. mellonella infected with A. baumannii clinical isolates. AHL-producing A. baumannii induced significantly greater mortality than did non-AHL-producing A. baumannii (P<0.01).