TABLE 2.

Mechanisms of aminoglycoside resistance in clinical isolates of P. aeruginosaa

Aminoglycoside resistance mechanismResistance tob:Incidence (%)c
Miller et al. (98)dMiller et al. (99)
AAC(6′)-IT, N, A1.1-18.8 (6.2)1.25
AAC(6′)-IIG, T, N2.1-70.3 (32.5)18.39
AAC(3)-IG0.6-31.9 (8.3)2.05
AAC(3)-IIG, T, N1.1-55.3 (4.5)e2.20
AAC(3)-IIIG, T0.1-7.1 (3.2)0.10
AAC(3)-VIG, T, N0.2-6.3 (2.6)0.15
AAC(3)-?G, N0.7-11.7 (4.5)0.60
ANT(2′′)-IG, T1.7-45.2 (16.9)11.87
ANT(4′)-IIT, A, I0.05
APH(3′)-VIA, I0.20
ImpermeabilityG, T, N, A, I4.3-23.7 (14.0)26.15
  • a Mechanisms of aminoglycoside resistance in clinical strains and their incidence in the indicated studies are shown. The most prevalent mechanisms are indicated in boldface type.

  • b Only the major antipseudomonal aminoglycosides are indicated. T, tobramycin; N, netilmicin; A, amikacin; G, gentamicin; I, isepamicin.

  • c The incidence of the indicated resistance mechanisms in aminoglycoside-resistant clinical strains of P. aeruginosa when they occur singly. The data do not include instances in which the indicated mechanisms occur in combination with other aminoglycoside resistance mechanisms.

  • d The indicated publication summarizes data from several studies, and the numbers presented reflect the range of incidences for each mechanism seen in these individual studies. The numbers in parentheses are the averages for all the studies.

  • e The average incidence reported excludes the 55.3% incidence reported for a single small study in Chile.