Emergence of carbapenem-resistant Acinetobacter baumannii as the major cause of ventilator-associated pneumonia in intensive care unit patients at an infectious disease hospital in southern Vietnam

Abstract

Ventilator-associated pneumonia (VAP) is a serious healthcare-associated infection that affects up to 30 % of intubated and mechanically ventilated patients in intensive care units (ICUs) worldwide. The bacterial aetiology and corresponding antimicrobial susceptibility of VAP is highly variable, and can differ between countries, national provinces and even between different wards in the same hospital. We aimed to understand and document changes in the causative agents of VAP and their antimicrobial susceptibility profiles retrospectively over an 11 year period in a major infectious disease hospital in southern Vietnam. Our analysis outlined a significant shift from Pseudomonas aeruginosa to Acinetobacter spp. as the most prevalent bacteria isolated from quantitative tracheal aspirates in patients with VAP in this setting. Antimicrobial resistance was common across all bacterial species and we found a marked proportional annual increase in carbapenem-resistant Acinetobacter spp. over a 3 year period from 2008 (annual trend; odds ratio 1.656, P = 0.010). We further investigated the possible emergence of a carbapenem-resistant Acinetobacter baumannii clone by multiple-locus variable number tandem repeat analysis, finding a blaOXA-23-positive strain that was associated with an upsurge in the isolation of this pathogen. We additionally identified a single blaNDM-1-positive A. baumannii isolate. This work highlights the emergence of a carbapenem-resistant clone of A. baumannii and a worrying trend of antimicrobial resistance in the ICU of the Hospital for Tropical Diseases in Ho Chi Minh City, Vietnam.

Fig. 1.

The changing aetiology of pathogens isolated from tracheal aspirates in ICU patients at the Hospital for Tropical Diseases in Ho Chi Minh City, Vietnam. (a) Proportion of selected bacterial isolates cultured from tracheal aspirates from 2000 to 2010. Black line, Acinetobacter spp.; grey line, K. pneumoniae; dashed black line, Streptococcus pneumoniae; dotted black line, Staphylococcus spp.; dotted grey line, Pseudomonas aeruginosa. (b) Histogram showing the proportion of Acinetobacter spp. (dark grey), Pseudomonas aeruginosa (light grey) and K. pneumoniae (black) cultured from tracheal aspirates showing resistance to imipenem from 2000 to 2010.

Fig. 2.

The distribution of OXA genes in 34 Acinetobacter spp. isolated from tracheal aspirates in ICU patients at the Hospital for Tropical Diseases in Ho Chi Minh City, Vietnam in 2010. (a) Histogram showing the number of Acinetobacter spp. (n = 34) producing PCR amplicons for OXA-51, OXA-58, OXA-23, OXA-24 and combinations thereof. Carbapenem-resistant isolates, dark grey; carbapenem-sensitive isolates, light grey. (b) Dendrogram created by MLVA using eight VNTR loci from 34 Acinetobacter spp. strains isolated in the ICU in 2010. The strain numbers are shown to the left of the dendrogram and the scale at the top of the diagram shows the percentage MLVA identity. Associated metadata data include the presence (black) or absence (white) of the OXA-51, OXA-58, OXA-23, OXA-24 and NDM-1 genes by PCR amplification, susceptibility to imipenem (IMP-R: susceptible, white; resistant, grey) and MLVA group (>90 % MLVA identity).