Candida-Acinetobacter-Pseudomonas Interaction Modelled within 286 ICU Infection Prevention Studies
1Rural Health Academic Center, Melbourne Medical School, University of Melbourne, Ballarat 3350, Australia.
Background:
Whether Candida interacts to enhance the invasive potential of Acinetobacter and Pseudomonas bacteria cannot be resolved within individual studies. There are several anti-septic, antibiotic, anti-fungal, and non-decontamination-based interventions to prevent ICU acquired infection. These effective prevention interventions would be expected to variably impact Candida colonization. The collective observations within control and intervention groups from numerous ICU infection prevention studies simulates a multi-centre natural experiment with which to evaluate Candida, Acinetobacter and Pseudomonas interaction (CAPI).
Methods:
Eight Candidate-generalized structural equation models (GSEM), with Candida, Pseudomonas and Acinetobacter colonization as latent variables, were confronted with blood culture and respiratory tract isolate data derived from >400 groups derived from 286 infection prevention studies.
Results:
Introducing an interaction term between Candida colonization and each of Pseudomonas and Acinetobacter colonization improved model fit in each case. The size of the coefficients (and 95% confidence intervals) for these interaction terms in the optimal Pseudomonas (+0.33; 0.22 to 0.45) and Acinetobacter models (+0.32; 0.01 to 0.5) were similar to each other and similar in magnitude, but contrary in direction, to the coefficient for exposure to topical antibiotic prophylaxis (TAP) on Pseudomonas colonization (-0.45; -0.71 to -0.2). The coefficient for exposure to topical antibiotic prophylaxis on Acinetobacter colonization was not significant.
Conclusions:
GSEM modelling of published ICU infection prevention data supports the CAPI concept. The CAPI model could account for some paradoxically high Acinetobacter and Pseudomonas infection incidences, most apparent among the concurrent control groups of TAP studies.
Insights
Candida interacts with Acinetobacter and Pseudomonas bacteria, increasing infection risk in ICUs. This Candida, Acinetobacter, and Pseudomonas interaction (CAPI) model explains high infection rates observed in studies of topical antibiotic prophylaxis.
Area of Science:
- Infectious Diseases
- Microbiology
- Critical Care Medicine
Background:
- Individual studies cannot determine if Candida enhances the invasive potential of Acinetobacter and Pseudomonas.
- ICU infection prevention strategies may variably impact Candida colonization.
- Collective data from ICU infection prevention studies can simulate a natural experiment to study Candida, Acinetobacter, and Pseudomonas interaction (CAPI).
Purpose of the Study:
- To evaluate the interaction between Candida, Acinetobacter, and Pseudomonas (CAPI) in intensive care unit (ICU) settings.
- To determine if Candida colonization influences the invasive potential of Acinetobacter and Pseudomonas.
- To assess the CAPI concept using existing ICU infection prevention study data.
Main Methods:
- Employed generalized structural equation models (GSEM) with Candida, Pseudomonas, and Acinetobacter colonization as latent variables.
- Utilized blood culture and respiratory tract isolate data from over 400 groups across 286 infection prevention studies.
- Tested eight candidate GSEM models to evaluate the CAPI concept.
Main Results:
- Model fit improved significantly with the inclusion of an interaction term between Candida and Acinetobacter, and Candida and Pseudomonas colonization.
- The interaction terms for Candida-Pseudomonas and Candida-Acinetobacter were similar in magnitude but opposite in direction to the effect of topical antibiotic prophylaxis (TAP) on Pseudomonas colonization.
- Topical antibiotic prophylaxis showed a significant negative impact on Pseudomonas colonization but not Acinetobacter.
Conclusions:
- Generalized structural equation modeling of published ICU data supports the Candida, Acinetobacter, and Pseudomonas interaction (CAPI) concept.
- The CAPI model helps explain unexpectedly high Acinetobacter and Pseudomonas infection rates, particularly in control groups of TAP studies.
- Findings suggest a complex interplay between fungal and bacterial colonization in ICU infections.
