Abstract
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.
Highlights
Candida colonization at the respiratory tract and elsewhere is associated with poor outcomes among high-risk ICU patients [1]. The reason for this association remains unclear as Candida itself is a rare cause of ventilator-associated pneumonia (VAP) and candidemia occurs infrequently in the ICU [2,3]
Defining the clinical relevance of the postulated Candida–Acinetobacter–Pseudomonas interaction (CAPI) is unlikely to be achieved within the constraints of a single centre study as there are several obstacles
generalized structural equation models (GSEM) modelling of Pseudomonas, Acinetobacter and Candida colonization, each as latent variables, versus group-level exposures, provide support to the CAPI concept
Summary
Candida colonization at the respiratory tract and elsewhere is associated with poor outcomes among high-risk ICU patients [1]. Several preclinical studies have implicated a potential interaction between Candida colonization and invasive infection with Gram-negative bacilli including Pseudomonas and Acinetobacter bacteria [4]. The collective observations within control and intervention groups from numerous ICU infection prevention studies simulates a multi-centre natural experiment of Candida colonization subject to various exposures and provides an opportunity to evaluate CAPI. 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. ICU infection prevention studies simulates a multi-centre natural experiment with which to evaluate. 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)
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