Unmasking VIM Pseudomonas aeruginosa: Threats in Critical Care
VIM-producing Pseudomonas aeruginosa isn’t just surviving in ICUs; it’s thriving. With mortality rates exceeding 30%, colonization risks hiding in drains, devices, and even donor milk, IPs must take proactive steps to outsmart this pathogen. Now is the time to double down on environmental controls, risk factor recognition, and surveillance strategies. Let’s break the biofilm cycle before the next outbreak takes root.
Unmasking VIM Pseudomonas aeruginosa
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Pseudomonas aeruginosa remains a problematic bug in hospital settings, contributing to a range of nosocomial infections. In the US, multidrug-resistant P aeruginosa causes 13% to 19% of health care–acquired infections (HAIs) annually.1 The pathogen can survive harsh conditions, and it has devised virulence mechanisms and resistance to a broad range of antibiotics. This is particularly the case for the strains that carry the Verona integron–encoded metallo-β-lactamase (VIM), an enzyme that confers resistance to carbapenems, often reserved as last-line antibiotic therapy. Multiple cases of VIM-positive P aeruginosa (VIM-PA), have been reported in intensive care units (ICUs), raising concerns for the patients and the staff. The mortality rate of these infections is quite alarming, usually exceeding 30%, depending on the site of infection and the underlying condition of the patient.2
The nature of the clinical cases often managed in the ICU and the therapeutic procedures carried out in this setting can create a breeding ground for formidable disease-causing microorganisms, such as P aeruginosa. Long hospital stays, severe illnesses, and deranged immune defenses are characteristic features of the typical ICU patient. These may encourage infection with VIM-producing P aeruginosa or even silent colonization, which can remain undetected until clinical deterioration or transmission to other patients occurs.
To develop effective guidelines for infection prevention and manage outbreaks, a deeper understanding of the risk factors that specifically lead to VIM-PA colonization and infection is needed. This piece highlights some of the environmental, patient-related, and provider-related issues in the ICU that can contribute to the growth of these superbugs.
Environmental Risk Factors
The environment in the ICU is a key contributor to colonization and infection by VIM-PA. In a retrospective study conducted in the Netherlands, researchers found that persistent environmental contamination by P aeruginosa was the primary source of bacterial transmission. In the study, 86.3% of the transmissions were attributed to a contaminated environment, compared with 13.7% of the cases that were attributed to cross-transmission.3
ICU Surfaces and Equipment
With P aeruginosa, routine disinfection protocols are sometimes insufficient, primarily due to the virulence and antimicrobial resistance patterns exhibited by these bacteria, particularly in biofilm formation. P aeruginosa can adhere to surfaces and employ other mechanisms such as quorum sensing and growth inhibition to perpetuate the biofilm and promote tolerance to antibacterial agents.
In the ICU environment, numerous high-touch surfaces can serve as reservoirs for VIM-producing P aeruginosa. Most health care workers will be concerned about countertops and medical trolleys, while ventilator buttons, bed rails, and infusion stands may receive less attention during routine cleaning despite being potent niches for these bugs.Ventilator circuits, bronchoscopes, urinary catheters, and extracorporeal membrane oxygenation lines can also harbor biofilms that protect VIM-PA from both immune clearance and disinfectants. If not rigorously sterilized or replaced, these devices can act as persistent sources of infection.
Sink Drains and Water Systems
P aeruginosa thrives in a wet environment, and sink drains provide a preferred niche for these bacteria, with splashes traveling a distance of up to 1 m from the basin.4 A study in a Swedish hospital established that sink drains harbored VIM-PA, and dispersing the biofilms in the drainage system led to control of an outbreak.5
In another study in Switzerland, the researchers went a step further and removed all sinks near the patients in the ICU, adopting a completely waterless model.6 They decided to go completely waterless after the initial attempts to replace the sink siphons led to reinfections in just a few weeks. In the waterless model, a handwashing sink was placed outside the ICU rooms, and disposable wipes and single-use hygiene kits were used. Oral medication was dissolved in spring water. Only after these interventions was the outbreak of the multidrug-resistant P aeruginosa curbed.
These studies underscore the importance of reconsidering the drainage architecture of ICUs and hospitals at large.
Staff and Visitor Movement
High patient-to-nurse ratios, poor hand hygiene, and a lack of adherence to personal protective equipment regulations among health care workers contribute to horizontal transmission. Additionally, family members and other visitors, especially in neonatal or long-term ICUs, can serve as vectors if proper infection control measures are not enforced.
Patient-Related Risk Factors
Prior Antibiotic Use and Prior Hospitalization
Patients with prior antibiotic exposure, especially to carbapenems or fluoroquinolones, are at a higher risk of VIM-PA colonization and infection. This is because overuse or prolonged use of these broad-spectrum antibacterial agents favors the colonization by resistant strains. The use of these drugs often leads to the elimination of susceptible strains, leaving behind undetectable and resistant strains that are then spread from patient to patient or colonize the environment. Antibiotic use within 3 months of admission to the ICU puts patients at risk of developing carbapenem-resistant P aeruginosa infections.7
Patients previously admitted to a hospital before their current ICU admission are more likely to develop VIM-PA infection and colonization due to the increased risk of exposure to these bacteria.1 Similarly, longer admission periods in the ICU can lead to a higher risk of colonization and infection. In the same breadth, long-term care facilities are also known to harbor many drug-resistant bacteria.
Patients coming to the ICU with an already established P aeruginosa colonization are more likely to have positive cultures later. In a study at the University of Maryland Medical Center, patients were tested for P aeruginosa colonization at admission and monitored. Patients colonized with P aeruginosa were over 6 times more likely to have a subsequent positive clinical culture than patients who were initially not colonized.8
Advanced Age
Advanced age is a known risk factor for developing HAIs mainly because of weakened immune function. Additionally, people of advanced age are more likely to have comorbidities and frequent exposure to health care settings, which directly translates to more exposure to disease-causing microorganisms. A 2010 study found that people above 86 years of age in a long-term care facility were more likely to develop drug-resistant strains of bacteria.9
In the ICU, older patients often spend longer periods on the ventilator. They are also likely to undergo more invasive procedures, leading to a higher risk of exposure to pathogens such as VIM-PA.
Anemia
A study conducted in 2 district hospitals in the United Kingdom identified anemia as a risk factor for P aeruginosa infection, with 53% of cases having hemoglobin levels below 11.5 g/dL.
This can be attributed to the fact that anemia is often associated with other factors, such as poor nutritional status, which can compromise the immune system. Anemia can also be caused by conditions such as bone marrow suppression, inflammatory conditions, and even cancer, which can all predispose patients to infections by drug-resistant bacteria.
Severity of Illness and Length of Stay
The severity of a patient’s illness correlates with the risk of acquiring VIM-PA. Patients with severe disease are more likely to undergo more invasive procedures, stay longer on the ventilator in the ICU, and receive more broad-spectrum antibiotics, all of which can increase the risk of colonization by VIM-PA.
Specific Clinical Conditions
Studies have shown that specific clinical conditions are more likely to be associated with P aeruginosa colonization. A 2006 study established that neurological disease, urinary tract infections, and renal failure were significant risk factors for metallo-β-lactamase(MBL) P aeruginosainfections.10
Chronic wounds, surgical sites, and burns provide a direct entry point for P aeruginosa. The organism’s ability to form biofilms on necrotic or moist tissue surfaces allows it to persist despite topical or systemic treatment. This is particularly problematic in ICUs, where pressure ulcers and surgical wounds are common.
Posttransplant patients are also at higher risk of developing carbapenem-resistant P aeruginosa infections when they are admitted to the ICU. This is due to their immunosuppressed states and the prolonged use of antibiotics. Studies have established that both solid organ and stem cell recipients are at a higher risk of colonization and infection by drug-resistant bacteria.11,12
Breast Milk Feeding Practices in Neonatal ICUs
Breast milk is a rich source of nutrition that also helps boost a newborn’s immune system. However, in cases where breast milk is expressed, proper handling and hygiene should be observed to protect the baby from exposure to pathogens. In the neonatal ICU (NICU), for example, improper handling of expressed breast milk can lead to colonization by bacteria.
In a study conducted in an Italian NICU, breast milk feeding was associated with colonization by a well-defined, imipenem-resistant, MBL-P aeruginosa strain.13
Conclusion
Colonization and infection with VIM-PA in the ICU are driven by an interplay of patient factors and environmental persistence, as well as clinical practice gaps, including inadequate handwashing techniques and suboptimal disinfection protocols. The nature of care offered in the ICU is inherently risky, meaning patients are constantly at risk of developing infections with resistant strains of bacteria. The invasive procedures and prolonged hospital stays, in addition to the nature of diseases, call for vigilance and appropriate infection prevention and control measures to disrupt the growth of disease-causing organisms that might be lurking.
References
1. Raman G, Avendano EE, Chan J, Merchant S, Puzniak L. Risk factors for hospitalized patients with resistant or multidrug-resistant Pseudomonas aeruginosa infections: a systematic review and meta-analysis. Antimicrob Resist Infect Control. 2018;7:79. doi:10.1186/s13756-018-0370-9
2. Peña C, Suarez C, Ocampo-Sosa A, et al; Spanish Network for Research in Infectious Diseases (REIPI). Effect of adequate single-drug vs combination antimicrobial therapy on mortality in Pseudomonas aeruginosa bloodstream infections: a post hoc analysis of a prospective cohort. Clin Infect Dis. 2013;57(2):208-216. doi:10.1093/cid/cit223
3. Pham TM, Büchler AC, Voor In ‘t Holt AF, et al. Routes of transmission of VIM-positive Pseudomonas aeruginosa in the adult intensive care unit-analysis of 9 years of surveillance at a university hospital using a mathematical model. Antimicrob Resist Infect Control. 2022;11(1):55. doi:10.1186/s13756-022-01095-x
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5. Fraenkel C-J, Starlander G, Tano E, Sütterlin S, Melhus Å. The first Swedish outbreak with VIM-2-producing Pseudomonas aeruginosa, occurring between 2006 and 2007, was probably due to contaminated hospital sinks. Microorganisms. 2023;11(4):974. doi:10.3390/microorganisms11040974
6. Schärer V, Meier MT, Schuepbach RA, et al. An intensive care unit outbreak with multi-drug-resistant Pseudomonas aeruginosa - spotlight on sinks. J Hosp Infect. 2023;139:161-167. doi:10.1016/j.jhin.2023.06.013
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8. Harris AD, Jackson SS, Robinson G, et al. Pseudomonas aeruginosa colonization in the intensive care unit: prevalence, risk factors, and clinical outcomes. Infect Control Hosp Epidemiol. 2016;37(5):544-548. doi:10.1017/ice.2015.346
9. Ghibu L, Miftode E, Teodor A, Bejan C, Dorobăţ CM. Factori de risc pentru infecţiile cu Pseudomonas aeruginosa rezistent la carbapeneme. Rev Med Chir Soc Med Nat Iasi. 2010;114(4):1012-1016.
10. Zavascki AP, Barth AL, Gaspareto PB, et al. Risk factors for nosocomial infections due to Pseudomonas aeruginosa producing metallo-beta-lactamase in two tertiary-care teaching hospitals. J Antimicrob Chemother. 2006;58(4):882-885. doi:10.1093/jac/dkl327
11. Giannella M, Bartoletti M, Conti M, Righi E. Carbapenemase-producing Enterobacteriaceae in transplant patients. J Antimicrob Chemother. 2021;76(suppl 1):i27-i39. doi:10.1093/jac/dkaa495
12. Freire MP, Camargo CH, Bubach L, et al. Recurrent outbreak of carbapenem-resistant IMP-1-producing Pseudomonas aeruginosa in kidney transplant recipients: the impact of prolonged patient colonization. Transpl Infect Dis. 2025;27(1):e14414. doi:10.1111/tid.14414
13. Mammina C, Di Carlo P, Cipolla D, et al. Nosocomial colonization due to imipenem-resistant Pseudomonas aeruginosa epidemiologically linked to breast milk feeding in a neonatal intensive care unit. Acta Pharmacol Sin. 2008;29(12):1486-1492. doi:10.1111/j.1745-7254.2008.00892.x
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