Acinetobacter and Endoscopy

Introduction

If you have conducted microbial surveillance via bacterial sampling and culturing on an endoscope, you may be familiar with Acinetobacter. While it lacks the instantaneous notoriety of Escherichia, Klebsiella, or Pseudomonas, Acinetobacter has been colonizing natural surfaces around humans since its inception and migrating ever closer. What began as a modest forest floor detritus consumer breaking down leaf matter has adapted and co-evolved to perfectly fill an open ecological niche within our very medical facilities which may even pose a threat to our patients’ safety. Through the lens of microbiology, and in the context of reprocessing and clinical endoscopy, this article will briefly discuss where Acinetobacter comes from, how it got to our medical spaces, and how to interpret its recovery.

Background Microbiology

Acinetobacter was first identified by Beijerinck in 1911, however it was then named Micrococcus calcoaceticus [1]. Since then, the genus Acinetobacter had undergone creation in 1954 and many taxonomic changes since [2]. To date, over 30 species exist within this genus, however due to their innate ability to adapt their phenotypes to their environments, precise species identification can prove challenging without the most sensitive genetic tests. In fact, Acinetobacter contains so many slightly different genetic strains, identification via chemotaxis or microscopy alone is ill-advised as many strains may present indistinguishably [3].

All species of Acinetobacter are gram-negative and, depending on growth phase, present coccobacillary or coccoid morphology and are easily cultivated on general growth agar. Their name, being Greek in origin, is attributed to their strange twitching motion though the genus is described as non-motile [2][3].

While many environments can support Acinetobacter spp. recovery from soil is indeed the most common native habitat [4]. There are certain species, however, which are considered to be transient commensal organisms to the human microbiome and even contribute to host immune system developments such as A. lwoffii and A. johnsonii [5][6]. While some species of this genus have had proper time and environments to evolve along with humans and our immune systems to represent a commensal relationship, there are those which have become opportunistic pathogens by nature such as A. nosocomialis, A. haemolyticus, A. pittii, and A. baumannii; which are not often part of the human microbiome, and their natural reservoirs remain outside of human biological systems, though frequently found around human-associated spaces [7].

Ecological Dispersal

With Acinetobacter being globally ubiquitous, a number of dispersal patterns and vectors could be assumed. To this end, an in-depth analysis of A. baumannii was conducted, selected for being an opportunistic pathogen in the form of HAI, globally dispersed, and not intrinsically part of the innate human microbiome. The study revealed that this species is remarkably adept at aerosolization and adapted to adhere to fungal spores as hitchhikers. The species is so well adapted to travel by air that it even forgoes the most common vectors such as insects, arthropods, and other aquatic animals, though it is possible to recover them in such environments. As a result of its high abundance in atmosphere, large cell counts of A. baumannii have even been isolated in remote glaciers and can frequently be heavily recovered in rainwater. Despite this, the study identified this species to be recovered in the highest ratios directly surrounding human-associated spaces [7]. A separate genetic analysis on A. baumannii also found their high prevalence directly around human areas, most notably hospital surfaces and air, as well as on the skin of hospital staff and patients [4].

Hospital Colonization

Acinetobacter is remarkably adept at surviving a range of extreme environments from high humidity to intense desiccation for long stretches of time. Additionally, possess remarkably, they also possess unique forms of defense against radiation, evolved in order to survive the trip on fungal spores higher in the atmosphere and whilst being bombarded with excess solar radiation. Strikingly [7], because of the combination, this positions Acinetobacter to perfectly colonize an otherwise voided niche of habitat: inside medical facilities, whose environment conditions are often lacking in freely available water and treated with radiation as a form of disinfection.

Not only can Acinetobacter adapt to extreme surface conditions, but they have also largely gained the required genes to adhere to human skin and become a commensal part of the skin microbiome, this is seen overrepresented in hospital staff and patients with extended hospital stays when compared to people who don’t frequently enter hospitals. The versatility of Acinetobacter’s gained ability to adhere to any surface or host in the hospital setting, and it’s historic dispersal by air provide ample opportunity to circulate bacteria in hospital systems.

Molecular Defenses

Another boon some species of Acinetobacter possess is in the form of genetic virulence factors. Particularly, observed in A. baumannii are at least 6 known genetic islands containing virulence factors related to biofilm, antibiotic resistance, and resistance to disinfectants and detergents among others promoting infection [8][9][10]. Nearly all Acinetobacter can produce biofilm, however A. baumannii have shown heightened abilities here as well. As a result, Acinetobacter biofilms have been reported from hospital surfaces and medical devices. This is attributable to A. baumannii having developed genes which allow for production of biofilm that can specifically defend against antibiotics, disinfectants, and desiccation. Because of the combination of these resistances and genetic advantages, A. baumannii in particular has become optimally suited to thrive under some of the most intense hospital disinfection systems [11].

Clinical Relevance

Of extreme clinical importance is the recovery of A. baumannii, A. nosocomialis, and A. pittii. While these are three distinct species, they share remarkably similar genomes, making them a challenge to discriminate. A. baumannii has been, and still remains to be, the most clinically impactful species of Acinetobacter, having been on a steady increase since 2019 in burden on hospitals across the USA, both for its ability to be adaptively infectious and ability to generate multi-drug resistance (MDR) [12]. Morbidity due to A. baumannii blood-stream infections can present quite high, as far as 58% in some outbreaks. While other named species in Acinetobacter may be opportunistic pathogens to the heavily immunocompromised, medical reports are few and rarely morbid when compared to A. baumannii Acinetobacters ability to employ horizontal gene transfer on a rapid scale are what support and drive this genus’ ability to develop or utilize MDR genes which has given this genus heightened notoriety as a HAI. Because the environmental strains are easily poised to opportunistically lean into parasitism through this schema, environmental monitoring of one’s facility would be the only accurate way to detect if such MDR threats currently exist.

Relation to Endoscopy

GI endoscopy has reported rare infections caused by Acinetobacter, though it can happen, typicallyfollowing upper procedures on immunocompromised peoples. When searching through literature Pseudomonas aeruginosa remains the most common culprit responsible for infections following procedure, and particularly responsible MDR outbreaks. Interestingly, Acinetobacter can often be reported as being recovered in clinical specimens, however not responsible for causing infection [13][14]. This can most likely be attributable to Acinetobacter’s propensity to develop biofilm, potentially harboring more pathogenic strains of bacteria. Of higher concern with Acinetobacter is its presence surrounding bronchoscopy or cystoscopy, since the rates of infection with Acinetobacter are higher following these procedures. Regardless of this however, A. baumannii has swiftly become one of the world's leading HAI threats, even prompting the WHO to call for new drug interventions to combat carbapenem-resistant strains [15].

Interpreting Microbial Surveillance Results

Our understanding of Acinetobacter’s origin is largely environmental and easily recovered in many soil types and can easily travel by air. This presents the opportunity for Acinetobacter to be recovered accidentally as an environmental contamination of your endoscope sample. As discussed earlier, Acinetobacter can be found in higher ratios of culture samples when sampling occurs on raining or humid days in less controlled hospital rooms, which could indicate poor air ventilation quality. Acinetobacter can also enter endoscope samples from the sampler’s clothes if they are not wearing proper protective equipment. Acinetobacter has also become a commensal skin organism specifically within hospital settings, making its occurrence common if staff do not follow proper hand-hygiene protocols.

Conclusion

Understanding Acinetobacter's evolution, ecological dispersal, and adaptation to clinical environments is crucial for interpreting microbial surveillance results in healthcare settings. While not as immediately notorious as other hospital-associated pathogens, Acinetobacter, particularly species like A. baumannii, A. nosocomialis, and A. pittii pose significant risks due to their ability to adapt, survive in harsh conditions, and develop multi-drug resistance. The recovery of Acinetobacter in clinical spaces, especially in relation to endoscopy, highlights the importance of distinguishing between environmental contamination of non-pathogenic varieties and patient-derived strains. However, with the trend of increased MDR gene expression and biofilm formation throughout a few Acinetobacter spp. caution is warranted in the recovery of benign environmental isolates. By enhancing environmental monitoring and understanding the specific species recovered, healthcare facilities can better manage the potential risks posed by this resilient bacterium, ensuring improved patient safety and infection control.

Sources and further readings

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  2. Doughari HJ, Ndakidemi PA, Human IS, Benade S. The ecology, biology and pathogenesis of Acinetobacter spp.: an overview. Microbes Environ. 2011;26(2):101-12. doi: 10.1264/jsme2.me10179. Epub 2011 Mar 18. PMID: 21502736.

  3. Visca P, Seifert H, Towner KJ. Acinetobacter infection--an emerging threat to human health. IUBMB Life. 2011 Dec;63(12):1048-54. doi: 10.1002/iub.534. Epub 2011 Oct 18. PMID: 22006724.

  4. Garcia-Garcera, M., Touchon, M., Brisse, S., & Rocha, E. P. C. (2017). Metagenomic assessment of the interplay between the environment and the genetic diversification of Acinetobacter. Environmental Microbiology, 19(12), 5010–5024. https://doi.org/10.1111/1462-2920.13949. Accessed August 2024.

  5. Ruokolainen, Lasse & Paalanen, Laura & Karkman, Antti & Laatikainen, Tiina & Hertzen, Leena & Vlasoff, Tiina & Markelova, Olga & Masyuk, Vladimir & Auvinen, Petri & Paulin, Lars & Alenius, Harri & Fyhrquist, Nanna & Hanski, Ilkka & Mäkelä, Mika & Zilber, Elmira & Jousilahti, Pekka & Vartiainen, Erkki & Haahtela, Tari. (2017). Significant disparities in allergy prevalence and microbiota between the young people in Finnish and Russian Karelia. Clinical & Experimental Allergy. 47. 10.1111/cea.12895.

  6. Ruokolainen L, Parkkola A, Karkman A, Sinkko H, Peet A, Hämäläinen AM, von Hertzen L, Tillmann V, Koski K, Virtanen SM, Niemelä O, Haahtela T, Knip M. Contrasting microbiotas between Finnish and Estonian infants: Exposure to Acinetobacter may contribute to the allergy gap. Allergy. 2020 Sep;75(9):2342-2351. doi: 10.1111/all.14250. Epub 2020 Mar 17. PMID: 32108360.

  7. Wilharm, Gottfried & Skiebe, Evelyn & Lopinska, Andzelina & Higgins, Paul & Weber, Kristin & Schaudinn, Christoph & Neugebauer, Christof & Goerlitz, Katharina & Meimers, Gideon & Rizova, Yana & Blaschke, Ulrike & Heider, Christine & Cuny, Christiane & Drewes, Stephan & Heuser, Elisa & Jeske, Kathrin & Jacob, Jens & Ulrich, Rainer & Bocheński, Marcin & Jerzak, Leszek. (2024). On the ecology of Acinetobacter baumannii - jet stream rider and opportunist by nature. 10.1101/2024.01.15.572815.

  8. Moubareck, C.A.; Halat, D.H. Insights intoAcinetobacter baumannii: A review of microbiological, virulence, and resistance traits ina threatening nosocomial pathogen.Antibiotics2020,9, 119.

  9. Harding, C.M.; Hennon, S.W.; Feldman, M.F. Uncovering the mechanisms of Acinetobacter baumannii virulence. Nat. Rev. Microbiol.2018,16, 91–102.

  10. Ridha, D.J.; Ali, M.R.; Jassim, K.A. Occurrence of Metallo-β-lactamase Genes among Acinetobacter baumannii Isolated from Different Clinical samples. J. Pure Appl. Microbiol. 2019,13, 1111–1119.

  11. Ahuatzin-Flores, Omar & Torres, Eduardo & Chavez, Edith. (2024). Acinetobacter baumannii, a Multidrug-Resistant Opportunistic Pathogen in New Habitats: A Systematic Review. Microorganisms. 12. 644. 10.3390/microorganisms12040644.

  12. “Antimicrobial Resistance Threats in the United States, 2021-2022.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 16 July 2024, www.cdc.gov/antimicrobial-resistance/data-research/threats/update-2022.html. Accessed August 2024.

  13. Deb A, Perisetti A, Goyal H, Aloysius MM, Sachdeva S, Dahiya D, Sharma N, Thosani N. Gastrointestinal Endoscopy-Associated Infections: Update on an Emerging Issue. Dig Dis Sci. 2022 May;67(5):1718-1732. doi: 10.1007/s10620-022-07441-8. Epub 2022 Mar 9. Erratum in: Dig Dis Sci. 2022 Jun;67(6):2691. doi: 10.1007/s10620-022-07502-y. PMID: 35262904.

  14. Kovaleva J, Peters FT, van der Mei HC, Degener JE. Transmission of infection by flexible gastrointestinal endoscopy and bronchoscopy. Clin Microbiol Rev. 2013 Apr;26(2):231-54. doi: 10.1128/CMR.00085-12. PMID: 23554415; PMCID: PMC3623380.

  15. Hernández-González, I. L., & Castillo-Ramírez, S. (2020). Antibiotic-resistant Acinetobacter baumannii is a One Health problem. The Lancet. Microbe, 1(7), e279. https://doi.org/10.1016/s2666-5247(20)30167-1.