Acinetobacter nosocomialis
1. Classification
a. Higher order taxa
Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales, Moraxellaceae, Acinetobacter
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NCBI: [1] |
Acinetobacter nosocomialis
2. Description and significance
Acinetobacter nosocomialis is a Gram-negative, non-motile, non-fermentative bacterium primarily recognized for causing hospital-acquired infections. It is known for its resilience in harsh environments, including hospital settings, due to its resistance to disinfectants and multiple antibiotics [1]. A closely related species (A. baumannii) has been extensively studied for its role in multidrug resistant infections, but recent research emphasizes the equally important role that A. nosocomialis can play in clinical infections, with some studies reporting similar mortality rates between the two species [2].
A. nosocomialis causes various infections, especially in immunocompromised patients or those with invasive medical devices such as catheters or ventilators [3]. Bloodstream infections and respiratory infections are among the most common infections, with high mortality rates reported in hospital settings [4]. Despite its pathogenic potential, A. nosocomialis remains understudied compared to other members of the genus Acinetobacter. The rise of multidrug resistance in A. nosocomialis has added to the challenge of treating infections caused by the bacterium. A. nosocomialis releases small particles called outer membrane vesicles, which help trigger inflammation and protect the bacteria from the body’s immune system. This makes infections harder to treat [5]. Scientists are exploring new treatments, such as bacteriophage therapy, to fight strains of A. nosocomialis that resist many antibiotics.
3. Genome structure
The whole genome of Acinetobacter nosocomialis has been sequenced using an isolate from a plastic-containing landfill [6]. The A. nosocomialis genome contains 3,850,149 bases, 3,525 of which are protein-coding sequences, and the GC nucleotide base content is 38.84% [6]. Some unique proteins that are encoded for are OXA-23 and OXA-58, which produce carbapenemases [7]. These enzymes break down β-lactams, serving as a major mechanism of carbapenem resistance in A. nosocomialis. Outer membrane protein A is another protein produced by A. nosocomialis, which contributes to biofilm formation [8].
4. Cell structure
Acinetobacter nosocomialis is Gram-negative, non-motile, non-spore-forming, and has a coccobacilli morphology [9]. The cell wall is difficult to de-stain, due to thicker peptidoglycan walls and therefore, often incorrectly appears to be Gram-positive. The A. nosocomialis cell envelope is also unique in that it causes inflammation through the activity of outer membrane vesicles and the proteins within those vesicles [8]. Outer membrane vesicles are also able to modify its outer membrane to limit drug penetration [10].
5. Metabolic processes
Acinetobacter nosocomialis, a chemoorganoheterotroph, derives its carbon and energy from organic molecules [1,3]. While it can survive in low-oxygen environments by utilizing alternative electron acceptors, this non-fermentative bacterium primarily relies on aerobic respiration to break down substrates and produce energy [1,12]. A. nosocomialis bacteria use amino acids and fatty acids as carbon sources, allowing it to thrive in environments like hospitals, where these substances might be found on surfaces or medical equipment [1,12]. Also synthesizes outer membrane vesicles, which have serine proteases, hemolysin, and outer membrane protein A [8]. By causing host inflammatory reactions and cytotoxicity, these vesicles are vital for the pathogenicity of A. nosocomialis[8]. A. nosocomialis use type VI secretion system (T6SS) to outcompete other microbes in nutrient-limited situations [3].
6. Ecology
Acinetobacter nosocomialis can inhabit medical devices like catheters and ventilators, rendering it a major contributor to hospital-acquired (nosocomial) infections [4,1]. It flourishes especially on medical devices in critical care units (ICUs) [1,4]. A. nosocomialis can potentially endure in natural conditions such as soil and water; nonetheless, but it is predominantly documented in hospital settings [3, 4]. A. nosocomialis is globally dispersed, with documented occurrences in Southeast Asia, North America, and Europe [1]. The bacterium flourishes at 37°C, the human body's temperature, and optimal growth occurs at neutral to slightly alkaline pH levels [8]. A. nosocomialis can persist on arid surfaces and withstand disinfectants [11, 4].
7. Pathology
Acinetobacter nosocomialis is an opportunistic pathogen of humans, particularly in immunocompromised patients in hospital settings, as well as to other bacteria and fungi [2,3]. The specific causes of virulence of A. nosocomialis have not been identified [8]. The bacterium can form biofilms on medical devices, such as urinary catheters, and can survive under low nutrient availability, dryness, and temperature changes [3]. The bacteria also utilizes outer membrane vesicles, secretory nanocomplexes that deliver virulence-associated proteins to host cells to damage them or induce programmed cell death. The outer membrane vesicles produced by A. nosocomialis are cytotoxic to human epithelial cells and cause inflammatory responses such as congestion and an increase in production of white blood cells within the host [5]. The OmpA protein synthesized by A. nosocomialis is linked to its pathogenesis, due to its role in the distribution of proteins necessary to the cellular envelope and the induced cytotoxicity in the OMVs [8]. The adhesins and pili that A. nosocomialis exhibit allow adherence to medical devices and tissues [4]. A. nosocomialis is also resistant to antibiotics such as broad-spectrum β-lactams and aminoglycosides [7], including carbapenems, polymyxins, sulbactam, and tigecycline [12] by overexpressing antibiotic efflux pumps [4]. In addition, A. nosocomialis uses the type VI secretion system (T6SS) to out compete other organisms and to fight off attacks from the host immune system [3].
8. The Acb Complex
A. nosocomialis is found in a group of bacteria known as the Acinetobacter calcoaceticus-baumannii (Acb) complex. The other bacteria found in the Acb complex include A. calcoaceticus, A. baumannii, A. pittii, A. seifertii, and A. dijkshoorniae [2]. Patients infected by the Acb complex can experience various infections including pneumonia, sepsis, and soft tissue infections. Antibiotic resistance in the Acb complex (especially to carbapenem) as well as the ability to evade human immunity accounts for the difficulty in developing reliable treatments [2]. Within the complex, varying amounts of each bacteria account for the severity of the infection, with A. nosocomialis being associated with a lower mortality rate than A. baumannii isolates [2]. Currently, different antibiotic treatments and therapies are being tested to treat multidrug resistant Acb complexes, such as TCUAN2 phage therapy and bacteriophage-derived endolysin [8].
9. Current Research
Current research on A. nosocomialis is focused on the frequent comparison between A. nosocomialis and other Acintobacter members. In a study done in Thailand, clinical outcomes were compared between patients with A. nosocomialis and A. baumannii [2]. It was found that both A. baumannii and A. nosocomialis had similar percentages of mortality, but A. nosocomialis had a lower percentage of patients who acquired a community-acquired infection [2]. In other studies done in Thailand, A. nosocomialis resistance to carbapenem was measured, with A. pittii and A. baumannii. When comparing A. pittii with A. nosocomialis, it was found that A. nosocomialis had a slightly higher resistance compared to A. pittii [7]. In the same experiment, researchers found that the production of certain OXA enzymes was a reason for carbapenem resistance [7]. When comparing both A. pittii and A. nosocomialis to A. baumannii, A. baumannii had much higher resistance to carbapenem in comparison to A. pittii and A. nosocomialis, leading to a higher mortality rate to patients infected with A. baumannii [4]. To combat the high resistance of Acinetobacter bacterium to carbapenems, recent studies have shown that using bacteriophages that target A. nosocomialis are effective in getting rid of A. nosocomialis in the bloodstream, therefore increasing survival. Isolating the bacteriophages TCUAN1 and TCUAN2 from sewer systems, these phages were injected into mice that were infected with A. nosocomialis [12]. It was found that mice that were treated with the phages showed less amounts of A. nosocomialis in their bloodstream and had a significantly much higher percent survival than the infected control mice [12]. With this developing research on phage therapy on antibiotic resistant bacteria, this kind of treatment could be very useful in combating resistant bacteria in hospital settings, where most A. nosocomialis infections occur.
9. References
[1] Wisplinghoff, H., Paulus, T., Lugenheim, M., Stefanik, D., Higgins, P. G., Edmond, M. B., Wenzel, R. P., Seifert, H. (2012). Nosocomial bloodstream infections due to Acinetobacter baumannii, Acinetobacter pittii and Acinetobacter nosocomialis in the United States. Journal of Infection, 64(3), 282-290. https://doi.org/10.1016/j.jinf.2011.12.008
[2] Nithichanon, A., Kewcharoenwong, C., Da-Oh, H., Surajinda, S., Khongmee, A., Koosakunwat, S., Wren, B. W., Stabler, R. A., Brown, J. S., Lertmemongkolchai, G. (2022). Acinetobacter nosocomialis causes as severe disease as Acinetobacter baumannii in northeast Thailand: Underestimated role of A. nosocomialis in Infection. Microbiology spectrum, 10(6), e02836-22. https://doi.org/10.1128/spectrum.02836-22
[3] Sun, Y., Wang, L., Zhang, M., Jie, J., Guan, Q., Fu, J., Chu, X., Chen, D., Li, C., Song, L., Luo, Z. Q. (2024). Acinetobacter nosocomialis utilizes a unique type VI secretion system to promote its survival in niches with prey bacteria. mBio, 15(7), e01468-24. https://doi-org.ezproxy.bu.edu/10.1128/mbio.01468-24
[4] Chusri, S., Chongsuvivatwong, V., Rivera, J. I., Silpapojakul, K., Singkhamanan, K., McNeil, E., & Doi, Y. (2014). Clinical outcomes of hospital-acquired infection with Acinetobacter nosocomialis and Acinetobacter pittii. Antimicrobial Agents and Chemotherapy, 58(7), 4172–4179. https://doi.org/10.1128/AAC.02992-14
[5] Nho, J. S., Jun, S. H., Oh, M. H., Park, T. I., Choi, C. W., Kim, S. I.,Choi, C. H., Lee, J. C. (2015). Acinetobacter nosocomialis secretes outer membrane vesicles that induce epithelial cell death and host inflammatory responses. Microbial pathogenesis, 81, 39-45. https://doi.org/10.1016/j.micpath.2015.03.012
[6] Seong, H. J., Yao, Z. Jang, Y. (2023). Complete genome sequence of acinetobacter nosocomialis GNU001, isolated from a plastic-containing landfill. ASM Journals, 12(1), e01077-22. https://doi.org/10.1128/mra.01077-22
[7] Singkham-in, U., Chatsuwan, T. (2018). Mechanisms of carbapenem resistance in Acinetobacter pittii and Acinetobacter nosocomialis isolates from Thailand. Journal of Medical Microbiology, 67(12). https://doi-org.ezproxy.bu.edu/10.1128/mbio.01468-24
[8] Kim, S. W., Oh, M. H., Jun, S. H., Jeon, H., Kim, S. I., Kim, K., Lee, Y. C., Lee, J. C. (2016). Outer membrane Protein A plays a role in pathogenesis of Acinetobacter nosocomialis. Virulence, 7(4), 413-426. https://doi.org/10.1080/21505594.2016.1140298
[9] Machado, R. A. R., Loulou, A., Bhat, A. H., Mastore, M., Terrettaz, C., Brivio, M. F., & Kallel, S. (2023). Acinetobacter nematophilus sp. nov., Alcaligenes nematophilus sp. nov., Enterobacter nematophilus sp. nov., and Kaistia nematophila sp. nov., isolated from soil-borne nematodes and proposal for the elevation of Alcaligenes faecalis subsp. faecalis, Alcaligenes faecalis subsp. parafaecalis, and Alcaligenes faecalis subsp. phenolicus to the species level. Taxonomy, 3(1), 148-168. https://doi.org/10.3390/taxonomy3010012
[10] Huang, L., Chen, T. L., Lee, Y. T., Lee, M. H., Kuo, S. C., Yu, K. W., Dou, H. Y., & Fung, C. P. (2014). Risk factors for imipenem-nonsusceptible Acinetobacter nosocomialis bloodstream infection. Journal of Microbiology, Immunology and Infection, 47(4), 311-317. https://doi.org/10.1016/j.jmii.2013.02.002
[11] Lai, H.-H., Liou, B.-H., Chang, Y.-Y., Kuo, S.-C., Lee, Y.-T., Chen, T.-L., & Fung, C.-P. (2016). Risk factors and clinical outcome of sulbactam nonsusceptibility in monomicrobial Acinetobacter nosocomialis bacteremia. Journal of Microbiology, Immunology and Infection, 49(3), 371-377. ClinicalKey. http://dx.doi.org/10.1016/j.jmii.2014.06.004
[12] Lai, MJ., Wu, WJ., Chin, YH., Chao, HJ., Chen, LK., Peng, SY., Chang, KC. (2023). Isolation and characterization of bacteriophages with activities against multi- drug-resistant Acinetobacter nosocomialis causing bloodstream infection in vivo. Journal of Microbiology Immunology and Infection, 56(5), 1026-1035. https://doi.org/10.1016/j.jmii.2023.07.012
Edited by [Jennifer Bhatnagar], student of [mailto:jmbhat@bu.edu Jennifer
Bhatnagar] for [http://www.bu.edu/academics/cas/courses/cas-bi-311/ BI 311
General Microbiology], 2020, Boston University.
[[Category:Pages edited by students of Jennifer
Bhatnagar at Boston University]]
