Acinetobacter lwoffii: Difference between revisions
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=1. Classification= | =1. Classification= | ||
==a. Higher order taxa== | ==a. Higher order taxa== | ||
Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales; Moraxellaceae; Acinetobacter; lwoffii [[#References |[1]]]. | Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales; Moraxellaceae; Acinetobacter; lwoffii [[#References |[1]]]]. | ||
=2. Description and significance= | =2. Description and significance= | ||
Acinetobacter lwoffii is a Gram negative, aerobic bacterium important in the skin microbiome and is found in the normal flora of the skin, oropharynx, and perineum [3]. A. lwoffii lives on the skin of healthy humans, in soil and plants, in frozen foods and poultry, and in human specimens, such as blood and urine [3]. However, it is dangerous upon entering the bloodstream as it is largely resistant to antimicrobials, meaning it can become dangerously pathogenic [3]. A. lwoffii is one of the most frequent species found in hospital samples, after Acinetobacter baumannii [3, 4]. A. lwoffii possesses the ability to survive and reproduce after desiccation in clinical and hospital environments at room temperature and is often a source of infection in hospital settings [5]. Current research is focused on what mechanisms make A. lwoffii resistant to antimicrobials and allow it to survive harsh environmental conditions. | |||
=3. Genome structure= | =3. Genome structure= | ||
Whole-genome sequencing has been performed on multiple strains of A. lwoffii. The genome of A. lwoffii WJ10621, a clinical strain of A. lwoffii that is resistant to several drugs, contains 3,419,011 bases and 3,394 predicted coding sequences, with a G+C content of 41.57% [6]. The genome contains 83 tandem repeat regions, 6 copies of the 5S rRNA gene, 7 copies of the 23S rRNA gene, and 6 copies of the 16S rRNA gene, as well as 91 predicted tRNA genes [6]. In this genome, 62 genes were assigned to the “resistance to antibiotics and toxic compounds” subsystem and 56 gene products showed at least 50% protein similarity with antibiotic resistance genes in the Antibiotic Resistance Genes Database (ARDB) [7]. A total of 26 genes coding for cobalt-zinc-cadmium resistance and 14 coding for multidrug resistance efflux pumps were predicted (6). This strain contains genes involved in amino acid metabolism (309 genes) and carbohydrate metabolism (243 genes) [6]. There are 84 predicted transposase genes distributed in the genome, which suggests the existence of frequent horizontal gene transfer events [6]. | |||
Whole-genome sequencing was also conducted on five strains of A. lwoffii (ED23-25, ED45-23, ED9-5a, VS15, and AK30A) that were isolated from permafrost sediments collected from different regions of Kolyma Lowland [8]. These environmental strains of A. lwoffii have five large plasmids that contain genes of heavy metal resistance. There are genes that encode resistance to salts of mercury, arsenic, chromium, copper, and cobalt-zinc-cadmium, such as the czc, mer, ars, and cop operon [8]. These genes encode for transporter proteins that regulate the amount of heavy metal in the cell by exporting excess amounts of heavy metals out of the cell. This transport system confers resistance to these heavy metals and allows A. lwoffii to survive in conditions of extreme heavy metal concentrations [8]. | |||
=4. Cell structure= | =4. Cell structure= | ||
A. lwoffii is a Gram-negative species of bacteria that is non-motile, meaning it does not have its own mechanism of movement. The shape of A. lwoffii bacteria is described as a coccobacilli, a mix between a round shape and a rod shape [3]. Under conditions of dessication, A. lwoffii tend to exist more as round cells, and may even increase the thickness of their cell walls [5]. | |||
=5. Metabolic processes= | =5. Metabolic processes= | ||
A. lwoffii is an aerobic bacterium incapable of fermentation [9]. It is psychrotrophic, meaning its optimal growth temperature is 7°C or higher (9). When tested with Kovac’s reagent, Acinetobacter species are oxidase negative [9]. They are catalase positive and nonmotile [9]. A. lwoffii is nitrate negative and O-F negative: however, A. lwoffii can use both ammonium and nitrate as nitrogen sources [10]. For carbon and energy sources, A. lwoffii is able to use a broad spectrum of organic compounds like ethanol, acetate and lactate [10]. However, most cannot metabolize glucose. In fact, when A. lwoffii are grown in a glucose-containing media, it acidifies the media via an aldose dehydrogenase [4]. A. lwoffiii can grow in low-pH environments, with optimum growth at around pH of 3.3 [9]. | |||
=6. Ecology= | =6. Ecology= | ||
A. lwoffii is commonly found in the normal flora of the human skin, oropharynx, perineum, as well as soil and plants all over the world [11, 12]. A. lwoffii has the ability to survive a wide range of temperatures, low pH, and dry conditions. It is often found in frozen food and poultry [13]. Strains of A. lwoffii are even found on the skin of newborns [4]. Compared to other rod-shaped bacteria, A. lwoffi is particularly successful at surviving in dry conditions and has been found to survive for up to 21 days under desiccation [5]. A. lwoffii is also resistant to sterilization methods such as disinfectants and irradiation [13]. | |||
=7. Pathology= | =7. Pathology= | ||
A. lwoffii is a pathogenic microbe in humans and other animals, presenting as infectious and resistant to many antibiotics, including ciprofloxacin, ceftazidime, cefepime, and piperacillin [6, 15]. It has become an increasing issue in hospital infections due to its antibiotic resistance and high rate of infection in immunocompromised patients [14]. A. lwoffii was identified in several papers as being the cause of hospital infections in the ICU or neonatal units, including gastritis [14, 15]. The resilience of A. lwoffii in conditions of dessication allows it to act as a prime pathogen in hospitals [5]. Infections resulting from this pathogen have presented clinically in humans as wound infections, meningitis, septicaemia, pneumonia, and gastroenteritis [13, 16, 17]. An association with A. lwoffii has been identified with gastroenteritis, as when food with the presence of A. lwoffii is consumed and reaches the gastrointestinal tract, it adheres and invades the epithelial cells of the gut leading to gastroenteritis [13]. A. lwoffii has also been identified as a pathogen in many infections of the bloodstream, particularly in cases involving catheters [18]. | |||
=8. Current Research= | =8. Current Research= | ||
While A. baumannii is the most common Acinetobacter species to cause infections, there have been increasing reports of A. lwoffii being reported as a pathogen [19]. Current research is focused on discovering mechanisms that make A. lwoffii resistant to disinfectants and allow it to survive harsh environmental conditions. A study contributing to such research is one that used whole genome sequencing of five permafrost strains of A. lwoffii to analyze the strains’ resistance genes [8]. These plasmids in the strains contained functionally active genes resistant to salts of heavy metals and arsenic. This shows how arsenic, mercury, and other heavy metals contribute to resistance in A. lwoffii. | |||
Similarly, research shows that plasmids from Acinetobacter strains are able to carry numerous different genes [19]. This allows the host cell to survive in extreme environmental conditions that are usually restricting in growth or are lethal for the cell. If a cell has genes responsible for antibiotic resistance, then they would be located on plasmids. Looking at plasmid content of A. lwoffii, they found 342 protein-coding genes. The results of this study concluded that A. lwoffii can be considered potentially useful in bioremediation. | |||
Another recent study on the analysis of A. lwoffii strains was conducted between permafrost-conserved strains. It revealed no difference between the ancient and modern strains in terms of gene content for resistance to heavy metals and arsenic [20]. The modern strains of A. lwoffii had more antibiotic resistance genes than that of the permafrost strains. When the modern strains were exposed to antibiotics, they accumulated resistance genes. This analysis indicates that the permafrost strains could be potentially pathogenic to humans due to thawing caused by global warming. | |||
=9. References= | =9. References= | ||
[1] | [1]Schoch C.L. et al. 2020. Taxonomy browser (Acinetobacter lwoffii). National Center for Biotechnology Information. Retrieved 20 November 2021 from https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=28090&lvl=3&lin=f&keep=1&srchmode=1&unlock | ||
[2] Berlau, J., Auckland, H., Malnick, H., Pitt, T. 1999. Distribution of Acinetobacter Species on Skin of Health Humans. European Journal of Clinical Microbiology Infectious Diseases. 18:179-183. | |||
[3] Bouvet, P.J.M., Jeanjean, S., Vieu, J., Dijkshoorn, L. 1990. Species, Biotype, and | |||
Bacteriophage Type Determinations Compared with Cell Envelope Protein Profiles for Typing Acinetobacter Strains. Journal of Clinical Microbiology 28(2):170-176. | |||
[4] Constantiniu, S., Romaniuc, A., Iancu, L.S., Filimon, R., Tarasi, I. 2004. Cultural and Biochemical Characteristics of Acinetobacter spp. Strains Isolated From Hospital Units. Journal of Preventive Medicine 12:35-42. | |||
[5] Houang E.T., Sormunen R.T., Lai L., Chan C.Y., Leong A.S. 1998. Effect of desiccation on the ultrastructural appearances of Acinetobacter baumannii and Acinetobacter lwoffii. Journal of Clinical Pathology 51:786-788. | |||
[6] Hu, Y., Zhang, W., Liang, H., Liu, L., Peng, G., Pan, Y., Yang, X., Zheng, B., Gao, G. F., Zhu, B., Hu, H. 2011. Whole-Genome Sequence of a Multidrug-Resistant Clinical Isolate of Acinetobacter lwoffii. | |||
Journal of Bacteriology 193(19):5549–5550. | |||
[7] Liu, B., Pop, M. 2009. ARDB - Antibiotic Resistance Genes Database. Nucleic Acids Research 37:D443-D447. | |||
[8] Mindlin, S., Petrenko, A., Kurakov A., Beletsky, A., Mardanov, A., Petrova, M. 2016. | |||
Resistance of Permafrost and Modern Acinetobacter lwoffii Strains to Heavy Metals and Arsenic Revealed by Genome Analysis. BioMed Research International 2016:1-9. | |||
[9] Hata, D.J. 2010. Molecular methods for identification and characterization of acinetobacter spp. Molecular diagnostics. Academic Press 26:313-326. | |||
[10] Poduch, E., Kotra, L.P. 2007. Acinetobacter Infections. xPharm: The Comprehensive Pharmacology Reference. Elsevier 1:1-9. | |||
[11] Ku, S. C., Hsueh, P. R., Yang, P.C., Luh, K. T. 2000. Clinical and Microbiological Characteristics of Bacteremia Caused By Acinetobacter lwoffii. European Journal of Clinical Microbiology & Infectious Diseases 19:501-505. | |||
[12] Bouvet, P.J.M., Grimont, P. A. D. 1986. Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemolyticus sp. nov., Acinetobacter johnsonii sp. nov., and Acinetobacter junii sp. nov. and amended descriptions of Acinetobacter calcoaceticus and Acinetobacter lwoffii. International Journal of Systematic Bacteriology 36(2):228-240. | |||
[13] Regalado, N. G, Martin, G., Antony, S. J. 2009. Acinetobacter lwoffii: Bacteremia associated with acute gastroenteritis. Travel Medicine and Infectious Disease 7:316-317. | |||
[14] Kumari M., Batra P., Malhotra R., Mathur P. 2018. A 5-year surveillance on antimicrobial resistance of Acinetobacter isolates at a level-I trauma centre of India. Journal of Laboratory Physicians 11:34-38. | |||
[15] Zavros, Y., Reider, G., Ferguson, A., Merchant, J. L. 2002. Gastritis and Hypergastrinemia Due to Acinetobacter lwoffii in Mice. American Society for Microbiology 70(5):2630-2639. | |||
[16] Cao S., Geng Y., Yu Z., Deng L., Gan W., et al. Acinetobacter lwoffii, an emerging pathogen for fish in Schizothorax genus in China. Transboundary and Emerging Diseases 65:1816-1822. | |||
[17] Kenchappa P., Sreenivasmurthy B. 2005. Epidemiological investigation of nosocomial Acintebacter infections using arbitrarily primed PCR and pulse field gel electrophoresis. Indian Journal of Medical Research 46:700-706. | |||
[18] Turton J., Shah., Ozongwu C., Pike R. 2010. Incidence of Acintobacter species other than A. baumannii among clinical isolates of Acinetobacter: evidence for emerging species. Journal of Clinical Microbiology 48:1445-1449. | |||
[19] Walter, T., Klim, J., Jurkowski, M., Gawor, J., Köhling, I., Słodownik, M., Zielenkiewicz, U. 2020. Plasmidome of an environmental Acinetobacter lwoffii strain originating from a former gold and arsenic mine. Plasmid 110:1-17. | |||
[20] Rakitin, A. L., Ermakova, A. Y. , Beletsky, A. V., Petrova, M., Mardanov, A. V., Ravin, N. V.. 2021. Genome Analysis of Acinetobacter lwoffii Strains Isolated from Permafrost Soils Aged from 15 Thousand to 1.8 Million Years Revealed Their Close Relationships with Present-Day Environmental and Clinical Isolates. Biology 10(871):1-15. | |||
Edited by Jobelle Manuel, Lydia Mahan, Alisandra von Lichtenberg, Ann Marie Hannoush, and Mary Le, students of [mailto:jmbhat@bu.edu Jennifer Bhatnagar] for [http://www.bu.edu/academics/cas/courses/cas-bi-311/ BI 311 General Microbiology], 2021, [http://www.bu.edu/ Boston University]. | |||
Latest revision as of 15:32, 6 December 2021
1. Classification
a. Higher order taxa
Bacteria; Proteobacteria; Gammaproteobacteria; Pseudomonadales; Moraxellaceae; Acinetobacter; lwoffii [1]].
2. Description and significance
Acinetobacter lwoffii is a Gram negative, aerobic bacterium important in the skin microbiome and is found in the normal flora of the skin, oropharynx, and perineum [3]. A. lwoffii lives on the skin of healthy humans, in soil and plants, in frozen foods and poultry, and in human specimens, such as blood and urine [3]. However, it is dangerous upon entering the bloodstream as it is largely resistant to antimicrobials, meaning it can become dangerously pathogenic [3]. A. lwoffii is one of the most frequent species found in hospital samples, after Acinetobacter baumannii [3, 4]. A. lwoffii possesses the ability to survive and reproduce after desiccation in clinical and hospital environments at room temperature and is often a source of infection in hospital settings [5]. Current research is focused on what mechanisms make A. lwoffii resistant to antimicrobials and allow it to survive harsh environmental conditions.
3. Genome structure
Whole-genome sequencing has been performed on multiple strains of A. lwoffii. The genome of A. lwoffii WJ10621, a clinical strain of A. lwoffii that is resistant to several drugs, contains 3,419,011 bases and 3,394 predicted coding sequences, with a G+C content of 41.57% [6]. The genome contains 83 tandem repeat regions, 6 copies of the 5S rRNA gene, 7 copies of the 23S rRNA gene, and 6 copies of the 16S rRNA gene, as well as 91 predicted tRNA genes [6]. In this genome, 62 genes were assigned to the “resistance to antibiotics and toxic compounds” subsystem and 56 gene products showed at least 50% protein similarity with antibiotic resistance genes in the Antibiotic Resistance Genes Database (ARDB) [7]. A total of 26 genes coding for cobalt-zinc-cadmium resistance and 14 coding for multidrug resistance efflux pumps were predicted (6). This strain contains genes involved in amino acid metabolism (309 genes) and carbohydrate metabolism (243 genes) [6]. There are 84 predicted transposase genes distributed in the genome, which suggests the existence of frequent horizontal gene transfer events [6].
Whole-genome sequencing was also conducted on five strains of A. lwoffii (ED23-25, ED45-23, ED9-5a, VS15, and AK30A) that were isolated from permafrost sediments collected from different regions of Kolyma Lowland [8]. These environmental strains of A. lwoffii have five large plasmids that contain genes of heavy metal resistance. There are genes that encode resistance to salts of mercury, arsenic, chromium, copper, and cobalt-zinc-cadmium, such as the czc, mer, ars, and cop operon [8]. These genes encode for transporter proteins that regulate the amount of heavy metal in the cell by exporting excess amounts of heavy metals out of the cell. This transport system confers resistance to these heavy metals and allows A. lwoffii to survive in conditions of extreme heavy metal concentrations [8].
4. Cell structure
A. lwoffii is a Gram-negative species of bacteria that is non-motile, meaning it does not have its own mechanism of movement. The shape of A. lwoffii bacteria is described as a coccobacilli, a mix between a round shape and a rod shape [3]. Under conditions of dessication, A. lwoffii tend to exist more as round cells, and may even increase the thickness of their cell walls [5].
5. Metabolic processes
A. lwoffii is an aerobic bacterium incapable of fermentation [9]. It is psychrotrophic, meaning its optimal growth temperature is 7°C or higher (9). When tested with Kovac’s reagent, Acinetobacter species are oxidase negative [9]. They are catalase positive and nonmotile [9]. A. lwoffii is nitrate negative and O-F negative: however, A. lwoffii can use both ammonium and nitrate as nitrogen sources [10]. For carbon and energy sources, A. lwoffii is able to use a broad spectrum of organic compounds like ethanol, acetate and lactate [10]. However, most cannot metabolize glucose. In fact, when A. lwoffii are grown in a glucose-containing media, it acidifies the media via an aldose dehydrogenase [4]. A. lwoffiii can grow in low-pH environments, with optimum growth at around pH of 3.3 [9].
6. Ecology
A. lwoffii is commonly found in the normal flora of the human skin, oropharynx, perineum, as well as soil and plants all over the world [11, 12]. A. lwoffii has the ability to survive a wide range of temperatures, low pH, and dry conditions. It is often found in frozen food and poultry [13]. Strains of A. lwoffii are even found on the skin of newborns [4]. Compared to other rod-shaped bacteria, A. lwoffi is particularly successful at surviving in dry conditions and has been found to survive for up to 21 days under desiccation [5]. A. lwoffii is also resistant to sterilization methods such as disinfectants and irradiation [13].
7. Pathology
A. lwoffii is a pathogenic microbe in humans and other animals, presenting as infectious and resistant to many antibiotics, including ciprofloxacin, ceftazidime, cefepime, and piperacillin [6, 15]. It has become an increasing issue in hospital infections due to its antibiotic resistance and high rate of infection in immunocompromised patients [14]. A. lwoffii was identified in several papers as being the cause of hospital infections in the ICU or neonatal units, including gastritis [14, 15]. The resilience of A. lwoffii in conditions of dessication allows it to act as a prime pathogen in hospitals [5]. Infections resulting from this pathogen have presented clinically in humans as wound infections, meningitis, septicaemia, pneumonia, and gastroenteritis [13, 16, 17]. An association with A. lwoffii has been identified with gastroenteritis, as when food with the presence of A. lwoffii is consumed and reaches the gastrointestinal tract, it adheres and invades the epithelial cells of the gut leading to gastroenteritis [13]. A. lwoffii has also been identified as a pathogen in many infections of the bloodstream, particularly in cases involving catheters [18].
8. Current Research
While A. baumannii is the most common Acinetobacter species to cause infections, there have been increasing reports of A. lwoffii being reported as a pathogen [19]. Current research is focused on discovering mechanisms that make A. lwoffii resistant to disinfectants and allow it to survive harsh environmental conditions. A study contributing to such research is one that used whole genome sequencing of five permafrost strains of A. lwoffii to analyze the strains’ resistance genes [8]. These plasmids in the strains contained functionally active genes resistant to salts of heavy metals and arsenic. This shows how arsenic, mercury, and other heavy metals contribute to resistance in A. lwoffii.
Similarly, research shows that plasmids from Acinetobacter strains are able to carry numerous different genes [19]. This allows the host cell to survive in extreme environmental conditions that are usually restricting in growth or are lethal for the cell. If a cell has genes responsible for antibiotic resistance, then they would be located on plasmids. Looking at plasmid content of A. lwoffii, they found 342 protein-coding genes. The results of this study concluded that A. lwoffii can be considered potentially useful in bioremediation.
Another recent study on the analysis of A. lwoffii strains was conducted between permafrost-conserved strains. It revealed no difference between the ancient and modern strains in terms of gene content for resistance to heavy metals and arsenic [20]. The modern strains of A. lwoffii had more antibiotic resistance genes than that of the permafrost strains. When the modern strains were exposed to antibiotics, they accumulated resistance genes. This analysis indicates that the permafrost strains could be potentially pathogenic to humans due to thawing caused by global warming.
9. References
[1]Schoch C.L. et al. 2020. Taxonomy browser (Acinetobacter lwoffii). National Center for Biotechnology Information. Retrieved 20 November 2021 from https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=28090&lvl=3&lin=f&keep=1&srchmode=1&unlock
[2] Berlau, J., Auckland, H., Malnick, H., Pitt, T. 1999. Distribution of Acinetobacter Species on Skin of Health Humans. European Journal of Clinical Microbiology Infectious Diseases. 18:179-183.
[3] Bouvet, P.J.M., Jeanjean, S., Vieu, J., Dijkshoorn, L. 1990. Species, Biotype, and Bacteriophage Type Determinations Compared with Cell Envelope Protein Profiles for Typing Acinetobacter Strains. Journal of Clinical Microbiology 28(2):170-176.
[4] Constantiniu, S., Romaniuc, A., Iancu, L.S., Filimon, R., Tarasi, I. 2004. Cultural and Biochemical Characteristics of Acinetobacter spp. Strains Isolated From Hospital Units. Journal of Preventive Medicine 12:35-42.
[5] Houang E.T., Sormunen R.T., Lai L., Chan C.Y., Leong A.S. 1998. Effect of desiccation on the ultrastructural appearances of Acinetobacter baumannii and Acinetobacter lwoffii. Journal of Clinical Pathology 51:786-788.
[6] Hu, Y., Zhang, W., Liang, H., Liu, L., Peng, G., Pan, Y., Yang, X., Zheng, B., Gao, G. F., Zhu, B., Hu, H. 2011. Whole-Genome Sequence of a Multidrug-Resistant Clinical Isolate of Acinetobacter lwoffii. Journal of Bacteriology 193(19):5549–5550.
[7] Liu, B., Pop, M. 2009. ARDB - Antibiotic Resistance Genes Database. Nucleic Acids Research 37:D443-D447.
[8] Mindlin, S., Petrenko, A., Kurakov A., Beletsky, A., Mardanov, A., Petrova, M. 2016.
Resistance of Permafrost and Modern Acinetobacter lwoffii Strains to Heavy Metals and Arsenic Revealed by Genome Analysis. BioMed Research International 2016:1-9.
[9] Hata, D.J. 2010. Molecular methods for identification and characterization of acinetobacter spp. Molecular diagnostics. Academic Press 26:313-326.
[10] Poduch, E., Kotra, L.P. 2007. Acinetobacter Infections. xPharm: The Comprehensive Pharmacology Reference. Elsevier 1:1-9.
[11] Ku, S. C., Hsueh, P. R., Yang, P.C., Luh, K. T. 2000. Clinical and Microbiological Characteristics of Bacteremia Caused By Acinetobacter lwoffii. European Journal of Clinical Microbiology & Infectious Diseases 19:501-505.
[12] Bouvet, P.J.M., Grimont, P. A. D. 1986. Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemolyticus sp. nov., Acinetobacter johnsonii sp. nov., and Acinetobacter junii sp. nov. and amended descriptions of Acinetobacter calcoaceticus and Acinetobacter lwoffii. International Journal of Systematic Bacteriology 36(2):228-240.
[13] Regalado, N. G, Martin, G., Antony, S. J. 2009. Acinetobacter lwoffii: Bacteremia associated with acute gastroenteritis. Travel Medicine and Infectious Disease 7:316-317.
[14] Kumari M., Batra P., Malhotra R., Mathur P. 2018. A 5-year surveillance on antimicrobial resistance of Acinetobacter isolates at a level-I trauma centre of India. Journal of Laboratory Physicians 11:34-38.
[15] Zavros, Y., Reider, G., Ferguson, A., Merchant, J. L. 2002. Gastritis and Hypergastrinemia Due to Acinetobacter lwoffii in Mice. American Society for Microbiology 70(5):2630-2639.
[16] Cao S., Geng Y., Yu Z., Deng L., Gan W., et al. Acinetobacter lwoffii, an emerging pathogen for fish in Schizothorax genus in China. Transboundary and Emerging Diseases 65:1816-1822.
[17] Kenchappa P., Sreenivasmurthy B. 2005. Epidemiological investigation of nosocomial Acintebacter infections using arbitrarily primed PCR and pulse field gel electrophoresis. Indian Journal of Medical Research 46:700-706.
[18] Turton J., Shah., Ozongwu C., Pike R. 2010. Incidence of Acintobacter species other than A. baumannii among clinical isolates of Acinetobacter: evidence for emerging species. Journal of Clinical Microbiology 48:1445-1449.
[19] Walter, T., Klim, J., Jurkowski, M., Gawor, J., Köhling, I., Słodownik, M., Zielenkiewicz, U. 2020. Plasmidome of an environmental Acinetobacter lwoffii strain originating from a former gold and arsenic mine. Plasmid 110:1-17.
[20] Rakitin, A. L., Ermakova, A. Y. , Beletsky, A. V., Petrova, M., Mardanov, A. V., Ravin, N. V.. 2021. Genome Analysis of Acinetobacter lwoffii Strains Isolated from Permafrost Soils Aged from 15 Thousand to 1.8 Million Years Revealed Their Close Relationships with Present-Day Environmental and Clinical Isolates. Biology 10(871):1-15.
Edited by Jobelle Manuel, Lydia Mahan, Alisandra von Lichtenberg, Ann Marie Hannoush, and Mary Le, students of Jennifer Bhatnagar for BI 311 General Microbiology, 2021, Boston University.
