Acinetobacter baylyi

A. baylyi under 10x ocular lens and 100x objective lens with crystal violet stain.

Acinetobacter baylyi
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Pseudomonadales
Family: Moraxellaceae
Genus: Acinetobacter
Species:
A. baylyi
Binomial name
Acinetobacter baylyi
Carr et al. 2003

Acinetobacter baylyi is a bacterial species of the genus Acinetobacter.[1] The species designation was given after the discovery of strains in activated sludge in Victoria, Australia, in 2003.[2] A. baylyi is named after the late Dr. Ronald Bayly, an Australian microbiologist who contributed significantly to research on aromatic compound catabolism in diverse bacteria, including strains of Pseudomonas, Alcaligenes, and Acinetobacter.[3] This strain was previously designated Acinetobacter sp. and Acinetobacter calcoaceticus. The new species designation in 2003 was found to apply to an already well-studied Acinetobacter strain known as ADP1 (previously known as BD413), a derivative of a soil isolate characterized in 1969.[4] Research has established A. baylyi as a model organism.[5][6]

As with other species of Acinetobacter, it is a nonmotile, Gram-negative coccobacillus. It grows under strictly aerobic conditions, is catalase-positive, nitrate-negative, oxidase-negative, and non-fermentative.[7] The species is naturally competent, meaning that it can take up free exogenous DNA from its surroundings and incorporate the DNA into its own chromosomal DNA by transformation.[8] Its natural transformation and homologous recombination are exceptionally efficient in comparison to all studied microbes, thus contributing to its experimental utility.[9]

A. baylyi has been observed as a novel, low-virulence nosocomial pathogen, despite lacking typical virulence-related genes, that is resistant to many common antibiotics. It is primarily acquired by patients who have immunosuppressing conditions like diabetes or malignancy. However, it is still treatable with alternative antimicrobial medications.[10][11] A. baylyi's survival depends on a bacterial "contact-dependent growth inhibition" (CDI) system that transports toxic self-produced proteins to the microbe's outer membrane to hinder the growth of neighboring cells. Despite aiding in A. baylyi biofilm formation, CdiA proteins do not contribute to enhancing the biofilm's attachment to host epithelial cells. A. baylyi has shown promise as a method for alternative fuel sources.[12]

Metabolism

A. baylyi metabolic pathways have been used for many studies in microbial metabolism, known for its fast growth rate and ability to be easily cultured.[8] A. baylyi can be cultured in media using organic carbon sources to survive such as succinate, pyruvate, acetate, and ethanol.[13] A. baylyi is also known as an omnipresent bacterium, meaning it can be found many places in nature.[2]

A. baylyi prefers to utilize organic carbon sources that can enter the citric acid cycle quickly, requiring few intermediate reaction steps. This is notably achieved by aromatic compounds. A. baylyi is able to utilize aromatic compounds as organic carbon and energy sources through the unique β-ketoadipate pathway. Aromatic compounds are first transformed into catechol and protocatechuate, which then are transformed into the citric acid cycle substrates succinyl-CoA and acetyl-CoA, respectively.[14][15]

A. baylyi's glucose metabolism is slower in comparison to its metabolism of organic compounds, as it lacks a gene encoding for pyruvate kinase, a vital enzyme in glycolysis for transforming phosphoenolpyruvate into pyruvate.[14][16][13][17] When glucose is the primary carbon source available, A. baylyi can metabolize glucose by first oxidizing it into gluconate, which feeds into the Entner-Doudoroff pathway. Without pyruvate kinase, A. baylyi has to use a work-around of transforming the phosphoenolpyruvate into oxaloacetate, then malate, which can then become pyruvate and enter the pyruvate dehydrogenase complex and later the citric acid cycle.[16]

Unlike other bacteria that can predominantly use L-amino acids, A. baylyi is an example of this metabolic tolerance for different compounds with its ability to utilize D-Asp and L-Asp amino acids as both a primary carbon and nitrogen source, thus opening the door to see how D-enantiomers can be used for bacterial growth.[18]

Experiments have shown that A. baylyi uses intracellular arginine to produce a biodegradable alternative to petroleum-based plastics known as polyaspartic acid. A. baylyi uses arginine to first produce cyanophycin polypeptides, a transient source of nitrogen, which can then be converted to polyaspartic acid.[19][20] Cyanophycin is predominantly formed when nitrogen sources are low, and said nitrogen is released by cyanophycinase when environmental nitrogen is limited.[20]

Genetics

One major characteristic of A. baylyi is its ability to take in free DNA from the environment. It does so by importing the DNA by natural transformation, a mechanism that incorporates exogenous DNA into its chromosome, characteristic of A. baylyi.[8] The genome of A. baylyi has been completely sequenced, and roughly 35% of A. baylyi's genome sequence is solely devoted for encoding the machinery required for efficient uptake.[21] This mechanism strongly depends on A. baylyi's DNA strand break repair system to ensure success of recombination with exogenous DNA.[22] Most bacteria struggle to achieve this exchange of adaptive traits from outside DNA via simple point mutations, so the ease at which A. baylyi can take in foreign DNA is beneficial to its survival.[23] Natural transformation contributes greatly to this bacteria's ability in antibiotic resistance and vaccination escape.[8][23] This also makes A. baylyi an ideal microbe for laboratory experiments.[8] Collections of multiple single-gene mutations, caused by deletions, on dispensable genes of the ADP1 strain have been constructed. With the knowledge of the entire genome sequence and the mutants, scientists are able to know the functions of the APD1 strain in both directions, which expands the capability of the strain for industrial and environmental applications.[24]

The facilitation of A. baylyi's ability in natural transformation, or horizontal gene transfer (HGT) processes, may be aided by the mechanisms of outer membrane vesicles (OMVs). OMVs are produced via vesiculation, the bulging of the outer membrane followed by the constriction and release of small, spherical structures from the bacterium, and are composed of various periplasmic components, including proteins and lipids, as well as some genetic material. OMVs play significant roles in intracellular communication, virulence/bacterial defenses, and adaptation to environmental stress. OMVs released by A. baylyi offer a mode of gene transfer that is not susceptible to degradation by nucleases, contributing to the microbe's high survival rate and antibiotic resistance; however, environmental stress factors can impact the efficiency of these OMVs, ranging from levels of vesicle release to genetic content and HGT abilities.[25]

Due to its increasing involvement in hospital infections and multi-drug resistance nature back in 2014, A. baylyi strains have also been closely associated with pathogenicity, bacterial adhesion, and biofilm formation. Biofilms arise from the aggregation of surface microbial cells enveloped within a matrix of extracellular polymeric substances. The biofilms of Acinetobacter strains have been associated with various infectious diseases, including cystic fibrosis or urinary tract infections, due to their ability to adhere to medical devices composed of plastic or glass.[7] A. baylyi's genetic transformation mechanisms may be attributed to its success as an infectious agent due to the optimal environment it creates with its biofilms.[26] It has been found that two possible genes may be significant to biofilm formation: Fimbrial-biogenesis protein (3317) and Putative Surface protein. These genes are very similar to the genetic mechanisms behind the antibiotic resistance characteristics of a similar strand, Acinetobacter baumannii.[7]

ADP1 Strain

A. baylyi, specifically the strain ADP1, has been used for over a quarter of a century in several molecular biology studies due to its strong ability to easily undergo genetic transformation.[8][16] For these reasons, A. baylyi is used in multiple laboratory techniques as a model organism. These include genetics, specifically gene duplication and amplification as well as bacterial metabolism.[8][17] The microbe has also been studied for its potential use an alternative triacylglycerol (TAG) source, as under nitrogen limiting conditions it is able to transform excess organic matter into wax esters and triacylglycerols (TAGs) as a lipid storage form through the isoenzymes wax ester synthase/diacylglycerol acyltransferase.[27][13] The concentration of wax esters and triacylglycerols that the ADP1 strain produces depends on the organic matter present in medium of which the A. baylyi is grown on.[13] While A. baylyi as a general microbe has shown some recent virulence, the A. baylyi ADP1 strain specifically has been used as a non-virulent control when comparing to other Acinetobacter bacteria, such as A. baumannii.[28]

Applications

A. baylyi is typically sourced from contaminated environments like diesel oil- and crude oil-contaminated soils, contaminated river waters, activated sludge, lignocellulosic biomass, and more. The microbe is able to utilize the variety of pollutants, especially kinds based on aromatic compounds, heavy metals, and aliphatic substances, as carbon sources. A. baylyi has potential use for cleaning up contaminated natural environments via degradation, especially with management and supplementation of other necessary nutrients.[29]

A. baylyi also has the potential as a non-toxic biosurfactant alternative, emulsan, helping to break apart aggregated hydrophobic compounds like oil. Emulsan serves a range of industrial functions from a basic degreaser to emulsification of oil for subsequent removal or aid in transport, as the oil's viscosity is decreased and can move more smoothly through pipes. Additionally, emulsified oil can act as another source of energy. then makes it easier to degrade the compounds and remove them from the environment, ranging from functions.[30]

A. baylyi's ability to create TAGs has been used as a potential alternative method of producing TAG-based products like cosmetics, oleochemicals, and biofuels. They are currently made with the TAG sources of vegetable oils, animal fats, and recycled greases.[12] A. baylyi is particularly notable with TAG production as it has low selectivity on what kind of alcohol-based substrate to use.[31]

It has been proposed to combine A. baylyi's abilities to survive in contaminated environments as well as natural transformation in order to use the microbe as a biosensor. By incorporating DNA in A. baylyi ADP1 strain that will generate bioluminescence when activated by pollutant degradation mechanisms, the monitoring of soils and water supplies would be elevated.[32]

One of the most abundant resources is lignin, a complex organic polymer in plants responsible for reinforcing the rigidity of the cell wall and making them "woody."[33] This is typically discarded during industrial processes as it is difficult to breakdown the lignin into something usable.[34] Similar to creating an A. baylyi mutant strain specifically for monitoring of cleanliness of soils and waterways, incorporating DNA in A. baylyi ADP1 would result in a further optimized ability to degrade difficult compounds like lignin and make it into a useable molecule, like lipids.[35] This will lead to more efficient use of lignin-containing plants like trees as well as provide an alternative fuel source to petroleum-based products.[34]

Pathophysiology

Virulence factors

A. baylyi has been on the rise as a pathogen, however, the exact cause is unclear. It is hypothesized that this is a result of A. baylyi's high natural transformation ability. [36] This is unusual as the most commonly used A. baylyi strain lacks pathogenic traits and virulence-related genes like toxins, invasins, and secretory systems. However, a portion of its genome encodes for hemolysin-like proteins, which are proteins that can shred blood cells (usually erythrocytes), but the function of this genome portion is still unknown.[37] This results in A. baylyi being considered a low-virulence pathogen. A. baylyi is an opportunistic pathogen, typically acquired within a hospital setting by patients who already have coexisting diagnosis like diabetes mellitus or malignancy.[36]

Survival

A. baylyi codes for a bacterial "contact-dependent growth inhibition" (CDI) system, a common feature of Gram-negative bacteria. Cognate transport CdiB proteins on A. baylyi's membrane export toxic CdiA proteins to the outer membrane, which undergo a reaction by outer membrane receptors to release the C-terminal toxic (CT) domain responsible for inhibiting the growth of neighboring cells. CdiA proteins also facilitate the growth of an A. baylyi biofilm, however, the proteins do not assist in strengthening the biofilm's attachment to host epithelial cells.[38]

Additionally, A. baylyi has a variety of other structural features that contributes to its survival, ranging from lipopolysaccharide (LPS) chains in their outer membranes to having thick capsules. The LPS chains serve to provide structural integrity, and the capsule protects the microbe from complement-mediated killing by complement proteins, a part of the innate immune system.[39][40] It is important to note that A. baylyi's strong ability to perform natural transformation is a potential reason for its increasing antibiotic resistance as it is able to uptake exogenous DNA that has an antibiotic resistance gene (ARG). This is particularly impactful to the beta-lactam type of drugs.[10][41] Beta-lactam drugs include a beta-lactam ring in their chemical structure, and examples include penicillins and cephalosporins.[42] These are ineffective against A. baylyi as the microbe has β-lactamase enzymes which can metabolize said medications.[10]

Prophylaxis and Treatment

Prophylaxis

The commonest bacteria of the Acinetobacter genus that cause infections in humans are Acinetobacter baumannii species. A. baylyi is not typically known to also be harmful to humans. The most recommended method in preventing acquiring or spreading A. baylyi pathogens is to thoroughly wash hands and under fingernails with water and soap, especially before and after interacting with medical devices, "high-touch" surfaces, and wound care.[43]

Treatment

Studies have shown that by targeting the LysR-type transcriptional regulators present in the A. baylyi's with antibiotics has shown to show significant decline in the growth of the bacteria.[11] Antibiotics like imipenem, aminoglycosides, levofloxacin, trimethoprim/sulfamethoxazole, and chloramphenicol have demonstrated the greatest effectiveness in treating A. baylyi bacterial infection. Antimicrobial therapy has also been shown to help infected patients recover from infections caused by A. baylyi.[10]

Imipenem is part of the carbapenem drug class, which are resistant to degradation from β-lactamase enzymes. The drug affects A. baylyi by saturating and out-competing nutrients from entering the cell through specific nutrient uptake channels on its outer membrane, therefore blocking the channels. It especially impacts A. baylyi's ability to intake basic amino acids L-Arginine, lysine, and ornithine.[44]

Aminoglycosides are a category of drugs that inhibit the growth of Gram-negative bacteria, specifically by preventing protein synthesis.[45] Examples include streptomycin, neomycin, and tobramycin. They arose in response to multi-drug-resistance bacterial strains like A. baylyi, as well as Pseudomonas aeruginosa, Klebsiella pneumoniae, and Escherichia coli. Aminoglycosides are effective medications as they are first able to displace magnesium and calcium ions from bridging liposaccharides on the outer cell membrane, causing the bacteria's cell membrane to shift around and create pores due to the lack of cell membrane support. However, these pores also let in the aminoglycosides, which can then bind to the A-site of the 16S ribosomal RNA component of the 30S ribosomal subunit, inhibiting protein synthesis.[46]

Levofloxacin is a third-generation fluoroquinolone, acting upon nucleic acid transcription and replication as a non-intercalating topoisomerase poison, inhibiting the formation of new cells as a concentration-dependent bactericidal agent.[47][48] As A. baylyi is a Gram-negative bacteria, levofloxacin will both stabilize the temporary complex formed between the DNA helix and GyrB of DNA gyrase (a topoisomerase II enzyme), not allowing the enzyme to dissociate from the DNA, as well as block GyrA to pull the DNA strand through the C-gate, preventing the newly transcribed and replicated DNA from super-coiling, thereby not allowing the DNA to be stored away in the newly formed cell and killing it.[49][50][51]

Trimethoprim/sulfamethoxazole, typically given as a combination therapy known as co-trimoxazole, are two drugs that work together to inhibit A. baylyi's and other bacteria's folate synthesis metabolic pathway. Sulfamethoxazole, a sulphonamide, works first in the pathway by acting as a competitive inhibitor of dihydropteroate synthetase--an enzyme that only bacteria have and not humans--and preventing the synthesis of dihydropteroate from dihydropteroate diphosphate and p-aminobenzoic acid (PABA) by mimicking PABA.[52] The dihydropteroate is then condensed with L-Glutamic acid into dihydrofolate via an ATP-requiring reaction catalyzed by dihydrofolate synthetase.[53][52] Trimethoprim works next by inhibiting dihydrofolate reductase, an enzyme found in both humans and bacteria from reducing dihydrofolate into tetrahydrofolate. While dihydrofolate reductase is an enzyme found in both humans and bacteria, trimethoprim is "100,000 times" more selective towards the bacterial enzyme. Sulfamethoxazole and trimethoprim do not directly kill the bacteria, instead preventing the cell from growing and dividing to allow the body's immune system to fight it off.[52]

Chloramphenicol inhibits A. baylyi's peptidyl transferase enzyme, which is responsible for extending the protein chain by moving it from the tRNA on the bacterial ribosomal 50S subunit P-site to the next tRNA-bonded amino acid at the ribosomal 50S subunit A-site. As the transfer can't occur, the ribosome is no longer able to "read" the mRNA chain and protein synthesis is halted.[54]

References

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  29. ↑ Gutnick, David L.; Bach, Horacio (2008). Gerischer, Ulrike (ed.). Acinetobacter molecular microbiology. Norfolk, UK: Caister Academic Press. pp. 239–240. ISBN 978-1-904455-20-2. OCLC 154685348.
  30. ↑ Gutnick, David L.; Bach, Horacio (2008). Gerischer, Ulrike (ed.). Acinetobacter molecular microbiology. Norfolk, UK: Caister Academic Press. pp. 241, 249. ISBN 978-1-904455-20-2. OCLC 154685348.
  31. ↑ Gutnick, David L.; Bach, Horacio (2008). Gerischer, Ulrike (ed.). Acinetobacter molecular microbiology. Norfolk, UK: Caister Academic Press. pp. 250–251. ISBN 978-1-904455-20-2. OCLC 154685348.
  32. ↑ Gutnick, David L.; Bach, Horacio (2008). Gerischer, Ulrike (ed.). Acinetobacter molecular microbiology. Norfolk, UK: Caister Academic Press. p. 253. ISBN 978-1-904455-20-2. OCLC 154685348.
  33. ↑ Kirk-Othmer, ed. (2001-01-26). Kirk-Othmer Encyclopedia of Chemical Technology (1 ed.). Wiley. doi:10.1002/0471238961.12090714120914.a01.pub2. ISBN 978-0-471-48494-3.
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