Alcaligenes xylosoxidans

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Class: Betaproteobacteria
Order: Burkholderiales
Family: Alcaligenaceae
Genus: Achromobacter (formerly Alcaligenes)
Species: Achromobacter xylosoxidans


After it was discovered the only difference between the Alcaligenes and Achromobacter motile strains was the reaction in litmus milk, the genus name Alcaligenes was changed to Achromobacter. [1] Achromobacter signifies colorless rodlet and xylosoxidans implies oxidizing xylose. Although Achromobacter strains had been previously described, Yabuuchi and Ohyama were the first to isolate Achromobacter xylosoxidans from ear discharge.[2]

Morphology and Cell Structure

Colonies are circular, flat to convex, smooth, and have an entire margin. The colonies tend to be colorless or grayish white. Cells are rod-shaped and Gram-negative. Individual cells are motile due to a peritrichous flagellar arrangement[3], and its movement is described as swimming. Achromobacter xylosoxidans also has the ability to form biofilms, which is important to its pathogenicity because it protects the bacterial cells from attacks by host cells.[4]

Nutrition and Growth

In the presence of nitrate or nitrite, the species grows anaerobically.[3]The bacteria are able to do so because they are capable of using denitrification for respiration and have the flexibility to use either nitrate or nitrite as the electron acceptor. [4] Bacteria of this species are chemoorganotrophic, meaning they oxidize organic compound electron donors to produce energy. Cells are limited to using only D-glucose as this organic source for energy.[3]

Achromobacter xylosoxidans has been shown to grow on several types of agars. When it was first isolated, it was grown successfully on Leifson's deoxycholate agar, Salmonella-Shigella agar, and nalidixic acid-cetrimide (NAC) agar.[2]The first two agars help differentiate Salmonella and Shigella species, and the NAC agar is often used to selectively isolate Pseudomonas species. This bacteria has also been grown on Mueller-Hinton agar, commonly used in experiments testing antibiotic resistance, at 37 degrees Celsius.[5] This species also thrives on nutrient agar.[3]

Genome (Betaproteobacteria)

A. xylosoxidans is a member of the Domain Bacteria, and it is more specifically classified as a Betaproteobacteria. To determine the genus of the species, the 16S rRNA gene was sequenced. This species can be identified by sequencing a specific set of 765 base pairs known as the internal mrdA fragment. One operon of this species, called the axyXY-oprZ operon, allows it to be resistant to aminoglycoside. The presence of this operon and the resistance it provides for the bacteria is significant because aminoglycoside is used in the treatment of cystic fibrosis.[5] The entire genome for Achromobacter xylosoxidans was sequenced by Jakobsen et al. (2013) and is accessible at the link While sequencing this genome, Jakobsen et al. recorded many details about the composition of the genome. It is composed of 6,916,670 base pairs, and has 6390 ORFs. ORFs, or open reading frames, refer to parts of the genome capable of being translated. There are also 6390 protein-coding genes. Out of the entire genome, the GC content is 67%, meaning the AT content is 33%.[4]


This species of bacteria is known to naturally occur in water and soil.[3]In one study, A. xylosoxidans was found to recruit copper in the soil and directly improve a plant's uptake of copper. In the experiment, the bacteria used 1-aminocyclopropane-1-carboxylic acid (ACC) as a nitrogen source, helping it produce indole acetic acid (IAA) and solubilize phosphate. It was these specific actions of the bacteria promoted the extra growth of the plant's roots, shoots, and biomass.[6] The interactions between A. xylosoxidans and other microbes is mainly in forming biofilms with other microbes that can lead to infections or illnesses in humans. For example, this species is often found in conjuction with several other pathogenic microbes in patients with cystic fibrosis.[7]


For a long period of time, it was assumed that this bacteria only posed the threat of sepsis to immunocompromised individuals. In fact, the species was considered to be of low pathogenicity to humans, generally targeting transplant recipients, individuals with renal failure, or individuals with other conditions that negatively impacted their immune system. After gathering more research on the species, it is now known as an opportunistic human pathogen, and can lead to several infections, including "endophthalmitis, keratoconjunctivitis, catheter-associated bloodstream infection, endocarditis, pneumonia, meningitis, and peritonitis"[8]

This pathogen utilizes three different secretion systems to infect: Type 2 Secretion System (T2SS), Type 3 Secretion System (T3SS), and Type 6 Secretion System (T6SS). The T2SS has the role of releasing toxins and proteases into the extracellular environment. The T3SS and T6SS are responsible for transport of the cell so it can come in contact with target cells. Once bound to the target cell, the T3SS can inject the virulence factors directly into the target cell.[4]

The bacteria is commonly found in cystic fibrosis patients. The mucus of an individual with cystic fibrosis is especially thick and deficient in oxygen, providing a suitable anaerobic environment for A. xylosoxidans to live in because it utilizes anaerobic respiration.[4]

A. xylosoxidans is often detected in hospitals, specifically in wet environmental areas. Examples include in respirators, incubators, and disinfectants. The species is resistant to a variety of antibiotics, making it difficult to combat when it is infecting an individual.[9]The threat of this bacterium is compounded by the fact that its antibiotic resistance is known to increase after it becomes infectious, and its patterns of antibiotic resistance change constantly.[4][9]In one study, A. xylosoxidans was linked to infection outbreaks in burn units.[9]Additionally, it is possible to transmit the infection from person to person.[7]

Despite its antibiotic resistance and adaptability, some successful treatments have been found against A. xylosoxidans. Combinations of antibiotics seem to be most effective in contesting the bacterial cells. Some helpful antimicrobial treatments include chloramphenicol-minocycline, ciproflaxin-imipenem, and cirpofloxacin-meropenem.[4]More recently, bacteriophages specific to this species have been sought out as a possible treatment option.

Current Research

Since A. xylosoxidans has eluded advancements in treatment through adaptation, scientists have been looking for ways to combat this bacterium. One paper by Ma et al. (2016) discussed the discovery of a potential treatment.[10] A medical approach that is continually being developed to fight microbes is using phage therapy. This involves the use of a lytic bacteriophage (a phage capable of destroying the target cell) that is specific to pathogenic microbes so it can target only those cells and destroy them. In their paper, the researchers admit that several phages for A. xylosoxidans have previously been discovered and fully sequenced, including phiAxp-1, JWAlpha, and JWDelta. In their experiment, a new phage specific to the bacterium was discovered called phiAxp-3. This phage was able to use any exposed LPS on the bacterium as the receptor site to bind to and enter the cell, eventually destroying the cell.[10]

Another paper determined that A. xylosoxidans can form biofilms on contact lenses and lead to eye infections.[11] Wearing contact lenses leads to a higher risk of being diagnosed with microbial keratitis and infectious corneal ulcers. These infections begin when microbes on the lens are able to penetrate the epithelial surface of the eye and invade the host. Formerly, it was widely accepted that the most common pathogens leading to eye infections were Pseudomonas aeruginosa, Serratia marcescens, and Staphylococcus aureus, respectively. However, this study found that species of the genus Achromobacter dominated the microbial community found on contact lenses and contact cases. Specifically, the Achromobacter-induced infections were described as slow growing, periodic infections that could lead to corneal ulcers. The dominance of this genus was attributed to its ability to form biofilms and its ability to survive in disinfectant solutions. Now that this information has been discovered, the treatment for corneal ulcers can be adjusted so it is more effective against the resistant Achromobacter species.[11]


  1. Hendrie MS, Hodgkiss W, Shewan JM. 1964. Consideration on organisms of the Achromobacter-Alcaligenes group. Ann. Inst. 15:43-59.
  2. 2.0 2.1 Yabuuchi E, Ohyama A. 1971. Achromobacter xylosoxidans n. sp. from human ear discharge. Japan. J. Microbiol. 15(5):477-481.
  3. 3.0 3.1 3.2 3.3 3.4 Vos, P., Garrity, G., Jones, D., Krieg, N.R., Ludwig, W., Rainey, F.A., Schleifer, K.-H. & Whitman, W.B. (eds., 2009). Bergey’s Manual of Systematic Bacteriology, 2nd ed., vol. 3, Springer-Verlag, New York, NY.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Jakobsen TH, Hansen MA, Jensen PO, Hansen L, Riber L, Cockburn A, Kolpen M, Ronne Hansen C, Ridderberg W, Eickhardt S, Hansen M, Kerpedjiev P, Alhede M, Qvortrup K, Burmolle M, Moser C, Kuhl M, Ciofu O, Givskov M, Sorensen SJ, Hoiby N, Bjarnsholt. 2013. Complete genome sequence of the cystic fibrosis pathogen Achromobacter xylosoxidans NH44784-1996 complies with important pathogenic phenotypes. PLoS One. 8(7):e68484
  5. 5.0 5.1 Bador J, Neuwirth C, Liszczynski, Mezier MC, Chretiennot M, Grenot E, Chapuis A, de Curraize C, Amoureux L. 2016. Distribution of innate efflux-mediated aminoglycoside resistance among different Achromobacter species. New Microbes New Infect. 10:1-5.
  6. Ma Y, Rajkumar M, Freitas H. 2009. Inoculation of plant growth promoting bacterium Achromobacter xylosoxidans strain Ax10 for the improvement of copper phytoextraction by Brassica juncea. J Environ Manage. 90(2):831-7.
  7. 7.0 7.1 Firmida MC, Pereira RHV, Silva EASR, Marques EA, Lopes AJ. 2016. Clinical impact of Achromobacter xylosoxidans colonization/infection in patients with cystic fibrosis. Braz J Med Biol Res. 49(4):e5097.
  8. Spilker T, Vandamme P, LiPuma JJ. 2012. A multilocus sequence typing scheme implies population structure and reveals several putative novel Achromobacter species. J Clin Microbiol. 50(9): 3010-3015
  9. 9.0 9.1 9.2 Schulz A, Perbix W, Fuchs PC, Seyhan H, Schiefer JL. 2016. Contamination of burn wounds by Achromobacter xylosoxidans followed by severe infection: 10-year analysis of a burn unit population. Ann Burns Fire Disasters. 29(3):215-222.
  10. 10.0 10.1 Ma Y, Li E, Qi Z, Li H, Wei X, Lin W, Zhao R, Jiang A, Yang H, Yin Z, Yuan J, Zhao X. 2016. Isolation and molecular characterization of Achromobacter phage phiAxp-3, an N4-like bacteriophage. Sci Rep. 6:24776.
  11. 11.0 11.1 Wiley L, Bridge DR, Wiley LA, Odom JV, Elliot T, Olson JC. 2012. Bacterial biofilm diversity in contact lens-related disease: emerging role of Achromobacter, Stenotrophomonas, and Delftia. IOVS. 53: 3896-3905.

Authored by Sara Frey, a student of CJ Funk at John Brown University