Wohlfahritiimonas chitiniclastica: Difference between revisions
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''Armillaria mellea'' | |||
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Revision as of 21:07, 9 December 2025
Classification
Higher order taxa
Domain: Bacteria [1][2].
Kingdom: Pseudomonadati [1][2].
Phylum: Pseudomonadota (Proteobacteria) [1][2].
Class: Gammaproteobacteria (g-proteobacteria) [3].
Order: Cardiobacteriales [1][2].
Family: Igantzschineriaceae [1][2].
Genus: Wohlfahrtiimonas [3].
Species
Wohlfahrtiimonas chitiniclastica [3]
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NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=47429&l vl=3&lin=f&keep=1&srchmode=1&unlock] |
Armillaria mellea
Description and significance
Wohlfahrtiimonas chitiniclastica is a Gram-negative, aerobic bacterium of the class Gammaproteobacteria [3]. It was first identified in 2008 from parasitic fly (Wohlfahrtia magnifica) larvae as a species within a new genus, Wohlfahrtiimonas [3]. To date, three species within the genus have been identified, with W. chitiniclastica being the only one involved in human infection [4]. W. chitiniclastica is a serious pest of livestock, and has been linked to myiasis, a condition where fly larvae infest living and necrotic tissue, particularly in wound infections caused by W. magnifica larvae [5][6][10]. Myiasis caused by W. chitiniclastica is particularly severe in people with chronic wounds, poor sanitation, or who are immunocompromised [7][8]. From its first isolation in 2008 to 2025, 44 cases of W. chitiniclastica infection have been reported globally [4]. From these previous case studies and current research, the genome structure, cell structure, basic metabolic processes, and virulence factors of W. chitiniclastica have been identified. Despite increasing clinical reports, the exact mechanism of pathogenesis and transmission routes by W. chitiniclastica remains unclear, thus inhibiting proper prevention and treatment [9].
Genome structure
Genomes of Wohlfahrtiimonas chitiniclastica have been sequenced from 28 strains found in different parts of the world, with 24 strains from human sources, and 4 from animal sources [10]. Genome sizes range from 1.99 to 2.18 million base pairs with a G+C content of 44.3 mol% [3][9]. All strains share housekeeping genes, including ribosomal proteins, as well as macrolide resistance genes including macA and macB genes and multidrug efflux systems [9]. In the accessory genome, conserved virulence factor B (cvfB) and antimicrobial resistance genes are found against tetracycline, aminoglycosides, sulfonamide, streptomycin, chloraphenicol, and beta lactamases [10]. Genes for toxin-antitoxin (TA) modules that mediate cell stress, including the relG toxin, the YefM-YoeB module, and PasTI modules, were identified [10]. Additionally, Type 2 Secretion (T2S) system genes for cellular and tissue degrading proteins, including proteases, cellulases, pectinases, phospholipases, lipases, were identified [9][10]. . Genes encoding for proteins involved in chitin degradation (which is found in insect exoskeletons) reflect the bacteria’s parasitic relationship with flies [3][9][10]. Strain BM-Y isolated from a zebra carries the blaVEB-1 gene cassette, which can express extended-spectrum β-lactamase (EBSL), resulting in reduced efficacy of β-lactam antibiotics [11].
Cell structure
Wohlfahrtiimonas chitiniclastica is Gram-negative, with rod-shaped cells that are approximately 1.5 -- 2.0 µm in length and 0.5 -- 1.0 µm in width [3]. Wohlfahrtiimonas chitiniclastica is strictly aerobic, non-motile, and non-spore-forming [8]. Colonies grown on nutrient agar at 35 ℃ are smooth, convex, glistening, and have entire edges [3][6].
Metabolic processes
W. chitiniclastica is a chemoorganoheterotroph, utilizing organic compounds for both carbon and energy [9]. It is a facultative anaerobe, allowing it to metabolize substrates through aerobic respiration and utilize byproducts of host inflammation [9]. W. chitiniclastica also secretes digestive proteins including proteases, cellulases, pectinases, phospholipases, and lipases, allowing better infectivity [9][10]. Wohlfahrtiimonas chitiniclastica produces chitinase enzymes, allowing it to break down chitin, a major component of insect exoskeletons and fungal cell walls, which helps W. chitiniclastica invade fly larvae and spread through myiasis [3][9]. Additionally, W. chitiniclastica is non-fermentative and is capable of metabolizing amino acids for growth [9].
Ecology
Wohlfahrtiimonas chitiniclastica was originally isolated from parasitic flies, specifically a primary laboratory culture of a third stage Wohlfahrtia magnifica larvae [3]. Wohlfahrtia magnifica is a serious pest of live vertebrates, primarily livestock, in Eastern Europe, the Mediterranean, and Middle Asia. However, increasing global cases, with infection cases in South America and Australia where Wohlfahrtia magnifica does not exist, indicate that W. chitiniclastica can be transmitted from other fly species in different regions, including Lucilia sericata, Lucilia illustris, Chrysomya megacephala, Hermetia illucens, and Musca domestica [5][6][10]. W. chitiniclastica infections have been documented with 21 cases in Europe, 15 cases in the United States, 6 in Asia, 1 in Australia, and 1 in Africa [5][10]. W. chitiniclastica is usually spread through the infestation of parasitic flies’ larvae, which infest mammals, including humans and livestock [10]. The variety of geographical location in which W. chitiniclastica has been identified indicates its ability to survive in various environmental temperatures [10].
Pathology
Wohlfahrtiimonas chitiniclastica has recently gained attention as a human pathogen capable of causing a spectrum of infections, from wound colonization to bacteremia and sepsis [8][12]. Infection occurs when fly larvae carrying W. chitiniclastica infest wounds [8][12]. Infection from environmental contact and food sources has also been described. In addition to W. chitiniclastica being a facultative anaerobe, its ability to survive in multiple environments increases risks for zoonotic transmission from animal to human hosts [10]. Populations with poor hygiene or immunosuppression are at higher risk due to skin barrier disruptions and impaired immune function [12]. Clinically, infections can present with local inflammation, pus, fever, and in severe cases, systemic inflammatory response leading to sepsis [5][6][7][8][12][13]. Both monomicrobial and polymicrobial infections have been reported, with polymicrobial cases more common [13]. Frequent co-pathogens reported alongside W. chitiniclastica include Ignatzschineria indica, Escherichia coli, Morganella morganii, Proteus mirabilis, Providencia rettegri, and Staphylococcus aureus [5][13][14]. Studies have identified virulence factors, such as conserved virulence factor B (cvfB) observed in all W. chitiniclastica isolates [9][10]. Deletion of cvfB resulted in decreased virulence, demonstrating its importance in the pathogenesis of W. chitiniclastica [9][10]. Toxin-antitoxin (TA) modules, including the relG toxin, the YefM-YoeB module, and PasTI modules were identified, which benefit bacterial survival by mediating stressors caused by nutrient limitations or antibiotics, for example [10]. Additionally, Type 2 Secretion (T2S) systems secrete proteins including proteases, cellulases, pectinases, phospholipases, lipases, which cause destruction of tissues and cells to allow for better infectivity [9][10].
Current Research
Recent studies have advanced the understanding of W. chitiniclastica regarding its antimicrobial resistance profiles, virulence factors, and genetic diversity. Whole-genome sequencing and plasmid analysis have revealed drug resistance mechanisms, including efflux pump genes that expel antibiotics from the cell and β-lactamase gene cassettes that break down β-lactam antibiotics [9][10]. These findings extend earlier characterizations of W. chitinclastica’s resistance traits, emphasizing the clinical challenge posed by its emerging antibiotic resistance [6][14]. Researchers are now using MALDI-TOF MS, a rapid protein-based mass-spectrometry method, which identify bacteria by their unique molecular “fingerprint,” along with 16S rRNA gene sequencing procedures to identify W. chitiniclastica [5][14]. Early diagnosis of W. chitiniclastica using MALDI-TOF is correlated with improved treatment outcomes, using the antibiotics carbapenems and fluoroquinolones [14]. Nevertheless, standardized treatment protocols remain underdeveloped due to the rarity of reported cases and the variation in the species’ antimicrobial susceptibility. Vaccine development has not yet been reported for W. chitiniclastica. However, recent genomic analyses have revealed the toxin-encoding gene relG in some strains, as well as the virulence factor cvfB, both of which may serve as potential targets for future drug development [14]. Epidemiological studies continue to clarify transmission dynamics, including the diversity of fly vectors implicated in the distribution of W. chitiniclastica across Europe, Australia, Asia, Africa, and the Americas [6]. Populations at increased risk of infection, such as individuals experiencing homelessness and those with chronic wounds, are exemplified by recent case studies, demonstrating the need to investigate improved infection control and prevention [8].
References
[1] Sayers, E., et al. (2019). GenBank, Nucleic Acids Research, 47(D1): D94–D99.
Edited by Susanna Dai, Lucca DeFulgentis, Jozef Janak, Joshua Mueller, Matisse Nash, students of [Jennifer Bhatnagar (jmbhat@bu.edu)]
for BI 311 General Microbiology, 2024, Boston University.
[[Category:Pages edited by students of Jennifer Bhatnagar at Boston University]]
