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Aeromonas
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Encompassing a diverse group of Gram-negative, non-spore-forming, cocco bacillary species, the genus Aeromonas is classified taxonomically in the family Aeromonadaceae, order Aeromonadales, class Gammaproteobacteria, phylum Proteobacteria, and domain Bacteria. Being one of the five genera (i.e., Aeromonas, Oceanimonas, Oceanisphaera, Tolumonas, and Zobellella) within the family Aeromonadaceae, the genus Aeromonas shares remarkable biochemical (e.g., cytochrome oxidase), ecological (aquatic), and pathological similarities to members of the families Vibrionaceae (Vibrio) and Enterobacteriaceae (Plesiomonas), and indeed was once included in the family Vibrionaceae. It was only in 1986 when the genus Aeromonas became a member of the newly established Aeromonodaceae family after detailed examination of rRNA and housekeeping gene sequences [1].
Aeromonas
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Chi-Jung Wu, Maria José Figueras, Po-Lin Chen, Wen-Chien Ko
Aeromonas species are gram-negative, oxidase-positive, facultative anaerobic rod-shaped bacteria in the family Aeromonadaceae that are ubiquitously distributed in aquatic environments and established pathogens of fish and marine animals.1 They are also associated with a wide spectrum of diseases in humans, including gastroenteritis, septicemia, skin and soft-tissue infections, biliary tract infection, and other uncommon infections.1 Human infections, predominated by gastroenteritis of either acute, self-limited diarrhea, or cholera-like illness, are increasingly recognized and reported, and their clinical variety is expanding. Although the involvement of aeromonads as enteropathogens has been questioned, their pathogenic role in causing human gastrointestinal infection is supported by accumulating evidence.1–3 Not only could aeromonads be isolated from different foods, but they could also be detected in returning travelers suffering from diarrhea. Globally three major species isolated from clinical, food, and water sources are Aeromonas hydrophila, Aeromonas veronii biovar sobria, and Aeromonas caviae. However, the list of newly identified Aeromonas species becomes longer and longer. In light of the rapidly evolving landscape around Aeromonas species, we present an overview on the clinical epidemiology, variation, and antimicrobial treatment of Aeromonas-induced gastroenteritis, the isolation of aeromonads from feces, and the putative virulence factors in aeromonads causing gastroenteritis, along with current evidence supporting the pathogenic role of aeromonads in human gastrointestinal infections.
Resistome and microbial profiling of pediatric patient’s gut infected with multidrug-resistant diarrhoeagenic Enterobacteriaceae using next-generation sequencing; the first study from Pakistan
Published in Libyan Journal of Medicine, 2021
Ome Kalsoom Afridi, Johar Ali, Jeong Ho Chang
A total of 14 bacterial families were identified in patients infected with MDR Enterobacter and ESBL producing E. coli while10 bacterial families were identified in healthy controls. The most abundant bacterial families in healthy controls were Bifidobacteriaceae (54.9%), Lachnospiraceae (12.6%), and Coriobacteriaceae (8.8%) while Enterobacteriaceae (40%), Bacteroidaceae (32%), and Ruminococcaceae (8.8%) were found abundantly in patients infected with MDR Enterobacter and ESBL producing E. coli. The other families identified in the gut microbiota of patients infected with MDR Enterobacter and ESBL producing E. coli are Clostridiaceae (5.1%), Bifidobacteriaceae (4.4%), Enterococcaceae (3.3%), Selenomonadaceae (1.8%), Sphingobacteriaceae (1.3%), Streptococcaceae (0.9%), and Aeromonadaceae (0.7%). Minor families identified in healthy controls were Lactobacillaceae, Erysipelotrichaceae, Eubacteriaceae, Streptococcaceae, Akkermansiaceae, Ruminococcaceae, Eggerthellaceae, Enterobacteriaceae, Leuconostocaceae, and Clostridiaceae (Figure 1B).
Integrated fecal microbiome–metabolome signatures reflect stress and serotonin metabolism in irritable bowel syndrome
Published in Gut Microbes, 2022
Zlatan Mujagic, Melpomeni Kasapi, Daisy MAE Jonkers, Isabel Garcia-Perez, Lisa Vork, Zsa Zsa R.M. Weerts, Jose Ivan Serrano-Contreras, Alexandra Zhernakova, Alexander Kurilshikov, Jamie Scotcher, Elaine Holmes, Cisca Wijmenga, Daniel Keszthelyi, Jeremy K Nicholson, Joram M Posma, Ad AM Masclee
In order to identify links between gut microbiota and corresponding metabolites, an extensive metabolic reaction network was constructed involving significantly increased and decreased gut microbial families and fecal metabolites in IBS patients (full network in Figure S5). A representation based on this network is presented in Figure 4a. In this interactive figure, the microbial families found to be increased in IBS (purple) and increased in HC (green) are shown on the left. In the figure, via the centralized enzymes, the pathways toward the fecal water metabolites on the right, again in purple increased in IBS, and green increased in HC, can be followed. Pathways for saccharolytic and proteolytic metabolic activity can be extrapolated from this graph. First, propionate-CoA transferase, a microbial enzyme involved in fatty acid synthesis and oxidation, found in 14 IBS- and 13 HC-associated bacterial families, can produce both acetate and lactate (both higher in HC, Figure 4b). CoA-bound forms of acetate or lactate are released and CoA-bound propionate is formed from free propionate (higher in IBS). Second, a general class of aspartoacylases that produce aspartate plus carboxylate from an acylaspartate-substrate (Figure 4c). The carboxylic acid metabolites, formate, and acetate can be produced by reactions mediated by this enzyme. Fecal aspartate and formate are both higher in IBS, whereas acetate is higher in HC. Specifically, N-formylaspartate amidohydrolase (Homo sapiens and microbial enzyme) produces both aspartate and formate. Six HC-associated microbial families (Aeromonadaceae, Clostridiaceae, Mycobacteriaceae, Rhizobiaceae, Campylobacteraceae, Propionibacteriaceae) have this enzyme and also 2 IBS-associated families (Alteromonadaceae, Burkholderiaceae). Third, alanine-lactate ligase, found in 5 HC and 3 IBS associated microbiota families, uses both alanine and lactate as substrates. However, alanine is found in higher concentrations in IBS and lactate higher in HC. A number of enzymes catalyze reactions involving multiple metabolites that are all associated with either IBS or HC. Lactate 2-monooxygenase produces acetate from substrate lactate, both higher in HC. However, valine N-monooxygenase can use both valine and isoleucine as substrate, both these branched-chain amino acids (BCAAs) are higher in IBS and can only be found in some species within the Mycobacteriaceae family. Last, carnosine synthase produces anserine from substrates beta-alanine and 3-methylhistidine (both higher in IBS, Figure 4d), whereas beta-alanine-histidine dipeptidase catalyzes the reverse reaction (Figure 4e). Homo sapiens, HC-associated Aeromonadaceae, Clostridiaceae, Mycobacteriaceae, Rhizobiaceae, Campylobacteraceae and Propionibacteriaceae, and IBS-associated Alteromonadaceae and Burkholderiaceae microbial families all have both of these enzymes.