Escherichia albertii

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Higher order taxa

Bacteria, Eubacteria; Proteobacteria; Gammaproteobacteria; Enterobacteriales; Enterobacteriaceae; Escherichia (1)


Escherichia albertii

2. Description and significance

Escherichia albertii is a recently characterized bacteria that acts as a human and avian enteropathogen (1). It was recognized as a unique pathogen in 2003 after being isolated from the stool of Bangladeshi children presenting with diarrhea and abdominal pain (2). E. albertii is a gram negative, rod shaped bacteria that closely resembles other members of the Escherichia genus, and has frequently been mischaracterized as Escherichia coli (1). E.albertii is a food-borne pathogen, and consumption of food contaminated with E.albertii can result in fever, diarrhea, abdominal pain, nausea, and vomiting (3). Additional research has confirmed the presence of E.albertii in farmed poultry carcasses following slaughter (4) and in chicken meat sold in retail grocery stores (5). Further research is needed to characterize and expand on the pathogenic nature and prevalence of E.albertii in order to prevent the occurence of diarrheal disease in humans.

3. Genome structure

The genome of E. albertii is very similar to the rest of the Escherichia genus, making it hard to distinguish between them (1). E. albertii has the eaeA gene, deeming it a part of Enterobacteriaceae. This gene helps the bacteria adhere to epithelial cells in tissues, ultimately modifying the cells and thus contributing to diarrhea (6). Each strain has an identical 353 base-pair fragment in their 16S rRNA genes (7). E. albertii showed 99.5-99.8% sequence similarity to the 16S rRNA in Escherichia coli (8). Its G + C content is 49.8%. E. albertii’s chromosomes average 4,777 kb, making it smaller in size than E. coli, whose chromosomes average 5,132 kb. E. albertii has an average of 7 rRNA operons and 86-97 tRNA genes, 75 of which are shared between all strains. The microbe has between 7-11 insertion sequence elements, which is less than that of E. coli, which have between 42 to 224 copies (8). Each strain of E. albertii has the gene cdtB, which shows the capability of encoding cytolethal distending toxin, CDT (8). Vulnerability to CDT can result in harmful modifications to the cell cycle (9). CDT can make the cell cycle stop and repair itself, even though there is no DNA damage. This can lead to the genetic makeup of the cell becoming unsteady and could potentially lead to malignant cells (9). It also encodes other virulence genes such as fimA, iucC, and aer. E. albertii encodes colicins B, D, E7, and M (8). The microbe demonstrates antibiotic resistance, with the greatest percentage of strains being tetracycline resistant at 62.7%. There are other high instances of streptomycin, piperacillin, and chloramphenicol resistance, with lower instances of ampicillin, norfloxacin, and furadantin resistance. 80.4% of strains demonstrate resistance to two or more antibiotics (10). The strain SP140150 carries genes mcr-1 and blaCTX-M-55 (10). The gene mcr-1 is a plasmid-mediated colistin resistance gene, which means that E. albertii is resistant to the antibiotic colistin (10). The gene blaCTX-M-55 is a part of the extended-spectrum beta-lactamase gene group, which are resistant to a range of antibiotics (10).

4. Cell structure

Interesting features of cell structure. Can be combined with “metabolic processes”E. albertii is a Gram-negative rod-shaped bacteria (1). It has a lower tolerance to heat, pH, and pressure than that of E. coli, making any means that kills off E. coli able to additionally kill off E. albertii (11). E. albertii is non-motile (1). E. albertii is capable of producing the protein intimin, which allows the microbe to attach to cells in the human intestines (12). Presence of fimbriae or other attachment mechanisms is unknown. Insight into its membrane, organelles, and molecular components are not known.

5. Metabolic processes

Biochemical properties help distinguish E. albertii from E. coli. A specific distinguishing characteristic is E. albertii’s general inability to ferment lactose, D-sorbitol, D-xylose, L-rhamnose, melibiose and dulcitol (1). In addition, E. albertii is unable to produce beta-D-glucuronidase (6). The most distinguishing biochemical process between the two Escherichia species is E. albertii’s inability to ferment D-sorbitol, a trait that is strongly associated to E. coli (8). Some other metabolic processes of E. albertii are its ability in some strains to ferment sucrose. It was previously known that E. albertii tested negative for sucrose fermentation; however, recently it has been discovered that 5 strains (19.2%) tested positive for sucrose fermentation and beta-galactosidase (1). The strains also fermented D-arabinose, D-fructose, D-galactose, D-mannose and ribose, but were unable to fertilize D-fucose, palatinose, sedoheptulose anhydride, L-sorbose, D-tagatose, D-turanose, and xylitol (8). E. albertii is unable to grow in KCN broth, cannot use malonate, and lacks acid production from D-xylose, D-arabitol, melibiose, and cellobiose (8).

6. Ecology

Since being reclassified as a new species part of the Escherichia group, more than half of the 282 E. albertii isolates were associated with diarrhea and/or gastroenteritis in humans (8). In addition, E. albertii has also been identified to cause mortality among birds, with the first notable incident being in December 2004 among redpoll finches (Carduelis flammea) in Alaska (11). In addition, presence of E. albertii has been noted in pig, cat, and environmental samples, and in raw meats as a contaminant (8). The exact prevalence of E. albertii are unknown; however, it is known to cause foodborne-illnesses by transmitting via food-borne routes including lettuce, ground beef, and turkey (3).

7. Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

8. Current Research

Currently, research is being done to better understand the prevalence of E.albertii in farmed poultry. In one study, researchers sampled 104 packages of retail chicken meat and found that 2 chicken livers (giblets) and 1 chicken meat sample tested positive for E.albertii. This study was the first to identify the presence of E.albertii in retail food (5). Given past evidence that supports food-borne transmission of E.albertii, this area is of interest to current researchers in order to properly identify and contain the pathogen in farmed poultry. A recent study focused on analyzing antibiotic resistance genes in E. albertii, specifically in a China providence. A variety of antibiotics, a double disk test and PCR were used to conclude that microbes that were positive for producing extended-spectrum β-lactamases (ESBLs) had higher resistance rates than non-ESBL producing microbes to antibiotics like norfloxacin and amoxicillin. The study found that additionally, all E. albertii that contained the MCR-1 genes were resistant to the antibiotic Colistin (10). This can contribute to human diseases that were once cured with antibiotics becoming untreatable. Another study conducted in 2017 observed how E. albertii strain can translocate from the intestinal lumen to Mesenteric Lymph Nodes and liver in a rat model, demonstrating for the first time, the initial steps of E. albertii colonization using rat intestinal mucosa (15). The results of the study allowed for a draft of the general E. albertii infection route in vivo, starting from the initial colonization until the spreading of bacteria. E. albertii is thought to cross the intestinal epithelium through infections of M-like cells in vitro to further identify translocation routes in vivo (12).

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Edited by [Sarah Ziobro, Sarah Tong, Sally Lakis, Miyu Niwa], students of Jennifer Talbot for BI 311 General Microbiology, 2015, Boston University.

9. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.