Edwardsiella tarda

A Microbial Biorealm page on the genus Edwardsiella tarda

Classification

Higher order taxa

Bacteria, Proteobacteria, Gamma proteobacteria, Enterobacteriales, Enterobacteriaceae

Species

NCBI: Taxonomy

Edwardsiella tarda

Description and significance

Edwardsiella tarda was the first species identified of the genus Edwardsiella, and was named after a renowned microbiologist P. R. Edwards (Janda, 1991). E. tarda was originally named Edwardsiella anguilimortifera, but it was ultimately changed to E. tarda because this name was used more often in scientific reports. E. tarda is a Gram-negative bacilli that belongs to the Enterobacteriaceae family and was first characterized in 1965 (Health, 2001). E. tarda has many traits that are characteristic of many enterobacteria such as E. coli. These characteristics include it being a facultative anaerobe, rod-shaped, and motile (Health 2001). Its motility is due to peritrichous flagella. Although Edwardsiella tarda was initially characterized more than thirty years ago, there is still very little known about this bacterium. E. tarda is known for causing diseases in both humans and fish, both of which can potentially be fatal if untreated. Though this may be the case, the likelihood of a serious infection is very slim. As a fish pathogen, it is of particular importance to aquaculture and the fishing industry, especially commercial fish farms. It may become more of a significant health issue to fish and humans alike, especially in light of emerging and increasing antibiotic resistance in fish pathogens, due in large part to overuse of antibiotics in fish farming (Greenlees et al., 1998; Lehane and Rawlin, 2000). Some studies have focused on using proteomics and molecular techniques to elucidate the mechanism of pathogenesis in Edwardsiella tarda (Rao et al., 2004). Studies such as these have allowed the characterization of novel toxin secretion pathways, such as the discovery of a type VI secretion system essential for E. tarda pathogenesis (Zheng and Leung, 2007). These types of analyses help us better understand bacterial pathogenesis in general, as well as provide new insights for fighting disease.

Genome structure

There are two genomes for strains of E. tarda in progress (documented in NCBI): strains ATCC 23685 and EIB 202 (Du, 2007). ATCC 23685 is a strain commonly found in normal human gut flora, while EIB 202 is a virulent strain that causes disease in many fresh water and marine fish (Du, 2007).

Cell structure and metabolism

E. tarda is a Gram-negative bacilli. E. tarda has many traits that are characteristic of many enterobacteria such as E. coli. These characteristics include it being a facultative anaerobe, rod-shaped, and motile (Health 2001). Its motility is due to peritrichous flagella. It is positive for glucose fermentation, but negative for lactose fermentation and is unable to grow on D-mannitol or D-sorbitol. E. tarda is also oxidase-negative and catalase-positive. It does not produce ureasebut is similar to salmonella in that it is able to generate hydrogen sulfide on laboratory media.

Ecology

Edwardsiella tarda is predominantly found in freshwater environments colonizing the guts of fish, including flounder living off the coasts of East Asia and catfish that live in regions of the United States. It can also be found in the intestinal tract of birds, reptiles, and mammals (Janda et. al, 1991). THey can be found as part of the human intestinal flora as well, although this seems to be rare, and is usually due to an infection or prolonged contact with contaminated water. Other factors that increase the risk of getting an infection include high iron concentration, very young or old age, or an immune incompetence.

Pathology

E. tarda is typically found in the normal gut flora of fish and humans, and can be an opportunistic pathogen in human, causing gastroenteritis and diarrhea (Verjan, 2005). E. tarda has a high affinity for red blood cells due to specific fimbriae that it produces. As a result, Edwardsiella tarda has hemagglutination properties (Sakai, 2003). The fimbriae are encoded in the genome as a region made of 534 base pairs (Sakai, 2003). Scientists have found that the hemagglutination properties of E. tarda is inhibited by N-acetylneuraminic acid and fetuin, but not D-mannose (Sakai, 2003). In the lab, E. tarda is easily grow on nutrient agar plates and nutrient broth. Though Edwardsiella tarda was first characterized in the 60’s, there have been few studies done to test its relative pathogenicity. However, the few research that has been conducted on it shows that it releases dermatotoxins that damage the skin. Studies also show that E. tarda is invasive in HEp-2 cell monolayers, and that it produces a cell-associated hemolysin and siderophores (Janda et al, 1991). Siderophores are iron-binding molecules produced by freshwater and marine bacteria. These siderophores are related to microbial virulence, and scavenge the iron inside of host cells, providing the microbial cell essential micronutrients (Janda et al, 1991). As there is iron deprivation in the host, the CAH (cell-associated hemolysin) of E. tarda provides iron by cleaving erythrocytes and releasing hemoglobin. Because E. tarda is so prevalent in the freshwater environment, it is easy to see why many of the organisms living within these areas will carry E. tarda within their intestinal tract. This microorganism is an opportunistic pathogen, and is able to live inside and outside of the host organism. One of the most common diseases among freshwater fish is hemorrhagic septicemia, also known as edwardsiellosis, which usually results in the death of the fish (Yousuf, 2006). This disease is usually prevalent in flounder. A few known epidemics of edwardsiellosis have been recorded, and can be devastating to the fish population, but if the infection is detected early, the epidemic may be easily avoided (Yousuf, 2006). In humans, E. tarda can cause gastroenteritis, which is infection in the stomach and intestines (Clarridge, 1980). This is especially true in areas where raw fish is a large part of their daily diet. E. tarda can also cause colitis and dysentery-like diseases in humans (Janda et al., 1991) as well as gastroenteritis, infections of wounds, gas gangrene associated with trauma to mucosal surfaces, and systemic disease such as septicemia and meningitis (Janda and Abbott, 1993). These gastroenteritis cases are usually misdiagnosed and attributed to other agents. The best way to avoid an E. tarda infection would is to not spend too much time in contaminated water, and practice good hygiene habits.

E. tarda can even be transferred to infants during the birthing process. Mowbray and her colleagues described a case where a 6-day old boy had E. tarda growing within its gastrointestinal tract since the time of birth. The strain of E. tarda was the same as the one found colonizing the mother’s vaginal and gastrointestinal areas, as demonstrated by both fingerprinting and antibiotic susceptibility analyses (Mowbray, 2002). The mother had spent time in contaminated lake water during her pregnancy, demonstrating that exposure of the mother to contaminated water poses a risk to newborn babies (Mowbray, 2002). The incidence of E. tarda infection in newborns is increasing. Before 2003, there were only two known cases of neonatal sepsis caused by Edwardsiella tarda (Mowbray, 2002). By 2003, however, there were a total of 300 cases of E. tarda infection, in which 83% of the patients had gastroenteritis. Studies showed that E. tarda is able to become part of the vaginal flora and then cause neonatal sepsis through infection at birth. Very little is known about the vaginal colonization of E. tarda, but there were only a handful of cases where patients had gynecologic infections (Mowbray, 2002).

Although Edwardsiella tarda may cause infection in humans – some of which can become lethal, there are many ways to prevent infection. E. tarda is still very susceptible to many antibiotics, including ampicillin, antifolates, chloramphenicol, ciprofloxacin, kanamycin, most β-lactams, and nitrofurantoin (Stock, 2001). On the other hand, these bacteria are very resistant to colistin, glycopeptides, lincosamides, streptogramins, and rifampin (Stock, 2001). Compared to the other species in the genus Edwardsiella, E. tarda is also resistant to oxacillin and benzylpenicillin (Stock, 2001).

Other types of treatment that would inhibit E. tarda’s growth include moist and dry heat, usually above 121˚C or above 160˚C respectively. Edwardsiella tarda is also susceptible to many disinfectants such as 70% ethanol, iodine, and formaldehyde (Stock, 2001).

Current Research

The sequencing of the genome is still in progress.

References

Clarridge, J. E., D. M. Musher, V. Fainstein, and R. J. Wallace. "Extraintestinal human infection caused by Edwardsiella tarda." J Clin Microbiol. (1980): 511-14.

DSMZ. “Bacterial nomenclature up-to-date.” 2004. < http://www.dsmz.de/microorganisms/bacterial_nomenclature_info.php?genus=EDWARDSIELLA&show_all_details=1>

Du, Meng, Chen, Jixiang, Zhang, Xiaohua, Li, Aijuan, Li, Yun, Wang, Yingeng “Retention of Virulence in a Viable but Nonculturable Edwardsiella tarda Isolate” Appl. Environ. Microbiol. 2007 73: 1349-1354

"Edwardsiella tarda." Edwardsiella tarda. 2002. UniProt Consortium. 11 Dec. 2008 <http://www.uniprot.org/taxonomy/636>.

Greenlees KJ, Machado J, Bell T, Sundlof SF. Food borne microbial pathogens of cultured aquatic species. Vet Clin North Am Food Anim Pract. 1998 Mar;14(1):101-12.

Health Canada. "Edwardsiella tarda - Material Safety Data Sheets (MSDS)." Public Health Agency of Canada. Jan. 2001. 10 Dec. 2008 <http://www.phac-aspc.gc.ca/msds-ftss/msds57e-eng.php>.

Janda, Michael J., Sharon L. Abbot, Susan Kroske-Bystrom, Wendy K. Cheung, Catherine Powers, Robert P. Kokka, and K. Tamura. "Pathogenic Properties of Edwardsiella Species." Journal of Clinical Microbiology 9th ser. 29 (1991): 1997-2001

Janda JM, and Abbott SL. Infections associated with the genus Edwardsiella: the role of Edwardsiella tarda in human disease. Clin Infect Dis. 1993 Oct;17(4):742-8.

Lehane L, Rawlin GT. Topically acquired bacterial zoonoses from fish: a review. Med J Aust. 2000 Sep;173(5):256-9.Links

MedicineNet. "Medical Dictionary." 10 Dec. 2008 <http://www.medicinenet.com>.

Mowbray, Erin E., George Buck, Kraig E. Humbaugh, and Gary S. Marshall. "Maternal Colonization and Neonatal Sepsis Caused by Edwardsiella tarda." 10 Oct. 2002. American Academy of Pediatrics. 11 Dec. 2008 <http://pediatrics.aappublications.org/cgi/content/full/111/3/e296>.

Rao PS, Yamada Y, Tan YP, and Leung KY. Use of proteomics to identify novel virulence determinants that are required for Edwardsiella tarda pathogenesis. Mol Microbiol. 2004 Jul;53(2):573-86.

Sakai, Takamitsu, Kinya Kanai, Kiyoshi Osatomi, and Kazuma Yoshikoshi. "Identification of a 19.3-kDa protein in MRHA-positive Edwardsiella tarda: putative fimbrial major subunit." FEMS Microbiology Letters 226 (2003): 127-33.

Stock, Ingo, Wiedemann, Bernd. “Natural Antibiotic Susceptibilities of Edwardsiella tarda, E. ictaluri, and E. hoshinae.” Antimicrob. Agents Chemother. 2001 45: 2245-2255

Verjan, Noel, Ikuo Hirono, and Takashi Aoki. "Genetic Loci of Major Antigenic Protein Genes of Edwardsiella tarda." Appl. Environ. Microbiol. 9th ser. 71 (2005): 5654-658.

Yousuf, RM, SH How, M. Amran, KT Hla, A. Shah, and A. Francis. "Edwardsiella tarda septicemia with underlying multiple liver abscesses." (2006): 49-53.

Zheng J, and Leung KY. Dissection of a type VI secretion system in Edwardsiella tarda. Mol Microbiol. 2007 Dec; 66(5):1192-206. Epub 2007 Nov 6.

Edited by student of Dr. Maia Larios-Sanz at University of St. Thomas