Edwardsiella tarda: Difference between revisions
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Edwardsiella tarda | ''Edwardsiella tarda'' | ||
==Description and significance== | ==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. | ''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. | 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== | ==Genome structure== | ||
| Line 23: | Line 24: | ||
==Cell structure and metabolism== | ==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. | ''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 | 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 urease but is similar to ''Salmonella'' in that it is able to generate hydrogen sulfide on laboratory media. | ||
==Ecology== | ==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). | ''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). It 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. | ||
Recent research has suggested the increasing presence of ''E. tarda'' in Antarctic wildlife including those animals that live outside aquatic systems. According to Leotta and colleagues, two reported cases of injured or wounded wildlife with ''E. tarda'' infections led to performing a study of the prevalence of E. tarda in the Antarctic wildlife. In their study, “The classic Edwardsiella tarda was isolated from 281 (15.1%) of 1,855 Antarctic wildlife samples obtained from southern giant petrels, brown skuas, greater sheathbills, Adelie penguins, gentoo penguins and chinstrap penguins from Potter Peninsula in 2000 and 2002. “ (Leotta et al., 2009). Samples of feces, eggs, and other means were taken from those various species. “[They] considered that ''E. tarda'' was a common bacterium in the feces of Antarctic birds and mammals, because no significant differences were found with regard to the areas and seasons investigated. This was supported by the fact that there were no significant differences in the distribution of positive rates obtained within the species evaluated. However, ''E. tarda'' was described as an opportunistic bacterial pathogen and has been commonly isolated from different healthy, sick and moribund Wsh, birds and reptiles in several ecosystems around the world.” (Leotta et al., 2009). The study concluded that the presence of ''E. tarda'' was common among many species in the Antarctic, although more tests had to be run to see other possible pathogenic traits. The presence of ''E. tarda'' even in smaller numbers as reported by this study only highlights the possibility of the spread of disease in Antarctic wildlife and further study may help with identifying and evaluating the condition of this and other ecosystems. | |||
==Pathology== | ==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). | ''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). E. tarda flagellar genes, fliC12, fliA and flhDC are essential for the number and length of flagellar filaments, and subsequently the swimming and swarming ability of E. tarda. These genes have also been shown to aid biofilm formation ability, adherence and internalization to Epithelioma papulosum cyprini (EPC) cells, and pathogenicity to zebrafish. E. tarda has been shown to be resistant to the bactericidal properties of host serum[1] by preventing serum complement activation via the alternative pathway[2]. This important virulence factor is facilitated by several host serum-induced proteins, including the novel putative zinc metalloprotease (Sip1)[3]. When used as a subunit vaccine, purified recombinant Sip1 (rSip1) effectively induced protection in flounder fish against E. tarda infection. The type III secretion system (T3SS) of E. tarda enables infection by translocating effector proteins into host cells[1]. The E. tarda T3SS gene cluster consists of 34 genes[1], including the esrA-esrB genes which contribute to the virulence of E. tarda. The gene esrB is responsible for the secretion of translocon proteins like EseB[1]. EseB mediates autoaggregation and subsequently biofilm formation of E. tarda by forming filamentous appendages on the bacterial surface[2].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. Many gram-negative bacteria (including E. tarda) use ferric uptake regulator (Fur) as an important transcriptional regulator. In E. tarda, Fur’s role is significant and multifaceted; Fur affects the growth, siderophore production, and acid tolerance of E. tarda, helps protect against oxidative stress and host serum, helps inhibit host immune response, and generally increases the overall virulence of the bacterium. 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. Pathogenic E. tarda was first isolated and documented in farmed striped catfish (Pangasianodon hypophthalmus) in fish sampled between October 2007 and May 2008 from a farm in the Bhimavaram district of Andhra Pradesh, located on the east coast of India. A higher prevalence of infection was observed in the summer as opposed to the winter[1]. 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). Two outbreaks of Edwardsiellosis were recorded in October 2013 and July 2014 in cage-cultured sharpsnout sea breams, Diplodus puntazzo, in a single commercial fish farm located in the Saronikos Bay of Eastern Greece. This was not only the first report of Edwardsiellosis in this species, but also the first report of E. tarda in cage-cultured fish in the Mediterranean, in general. | ||
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). | 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. | ||
Other types of treatment that would inhibit E. | |||
''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). E. tarda has hemolytic properties which can cause reddening and systemic hemorrhagic septicemia in infected fish. Hemolysis is facilitated by the pore-forming cytotoxic protein, Cytolysin A (ClyA), which is encoded by the clyA gene. Eha protein was found to act as an important transcriptional regulator of clyA, and thus also of general hemolytic activity in E. tarda. | |||
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). | |||
In their article, “Human Edwardsiellosis Traced to Ornamental Fish,” Vandepitte et. Al review the pathogenic role of ''Edwardsiella tarda'' and the role of that “ornamental” fish play in transmitting infections. ''E. tarda'' can cause human Edwardsiellosis, an intestinal infection. It is most prevalent in tropical areas such as Singapore, Vietnam, and Cuba. The article reviewed a case report involving a two month old infant male in suburban Belgium, and had two days of vomiting. The infant did not have a fever and the stool cultures were normal. Following this initial exam it was the reported that the infant experienced diarrhea, and unformed stools that had a yellowish color and contained mucus. This time the stool culture came back positive for E. tarda. This was the first documented case of a human Edwardsiellosis in Belgium. | |||
The patient was then followed for two months, in which the diarrhea continued and additional stool cultures remained positive for ''E. tarda''. Antibiotics where prescribed for two weeks, after which the stool cultures were normal. The patient’s home was found to have an aquarium which contained ornamental fish. A ''Pterophyllum scalarem'', a tropical fish that originates in Brazil, was retrieved. The fish was was cultured and tested positive for Citrobacter freundii, ''Aeromonas hydrophila'', and ''E. tarda''. The authors write, “The introduction of ornamental fish into pediatric hospitals presents a potential hazard for neonates and young infants” (Vandepitte 166) because they are potential vehicles for transmission. This case study brings to light that contact with tropical fish, even in an aquarium setting, may increase your risk of transmitting and/or becoming infected by bacterial pathogens such as ''E. tarda''. | |||
==Current Research== | ==Current Research== | ||
The sequencing of the genome is still in progress. | |||
In the article "Detection of different quorum-sensing signal molecules in a virulent ''Edwardsiella tarda'' strain LTB-4", researchers describe the possible quorom sensing molecules used by virulent strains of ''Edwardsiella tarda''. The specific strain studied was LTB-4 which was isolated from the brain of a turbot, this fish as well as zebrafish are commonly infected with E. tarda. Quorom sensing is a process through which bacteria regulate gene expression in response to population density. ''E. tarda'' LTB-4 was found to possess two systems of quorom sensing; the N-acylhomoserine lactone (AHL) system and the autoinducer-2 (AI-2) system. Four types of AHLs were identified in ''E. tarda'' LTB-4: C4-HSL, C6-HSL, 3-oxo-C6-HSL, and another uncharacterized AHL molecule. AHL molecules accumulated during the entire growth phase of the culture, but ceased production at peak levels; at this point the AHL levels recovered to even higher levels. The autoinducer system was found to produce molecules at low densities, but not during stationary phase when cell density was highest. Interestingly, the virulence of other bacteria is highest at this point when AI-2 production is at a peak, further investigation could show whether this is true or not in ''E. tarda'', and is a possible pathway to be manipulated for treatment. | |||
==References== | ==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. | |||
Han, Y., et al. "Detection of different quorum-sensing signal molecules in a virulent ''Edwardsiella tarda'' strain LTB-4." Journal of Applied Microbiology 108.1 (2010): 139-147. Academic Search Premier. EBSCO. 21 Apr. 2010. | |||
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. | |||
Vandepitte, J., P. Lemmens, and L. De Swert. "Human Edwardsiellosis Traced to Ornamental Fish." Journal of Clinical Microbiology 17 (1983): 165-67. Web. <http://jcm.asm.org/cgi/reprint/17/1/165.pdf>. | |||
Leotta, G., Piñeyro, P., Serena, S., and Germán, V. “Prevalence of Edwardsiella tarda in Antarctic wildlife” Polar Biology. 2009. Volume 35. p. 809-812. | |||
Edited by students Hans Han, Michael Le, Andy Nguyen, and Michael Pham under the supervision of [mailto:lariosm@stthom.edu Dr. Maia Larios-Sanz] at the University of St. Thomas | |||
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Latest revision as of 14:03, 13 May 2016
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 urease but 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). It 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.
Recent research has suggested the increasing presence of E. tarda in Antarctic wildlife including those animals that live outside aquatic systems. According to Leotta and colleagues, two reported cases of injured or wounded wildlife with E. tarda infections led to performing a study of the prevalence of E. tarda in the Antarctic wildlife. In their study, “The classic Edwardsiella tarda was isolated from 281 (15.1%) of 1,855 Antarctic wildlife samples obtained from southern giant petrels, brown skuas, greater sheathbills, Adelie penguins, gentoo penguins and chinstrap penguins from Potter Peninsula in 2000 and 2002. “ (Leotta et al., 2009). Samples of feces, eggs, and other means were taken from those various species. “[They] considered that E. tarda was a common bacterium in the feces of Antarctic birds and mammals, because no significant differences were found with regard to the areas and seasons investigated. This was supported by the fact that there were no significant differences in the distribution of positive rates obtained within the species evaluated. However, E. tarda was described as an opportunistic bacterial pathogen and has been commonly isolated from different healthy, sick and moribund Wsh, birds and reptiles in several ecosystems around the world.” (Leotta et al., 2009). The study concluded that the presence of E. tarda was common among many species in the Antarctic, although more tests had to be run to see other possible pathogenic traits. The presence of E. tarda even in smaller numbers as reported by this study only highlights the possibility of the spread of disease in Antarctic wildlife and further study may help with identifying and evaluating the condition of this and other ecosystems.
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). E. tarda flagellar genes, fliC12, fliA and flhDC are essential for the number and length of flagellar filaments, and subsequently the swimming and swarming ability of E. tarda. These genes have also been shown to aid biofilm formation ability, adherence and internalization to Epithelioma papulosum cyprini (EPC) cells, and pathogenicity to zebrafish. E. tarda has been shown to be resistant to the bactericidal properties of host serum[1] by preventing serum complement activation via the alternative pathway[2]. This important virulence factor is facilitated by several host serum-induced proteins, including the novel putative zinc metalloprotease (Sip1)[3]. When used as a subunit vaccine, purified recombinant Sip1 (rSip1) effectively induced protection in flounder fish against E. tarda infection. The type III secretion system (T3SS) of E. tarda enables infection by translocating effector proteins into host cells[1]. The E. tarda T3SS gene cluster consists of 34 genes[1], including the esrA-esrB genes which contribute to the virulence of E. tarda. The gene esrB is responsible for the secretion of translocon proteins like EseB[1]. EseB mediates autoaggregation and subsequently biofilm formation of E. tarda by forming filamentous appendages on the bacterial surface[2].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. Many gram-negative bacteria (including E. tarda) use ferric uptake regulator (Fur) as an important transcriptional regulator. In E. tarda, Fur’s role is significant and multifaceted; Fur affects the growth, siderophore production, and acid tolerance of E. tarda, helps protect against oxidative stress and host serum, helps inhibit host immune response, and generally increases the overall virulence of the bacterium. 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. Pathogenic E. tarda was first isolated and documented in farmed striped catfish (Pangasianodon hypophthalmus) in fish sampled between October 2007 and May 2008 from a farm in the Bhimavaram district of Andhra Pradesh, located on the east coast of India. A higher prevalence of infection was observed in the summer as opposed to the winter[1]. 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). Two outbreaks of Edwardsiellosis were recorded in October 2013 and July 2014 in cage-cultured sharpsnout sea breams, Diplodus puntazzo, in a single commercial fish farm located in the Saronikos Bay of Eastern Greece. This was not only the first report of Edwardsiellosis in this species, but also the first report of E. tarda in cage-cultured fish in the Mediterranean, in general. 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). E. tarda has hemolytic properties which can cause reddening and systemic hemorrhagic septicemia in infected fish. Hemolysis is facilitated by the pore-forming cytotoxic protein, Cytolysin A (ClyA), which is encoded by the clyA gene. Eha protein was found to act as an important transcriptional regulator of clyA, and thus also of general hemolytic activity in E. tarda.
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).
In their article, “Human Edwardsiellosis Traced to Ornamental Fish,” Vandepitte et. Al review the pathogenic role of Edwardsiella tarda and the role of that “ornamental” fish play in transmitting infections. E. tarda can cause human Edwardsiellosis, an intestinal infection. It is most prevalent in tropical areas such as Singapore, Vietnam, and Cuba. The article reviewed a case report involving a two month old infant male in suburban Belgium, and had two days of vomiting. The infant did not have a fever and the stool cultures were normal. Following this initial exam it was the reported that the infant experienced diarrhea, and unformed stools that had a yellowish color and contained mucus. This time the stool culture came back positive for E. tarda. This was the first documented case of a human Edwardsiellosis in Belgium. The patient was then followed for two months, in which the diarrhea continued and additional stool cultures remained positive for E. tarda. Antibiotics where prescribed for two weeks, after which the stool cultures were normal. The patient’s home was found to have an aquarium which contained ornamental fish. A Pterophyllum scalarem, a tropical fish that originates in Brazil, was retrieved. The fish was was cultured and tested positive for Citrobacter freundii, Aeromonas hydrophila, and E. tarda. The authors write, “The introduction of ornamental fish into pediatric hospitals presents a potential hazard for neonates and young infants” (Vandepitte 166) because they are potential vehicles for transmission. This case study brings to light that contact with tropical fish, even in an aquarium setting, may increase your risk of transmitting and/or becoming infected by bacterial pathogens such as E. tarda.
Current Research
The sequencing of the genome is still in progress.
In the article "Detection of different quorum-sensing signal molecules in a virulent Edwardsiella tarda strain LTB-4", researchers describe the possible quorom sensing molecules used by virulent strains of Edwardsiella tarda. The specific strain studied was LTB-4 which was isolated from the brain of a turbot, this fish as well as zebrafish are commonly infected with E. tarda. Quorom sensing is a process through which bacteria regulate gene expression in response to population density. E. tarda LTB-4 was found to possess two systems of quorom sensing; the N-acylhomoserine lactone (AHL) system and the autoinducer-2 (AI-2) system. Four types of AHLs were identified in E. tarda LTB-4: C4-HSL, C6-HSL, 3-oxo-C6-HSL, and another uncharacterized AHL molecule. AHL molecules accumulated during the entire growth phase of the culture, but ceased production at peak levels; at this point the AHL levels recovered to even higher levels. The autoinducer system was found to produce molecules at low densities, but not during stationary phase when cell density was highest. Interestingly, the virulence of other bacteria is highest at this point when AI-2 production is at a peak, further investigation could show whether this is true or not in E. tarda, and is a possible pathway to be manipulated for treatment.
References
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Edited by students Hans Han, Michael Le, Andy Nguyen, and Michael Pham under the supervision of Dr. Maia Larios-Sanz at the University of St. Thomas
Edited by Students Diana Deavila, Gaurav Rana, Kevin Kamis, Anthony Savushkin, Lauren White, and Ryan Winslow Students of Mary Glogowski Loyola University Chicago
