Tuesday, 18 March 2008

Either Human or Fish

Vibrio vulnificus is an aquatic bacterium from warm and tropical ecosystems that produces diseases in humans and aquatic snimals (Tison et al., 1982; Oliver, 1989; Amaro & Biosca, 1996). Human vibriosis occurs after eating contaminated seafood or exposing open wounds to seawater (Veenstra et al., 1992; Strom & Paranjpye, 2000), and fish vibriosis after immersion in contaminated water or contact with diseased animals or carriers (Amaro et al., 1995; Marco-Noales et al., 2001; Valiente & Amaro, 2006). The species has been subdivided into three biotypes on the basis of differences in biochemical properties, such as indole production and cellobiose fermentation, as well as serological and genetic traits and host range (Tison et al., 1982; Bisharat et al., 1999, 2007). Biotypes 1 (BT1) and 3 (BT3) are considered human pathogens and biotype 2 (BT2) pathogens of aquatic animals (Tison et al., 1982; Song et al., 1990; Biosca et al., 1996, 1997; Bisharat et al., 1999; Fouz et al., 2002, 2006a; Fouz & Amaro, 2003) in spite of the fact that several human cases of wound infection and sepsis due to BT2 have occurred worldwide (Veenstra et al., 1992; Amaro & Biosca, 1996; Dalsgaard et al., 1996). BT2 was first isolated in Japan in 1976 (Muroga et al., 1976) and was described in 1982 by Tison et al. (1982). The first cases in Europe were recorded in 1989 in Spanish eel farms (Biosca et al., 1991). Later, the disease spread to other countries such as Sweden, The Netherlands and Denmark (Høi et al., 1998; Dalsgaard et al., 1999), always affecting eels cultured in brackish water. BT2 is heterogeneous and can be subdivided into different serovars (Martin & Siebeling, 1991; Biosca et al., 1996, 1997; Høi et al., 1998; Fouz & Amaro, 2003). The first described, serovar E (SerE) (equivalent to serovar O4 according to the serotyping system of Martin & Siebeling, 1991), is clearly related to both highly virulent epizootics and human infections (Veenstra et al., 1992; Amaro & Biosca, 1996; Dalsgaard et al., 1996). This serovar seems to be genetically homogeneous regardless of origin, either human or fish (Gutacker et al., 2003). The last serovar described, serovar A (SerA), emerged in Southern Europe in 2000 (Fouz & Amaro, 2003), affecting eels cultured in fresh water that had been vaccinated against SerE (Fouz et al., 2001). SerA spread to the Danish eel farming industry in the summer of 2004, also affecting eels cultured in fresh water (Fouz et al., 2006a). Two additional serovars, O3 and O3/O4 (SerO3 and SerO3/O4), were only isolated once from diseased eels as secondary pathogens in Denmark in the mid-1990s (Høi et al., 1998). They were Abbreviations: BT, biotype; ECP, extracellular product; GR, growth rate; Hb, haemoglobin; RAPD, random amplified polymorphic DNA; Ser, serovar; SS, sterile saline; UPGMA, unweighted pair group method with arithmetic means. For this reason, their inclusion in BT2 is controversial. To gain insight into the virulence factors that are essential for eel pathogenicity, genomes of selected strains belonging to the different biotypes, both virulent and avirulent for eels, were compared by suppression subtractive hybridization (Lee et al., 2005). This study demonstrated that all virulent BT2 strains analysed, irrespective of the serovar, shared plasmid-borne genetic sequences that could be considered as virulence markers for fish (Amaro et al., 2006).

'Phenotypic and genotypic characterization of a new fish-virulent Vibrio vulnificus serovar that lacks potential to infect humans', "Microbiology" 153 (2007)1926-1934.

No comments: