Aeromonas spp. are Gram-negative, non-spore-forming and facultative anaerobic bacteria that are isolated from CDK inhibitor aquatic environments and human clinical specimens (Janda & Abbott, 1998). The role of aeromonads as causative agents of gastroenteritis in humans is not fully understood. However, there is strong evidence that at least some strains can cause gastroenteritis, especially in susceptible populations (Kirov, 1997). For testing the virulence of Aeromonas isolates, current methods use testing of bacterium-free culture supernatants for a range of extracellular products such as proteases,

hemolysins, cytotoxins and enterotoxins or testing of the bacterial isolates for genes coding for virulence factors (Kingombe et al., 1999; Abdullah et al., 2003; Chacon et al., 2003). Aeromonas veronii biovar veronii is commonly isolated from aquatic environments and also from intestinal and extraintestinal infections in humans (Holmes et al., SCH772984 molecular weight 1996; Janda & Abbott, 1996, 1998; Joseph, 1996).

Very few studies have been conducted on A. veronii and sparse information is available on the virulence factors of this bacterium. Virulence factors such as enterotoxin, hemolysin, serum resistance and inducible chitinase production have been reported to play a role in the pathogenicity of A. veronii isolates (Singh, 1999; González-Serrano et al., 2002; Rahman et al., 2002). However, strains lacking these virulence genes have been shown to produce enterotoxicity in suckling mouse test, suggesting that factors other than hemolytic toxins contribute to the virulence of Aeromonas (González-Serrano et al., 2002). Because, at present, there is no definitive criterion for identifying enteropathogenic aeromonad isolates, it is difficult to define the etiological

role of a particular Aeromonas strain when it is isolated from a diarrheal sample. Vibrio parahaemolyticus is a Gram-negative, halophilic bacterium and is implicated in several cases of seafood-borne gastroenteritis globally (Fujino et al., 1953). It was observed in the late 1960s that 90% of the clinical strains produced β-hemolysis on a high-salt blood agar (Wagatsuma agar), the reaction being referred to as the Kanagawa phenomenon (K), with hemolytic isolates being designated K+ and non-hemolytic K− pheromone (Sakazaki et al., 1968; Miyamoto et al., 1969). K+ activity is due to a high level of the production of a thermostable direct hemolysin (TDH), encoded by the tdh gene (Nishibuchi et al., 1991; Okuda & Nishibuchi, 1998). In a later report, V. parahaemolyticus K− strains, isolated during an outbreak of gastroenteritis in the Maldives in 1985, possessed a TDH-related hemolysin (TRH) encoded by the trh gene rather than the tdh gene (Honda et al., 1987, 1988). The trh sequence is about 70% similar to the tdh sequence (Nishibuchi et al., 1989).