INTRODUCTION
The genus Aeromonas consists of ubiquitous gram-negative rods that are widely distributed in freshwater, estuarine, and marine environments worldwide [1,2]. Aeromonas species grow at a range of temperatures but are isolated with increased frequency during warmer months (May through October in the Northern hemisphere). The organism is frequently isolated from retail produce sources and meat products [3]. For over 100 years, aeromonads have been recognized as the cause of a wide spectrum of disease syndromes among warm and cold-blooded animals, including fish, reptiles, amphibians, mammals, and humans [4,5].
MICROBIOLOGY
The genus Aeromonas was part of the family Vibrionaceae until the mid-1980s, when phylogenetic evidence from molecular studies supported separating out the genus as the family Aeromonadaceae [2,6,7]. The genus has traditionally been divided into two major groups of species: motile, mesophilic species that can cause human disease and non-motile, psychrophilic species that generally only cause disease in fish. The genus currently includes 17 validated phenotypic species from among 19 genotypic DNA hybridization groups. To date, only eight of these named species have been associated with human disease (table 1) and all are motile, mesophilic species [8].
Aeromonas species are oxidase positive and ferment glucose. The organisms grow at a range of temperatures from 0 to 42?C.
PATHOGENESIS
The virulence of Aeromonas species is likely multifactorial. Possible virulence factors include toxins (cytotoxic and cytotonic), proteases, hemolysins, lipases, adhesins, agglutinins, pili, enterotoxins, various enzymes, and outer membrane arrays, such as an S-layer and capsule. Other factors that may contribute to virulence include VacB [9], enolase [10], and the presence of a Type VI secretion system [11-18]. It is difficult to determine which and how many aeromonads contain these putative virulence factors. In addition to the presence of virulence factors in the organism, the host immune response to infection influences the severity of infection [19].
The genus Aeromonas consists of ubiquitous gram-negative rods that are widely distributed in freshwater, estuarine, and marine environments worldwide [1,2]. Aeromonas species grow at a range of temperatures but are isolated with increased frequency during warmer months (May through October in the Northern hemisphere). The organism is frequently isolated from retail produce sources and meat products [3]. For over 100 years, aeromonads have been recognized as the cause of a wide spectrum of disease syndromes among warm and cold-blooded animals, including fish, reptiles, amphibians, mammals, and humans [4,5].
MICROBIOLOGY
The genus Aeromonas was part of the family Vibrionaceae until the mid-1980s, when phylogenetic evidence from molecular studies supported separating out the genus as the family Aeromonadaceae [2,6,7]. The genus has traditionally been divided into two major groups of species: motile, mesophilic species that can cause human disease and non-motile, psychrophilic species that generally only cause disease in fish. The genus currently includes 17 validated phenotypic species from among 19 genotypic DNA hybridization groups. To date, only eight of these named species have been associated with human disease (table 1) and all are motile, mesophilic species [8].
Aeromonas species are oxidase positive and ferment glucose. The organisms grow at a range of temperatures from 0 to 42?C.
PATHOGENESIS
The virulence of Aeromonas species is likely multifactorial. Possible virulence factors include toxins (cytotoxic and cytotonic), proteases, hemolysins, lipases, adhesins, agglutinins, pili, enterotoxins, various enzymes, and outer membrane arrays, such as an S-layer and capsule. Other factors that may contribute to virulence include VacB [9], enolase [10], and the presence of a Type VI secretion system [11-18]. It is difficult to determine which and how many aeromonads contain these putative virulence factors. In addition to the presence of virulence factors in the organism, the host immune response to infection influences the severity of infection [19].
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