Aeromonas and Plesiomonas Species

Abstract

Recent studies have identified previously unknown Aeromonas virulence mechanisms that may contribute significantly to human pathogenicity. This chapter reviews existing knowledge of Aeromonas virulence factors and host responses and future directions that may provide a more detailed understanding of Aeromonas-associated human diseases. Aeromonas extraintestinal diseases (peritonitis, endocarditis, pneumonia, conjunctivitis, and urinary tract infections) are more common and varied than those caused by Plesiomonas shigelloides (cellulitis, arthritis, endophthalmitis, and cholecystitis). Aeromonas spp., therefore, may produce different types of cytotonic enterotoxins that are functionally similar. It is plausible that the expression of various virulence factors of Aeromonas may be controlled by quorum sensing. The major signal molecule synthesized by the ahyI locus in A. hydrophila was N-(butanoyl)-L-homoserine lactone (BHL), also referred to as C4-HSL, with N-acylhomoserine lactone (AHL) synthesized in relatively smaller amounts. At present, it is not possible to identify the disease-causing strains because of our incomplete understanding of Aeromonas virulence mechanisms. Some of the confusion surrounding Aeromonas enterotoxins has been resolved, and several new virulence factors have been described. The case for Plesiomonas’s being an enteric pathogen is less convincing than that for Aeromonas spp. Although Plesiomonas species has been isolated from diarrheal patients and has been incriminated in several large water- and foodborne outbreaks, no definite virulence mechanism has been identified in most strains associated with gastrointestinal infections.