Disease dynamics in the wild are influenced by a number of ecological and evolutionary factors not addressed by traditional laboratory-based characterization of pathogens. Here we propose the oyster, Crassostrea gigas, as a model for studying the interaction of the environment, bacterial pathogens, and the host in disease dynamics. We show that an important first step is to ask whether the functional unit of pathogenesis is a bacterial clone, a population, or a consortium in order to assess triggers of disease outbreaks and devise appropriate monitoring tools. Moreover, the development of specific-pathogen-free (SPF) oysters has enabled assessment of the infection process under natural conditions. Finally, recent results show the importance of microbial interactions and host genetics in determining oyster health and disease.
Involvement of Vibrios in Oyster DiseaseVibrios are ubiquitous marine bacteria that are ecologically and metabolically diverse members of planktonic and animal-associated microbial communities [1,2]. They have been called 'opportuni-trophs ' [3] due to their high metabolic versatility and genetic variability coupled with chemotaxis and quorum sensing (see Glossary), all of which allow high colonization potential [4,5]. Vibrios encompass the ancient and well-studied human pathogen, Vibrio cholerae, as well as some less thoroughly characterized opportunistic pathogens capable of infecting humans, including Vibrio parahaemolyticus and Vibrio vulnificus [2]. Even less well understood are the consequences of Vibrio infections in other animals, including fish, coral, shrimp, and mollusks; however, infections in these organisms can have important environmental and economic consequences [6]. In particular, vibrios have been suggested to be responsible for repeated mortality outbreaks in oyster beds (Crassostrea gigas) in France that have resulted in losses of up to 80-100% of production (Box 1). However the onset and progression of disease in the wild has been difficult to follow in the past. Hence, it is often not clear whether vibrios isolated from diseased oysters are the causative agent, secondary opportunistic colonizers, or commensals [7].Vibrios appear to employ a diversity of molecular mechanisms to infect oysters, albeit our knowledge is based mainly on very few model strains. For example, infection with Vibrio tasmaniensis LGP32 [8] involves an intracellular phase in hemocytes, which are the oyster's immune-competent cells, and resistance to (i) antimicrobial peptides (AMPs), (ii) reactive oxygen species (ROS) and (iii) copper [9][10][11][12]. Vibrio aestuarianus, by [ 1 5 _ T D $ D I F F ] contrast, interacts with hemocytes extracellularly and inhibits their phagocytotic abilities [13,14]. A common theme, however, is that metalloproteases have been linked to toxicity in V. tasmaniensis, V. aestuarianus, Vibrio corallilyticus, and Vibrio tubiashi [13,15,16]. Nonetheless, the disruption of
TrendsKnowledge of the genetic structure of the Vibrio population provides a framework for mapping d...