Factors Involved in the Dissemination of Disease in Fish Populations

Microbial pathogens have preyed on fish for eons and have coevolved with them. These cohabitants have, in a general way, established an overall equilibrium with their hosts in their natural habitat.

However, this equilibrium is unstable and, when viewed at a regional or local rather than at a global level, may result in epizootic disease.

With the advent of fish culture and the development of the science of microbiology in the 19th century, more attention was paid to the occurrence of epizootic diseases in cultured fishes.

The development of aquaculture has shifted the focus from the health of fishes in ecosystems (which is indirectly affected by anthropogenic involvement) to direct oversight and manipulation of captive populations.

The artificial rearing of fishes has led to the exacerbation of diseases that previously existed in wild populations. Currently, a contentious issue is the question of whether cultured fish are the source of diseases inimical to wild, especially endangered, populations of fish (most notably salmonids).

Similarly, those in the aquaculture community are concerned about the converse: are wild fish transmitting disease to cultured fishes?

These are among the plethora of unanswered questions about dissemination of disease in fish populations. Fortunately, the intricate complexities of ecosystems and the somewhat less complex culture environment, intimidating as they are, may yield some answers if approached rationally.

The objective of this paper is to review some of the most important factors that determine the establishment and course of infectious diseases in fish populations.

It has been long understood that intercalations of host, agent, and environmental factors determine, to a large extent, the course of disease in wild or cultured fish. The relationships among these variables have been analysed empirically; it is apparent that mathematical methods can be applied to the study of diseases caused by a variety of pathogens in a variety of host population structures.

In this sense, fish are no different from humans and other terrestrial animals when we address the factors which affect how diseases impinge on a population; they are simply wetter.

Mathematical models are used commonly for the estimation of the dynamics of fish populations (e.g., Weatherly and Gill 1987), especially commercially exploited species. There have been few similar studies for the diseases of fishes and their impacts on specific populations.

Disease dynamics have been studied extensively in humans and to a lesser extent in other animals, including populations of some wild animals (reviewed in Anderson and May 1979, 1982; May and Anderson 1979; Grenfell and Dobson 1995).

Models derived from mathematical simulations, however, vary in their ability to emulate real world situations, in part because they are dependent on the accuracy of the data used to construct the

models. Simple deterministic models (those based on preselected variable values) can generally predict the course of disease; more complex deterministic and stochastic models (those which incorporate probabilities of parameter values) incorporating myriad variables are closer to reality.

For fishes, there have been a few mathematical treatments of the disease processes in feral populations of Atlantic herring Clupea harengus affected by Ichthyophonus hoferi in the North Sea (Patterson 1996) as well as of lymphocystis in European flounder Platichthys flesus in the same region (Lorenzen et al. 1991).

Laboratory experiments have been carried out to defineparameters of disease dynamics for infectious pancreatic necrosis disease in cultured trout (Bebak 1996) and for Gyrodactylus in guppies Poecilia reticulata (Scott and Anderson 1984).

Thus, some preliminary work has been done in developing sophisticated models of disease for fish. However, even with some rudimentary experimental work and conservative assumptions, basic models of diseases can be constructed which may reflect the process of a wide variety of diseases in fish. More complex models can then be refined from these preliminary efforts.

Author:

PAUL W. RENO