The population density, although not strictly an environmental parameter, is crucial to the dissemination of disease because a prime factor in epizootic disease is the frequency of contact between infectious and susceptible animals. Whether
the contact is direct or indirect, from fish to fish or through an intermediate host, infection cannot occur unless the susceptible animal comes in contact with the pathogen.
Because the total amount of a given pathogen in the water is determined by both the quantity released by an individual and the total number of fish in the area, population density can affect pathogen transmission.
Other environmental factors may also influence the disease process by virtue of their impact on the survival of the pathogen in the environment or by affecting the host defense mechanisms.
For example, temperature also plays a significant role in disease development. Although such diseases as vibriosis, enteric redmouth, and furunculosis tend to occur at temperatures exceeding 108C, marine flexibacteriosis and freshwater cold-water disease occur at temperatures below 108C (Roberts 1986).
In addition, water flow and water chemistry can affect disease.
Fast flow rates may either shorten the contact between a host and pathogen or disseminate pathogens more effectively than slow flow rates.
Chemical components in the water can directly inactivate some sensitive agents. A population of fish under invasion from a pathogen comprises three mutually exclusive cohorts that can change relative to each other during the course of disease. The susceptible group (S) is composed of those individuals that can become infected on contact with a pathogen.
Their susceptibility is dependent on a general level of resistance that is inadequate to prevent the pathogen from invading the host. This level is predicated on species and innate stock resistance, as
mentioned above, as well as prior exposure and the development of acquired immunity by humoral or cellular responses that confer protection.
The infected cohort (I) is made up of susceptible individuals that have contacted the pathogen and become infected. During the initial phase of the infectious process, the latent or prepatent phase, the host is infected but incapable of transmitting the pathogen to other susceptible fish.
Subsequent to this period the infected host becomes infectious for a period characteristic of a particular host– pathogen system. This capacity for infecting others, the infectious state, may occur prior to the development of overt signs of disease or after signs appear.
Another temporal factor associated with the infectious group is the duration of infectiousness. It is intuitively obvious that the longer an individual remains infectious, the greater the probability that it will transmit a pathogen to other susceptible in the population.
Likewise, the shorter the duration of infectiousness, the lower the probability that the pathogen will be disseminated to others in the population. The duration of infectiousness for fish pathogens has not been explicitly studied, but as shown in Table 1, an estimated length of infectiousness for selected pathogens of salmonids varies from weeks to years.
In most disease states, the host develops immunity after some period of infection. Those that become immune or refractory to reinfection are no longer a component of the susceptible population and become members of the removed cohort (R).
As mentioned above, however, not all pathogens induce immunity, and therefore, even individuals that have been previously infected by these pathogens may become reinfected upon later exposure.
Unfortunately, unlike several childhood viral diseases of humans that have been extensively studied, the immunity induced to fish pathogens is not lifelong; thus at some point, immune animals revert to their susceptible status.
The only permanently non susceptible members of the removed cohort are those that have died. The proportion of these individuals is strictly associated with the specific disease mortality rate, which can vary markedly from episode to episode of disease.
Author:
PAUL W. RENO
