Although the basic reproductive rate of the pathogen is the primary component of the dynamics of disease, many other factors influence that component. Some of the main factors are discussed below.
Population density:
—Because the potential for development of disease in a population depends on the contact rate between infectious and susceptible animals, the frequency of that contact is dictated by the population density.
In any population, successful introduction of a pathogen depends on the host density being greater than a characteristic threshold density (Nt); if the host population density is below this level, no disease will occur (Grenfell and Dobson 1995).
This spatial factor is inversely dependent on b: the greater the value of b, the smaller the critical population size for disease establishment, since transmission is more efficient.
If S were plotted against I (Figure 4), the threshold density would be the point below which no new infection occurred (incidence 5 0; for the hypothetical example presented, Nt 5 625).
The number of infectious animals would begin to decrease until either a steady state occurred (enzootic infection) or the pathogen was eliminated from the population. Another parameter that relates to the density threshold is the duration of infectiousness.
With a longer period of infectiousness, more potentially effective contacts will occur and the threshold density will decrease. Therefore, quickly resolved acute diseases, such as the gramnegative septicemias of fish (Roberts 1986), may not remain in the population and may require a host population increase beyond the threshold density to become established again.
Conversely, diseases with protracted infectious periods have a longer opportunity to effect transmission to susceptibles and would not require as high a host density as acute infections. For fish pathogens such as R.salmoninarum and IPNV, which are known to be harboured for long periods of time, this would imply that the Nt for these pathogens is small.
However, long-term infections may not be transmitted over long periods of time, as for example in tuberculosis of humans (Brook and Madigan 1988).
Vertical transmission:
Another survival mechanism that pathogens have evolved is their ability to be passed directly from parent to progeny, that is, vertical transmission.
There are several important diseases of fish in which this mechanism is operative, such as IPNV (Wolf 1988), IHNV (Mulcahy and Pascho 1985), channel catfish virus (Wolf 1988), and R. salmoninarum (Brown et al. 1990); and there are several others in which it is suspected, such as pike fry rhabdovirus (Roberts 1986) and Flavobacterium psychrophilium (W. Cox, California Department of Fish and Game, and R. P. Hedrick, University of California-Davis, personal communication).
Because of the increasedability to transmit the pathogen under these circumstances, a low threshold population density is often sufficient to initiate an epizootic or maintain an enzootic state.
In essence, the vertically infected fish serve as an initiating point for infection and, if conditions are favourable for the development of disease, epizootics can ensue.
Another factor that comes into play with the success of vertical transmission is the likelihood that animals acquiring a pathogen from parents tend to harbour them for long periods, as in the examples cited above, and can extend the duration of infectiousness.
Author:
PAUL W. RENO
