Swinton, J., & Gilligan, C.A. Phil. Trnas. R. SOc. Lond. B (1996).

"Dutch elm disease and the future of the elm in the U.K.: a quantitative analysis".

Reviewed: 10/14/11

Dutch elm disease and its effects on the native populations within Great Britain have been a problem for longer than a century.  Separate epidemics in the last century have been caused by two related strains of fungal pathogen, O. ulmi and O. novo-ulmi. The fungus is shuttled between recently dead trees, that function as a breeding grounds, by a beetle vector. The authors of this article have developed a model to look at the long-term predictions possible from a simple density based characterization of elm trees and their transition to infection and otherwise.
I have already mentioned that recently deceased trees function as a breeding ground for the vector that helps propagate the fungus in the system. However, long-dead trees are no longer able to fulfill this role and this time dependency was accounted for in the model parameters. A couple of assumptions were made by the authors when developing the basics of their model equations. One was that the vector density was proportional to the number of dead trees total based on previous research in the system of study. This allowed for simplification in the equations for overall force of infection.
The model was run against data collected by the National Forestry Commission of Britain in the 1970's, however only non-woodland systems were looked at in order to minimize sampling uncertainty. The most interesting results from their model showed how endemic levels of pathogen could be maintained in the tree populations depending on their lethality and the transmission levels. High lethality, it seems, actually causes a pulse in the system that could allow for recovery of the host tree populations and a lower overall level of endemic infection. This is also related to the reproductive rate of the fungal pathogen, where a low R-naught for the pathogen requires a very high degree of lethality to even reach a point where persistence is possible.
There are however several possible ways in which the model presented was confusing and could be improved. The authors posit that competition between the two fungal species plays a role in the long-term disease dynamics, yet they run their model without the inclusion of the less-aggressive species, O. ulmi, even when it became clear that their was a serious underestimation of infected and dead trees occurring in their model when compared to the data collected by the Forestry Commission. This study would also benefit from a greater amount of information on the life-history traits of both the tree genus and the fungi. The parameter estimates used in their models were chosen using a best-guess method in the absence of data pertaining to the life-history of the trees at juvenile and adult stages and transmission estimates for the pathogens. The fungi themselves have two roles in natural systems, saprophytic and  parasitic; a better understanding of the transition between these two states would be of use in future studies.