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PATHOGENIC EFFECTS OF PLANT DISEASE AGENTS ON VECTOR INSECTS: AN INTRODUCTION

This Conference has so far emphasized an interdisciplinary approach to pathobiology, and this session is no exception. The various authors deal with such diverse pathogens as small RNA viruses of plants, spiroplasmas of plants and insects, walled prokaryotes of plants and insects, and nuclear polyhedrosis viruses (NPV) of insects. In indicating the hosts of these pathogens, I have reflected the current view that the pathogens are indeed confined to “usual” hosts. In retrospect, it seems that one central thread throughout this session is the current degree of uncertainty with respect to the limits of host ranges and specificities of pathogenic organisms. I am reminded of earlier work, in which we discovered, purely by accident, that acholeplasmas (which had been regarded before that time as saprophytes or commensals of vertebrates) multiplied in insects. It had been our intention to use them as control mycoplasmas, which were not expected to multiply! They did not, however, in our hands, cause plant disease. A central feature of host relationships is the necessity for pathogenic organisms to be adapted to each of the microenvironments of a biologic cycle. Perhaps what we are learning is that whereas organisms may be adapted to some of these microenvironments, the chance occurrence of the entire series of adaptations that might enable an organism to maintain itself in a reservoir in nature is a rare event. Such adaptations, in fact, apparently occur on an evolutionary time scale rather than on a contemporary one. Certainly, the production, licensing, and use of live vaccines depend on the rapid drift away from pathogenicity in different in vivo systems. With our spiroplasmas, we also observe such a drift after passage of the corn stunt agent in Drosophila; the ability to complete the biologic cycle in leafhoppers and plants is lost. The existence of plant viruses that apparently do not multiply, but that are acquired from and transmitted to plants by the circulative route, should be of considerable importance in studies on host specificity of viruses. True insect viruses have great potential as cornerstones in integrated insect control programs, so that their host range capabilities are of special interest. Detailed knowledge of the manner in which they infect cells is an a priori requirement for such an assessment. The careful observations of Hirumi et al. on one NPV-host cell system further this understanding. But, what is the range of potentially infectable cells? This important question is now being addressed by McIntosh et al., and the progress of this group, as reported here and in forthcoming publications, will have bearing on the speed with which insect viruses are made available for agricultural purposes. Perhaps, the NPV (baculovirus) and granulosis groups, which have no known counterparts as plant or vertebrate pathogens, will prove to be unable to replicate in vertebrate cells. In any event, there is good reason to hold high hope that potentially useful viruses will prove to be as safe as live vaccines for human use.