Effect of dose, pre-mortem host incubation temperature and thermal behaviour on host mortality, mycosis and sporulation of Metarhizium anisopliae var. acridum in Schistocerca gregaria

The effects of dose pre-mortem host incubation temperature and thermal behaviour on mortality, mycosis and sporulation of Metarhizium anisopliae var, acridum in the desert locust, Schistocerca gregaria (Forskal) were assessed in the laboratory. While all factors were important in determining locust mortality rate, they had little influence on rates of mycosis and sporulation following host death. Mortality rates at constant incubation temperatures between 15 and 30 degreesC broadly reflected the temperature-related vegetative growth profile of the fungus, with higher doses causing quickest mortality and generally high ( > 80%) levels of dose-independent mycosis. At 35 degreesC, locusts were able to suppress infection for several weeks, the effect of close on mortality was less apparent and no mycosis was observed, despite being more amenable for basic pathogen development compared with 15 degreesC. When locusts were presented with an intermittent cooler period (20/35 degreesC), dose-dependent mortality was more rapid with relatively high (> 70%) dose-independent rates of mycosis. However providing a thermal gradient of 25-50 degreesC in place of 35 degreesC, allowed locusts to suppress infection for some weeks and reduced mycosis rates slightly, demonstrating the therapeutic advantages of host thermoregulation. Despite this, there was little evidence that hosts could escape infection indefinitely, demonstrated by the rapid mortality and mycosis rates when the temperature was reduced to 30 degreesC. The importance of dose and pre-mortem host incubation temperature for the conidial yield resulting from mycosed cadavers was assessed. Inoculating dose was unimportant and no consistent trend of the incubation conditions on conidial yield was found, suggesting these were also unimportant, as long as the pathogen could grow sufficiently well to kill the host. Implications for secondary cycling of the pathogen in the field are discussed.