Demography and population models for Hieracium Pilosella in New Zealand
Degree GrantorUniversity of Canterbury
Degree NameDoctor of Philosophy
Hieracium pilosella has become a major concern in the high country grasslands of New Zealand. This thesis provides an understanding of the population dynamics of H. pilosella in an area which has supported the weed as a major component of the vegetation for more than 30 years. The study uses a combined modelling and experimental approach to determine vital rates and regulatory mechanisms. It then uses these to predict the rate of spatial spread, change in density, and the likely impact of biological control. Mature populations of H pilosella at Mt. John were found to be regulated by the interaction between density-dependent mortality and density-independent reproduction. The addition of water and/or fertiliser caused an increase in the reproductive vigour of the plant and a decrease in density while simulated grazing (i.e. mowing) had little effect on the population. A link was found between reproductive vigour and rosette size or age (50% of first year rosettes reproduced while only 11 % of older rosettes did), although the reproductive threshold size (23 mm diameter) appeared to be independent of age. Rosettes grown on soil which had previously supported H pilosella had lower growth and reproductive rates and produced fewer stolons of shorter length. However, there was little support for either the allelopathic or aluminium toxicity hypotheses for these lower growth rates. Spatial population models suggested that in the early stages of colonisation, H pilosella vital rates are such that it has the potential to occupy 100% of available space but as the population matures, vital rates change and it is unable to occupy all available space, probably because of intraspecific competition and a limit on plant size. Spread of patches was predicted to be 0.5 - 0.8 cm/yr by both explicit spatial simulation models and analytical diffusion models. Both spatial and non-spatial models predicted that the most effective agent for biological control would be one which caused an increase in mortality rather than a decrease in fecundity; to reduce a population by more than 50% a control agent would have to either increase mortality by 10 - 15 % or decrease daughter production by 80%.