Camellias are popular ornamental plants grown for their verdant evergreen foliage and spectacular flowers, which come in many colours, sizes and forms. The fungal pathogen (Ciborinia camelliae), which causes camellia flower blight, is considered the most serious disease of the camellia genus as it attacks the flowers, causing them to turn brown and fall early. The pathogen was described in Japan in 1919, spread to the USA in 1938 and was discovered in New Zealand in 1993. Relatively little research has been done on the pathogen or the disease that it causes. Chemical and cultural control methods have not proved particularly effective. The fungus was isolated from sclerotial medulla and isolates grew significantly better on Camellia Petal PDA, Oxoid PDA, Difco PDA and Oxoid MEA than on Homemade PDA, expired Oxoid PDA and Merck PDA. Cultures were maintained on Difco PDA and optimum temperatures for growth and sclerotial formation were between 15°C and 20°C. Surveys of the North Island in 1997 and both North and South Island in 1998 found the pathogen was more widely distributed than previously thought. It is widespread in the central, western and lower North Island and present in the north of the South Island and Christchurch. Although the outbreaks in Auckland and in Christchurch were probably the result of the transfer of infected material, dispersal by windborne ascospores appears to be the main method of spread. Conditions that stimulate sclerotial germination out of season were investigated using both protocols established for other fungi and novel methods that involved incubation at various temperatures, combinations of temperatures, and light. Artificial stimulation of germination was not achieved. Infection of petals was investigated using agar plug inoculation and, during the disease season, ascospores. Wounding was required for infection from plug inoculum but not from ascospores. Younger buds appeared to have more resistance to both types of inoculum. Ascospore inoculations of species and varieties showed that there were levels of resistance within the genus but this was not quantified. Several potential biocontrol agents, effective against the ascospore stage, were isolated but could not be evaluated due to the limited ascospore production season. Further research is required to study the pathogen/host interaction, the infection process, levels of resistance and mechanisms of resistance. Breeding for resistance appears to be possible and offers the best long term prospects for the control of this disease.