Olive disease models
The olive (Olea europaea L.), grown on over 8 million hectares, is the second most important oil fruit tree crop worldwide after oil palm and its cultivation is traditionally concentrated in the Mediterranean area. The total olive oil production for the 2006–2007 season was 2.859,500 tons (International Olive Oil Council (IOOC) data). Southern European countries account for about 74.9% of the world production, with Spain being the main producer (38.7%), followed by Italy (21%) and Greece (12.9%). Other important olive oil producers are Turkey, Tunisia and Syria (17.1%) as well as Jordan, Morocco and Algeria.
Peacock spot is also known as Olive scab and leaf spot and is widespread in all the major olive growing regions of the world (Obanor et al. 2005). Symptoms have been found to occur mainly on leaves and appear as dark green to black spots surrounded by a yellow halo similar to the eye spot on peacock’s feathers; hence, the name peacock spot (Graniti 1993; Shabi et al. 1994). Peacock spot is considered to be the most important olive grove disease in Spain (Trapero and Blanco, 2008). Crop losses arise mostly from defoliation of infected trees, poor growth and dieback of defoliated branches and reduced fruit yield (Graniti 1993; Viruega et al. 1997). Heavy defoliation has been reported to cause a delay in ripening and a decrease in oil yield in Italy (Graniti 1993) and New Zealand (MacDonald et al. 2000).
Olive scab or leaf spot, caused by the fungus Spilocaea oleagina, is widespread in the Mediterranean region. Losses arise mostly from the defoliation of severely infected trees, with consequently reduced yield.
Symptoms are mainly confined to leaves and appear as dark brown, circular, zonate spots surrounded by yellow haloes (‘peacocks eye’). S. oleagina shows a typical subcuticular growth, forming flat colonies within the cutinized layer of the thick epidermal cell wall. This habit has been associated with a defence reaction of the host involving mobilization and breakdown of the phenolic glucoside oleuropin and inhibition of pectolytic enzymes produced by the pathogen. The disease is particularly severe in densely planted groves of susceptible olive cultivars and in nurseries. Infections may occur throughout the year, except during hot and dry summers, when favorable temperatures (opt. 16–21°C) and rain occur. Conidia, formed at the apex of short ampulliform conidiophores, are usually carried by rain droplets, but recent data show that humid air currents and insects also contribute to limited aerial dissemination. Usually, the incubation period is about 2 weeks; however, if the infection is followed by a hot season, it may last several weeks. Spots already formed in spring may stop growing in summer and resume their growth and sporulation in autumn. Chemical control schedules include fungicide (especially copper) treatments during the main infection seasons (spring and autumn).
Disease Life Cycle
Heavily infected leaves and fruits on the ground, as well as on those that remained on the tree, are a source of inoculum for the current season or allow over-wintering of the fungus. The pathogen is known generally to survive unfavorable conditions, e.g. dry, hot weather, in fallen leaves as well as in infected leaves on the tree. The conidia formed in leaves on the tree can survive for several months; although once they have separated from the conidiophores they lose their germination ability in less than a week (Viruega and Trapero 1999). Following a period of moist warm weather new batches of conidia are readily produced on the foliar spots. Viable conidia are also produced in fallen leaves. However, their role as inoculum to produce new infections is considered to be negligible (Trapero and Blanco 2008). This study has shown that the disease generally is favoured by cool weather; however, the warm and humid weather during the summer of 2009 was also observed to encourage disease occurrence. These observations support those of Viruega and Trapero (1999), who found that in Spain leaf infections can remain latent over summer without causing any leaf drop and are the main source of inoculum for autumn–winter infection. Observations also indicated that young leaves were very susceptible to infection in spring, and that foliage in lower parts of trees was more frequently infected. This is consistent with the pathogen’s requirement for high humidity to develop. Germination requires 98% humidity, with temperatures in the range of 0–27°C (Trapero Cassas 1994). In Australia, the disease can be inactive during the hot and dry summers. Germination of the spores is restricted at temperatures above 30°C. The percentage of germinating conidia decreases linearly in proportion to leaf age, being 58% at 2 weeks and 35% at 10 weeks. Temperature significantly affects the frequencies of conidium germination on wet leaves from 5°C to 25°C. The per cent germination increases from 16.1, 23.9, 38.8 to 47.8 and decreases again to 35.5% after 24 h. Formation of appressoria occurred 6 h after the first signs of germination. The percentage of germlings with appressoria increases with increasing temperature to a maximum of 43% at 15°C. No appressoria are formed at 25°C after 48 h of incubation. Increasing wetness duration causes increasing numbers of conidia to germinate at all temperatures tested (5–25°C). The minimum leaf wetness periods required for germination at 5, 10, 15, 20 and 25°C were 24, 12, 9, 9 and 12 h, respectively. At 20°C, a shorter wetness period (6 h) is sufficient if germinating conidia were then placed in 100% RH, but not at 80 or 60%. However, no conidia germinate without free water even after 48 h of incubation at 20°C and 100% RH. The graphical presentation of the Peacock spot model shows the leaf wetness, relative humidity and air temperature together with the results for infection progress and infection severity. The graph below indicates an infection starting on December 17th at 19:00 and finishing by 100% on December 18th at 11:00. The infection severity is calculated after a longer moist period and it increases in steps to 4, which means the highest calculated severity for this infection period.
- Graniti A (1993) Olive scab: a review. OEPP/EPPO Bulletin 23, 377–384.
- MacDonald AJ, Walter M, Trought M, Frampton CM, Burnip G (2000) Survey of olive leaf spot in New Zealand. New Zealand Plant Protection 53, 126–132.
- Obanor EO, Walter M, Jones EE, Jaspers MV (2005) In vitro effects of fungicides on conidium germination of Spilocaea oleagina, the cause of olive leaf spot. New Zealand Plant Pathology 58, 278–282.
- Schubert K, Ritschel A, Braun U (2003) A monograph of Fusicladium s.lat. (Hyphomycetes). Schlechtendalia 9, 71–132.
- Shabi E, Birger R, Lavee S, Klein I (1994) Leaf spot (Spilocaea oleaginea) on olive in Israel and its control. Acta Horticulturae 356, 390–394.
- Trapero Cassas A (1994) El repilo del olivo. Agricultura 746, 788–790.
- Trapero A, Blanco MA (2008) Enfermedades. pp. 557–614. In ‘El cultivo de olivo. 6th edition.’ (Eds D Barranco, R Fernández-Escobar, L Rallo) 846 pp. (Coedición Junta de Andalucía/Mundi-Prensa: Madrid, Spain)
- Viruega JR, Lique F, Trapero A (1997) Caída de aceituhas debida a infectciones del pedunculo por Spilocaea oleagina, agente del Repilo del olivo. Fruticultura Profesional 88, 48–54.
- Viruega JR, Trapero A (1999) Epidemiology of leaf spot of olive tree caused by Spilocaea oleagina in southern Spain. Acta Horticulturae 474, 531–534.
Check which sensor set is needed for monitoring this crop’s potential diseases.