Peach Leaf Curl

Appearance

Leaves will also undergo chlorosis, turning a pale green or yellow, and later show a red or purple tint. Fruit can either drop prematurely or show surface distortions. Severe infection can also produce lesions on the flowers. The host tree will experience defoliation if the leaves are badly diseased. If a seedling is severely infected, it may die. Almond trees display similar symptoms.

Behavior

"Taphrina deformans" infects species of the genus "Prunus" and "P. persica" ). It is best known as the causative agent of peach leaf curl in peaches and nectarines. It has been observed that this fungus also infects the fruits of some South American trees like "Ocotea puberula", "Nectandra megapotamica" and other Lauraceae species. An additional form has been identified which infects apricots. Some researchers posit that these forms are separate varieties altogether, which is supported by recent genetic evidence based on hybridization. Furthermore, almond strains of "T. deformans" seem to be unable to induce peach leaf curl on peach trees, and vice versa.

Infected leaves develop a whitish bloom as the infection progresses. This bloom consists of asci that break through the cuticle of the leaf by way of lysis. One ascus contains eight ascospores, which are ejected in early summer and moved by rain and wind. This fungus is believed to survive the winter by staying on the surface of the new host plant, such as on bark or buds. In the spring, new buds are infected by the conidia as the leaves emerge from the buds. The disease does not occur every year, as it requires a minimum of 3mm of rainfall followed by at least 12 days during which the developing conidia remain damp and at temperatures below 19 °C.Smith, S.E. What is Peach Leaf Curl? 2009. WiseGEEK. 14 Apr 2009 The fungus has higher infection rates following cooler, damper winters.

"Taphrina deformans" hyphae growing in intercellular spaces secrete polysaccharide-degrading enzymes, such as cellulase, causing partial dissolution of the host cell wall. This process also results in changes in the plasma membrane.
"T. deformans" also produces the auxin indole-3-acetic acid from L-tryptophan via indole-3-pyruvic acid and indole-3-acetaldehyde. This process is thought to be responsible for the hyperplastic effect of the infection.