Wounding of trees by debarking during the vegetative period sometimes results in the formation of callus tissue which develops over the entire wound surface or on parts of it. This light and transmission electron microscopy study of living lime trees found that the formation of such a surface callus is subdivided into three stages. During the first stage, numerous cell divisions take place in regions where differentiating xylem remains at the wound surface after debarking. This young callus tissue consists of isodiametric parenchymatous cells. Cambium cells, sometimes also remaining at the wound surface, collapse and do not contribute to callus formation. During the second stage, cells in the callus undergo differentiation by forming a wound periderm with phellem, phellogen and phelloderm. In the third stage, a cambial zone develops between the wound periderm and the xylem tissue laid down prior to wounding. This process is initiated by anticlinal and periclinal divisions of a few callus cells only. Later this process extends tangentially to form a continuous belt of wound cambium. Subsequently, this cambium produces both wound xylem and wound phloem and thus contributes to further thickening.

Bacteria were isolated from necrotic lesions on a horse chestnut tree (Aesculus hippocastanum) with bleeding canker in Hamburg, Germany. Sequencing of the rDNA-ITS region revealed great similarity to pathovars of Pseudomonas syringae. Pseudomonas syringae pv. aesculi was identified by sequence homology of the gyrase B gene. This is the first report of P. syringae pv. aesculi in Germany. Phytophthora was not detected.

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A molecular technique was used to detect the bacterium Pseudomonas syringae pv. aesculi in horse chestnut trees (Aesculus hippocastanum), affected by the recently recognized European ÔPseudomonas horse chestnut bark diseaseÕ. The technique helped identify the pathogen within 6 h of sample preparation including DNA extraction, polymerase chain reaction (PCR) and electrophoresis until gel documentation. PCR primer pairs derived from the gyrase B gene sequence were used. Because of the great similarity in the gyrase B gene sequences of the numerous closely related P. syringae pathovars, the primers were not only totally specific to the pathovar aesculi, but also detected a few other pathovars.The assumption that other bacteria should not occur at least near to a necrotic lesion of a horse chestnut tree was corroborated by sequence identity of the PCR products obtained with the gyrase B gene sequence of P. syringae pv. aesculi. KochÕs postulates were fulfilled for an isolate of P. syringae pv. aesculi obtained from a diseased horse chestnut tree sampled in Hamburg in 2007.

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