No known vector.

No specific signs are present.

The early symptoms of this disease tend to be limited to 'bleeding' lesions; scattered drops of rusty-red, yellow-brown, or almost black, gummy liquid ooze from small and large patches of dying bark on the stems or branches of infected horse chestnuts.

These bleeding patches may be associated with the base of the tree at the soil surface or may start higher up the trunk at about one meter, and then extend upwards. Early in the year (spring), the exudates from bleeding patches are a dark color but transparent. As the weather becomes warmer, bleeding from infected tissues becomes more copious and runs some way down the tree. At this time, it is often a conspicuous rusty-color and no longer transparent but cloudy or opaque. Under dry conditions (summer), this exudate dries to leave a dark, brittle crust near the point of exit in the bark. Renewed bleeding may be seen later in the year, often in autumn. This suggests that the pathogen activity is greatest under moist, mild conditions of spring and autumn.

After some months, the center of the bleeding bark patch may become cracked. Cracking of bark and disfigurement of trees is common. In time, fruiting bodies of wood rotting fungi often appear on the surface of the dead bark, protruding out of the bark cracks.

Over three-to-four years and particularly if a tree has multiple bleeding cankers, the areas of dead phloem and cambium underneath the bleeding areas may coalesce and extend until they encircle the entire trunk or branch. When this happens, crown symptoms become visible, typically consisting of yellowing of foliage, premature leaf drop, and eventually, crown death. Sometimes, part of the crown will fail to flush, and later in the year the remaining foliage withers and dies. In trees with chronic dieback caused by the disease, the leaves may be smaller, and seem thinner and more flaccid than the foliage of healthy trees.

The inner bark (phloem) under the bleeding patches is usually necrotic or dead, with an orange-brown color, which is often clearly mottled or zoned. Underneath, the wood may be stained blue-black.

Molecular: Green et al. (2009) developed a real-time PCR for detection of Pseudomonas syringae pv. aesculi in plant tissues. This PCR assay can be used as a preliminary screen for Pseudomonas syringae occurring on horse chestnut.

Bleeding on the trunk and branches, necrotic phloem, foliar discoloration, and dieback of horse chestnut has also been seen with Phytophthora spp. (cactorum and citricola) in Europe. In the United States, the same pathogens have also been found to cause bleeding cankers on maple, birch, sweet gum, oak, and willow. Phytophthora ramorum also has been found to cause bleeding cankers on certain broadleaf species in England, including a single specimen of horse chestnut.

Strain Isolation: Pseudomonas syringae pv. aesculi is fluorescent on King's B medium. Strain isolations were performed onto King's B medium (King et al., 1954) from the margins of fresh or dry lesions found on horse chestnut trees (Bultreys et al., 2008).

Biochemical: Pseudomonas syringae pv. aesculi produces Levan on sucrose nutrient agar, is negative for Oxidase, is non-Pectolytic (does not cause rot in potato), is negative for Arginine dihydrolase, and induces a hypersensitive response on Tobacco (LOPAT Group I, +---+) (Webber et al., 2007; Young, 2010). Pseudomonas syringae pv. aesculi produces coronatine, a chlorosis inducing phytotoxin produced by several other pathovars of P. syringae (Bereswill et al., 1994; Bultreys et al., 2008). Pseudomonas syringae pv. aesculi also produces indole-3-acetic acid (IAA, auxin) (Glickman et al., 1998).

Molecular: Bultreys et al. (2008) identified Pseudomonas syringae pv. aesculi through pyoverdin-based tests, including visual, spectrophotometric and high performance liquid chromatography, the induction of potato rot, and extragenic palindromic (REP)-PCR. The modified PCR test detecting the cfl gene involved in coronatine synthesis was also used in identification (Bultreys et al., 2008).

Schmidt et al. (2009) developed a 'fast' molecular detection method, which included DNA extraction, polymerase chain reaction (PCR), and electrophoresis until gel documentation. The PCR primers were derived from the gyrase B gene. This primer, however, also amplified pathovar aptata and pathovar morsprunorum due to great similarity in the gyrase B gene sequence of closely related pathovars. The authors thought that the differing host ranges would aid in the identification of these pests from pathovar aesculi, because the other pathovars should not occur near a lesion of a horse chestnut tree. The test identified the pathovar from a tree sample within 6 hours of starting laboratory work.