Symptoms and Control Methods of Red Pine Bark Rot and Resin Flow Disease

[Distribution and Damage] This disease occurs in red pine (Pinuskoraiensis) plantations throughout the three northeastern provinces. In the Yanbian area of Jilin Province, the cities (counties) of Yanji, Hunchun, Helong, Wangqing, Dunhua, Antu, Longjing and others have relatively severe incidence, with a general incidence rate of 20%-30%, severely affected stands at 50%-60%, and in individual stands at the Mao'ershan Forest Farm in Yanji City, the incidence rate reaches as high as 98.6%.

The pathogen attacks the phloem and cambium of the trunk and lateral branches of young red pines, even penetrating deep into the surface xylem of the sapwood, causing the tissue to rot and die with a brown discoloration, seriously affecting the growth of diseased trees, with some leading to death. According to surveys, severely diseased trees lost 51.1% of height growth and 42.4% of diameter at breast height growth. The sunken diseased parts of the trunk cause timber defects, affecting the production of finished wood, making this an important disease harming young red pine plantations.

[Symptoms] The pathogen infects the trunk and lateral branches by invading through wounds in the bark. After lateral branches are infected, the phloem turns brown and rots, initially forming local lesions; the overall appearance of the branch shows no change and can only be detected by peeling back the bark. The pathogen quickly spreads throughout the entire branch, the needles turn yellow-green, and by the following spring the entire branch dies, with resin droplets at the boundary between diseased and healthy tissue. On the main trunk, the initial infection sites are mostly on the bark at the base of diseased lateral branches or at mechanically injured areas. In the early stage of the disease, there is no obvious change on the surface of the diseased area, but peeling back the phloem reveals a yellow-brown color. After reaching the deeper phloem, large amounts of resin continuously exude from the lenticels, dripping and clinging to the bark. The diseased area expands laterally around the trunk to form ring-shaped bark rot, and develops both upward and downward and deeper into the cortical layers. Infected young trees suffer from the disease for many consecutive years, and as the disease history lengthens, the exuded resin accumulates more and more, until the surface of the diseased area is covered with a layer of resin. On severely diseased trees that have been affected for several consecutive years, the diseased area can reach 50-60 cm in length, or even over 1 m. Because the cambium in the diseased area is destroyed and loses its capacity for regeneration, the diseased part of the trunk gradually becomes sunken and narrowed, and the rotten bark shrinks, cracks, and becomes rough and brown. In the most severe cases, the trunk becomes deformed with a thick upper part and a thin lower part. When the cambium in the ring-shaped rotten bark area completely dies, the severely diseased young tree dies, showing death symptoms in April and May. By mid-June, densely packed papillate brown false stromata and pycnidia form on the dead diseased branches and trunk bark. On naturally dead diseased branches and trunk bark, the sexual fruiting bodies are mostly produced. Sexual and asexual forms grow together and are difficult to distinguish with the naked eye. On severely diseased living trees, the dry bark of the diseased area also has scattered asexual and sexual fruiting bodies, with the asexual form being more numerous, covered by resin, and visible upon careful examination after scraping off the resin layer (Color Plate 14).

[Pathogen] The sexual stage of the pathogen, Leucostomakunzei (Fr.) Munk, forms false stromata that are flat-topped and conical, initially embedded in the bark, later breaking through the epidermal ostiole to become exposed. They are composed internally of dirty-white loose tissue, with 4 to more than 30 oval perithecia with long necks arranged in a nearly circular, closely packed manner at the base. The necks gather together, and the papillate ostioles are exposed outside the bark to form a disc-shaped ectostroma. The boundary between the false stroma and the host tissue is distinct, with a black line band at the basal margin. The false stroma is 882-1311 μm wide and 694-977 μm high; the ectostroma is 240-700 μm wide. The perithecia are oval with long necks, leathery, maturing to green-brown or brown, measuring 244-330 μm × 289-366 μm, with a neck length of 599-688 μm and a thickness of 33-55 μm. The asci are club-shaped, thin-walled, colorless, slightly thicker in the middle, with a bluntly rounded apex and a gradually narrowing base, sessile, measuring 21.3-27.5 μm × 4.3-5.0 μm. Each contains 8 ascospores arranged irregularly in two or three rows. The ascospores are sausage-shaped, single-celled, colorless, measuring 7.0-7.8 μm × 1.0-1.5 μm.

The pycnidia of the asexual stage are spherical or flattened spherical, brown and carbonaceous, initially embedded in the bark, later breaking through the epidermis with only the ostiole exposed. The locule cavity is irregular with multiple interconnected chambers sharing a common ostiole. It measures 696-1035 μm wide and 614-864 μm high. The conidiophores are borne peripherally within the locule cavity, branched, with 1-3 dichotomous branchings, tapering at the apex, colorless, non-septate, measuring 19.4-32.4 μm long and 1.1-1.6 μm thick. The conidia are sausage-shaped, single-celled, colorless, measuring 3.0-5.1 μm × 0.6-0.9 μm.

This fungus germinates spores and grows colonies relatively quickly on PDA and various other culture media, and pure cultures are easily obtained by conventional tissue and spore isolation methods. The colony is initially white and felt-like, turning brownish when mature. When cultured at 23-27°C under lateral light for about 25 days, granular pycnidia form on the colony surface, mostly solitary, initially white, and after another 10-20 days they mature and turn brown, exuding milky turbid conidial tendrils from the ostioles.

The temperature range for ascospore and conidial germination is 15-30°C, with the optimum at 20-25°C. The temperature range for colony growth is 5-35°C, with the optimum at 25°C. The pH range for ascospore and conidial germination is 3.5-8.5, with the optimum at 4.5-6.0. The pH range for colony growth is 3.0-8.0, with the optimum at 3.5-4.0. Spore germination rate is closely related to nutritional conditions; ascospores and conidia do not germinate when cultured in hanging drops of plain water. When cultured at 25°C for 48 hours, on 2% agar medium the germination rate is 53%; on 2% agar plus 98% pine bark extract the germination rate is 78.6%; on 2% agar plus 78% potato extract plus 20% pine bark extract the germination rate is 91.8%. When nutrition is sufficient, conidia become round upon germination, and ascospores become gourd-shaped. When nutrition is poor, conidia and ascospores become elongated-oval or swollen and elongated upon germination, with germ tubes emerging from both ends or one end of the spore.

Using pure cultures and spore suspensions obtained from isolation and culture, inoculations were made on healthy young trees of red pine, black pine, Japanese red pine, Scots pine, Changbai larch and others by punching, needle prickling, and scorching methods. The results showed that inoculation of red pine, except for the wound-free treatment, resulted in a 100% disease incidence rate, while inoculations of other tree species did not develop the disease. The incubation period from inoculation to the appearance of bark rot and resin flow was about 100 days.

[Occurrence Pattern] The fungus overwinters as mature and immature false stromata, pycnidia, and mycelium. After late April, when the daily average temperature reaches above 10°C, on every rainy day, the mature false stromata and pycnidia release spores, which are dispersed by wind and rain, serving as the primary infection source of this disease. In early June, new false stromata and pycnidia form on the current year's dead diseased branches, trunks, and the dry bark of diseased areas on severely diseased trees, gradually maturing and releasing spores by early July, serving as the secondary infection source of this disease. The spore dispersal period lasts from late April to late September, as long as 5 months. The number of spores dispersed is closely related to rainfall, temperature, and humidity. From mid-June to late July, with high rainfall, temperature, and humidity, this is the peak period of spore dispersal for this fungus, during which several dispersal peaks occur. Based on spore trapping with glass slides in the forest and microscopic examination of sections, the production and maturation periods of the sexual and asexual fruiting bodies of this fungus are irregular, and within the same stroma, the maturation periods of individual perithecia, and within the same perithecium, the maturation periods of individual asci, are all irregular. When asci mature, their walls disintegrate and dissolve, and in mature perithecia, large numbers of individual ascospores can be seen mixed together with many asci. On dead diseased young trees, both sexual and asexual spores can be released from July of the current year to July of the third year.

The occurrence and epidemic of this disease are closely related to stand age, slope aspect, soil, stand composition, canopy density, tree vigor, and management measures. The disease can occur in stands aged 10 to 30 years, with stands aged 15 to 25 years being most severely affected. Sunny slopes and semi-sunny slopes are more severely affected than shady slopes; pure stands are more severely affected than mixed stands. Stands with heavy clay soil and low available nitrogen content are more severely affected. Stands with a canopy density of about 0.8 are lightly affected, while stands with excessive canopy density cause poor tree growth and are severely affected. Stands with relatively low canopy density, due to strong light within the stand, favor the occurrence of pests such as the red pine adelgid and the pine aphid, which create many tiny wounds on the trunk bark, facilitating infection by this disease, and therefore the disease is also relatively severe. Long-term absence of thinning and tending after afforestation results in many suppressed and dying trees in the stand, or thinning and tending carried out too late, and some stands combined with unreasonable heavy pruning, such stands are severely affected. In contrast, stands where timely thinning and tending are carried out and a canopy density of about 0.8 is maintained are lightly affected. Therefore, all factors that cause poor tree growth and produce large numbers of wounds on weakened trees are the predisposing factors for the occurrence and epidemic of this disease.

[Control Measures] This pathogen is a weak parasite. Control methods should focus primarily on silvicultural measures, supplemented by chemical control. For red pine plantations, tending and management should be strengthened, with timely thinning and tending carried out according to the growth and development patterns of young stands, maintaining appropriate density, improving the sanitary environment within the stand, and enhancing tree vigor to prevent the occurrence of this disease. According to surveys, the rough-barked type of red pine not only grows faster than the thin-barked type but also has stronger resistance to red pine bark rot and resin flow disease. Attention should be paid to selecting and breeding superior fast-growing resistant varieties of red pine for production application. Afforestation should match species to site conditions, and mixed forests should be vigorously established.

For affected stands, in conjunction with thinning and tending, dead diseased branches, trunks, and dying severely diseased trees should be removed and transported out of the forest to be burned, reducing infection sources. For retained diseased trees, a water solution of 1% NaOH plus 25% Ca(OH)2 applied in spring after scraping off the rotten bark can achieve ideal results. When scraping the bark, care should be taken to protect the cambium, scraping to the boundary between diseased and healthy tissue, and the application range should extend 5-10 cm into the healthy area. With strict operation, the damage of this disease can be controlled after the first year of treatment, and with appropriate supplementary treatment in the second year, it can be cured. This method is especially suitable for large-scale application on severely diseased young trees with a diameter at breast height under 10 cm, and the trees are safe with no phytotoxicity. Pine tar, pine tar plus diesel oil at 1:1, and 10% chlorothalonil oil formulation can also be applied for treatment, all achieving relatively good results. However, it should be noted that applying oil-based chemical treatments to severely diseased young trees with a treatment length exceeding 50 cm can easily cause phytotoxicity, or even death, so treatment can be applied in stages, section by section.