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Cool, wet weather has prevailed across much of Kentucky over the past week or so, increasing the risk of diseases on tobacco transplants.
The current conditions are particularly favorable for collar rot and target spot. We have confirmed a case of collar rot from a greenhouse in central Kentucky within the past few days, so the focus of this week’s article will be on recognition and management of this disease.
Collar rot shows up in float beds in the spring, when sclerotialocated outside the float system germinate produce cup-shaped fruiting bodies called apothecia. Apothecia then produce spores (ascopores) that are dispersed on wind currents. When ascosporesland on susceptible tissue, they germinate if sufficient moisture is present. Germinated ascospores produce hyphae (fungal “threads”) that penetrate tissue and begin the infection process.
The first symptoms of collar rot are small, dark green, water-soaked lesions that appear at the bases of stems. In most cases, this disease becomes apparent when clusters of infected transplants collapse, leaving open holes in the plant canopy. These clusters or “foci” are usually grapefruit sized (4-6” in diameter). Stems of affected seedlings generally show a wet necrosis that is amber-to-brown in color, beginning at the base of the plant and extending upward. Signs of the causal agent Sclerotinia may be present on symptomatic plants or on debris in float trays. These signs include a white, cottony mycelium (fungal mass), present if humidity is high, and irregulary shaped, black sclerotia. Sclerotia resemble droppings and are the primary survival structure of S. sclerotiorum and are the primary source of inoculums for outbreaks in subsequent years.
Plants that are 5-7 weeks old are most susceptible to collar rot. We often see the first cases shortly after plants are first clipped following a period of disease –favorableweather. Cool temperatures ( 60 to 75 degrees F), high humidity, and overcast conditions, like those that have been common in Kentucky for the past week, are ideal for development of this disease. It’s also important to note that S. sclerotiorumis an efficient colonizer of dead plant matter and weakened or injured tissue, and these are usually the first to be attacked. The fungus will then move from these areas to nearby healthy plants as long as cool temperatures and high humidity prevail. This is one of the ways that secondary spread of the collar rot pathogen takes place, since S. sclerotiorumdoes not produce airborne spores on infected tissue. The other way in which secondary spread can occur is through dispersal of infected tissue- a possible event when infected plants are clipped.
There are no fungicides labeled for control of Sclerontiniacollar rot on tobacco transplants, making this a difficult disease to manage. Sound management practices are the only options that a grower can use to fight collar rot. Adequate ventilation and air circulation are a primary concern, since these limit the duration of leaf and stem wetness. Growers should manage stem wetness. Growers should manage temperatures to promote healthy plants and minimize injury. The latter is important because injured tissues are more susceptible to S. sclerotiorum. Fertility should be kept at around 100 ppm (N); excessive levels of N can lead to a lush, dense canopy that will take longer to dry and will be more susceptible to attach by the collar rot pathogen.
Plant debris should not be allowed to build up in transplant trays or remain in contact with seedlings. Clip seedlings at a low blade speed with a well-sharpened, high-vacuum mower to ensure complete removal of leaf pieces in the least injurious way possible.
Frequent clippings will reduce the amount of tissue that must be removed by the mower and will cause less plant injury and lead to less leaf material left on the transplants. Clippings and diseased plants should be discarded a minimum of 100 yards from the transplant facility, or buried.
Home gardens should not be planted near transplant facilities, and keep a wee-free zone around float beds. Over 300 species of plants, including many weeds, are hosts to S. sclerotiorum, making many weeds potential hosts for this pathogen.