by Carl Cantaluppi
Blossom end rot is a serious nonparasitic, noninfectious disorder of greenhouse and field tomatoes, caused by low levels of calcium. It is not associated with soil contact or with damage to other plant parts. This disorder is usually most severe following extremes in soil moisture (either too dry or too wet). These conditions result in a deficiency of calcium available to the maturing fruit.
This first visible symptom of the disorder is a small darkened or water-soaked area around the blossom end of the fruit, appearing about the time the fruit begins to ripen. The spot darkens, enlarges and becomes sunken as the fruits mature.
Large lesions may show concentric rings. The affected tissue is leathery and firm unless invaded by secondary decay organisms. Blossom end rot usually causes the fruit to ripen prematurely and to be inedible. The affected fruit areas tend to become infected with secondary pathogens, which appear as black, felt-like growth on the fruit. The affected area may be a speck to more than half of the fruit.
The calcium deficiency producing blossom end rot is most often a result of climatic or cultural problems. It is related to several factors, including calcium, nitrogen and soil moisture levels. The severity of this condition can be compounded when two or more of these factors interact with each other. It can occur even when there is abundant calcium in the soil and tissue tests show high levels of calcium in the plant.
The physiology of the plant may contribute to the disorder. Dissolved in water, calcium is taken up and moves through the vascular system (xylem) from the roots to the leaves. Since calcium is transported only in the water-conducting tissues, when water uptake is reduced, calcium uptake is reduced. Under high moisture stress, the water containing calcium and other minerals moves rapidly to the leaves. Most water is lost (transpired) through the leaves and most of the calcium is found in the leaves after transpiration has occurred. Fruit does not transpire as much as leaves; thus, less calcium is deposited there, resulting in a localized calcium deficiency in the fruit.
Because calcium has to be taken up from the soil by the roots, calcium sprays on the leaves and fruit are ineffective in preventing blossom end rot.
Ninety percent of the calcium that the mature fruit will contain is in the fruit by the time the waxy suberin layer has formed, when the fruit is about thumbnail size. When this calcium deficiency occurs in the end of the fruit, it causes cells to collapse producing the sunken lesion symptom of blossom end rot.
Blossom end rot usually appears on the first fruit cluster of a plant due to the combination of rapid plant growth with a large leaf area for water transpiration, water stress and fruit enlargement. It often occurs when plants have grown rapidly during the early part of the season and then are subjected to long periods of dry weather when fruits are at an early stage of development.
Also, water stress during early fruit enlargement can cause blossom end rot because the fruits are the last to receive adequate calcium. An alternation of excessively dry and excessively wet soil conditions generally increases the problem. The tomato fruit requires more calcium for development than the leaves and stem of the plant.
In field tomatoes, the disorder can be more serious on the windward side of a field rather than the leeward side and can be more serious on staked plants rather than non-pruned prostrate or caged plants. In addition, plants set out too early in cold soil causes slow water uptake, allowing blossom end rot to show up early. Plants cultivated closely are more susceptible to blossom end rot due to having a reduced root system available for water transport.
Another cause of blossom end rot is over-fertilization, especially with nitrogen, which stimulates vegetative growth. Excessive vegetative growth increases the rate of transpiration.
Tomato varieties differ in their resistance to blossom end rot. In general, pear or plum tomatoes used for processing and canning are most prone to this disorder.
Factors affecting blossom end rot
Although blossom end rot is the result of a calcium deficiency in fruit, environmental conditions that interfere with uptake and availability of water and nutrients can contribute greatly to symptom expression. Such conditions include water stress, excessive salinity and root damage from infectious diseases. Salinity decreases total calcium uptake and fruit calcium content by restricting water uptake. Xylem development inside the fruit is also restricted by salinity, decreasing the fruit’s ability to transport calcium to the distal end.
Excessive nitrogen fertilizer also can contribute to blossom end rot by promoting vigorous vine growth and depleting available calcium in the soil. It has been reported that calcium uptake is reduced where nitrogen is applied in the ammonium form (urea or anhydrous ammonia). The ammonium ion competes with the calcium ion for uptake.
Applying lime several months prior to planting in low-calcium fields can help prevent blossom end rot. For greenhouse tomatoes, make sure that adequate calcium is present by injecting calcium chloride through the irrigation system. Do not use calcium nitrate if tissue analysis shows adequate nitrogen present.
Cultivars that grow quickly and produce large amounts of foliage tend to be more susceptible to blossom end rot. Therefore, reducing nitrogen levels in the field will help reduce blossom end rot. Avoid ammoniacal forms of nitrogen that compete with calcium. Incidence of blossom end rot may increase where there is a low ratio of calcium to certain other nutrients such as potassium and nitrogen. The use of 5-10-10 fertilizer in place of 10-10-10 or 13-13-13 on tomatoes will help reduce the nitrogen problems associated with blossom end rot.
The field transplants should not be subjected to severe “hardening-off” before transplanting. Seedlings grown in the field at a steady rate are less susceptible to blossom end rot. But windy conditions in the spring coupled with low relative humidity can cause the high transpiration rates that can induce blossom end rot. Fluctuations in soil moisture during periods of rapid plant growth create moisture stress and limit calcium distribution to the fruit.
Removing affected fruits when symptoms are first observed may promote subsequent sound development of other fruit on the plant. By the time a second set of fruits begins developing, the plant has an expanded and developed a root system capable of gathering and delivering calcium to the fruiting structures.
In the field, select sites that have deep, well-drained soils. A large well-formed root system is better able to take up calcium and other minerals.
Tomatoes grown on land that has not been limed for two years or more are prime candidates for blossom end rot. Soil test to determine soil pH and soil nutrient levels annually and adjust the pH to 6.5 as needed.
Mulch plants to conserve moisture in the field and to provide a more uniform water supply. Straw, pine straw, ground leaves or newspapers are all good mulches. Mulches conserve and maintain a uniform moisture supply, thereby helping to reduce blossom end rot. Under drought conditions, plastic mulch may overheat the soil and increase blossom end rot if plants are not watered properly. Adequate soil moisture throughout the season through mulching and water management is essential for avoiding the disorder. Avoid cultivation and hoeing. If cultivation is necessary, it should be shallow to avoid root pruning.
Avoid severe pruning of plants. Severely pruned tomato plants are more prone to develop blossom end rot than unpruned plants.
Keep water supply uniform and regular. Irrigate plants thoroughly and often enough to maintain a constant water supply without water logging the plants. Tomato plants require 1.0-1.5 inches of water per week during growth and fruiting depending on soil type and weather conditions. Extreme fluctuations in soil moisture can cause an increase of blossom end rot. Preventing moisture stress is important to control blossom end rot, especially during fruit set and fruit enlargement.