In the beginning of the nineteen fifties bacterial blight caused much damage to pea crops in South Africa, particularly to those grown for seed production. A study has been made of the causal organism and the conditioning factors of the disease, special attention being paid to frost as a predisposing factor.
The symptoms of the disease vary according to weather conditions during and after infection. In dry weather with occasional frost they usually start on the stem near the soil and extend upwards to stipules and leaflets, where a characteristic fan- like pattern develops. In rainy weather they appear as scattered spots on the stems and leaves. The bacterium that causes the disease was identified as Pseudomonas pisi
Although frost is not essential to infection, the susceptibility of pea plants increased considerably when they were frosted before inoculation. There was no correlation between the increase in susceptibility and the amount of permanent frost injury. In freezing experiments with pods alone, it was confirmed that frost is a predisposing factor for infection, but frost cracks in the tissue were not a prerequisite. A second effect of frost is that the disease spreads more rapidly in tissue that has been frosted. Stem lesions did not spread far on the stems of plants in experimental fields as long as the temperature remained above freezing point. After a frost, however, the disease spread for a considerable distance on the stems and to the stipules, on which the typical fan-like symptoms developed. These results were confirmed in experiments with artificially frosted plants. A possible explanation is that the pathogen spreads in the temporarily enlarged, water-filled intercellular spaces of the stems and leaves that have been exposed to frost.
Because frost is a predisposing factor and because the optimum temperature for the development of symptoms is relatively high (about 25°-30°C), the winter climate in the seed producing areas of South Africa where frost in the early winter morning is followed by high day temperatures, is very conducive to the disease.
The time of planting had a considerable effect on the occurrence of the disease; it was much more severe in crops planted in April than in those planted in the second half of May or later. The difference in susceptibility between crops planted at different times is probably caused by the fact that early planted peas are more sensitive to frost than those that are planted later. Furthermore it was found in glasshouse experiments that pea plants that were grown at high temperatures were more susceptible to blight than those grown at low temperatures. The differences in susceptibility were correlated with the stomatal frequency. These results may also partially explain the differences in susceptibility between early and late plantings. Varietal resistance investigated in cultivar trials was not consistent over the years. Pea plants suffering from lack of water were more sensitive to frost than plants that were regularly irrigated, but not much difference in the occurrence of blight was found between peas grown at different irrigation levels.
Bacterial blight is a seed-borne disease and the pathogen remains viable in infected seed from one season to the next. Only if moderate frost occurs when the seeds are swelling in the pods and if there is a source of inoculum nearby, the pods and seeds may become infected in normal dry winters. Because the South African isolates of the pathogen do not easily move in the wood vessels, it is unlikely that seeds from apparently healthy pods will be infected, even if they are borne on diseased plants.
In South Africa no other natural host plant for Ps. pisi was found. In a pea field the spread of the disease was erratic, no obvious connection was found between new and already existing infections.
The following preventive measures are recommended: (a) plant at the right time of the year, (b) avoid frost pockets and (c) plant government certified seed.
Experiments were done to investigate how frost renders the plants more susceptible to infection. One of the effects of frost is that the plant tissue becomes water-soaked on thawing. Water-soaking, induced either by injecting the stems with sterile water or by bruising the leaflets, rendered pea plants considerably more susceptible to infection, probably because the pathogen penetrated the water- soaked tissue more easily. In experiments to study the effect of frost on the establishment of the pathogen it was found that the growth rate of Ps. pisi
in pea plants, that had been exposed to frost, did not differ much from the growth rate in non-frosted plants. Neither did prolonged watersoaking of plant tissue have a favourable effect on the multiplication of Ps. pisi
. Saprophytes did, however, multiply rapidly in water-soaked leaves while they remained stationary in normal plant tissue. During the first day of incubation the growth of Ps. pisi
in intercellular fluid from non-frosted pea plants, which had been infiltrated with distilled water, showed a lag phase, even though the fluid was inoculated with actively dividing bacteria. In one case a decrease in the concentration of Ps. pisi
was observed. In intercellular fluid from plants which had been frosted, the lag was less distinct than in fluid from infiltrated plants of the same planting, or it was entirely absent. After the lag phase little difference was observed between the growth rate of Ps. pisi
in intercellular fluid from plants that had been frosted and that in intercellular fluid from infiltrated, non-frosted plants.
The results described above show that the effect of frost on infection is primarily, that by inducing water congestion of the tissue it facilitates the invasion of the plants by the pathogen; and in the second place compounds, exuding into the intercellular spaces from cells which have been exposed to frost, favour the establishment of the bacteria.
The Ps. pisi
strain tested did not produce polygalacturonase, pectinlyase or the cellulolytic Cx enzyme in artificial media or in intercellular fluid. Ps. pisi
did, however, produce caseinolytic enzymes, but it is doubtful whether they are important as a virulence factor, because they were also found in sterile intercellular fluid.