Agriculture Reference
In-Depth Information
characteristic fan-shaped lesions. Stem lesions may develop to the extent that they
cause shoot death and this can delay and reduce seed production, so causing yield
loss.
The disease progresses during wet weather and bacteria oozing from disease
lesions are readily spread to healthy tissues or to neighbouring plants in wind-driven
rain. Bacteria enter tissues through stomata and damaged cells, so infection is
readily spread by machinery moving within and between crops and by animals
(including birds) feeding in diseased crops.
Seeds usually become infected directly from pod lesions during wet weather but
they may also become contaminated by bacteria-laden dust during harvesting, or
from cleaning and grading equipment. Dry conditions and high temperatures during
crop growth lead to a reduction in disease development and seed infection.
Seedborne bacteria may remain viable for several seasons but populations decline
during storage. Seed infection may occur in the apparent absence of field symptoms.
The pathogen has a well defined race structure and races can be determined by stem
inoculation of the pathogen into a defined set of differential pea varieties (Taylor
et al.,
1989) or using DNA sequence analysis (Cournoyer
et al.,
1996).
Pea blight was not known in the UK until 1985, when it was found in a seed crop
of Belinda combining peas during a routine inspection (Stead and Pemberton, 1987).
Prior to 1985 the disease had been subject to import (quarantine) regulations and had
been detected only occasionally in imported seed lots of combining and vining peas.
Following the 1985 outbreak, an action plan was drawn up to obtain general
control of the disease and, specifically, to exclude it from certified seed (Stead and
Pemberton, 1987). Samples of all breeders' seed, pre-basic and basic seed lots (i.e.
seed intended for further multiplication) had to be laboratory tested for
P. syringae
pv.
pisi
. In addition, all seed crops were inspected for symptoms of pea blight during
growing crop inspections. Where there was evidence that a particular seed line was
infected, steps were taken to eliminate that line from further seed multiplication.
In the period 1986-1990, over 5500 seed samples were tested in four UK seed
testing stations (Roberts
et al.,
1991). The results showed that
P. syringae
pv.
pisi
was relatively widely distributed in UK pea seed, with around 10% or more of
samples giving positive results in each of the five years. Infection fluctuated from
year to year and seed that was not subject to statutory testing (the final year of
certified seed and all farm-saved seed) showed a general increase in infection to
reach relatively high levels (more than 40% of samples infected) by 1988.
There was a sharp increase in the frequency of infected stocks between 1987 and
1989 and this suggested that some seed stocks were contaminated from sources
other than the parent seed (for example, by harvesting, cleaning or grading
equipment) or that the testing programme failed to detect some infected stocks. The
testing programme may have failed to identify infection in early generation seed for
two reasons. First, only a single sample was required from each crop and this may
not have been sufficiently representative when some crops consisted of several
hundred tonnes of seed. Second, tests on the required sample size of 1 kg
(approximately 3000 seeds) would not have detected infection in some stocks where
fewer than 0.1% of seeds were infected.
