An epidemic of the ergot fungus (Claviceps purpurea (Fr.)
Tul),
a non-systemic floral pathogen, appeared in
populations of Spartina anglica C. E. Hubb in Poole Harbour in
the 1980s.
Over 70% of inflorescences were
infected between 1985 and 1995. Between 1983 and 1995, there was no
consistent pattern in the rank order of sites
with respect to the proportion of inflorescences infected, and variation
in the amount of infection was not related
to inflorescence density. Among years, there was significant variation
in the total biomass of ergot per
inflorescence, but no significant difference in the number of ergots
per inflorescence. Log–log regressions of total
weight of ergot per inflorescence against the number of ergots per
inflorescence showed that in all years resources
for each additional ergot were limited.
There was no statistically significant difference between the number
of
seed set on infected and uninfected
inflorescences in 1985 or 1995. Further analysis showed that, compared
with uninfected inflorescences, there was
higher seed output from inflorescences with fewer than 10% of spikelets
infected, which balanced reduced seed
output from heavily infected inflorescences. At high levels of ergot
infection, a lower proportion of uninfected
spikelets set seed, compared with spikelets on uninfected inflorescences.
This suggests that conditions which
favour ergot growth are detrimental to seed production. Compared with
uninfected inflorescences, mean and total
seed weights were significantly lower in inflorescences with >10% of
spikelets infected.
The fungus Fusarium heterosporum Nees ex Fr. was found in
association with the ergots on Spartina. There was
a significant positive correlation between the average severity of
Fusarium infection and the number of ergots on
an inflorescence. There was a non-significant negative correlation between
severity of Fusarium and mean ergot
weight, when ergot number per inflorescence was held constant. These data
suggest that any negative effect of Fusarium on Claviceps
is small.
The high, and temporally and spatially uniform levels of ergot
infection probably result from genetic uniformity
of Spartina and the lack of zonation in the salt marshes of Poole
Harbour.
This situation is likely to persist for the foreseeable future.