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Effects
of Stressors on Mortality Rates in Lobsters (Homarus americanus) Infected With a Bacterial PathogenRichard A. Robohm1 and Andrew F. J. Draxler2 1NOAA, NMFS, Northeast
Fisheries Science Center, Milford Laboratory, 212 Rogers Ave., Milford CT
06460; 2James J. Howard Laboratory, Magruder Road, Highlands NJ
07732 The cause of
unprecedented lobster mortalities in western Long Island Sound (LIS) in 1998 and
1999 was not established. A parasitic
amoeba found in both moribund and non-moribund lobsters may, in association
with environmental conditions, contribute to deaths; however, controlled
laboratory studies with this organism cannot be done because the amoeba could
not be cultured in vitro. We report here the use of a surrogate, Aerococcus viridans (a bacterial
pathogen of lobsters), to help reveal whether increased, but environmentally
realistic, levels of temperature, hypoxia, sulfide, and ammonia can heighten
susceptibility to microbial infection.
Lobsters from commercial harvesters were acclimated for seven days to
conditions of temperature and bottom light that exist in western LIS in
September and to the salinity at the Howard Laboratory. Each lobster was injected in the ventral
sinus with 1x103 or 1x106 A. viridans or
saline. Experimental conditions for
temperature and concentrations of oxygen, sulfide, and ammonia were generated
in a flow-through system of sealed tanks.
Lobsters were monitored twice daily for behavioral response and
viability. At appropriate intervals,
lobsters were transported to the Milford Laboratory to enumerate bacteria in
the hepatopancreas and hemolymph. At adequate oxygen levels (200 mM), exposure to 6 mM sulfide and 24
mM ammonia accelerated the 50% mortality rate in
lobsters from 12 days to 6.6 days; at lower oxygen levels (80>mM) mortalities were further accelerated to about
3 days. The lower oxygen levels alone
were sufficient to accelerate lobster deaths regardless of the presence of
sulfide and ammonia. Temperature (14.5°C vs. 19.5
°C) and bacterial doses had moderate effects on
mortality. Bacteria in the hemolymph
and hepatopancreas of non-stressed lobsters reached 1x109 g-1
within 10 days; whereas counts in dying, stressed lobsters were 1x103
to 1x106 g-1 (lower than counts in non-stressed, infected-but-living animals at
the same time interval). Additional
experiments are in progress to separate the effects of sulfide and ammonia and
to examine whether the same effects are seen in lobsters infected with Vibrio fluvialis.
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