A plankton bloom had nearly wiped out a companies’ Chinook brood on the
West Coast with only a few weeks to go until stripping. Luckily, there
were fish on Campbell River sites that could be used at the West Coast
hatchery. So, the broodstock manager oversaw the loading of the females
into tanks on a Beaver (single engine bush plane). One-third SW was
used, a little TMS for good measure and an oxygen bottle on a Point-Four
micro bubble bar. All was fine.
While passing over Courtenay en route to the Alberni canal the weather
started getting rough, the tiny plane was tossed, if not for the courage
of the fearless crew, the broodstock would be lost. Over a large
airpocket, the fish, water, tanks, O2 bottle and broodstock manager
experienced zero gravity. While this is normal for astronauts and fish,
all here were subject to the regaining of gravity in a profound way. The
rest of the transport was equally ugly because the canal was fogged in
and it was a 30 min wave-topper to get to the hatchery.
On arrival, the fish were unceremoniously dumped into freshwater that
was colder than the transport water. Needless to say, egg quality was
not great for the survivors of the plankton bloom or the transport. To
boot, the plankton survivors were mercilessly and repeatedly attacked by
sea lions.
Physical trauma of these actions aside, it is no great stretch of the
imagination to suggest that the stress of events impacted egg quality.
At issue is the nature of the stress response and how it affects fish
health. The stress response is a behavioural and physiological reaction
of the fish to a perceived threat or insult.
There are two parts to the stress response: 1) the catecholamine
release (adrenaline rush) and 2) the cortisol response. The former
results in a heightened state of activity coupled with an escape
response, while the latter has a slower response time. This slower
response is similar to the maturation process in that it is mediated by
the lower brain (hypothalamus), acts on the pituitary and involves the
release of chemical messengers that affect the interrenal cells of the
kidney (Figure 1).
This endocrine cascade from hypothalamus to pituitary to interrenal
gland is the HPI axis. The hypothalamus releases corticotropin-releasing
factor (CRF) along nerves that trigger the liberation of corticotropic
hormone (CTH) from the pituitary into the blood. The CTH binds to cells
in the kidney called interrenal cells. These cell, akin to the adrenal
cortex in mammals, release glucocotricoids. In fish, this is cortisol.
Cortisol is a nasty brute, or a vital hormone, depending on the view.
The
normal mechanism of action for cortisol is similar to the BC Liberal
budget: it stems non-essential metabolic services to combat the current
crisis for a long-term goal. Instead of a Finance Minister, cortisol is
the hit man. Cortisol depletes liver glycogen (stored sugars); changes
free fatty acid levels in the blood, increases plasma glucose, inhibits
protein synthesis and suppresses the immune response mechanisms. In
essence, the cortisol response is aimed at providing energy to escape
further insult; everything non-essential to keeping the fish immediately
out of danger is put on hold.
The metabolic effects aside, there are two key health impacts of the
cortisol response as it pertains to broodstock: immunity and
reproduction.
Spawners are full of steroids; that’s what makes them spawners. Besides
making gametes, androgens (estrogens and testosterone) are known to
repress immune function. If one has ever had the pleasure of witnessing
a chum salmon spawning run, they are aware of the state of decay in
senescent (aged) fish.
Androgens, like cortisol, are steroids and they both have the effect of
decreasing the ability of white blood cells to produce antibodies.
Cortisol also affects the total number of white blood cells and the
immune organs (Maule, et al., 1989). Dr. Carl Schreck, a guru of stress
and cortisol effects postulates that broodstock in the later stages of
maturation may be vulnerable to stress-induced diseases because of
elevated androgens and cortisol (Schreck et al., 2001).
The message here is that broodstock are at an immunological
disadvantage because of the maturation process. Any additional immune
suppression as a result of stressors is double indemnity.
The second point is of stress effects during maturation. For
consideration here, assume that stressors are predation, handling,
transport or environmental issues and the like. Rolf (1982) points out
that there are two responses to stressors: 1) sacrifice egg number and
keep the body healthy (growing and fully functional) and 2) sacrifice
the body and maximize gamete production. Typically, the response to
stress early in vitellogenesis (egg building) is the first example, and
the response to stress late in the spawning season is the second.
Stressors, whether mechanical (handling) or environmental (water
quality) will effect gamete quality. Sometimes the effect is an earlier
or later spawning time, but it is always associated with reduced egg
performance (see Schreck et al. 2001). Stress, no matter when it occurs,
negatively affects reproductive performance. The issue is managing fish
health and husbandry to maximize animal care and productivity.