Measuring and scoring vitality impairment

Associations between vitality impairment and mortality in Tanner and snow crab; Stoner et al. 2008.

At the risk of repetition and irrelevance, I will repeat my short history with vitality impairment and mortality.  I began by trying to find out what kills fish. The word fish applies to all animal types in a fishery. We chose to do this in the lab for control reasons, given the common confounding of stressors in fisheries (Davis 2002). All sorts of objections were made by field people that the work was irrelevant because it did not include field conditions. Well we focused on the fish and their capabilities, in an effort to formulate hypotheses that could be tested in the field. We found that each species and size of fish has different sensitivities to stressors and that stressors of importance were different for species.  We also found that some stressors (temperature and hypoxia) could kill fish without apparent macro-injury. After killing many fish, we endeavored to identify characteristics (traits) of fish and fisheries that could be correlated with mortality as predictors, given the difficulty of holding fish and measuring delayed mortality in the field. We tried many traits; muscle and plasma physiology, stressors, volitional behavior, injury, and reflex actions.

Effects of fishing gear, temperature, and fish size on sablefish mortality, NOAA.

Muscle and plasma physiology were not correlated with mortality because these are alarm responses that can be adaptive or maladaptive responses to stressors. In specific contexts, lactate and CO2 may be useful where hypoxia or fatigue are a concern.  

Stressors are an approach that has garnered enthusiasm. However their effects can be confounded and difficult to model given the relatively unlimited combinations of factors that are possible in a fishery; seasonal effects, gear type and deployment times, catch type and amount, sorting and discarding.  

Volitional behavior is not correlated with mortality because it is subject to variation that is not directly linked to mortality, such as changes in perception, motivation, fear, and attraction; all which confound the relationship of behavior and mortality.  

Injury is often correlated with mortality, especially in accidental death.  However not all mortality is correlated with injury, as in the effects of temperature and hypoxia, for which micro-injury may be evident (apoptosis) but difficult to measure in the field. Often the effects of injury, temperature, and hypoxia are confounded making interpretations of their effects on mortality difficult.

Single reflex actions are often not correlated with mortality when they are part of systems not central to body function and regulation directly related to mortality. They may be important for complex behaviors; predator avoidance, feeding, habitat choice, migration and these can have indirect effects on mortality. 

We reasoned that fish had a quality called vitality and that vitality was correlated with mortality. However, for an individual fish this relationship is binomial. The fish is alive or dead. So decreasing vitality results in sublethal effects on behavior until a threshold is reached and the probability for death increases rapidly. In statistical groups of fish, decreasing vitality is log-linearly related to mortality.

At this point we chose to not measure the strength of reflex actions (because of confounded size effects); instead to score the presence or absence of several reflex actions as an expression of reflex action impairment and loss of vitality. Reflex actions are fixed behavior patterns based on neural, muscle, and organ functions which do not vary with changes in perception, motivation, fear, and attraction.  We chose to focus on several types of reflex actions to increase the probability that reflex actions key to body regulation were included. Later work has shown that the orientation reflex is such a key reflex, often correlated with morbidity and mortality associated with hypoxia and fatigue. 

Previous work with vitality scoring in fisheries had developed the semi-quantitative analysis method (SQA) of scoring fish activity and injury, which was used in tagging studies and in Pacific halibut discard mortality estimation (ICES 2014). The method observes the sequential loss of operculum clamping and startle to touch and increased injuries from minor to major and bleeding; with ordinal scoring (1-4) for severity of impairment. The vitality score is readily incorporated in multivariate models that may identify stressors of importance to mortality and model mortality based on those stressors. RAMP can be scored in a similar manner as SQA and included in multivariate models. RAMP scores severity of impairment by noting the sequential loss of several types of reflex action and inclusion of injury types. Scores range from 0 to a maximum which is the number of trait types observed for presence/absence. Strength of action and extent of injury are not included because of the confounding effects of size. The effect of size is included in the model explicitly as fish length or weight. Smaller fish will have more vitality impairment than larger fish, when exposed to equivalent stressors.

RAMP is a simple extension of the SQA concept that includes more testing for reflex actions. SQA and RAMP are similar scoring systems that differ by emphasis. SQA and RAMP score activity, responsiveness, and injury to quantify levels of vitality impairment. RAMP simply includes more information about types of reflex actions in an effort to include reflex actions that are central to body regulation over a range of stressor conditions.

The primary reason for inclusion of more reflex action information in RAMP is the observation that some reflex actions are central expressions for status of body regulation. Given the binomial nature of mortality observations, we need to know why fish die. They die for many reasons which all seem to point to the loss of physiological regulation; either homeostatic or allostatic regulation. How do we measure regulation?  Allostasis shows us that consideration of homeostatic set points is not sufficient to predict mortality. My view is that vitality is correlated with physiological regulation and that impairment of vitality and regulation leads to mortality when physiological bounds of the species are exceeded. Until we can directly measure the causes for mortality, we rely on measures for vitality based on activity, responsiveness, and injury.

For predicting mortality, I chose to measure vitality over modeling stressors because of the direct relationship between vitality impairment and mortality. Stressor interactions in fisheries can make interpretation of stressor effects on mortality difficult to interpret. Information about stressors in multivariate models for mortality can be used to identify changes in the design of fishing gears that reduce bycatch mortality. Then vitality impairment can be used to evaluate reduction in discard mortality associated with new gears.