Search

Rapid evolution of pest, pathogen, and wildlife populations can have undesirable effects, for example, when insects evolve resistance to pesticides or fishes evolve smaller body size in response to harvest. A destructive invasive species in the Laurentian Great Lakes, the sea lamprey ( Petromyzon marinus) has been controlled with the pesticide 3-trifluoromethyl-4-nitrophenol (TFM) since the 1950s. We evaluated the likelihood of sea lamprey evolving resistance to TFM by ( i) reviewing sea lamprey life history and control; ( ii) identifying physiological and behavioural resistance strategies; ( iii) estimating the strength of selection from TFM; ( iv) assessing the timeline for evolution; and ( v) analyzing historical toxicity data for evidence of resistance. The number of sea lamprey generations exposed to TFM was within the range observed for fish populations where rapid evolution has occurred. Mortality from TFM was estimated as 82%-90%, suggesting significant selective pressure. However, 57 years of toxicity data revealed no increase in lethal concentrations of TFM. Vigilance and the development of alternative controls are required to prevent this aquatic invasive species from evolving strategies to evade control. [ABSTRACT FROM AUTHOR]

For over 50 years, invasive sea lampreyPetromyzon marinuspopulations have been controlled in the Great Lakes using the pesticide 3-trifluoromethyl-4-nitrophenol (TFM), which is applied to streams containing larval sea lampreys. The specificity of TFM is due to the sea lamprey's relative inability to detoxify it using glucuronidation; this inability causes death by interfering with the production of ATP, the main energy currency of cells. TFM treatments typically last 12 h, but given the sea lamprey's relative inability to detoxify TFM we predicted that TFM-induced homeostatic disturbances and toxicity would occur following shorter periods of exposure. Accordingly, we exposed larval sea lampreys to the 12-h LC99.9 (i.e., the concentration lethal to 99.9% of the test subjects over 12 h) of TFM for 4 or 6 h and monitored the survival and replenishment of energy stores and metabolite concentrations in surviving sea lampreys over a 24-h depuration period. Minimal mortality (∼20%) was observed during the post-TFM recovery, despite respective 50% and 70% reductions in brain and liver ATP, 70–90% decreases in brain phosphocreatine (PCr), and 30–50% reductions in brain and liver glycogen with corresponding increases in lactate. While relatively resistant to TFM, muscle still underwent a 55% decline in PCr. However, energy stores and metabolites returned to preexposure levels 4–12 h after TFM exposure. We conclude that sea lampreys can rapidly restore homeostasis following shorter-term TFM exposure. The resilience of sea lampreys to shorter-term TFM exposure suggests that there is no merit in reducing TFM treatment times from 12 h, which could lead to “treatment residuals” that survive lampricide treatments. This capacity to reverse TFM-induced perturbations also suggests that larvae seen emerging from the stream substrate late in a treatment, or that find refuge near streambanks or in isolated pools, could be another source of treatment residuals, leading to increased sea lamprey parasitism of sport and commercial fisheries in the Great Lakes. Received November 7, 2011; accepted July 10, 2012 [ABSTRACT FROM PUBLISHER]

Although treatment of streams with the lampricide 3-trifluoromethyl-4-nitrophenol (TFM) has been highly effective for sea lamprey (Petromyzon marinus) population control in the Great Lakes, little is known about its mechanism(s) of toxicity. We investigated two hypotheses of TFM toxicity in larval sea lamprey exposed to TFM for 12 h. The first was that TFM interferes with oxidative ATP production by mitochondria, causing depletion of fuel stores in the body. The second was that TFM interferes with gill-mediated ion exchange, which eventually causes circulatory collapse. While exposure of larvae to TFM (2 mg·L–1) did not disturb tissue ATP stores, it led to a sustained 60% reduction in phosphocreatine (PCr) after 6 h. This was accompanied by 6- to 10-fold increases in plasma and tissue lactate, which persisted through 12 h. By 12 h, plasma glucose was nearly depleted in the five surviving lamprey, but TFM caused no appreciable changes in plasma Cl–, haematocrit, haemoglobin, or ammonia concentration. We conclude that TFM-mediated gill damage and ionic failure are not underlying mechanisms of TFM toxicity. Rather, TFM likely interferes with oxidative ATP production, leading to reduced tissue PCr stores and eventually profound hypoglycaemia that starves the nervous system of glucose, causing death. [ABSTRACT FROM AUTHOR]