37 7th Veterinary Report - Department of Primary Industries ...

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Silver Perch Kill, Bass Deformity and Neurologic Syndromes The veterinary investigation commissioned by the Noosa Fish Health Investigation Task Force (NFHITF) into the Sunland Fish Hatchery silver perch fish kill, golden perch neurological abnormalities and Australian bass deformities has examined the available sources of information and has come to validated conclusions which specifically address the fish health problems. Silver Perch Fish Kill The field and laboratory evidence are consistent with the silver perch at high risk of being exposed to very low sublethal but toxic doses of beta‐cyfluthrin pesticide. The pesticide, in combination with gill hyperplasia pathology caused by gill flukes and heavy metals was a significant stress to the fish. When high environmental temperatures occurred concurrent with pesticide spray drift, the chain of events produced a major fish kill at the hatchery pond of silver perch. The current laboratory and veterinary epidemiological data is supported through spray drift modeling conducted by the Australian Pesticides and Veterinary Medicines Authority (APVMA) AgDRIFT model. AgDRIFT demonstrated that all fish ponds on the hatchery would receive pesticides including beta‐cyfluthrin even when applied under current pesticide label conditions. The potential averaged initial concentrations of pesticides achieved in the fish hatchery water storages by spray drift were : o Without buffer o With buffer Cardendazim 0.013 – 0.162 µg/L Methidathion 0.027 – 0.323 µg/L beta‐cyfluthrin 0.00068 – 0.0082 µg/L Cardendazim 0.007 – 0.079 µg/L Methidathion 0.013 – 0.158 µg/L beta‐cyfluthrin 0.0006 – 0.004 µg/L By extrapolating from literature sources, the toxicity end points for silver perch when based on the Bluegill sunfish demonstrate a number of toxic exposure scenarios : 1. The 10% lethal concentration of beta‐cyfluthrin has the potential to cause temperature stress effects at an exposure of 0.087 – 0.15 µg/L. 2. Swimming abnormality in fish can be due to toxic effects at 0.7 – 5% of the lethal concentration at an exposure of 0.0006 – 0.0075 µg/L beta‐cyfluthrin. 3. An estimated safe level for exposure to beta‐cyfluthrin for silver perch is up to 0.00087 µg/L. From these, an estimated cyfluthrin exposure level of the order of 0.00087 – 0.15 µg/L (ppb) cyfluthrin could contaminate the pond sufficient to result in a sublethal toxic effect on silver perch resulting in fish temperature tolerance and swimming behaviour changes. Given that the AgDRIFT model exposure level is estimated to be 0.0006 ‐ 0.0082 µg/L (ppb), this fitted within the range for sublethal toxicity. On its own this range of beta‐cyfluthrin exposure would not be expected to result in temperature stress effects or mortalities. However fish with pre‐existing pathology such as gill hyperplasia when linked with successive heat waves would stress the fish beyond the point of survival. By addressing the significant and additional stress factors in an epidemiological framework of cause and effect, the veterinary risk assessment arrived at a more realistic estimation of the toxic impact for the pesticide. Thus the veterinary risk assessment indicated that the AgDRIFT beta‐cyfluthrin exposure is between 4.6 and 9.4 times the approximate cyfluthrin No Observable Effect Concentration (NOEC) for silver perch. This translates to a significant health risk to the silver perch fish. The concept of a causal web involving multiple stressors on the fish and ecosystem health is a well recognised phenomenon by ecotoxicologists Carson (1962) and Heath (1998) because sublethal toxic effects at extremely low concentrations can have significant consequences in the aquatic environment particularly where species are exposed to many different stressors occurring concurrently. The available information from the veterinary investigation show that the silver perch have been exposed to a Report to Noosa Fish Health Investigation Task Force 7th Veterinary Report Executive Summary of Veterinary Investigations Page 6 of 27
toxic level of beta‐cyfluthrin which was undetectable with current laboratory test sensitivities, in the water samples or in fish tissue samples but yet significantly contributed to the eventual deaths of the fish . Australian Bass Deformity Histology has confirmed the lesions described by Sunland Hatchery in that fish formed twin bodies/heads. The early deformities appear to indicate interferance with the control mechanisms governing distribution of the cells in the embryo rather than causing the death of embryonic cells. This may involve abnormalities with the hormonal control mechanisms of the blastomere and if it is due to a chemical compound its source may need to be considered as originating in the yolk material (ie. broodstock source) or in the water source used for the spawning of these eggs. Given that broodstocks from a non‐Noosa River source produced normal fry using the same water as that used for the broodstocks producing defective fry, the Noosa broodstock may more likely be the source of the problem. If these deformity lesions exist in the Noosa River bass over several breeding seasons, the implication would be a significant decline in the recruitment rate of juvenile fish in the hatchery and an eventual loss of the population of bass in the river unless intervention through the stocking of viable fry occurs. There is a requirement to examine the role of pesticides as teratogens in aquatic species. For example, atrazine has been shown to cause embryonic teratogenic effects in catfish (Berge et.al. 1983). Non‐pesticide teratogens such as heavy metals also need to be considered in the context of the aquatic environment of teratogenic effects. In the context of the veterinary epidemiology the issue of discovery of deformed Australian Bass at Sunland Hatchery is not related to husbandry or hormonal issues because the hatchery succesfully spawned normal bass fry when broodstock from the wild other than from the Noosa River were used for breeding. This is a critical epidemiological pointer that should guide the investigation into potential issues with the Noosa River which may be impacting the recruitment and replenishment of fish stocks over a period of years. To this end, the spray drift modelling data on the hatchery and nut farm are not directly relevant to the risk assessment of embryonic deformities reported by the hatchery. The epidemiological evidence suggests that since beta‐cyfluthrin and methidathion are much more toxic than carbendazim and that the frequency of carbendazim application is product label restrained to a maximum of 2 applications, together with the spray record indication that carbendazim was only used in 2007 (and not prior in 2005 or 2006), the likelihood of carbendazim being a major cause of fish kills is low. Golden Perch Neurological Derangement A histological lesion of spinal inflexion and fracture is not in‐consistent with reports of partially atropine responsive treatment of neurological problems with fish and supports the real risk of exposure to organophosphate type pesticides. Spray log data confirmed that methidathion was used in the period associated with observation of spinning or convulsive symptoms in the fry particularly after water from ouside the hatchery building ie. from the blocked tanks that have been modelled by AgDRIFT to receive pesticides including levels of methidathion in the range of 0.027 to 0.323 µg/L based on a reported 2008/09 application rate of 1030 L/ha. However the spray records showed that methidathion was not applied in that period. Rather methidahion was used in 2007 and the application rate from spray records indicated that up to 1396 L/ha was used at the time of the neurological symptoms observed in the fish fry held in tanks inside the hatchery or from broodstocks which were in the ponds during the spray period. This would potentially result in a 35.5% increase of drift concentration of 0.037 – 0.438 µg/L. The LC50 95h for the most sensitive species of Bluegill sunfish is 0.9 – 5.1 µg/L (averaged 2.2 µg/L). Given that the golden perch (and silver perch) fry did not suffer an acute fish kill but continued with neurological symptoms for several days and recovered in 72h with atropine therapy – the exposure profile of methidathion is up to 49% that of the acute mortality but still below. There is therefore a significant risk of exposure leading to clinical signs consistent with acute toxicity without causing a mass fish kill. It is interesting to note from an epidemiological perspective that all 3 syndromes of fish at Sunland Hatchery can be explained by exposure to 3 classes of pesticides. This would be improbable if husbandry, water quality, nutritional, bacterial, viral, fungal or parasitic disease were a problem at the hatchery. For example, it would be highly improbably for a single pathogen to manifest the 3 different syndromes of acute fish kills, neurological symptoms and embryonic fish deformities as no such pathogen exists. Different pathogens would need to be present all together at a virulent level on the farm and this is not the case after the veterinary sampling and testing for viral, fungal, bacterial and parasitic agents. Further for husbandry to be an issue, it would have to be so far removed from industry standards as to be unsustainable. This is just not the case with Sunland Hatchery which has been for 26 years a reliable producer of quality fish for many stocking groups and including the Queensland Government. What the epidemiology consistently points to is an issue with pesticide use activity for the period 2005 onwards, this being the time of onset of a series of fish kills, losses and health problems. Report to Noosa Fish Health Investigation Task Force 7th Veterinary Report Executive Summary of Veterinary Investigations Page 7 of 27
Page 1 and 2: Report to Noosa Fish Health Investi
Page 3 and 4: Veterinary Investigations Executive
Page 5: Develop effective tools for sensiti
Page 9 and 10: Mullet Deformities Syndrome Mullet
Page 11 and 12: B. As the hatchery is a commercial
Page 13 and 14: Summary Risk Assessment Statement T
Page 15 and 16: The recommendations of this report
Page 17 and 18: B. Nonylphenol, though not a pestic
Page 19 and 20: 14.12.09 10.2.2010 6.1.2010 09‐1
Page 21 and 22: Ferguson, H.W. (2006). Systemic Pat
Page 23 and 24: NRA (2002). Public Release Summary
Page 25 and 26: Weiss, S.J. (1989). Tissue destruct
Page 27: Troy Ziesemer Roger Arbuckle Gwen G

37 7th Veterinary Report - Department of Primary Industries ...

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