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<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Prepared on 7 March 2010 by :<br />

Dr. Roger SM CHONG BVSc MACVSc<br />

Principal <strong>Veterinary</strong> Officer (Aquatic Animal Biosecurity)<br />

Biosecurity Queensland<br />

<strong>Department</strong> <strong>of</strong> Employment, Economic Development and Innovation<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 1 <strong>of</strong> 27


Contents<br />

<strong>Veterinary</strong> Investigations Executive Summary ………………………………………………………………………………………..3<br />

Silver Perch Kill, Bass Deformity and Neurologic Syndromes …………………………………………………………………..6<br />

Mullet Deformities Syndrome …………………………………………………………………………………………………………………9<br />

Bass Fry Kill Syndrome ……………………………………………………………………………………………………………………………10<br />

Golden Perch Loss Syndrome ………………………………………………………………………………………………………………….12<br />

Australian Bass Growth Retardation Syndrome ……………………………………………………………………………………..14<br />

Silver Perch Larval Malformation,Discoordination and Acute Death Syndrome ……………………………………..16<br />

Supporting Documents ………………………………………………………………………………………………………………………….18<br />

Literature ………………………………………………………………………………………………………………………………………………20<br />

Acknowledgements ……………………………………………………………………………………………………………………………….26<br />

Photos cover page :<br />

Upper 1 st row ‐left – Silver perch deaths associated with spraying activity.<br />

Upper 1 st row‐right – Australian Bass twin body deformity from Noosa broodfish – histology.<br />

Upper 2 nd row left – Mullet embryo with three tails from Noosa broodfish.<br />

Upper 2 nd row right – Noosa mullet broodfish which produced deformed progeny.<br />

Lower 1 st row left – Fish pond and macadamia trees.<br />

Lower 1 st row right – Australian bass fingerlings with retarded growth.<br />

Lower 2 nd row left – Australian Bass fry from non‐Noosa broodfish, no deformities.<br />

Lower 2 nd row right – Golden perch gills with hypertrophic pathology, associated with nonylphenol exposure.<br />

(Photos with are Copyright 2010 Gwen Gilson.)<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 2 <strong>of</strong> 27


<strong>Veterinary</strong> Investigations Executive Summary<br />

The Noosa Fish Health Investigation Task Force was a unique and timely opportunity to study and record the risks<br />

and effects <strong>of</strong> agrichemicals and pesticides on fish health. It was a complex investigation which utilised the<br />

strengths <strong>of</strong> veterinary science with its multidisciplines <strong>of</strong> epidemiology, pathology, parasitology and toxicology.<br />

As a result, a clearer understanding <strong>of</strong> the fish health syndromes was achieved in the past year. The interplay <strong>of</strong><br />

the risk factors involved with agrichemical use and the responses <strong>of</strong> a highly sensitive group <strong>of</strong> animals – fish, has<br />

been methodically described as six major syndromes. This provides a practical foundation from which to harness<br />

and apply effective solutions. It will ensure that the health <strong>of</strong> the horticultural, aquacultural and ecological assets<br />

<strong>of</strong> the Noosa river catchment are sustainably protected into the future from inadvertant agrichemical<br />

contamination.<br />

Silver Perch Kill, Bass Deformity and Neurologic Syndromes<br />

Silver Perch Kill<br />

The epidemiological evidence was consistent with the silver perch being at high risk <strong>of</strong> acute exposure to very<br />

low sublethal but toxic doses <strong>of</strong> beta‐cyfluthrin pesticide. The pesticide, in combination with gill hyperplasia<br />

pathology caused by gill fluke parasites and moderate level background heavy metals was a significant additional<br />

stress to the fish. When high environmental temperatures occurred concurrent with pesticide spray days, the<br />

combined interplay <strong>of</strong> risk factors produced a major fish kill at the hatchery pond <strong>of</strong> silver perch. The fish were<br />

normal right up till the week <strong>of</strong> beta‐cyfluthrin spraying by the macadamia plantation.<br />

Australian Bass Deformity<br />

Pathology confirmed the two headed deformity in fish embryos reported and this appeared to indicate<br />

interferance with the control mechanisms <strong>of</strong> the embryonic cells. The implication would be reproductive failure<br />

<strong>of</strong> the bass population in the Noosa river as fewer young fish are produced or survive. Normal bass fry were<br />

produced by Sunland Hatchery when non‐Noosa broodstocks are used; which strongly points to the Noosa river<br />

as being the source <strong>of</strong> potential chemical toxins with mutagenic and genotoxic properties.<br />

Golden Perch Neurological Derangement<br />

A pathological lesion <strong>of</strong> spinal inflexion and fracture was consisitent with reports <strong>of</strong> partially atropine responsive<br />

treatment <strong>of</strong> spinning problems with fish larvae at Sunland Hatchery. This supports the real risk <strong>of</strong> exposure to<br />

organophosphate type pesticides. Spray log data confirmed that methidathion (an organophosphate) was used in<br />

the period associated with observation <strong>of</strong> spinning or convulsive symptoms in the fry particularly after water<br />

from ouside the hatchery building was used in spawning tanks.<br />

Mullet Deformities Syndrome (MDS)<br />

MDS pathology is very similar to the two headed bass syndrome because three tails or axial multiplication<br />

occurred. The serious implication is that a common agent is causing reproductive damage to more than one<br />

species <strong>of</strong> fish in the Noosa river. MDS was clinically presented as resulting in the failure <strong>of</strong> normal, full‐term<br />

development <strong>of</strong> fertilised mullet eggs. Carbendazim and atrazine agrichemicals were detected in the catchment<br />

at very low levels which appear to be innocuous, but is it ? given the epidemiological evidence <strong>of</strong> a potential<br />

common link.<br />

Bass Fry Kill Syndrome<br />

Evidence <strong>of</strong> liver and red blood cell pathology in affected fish pointed to potential methoxifenozide<br />

contamination <strong>of</strong> algal feeds held in uncovered tanks outside from spray drift <strong>of</strong> macadamia operations leading<br />

to acute deaths <strong>of</strong> hatched Australian Bass. Fish that were not fed the algae on the days <strong>of</strong> agrichemical spraying<br />

did not experience similar mortalities.<br />

Golden Perch Loss Syndrome<br />

Parasitology detected an external parasite Costia sp. protozoan as the main cause <strong>of</strong> low survival from 10,000 fry<br />

stocked in a pond. Interestingly, pathology also detected toxic injury to gill, liver and red blood cells not related<br />

to Costia sp.. Carbendazim, nonylphenol, trichlorphon/dichlorvos, 4‐t‐octylphenol, bisphenol A and urea<br />

agrichemical residues were detected from water storage locations on the Gilson Rd. hatchery. This was clear<br />

evidence <strong>of</strong> contamination from macadamia spray drift for carbendazim, nonylphenol and<br />

trichlorphon/dichlorvos.<br />

Australian Bass Growth Retardation Syndrome (ABGRS)<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 3 <strong>of</strong> 27


ABGRS resulted in a statistically significant (P


Develop effective tools for sensitive monitoring <strong>of</strong> river ecosystems from the potential risks <strong>of</strong><br />

agrichemical run‐<strong>of</strong>f.<br />

Where agrichemicals are found to have unacceptable toxicity risks to the ecosystem under practical<br />

conditions <strong>of</strong> use, withdrawal from market is an option.<br />

Until clear outcomes are in progress, the Sunland Hatchery will continue to manage the agrichemical<br />

contamination risks experienced whch resulted in the last five years <strong>of</strong> fish health and production failures<br />

through support from Biosecurity Queensland and the hatchery’s private veterinarian ‐ Dr. Matt Landos, using a<br />

Hatchery Spray Drift Protection Program. This program entails ‐<br />

a. Protection <strong>of</strong> all water sources within an enclosed structure.<br />

b. Protection <strong>of</strong> all fish and algae production units with screens or covers to minimise drift <strong>of</strong><br />

pesticide and other agricultural chemicals.<br />

c. Use <strong>of</strong> an alternate site for the sustainable production <strong>of</strong> grow out sized fish.<br />

d. Use <strong>of</strong> an alternate site for the production <strong>of</strong> food items for larval fish eg. algal and<br />

zooplankton.<br />

This program has successfully resulted in the production <strong>of</strong> healthy and fecund Australian Bass, silver perch and<br />

golden perch fingerlings for sale in late 2009 and early 2010. However, this mode <strong>of</strong> biosecurity adds<br />

considerable costs to the production <strong>of</strong> fish for restocking groups and aquaculturists because <strong>of</strong> increased labour<br />

inputs to carting clean water from the Ringtail ponds, transportation <strong>of</strong> normal fish to Ringtail, decontamination<br />

procedures for utensils and equipment <strong>of</strong> the hatchery at Gilson road and increased monitoring <strong>of</strong> macadamia<br />

plantation spray activity.<br />

Prepared on 7 March 2010 by :<br />

Dr. Roger SM CHONG BVSc MACVSc<br />

Principal <strong>Veterinary</strong> Officer (Aquatic Animal Biosecurity)<br />

Biosecurity Queensland<br />

<strong>Department</strong> <strong>of</strong> Employment, Economic Development and Innovation<br />

Pr<strong>of</strong>itable <strong>Primary</strong> <strong>Industries</strong> for Queensland<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 5 <strong>of</strong> 27


Silver Perch Kill, Bass Deformity and Neurologic Syndromes<br />

The veterinary investigation commissioned by the Noosa Fish Health Investigation Task Force (NFHITF) into the<br />

Sunland Fish Hatchery silver perch fish kill, golden perch neurological abnormalities and Australian bass<br />

deformities has examined the available sources <strong>of</strong> information and has come to validated conclusions which<br />

specifically address the fish health problems.<br />

Silver Perch Fish Kill<br />

The field and laboratory evidence are consistent with the silver perch at high risk <strong>of</strong> being exposed to very low<br />

sublethal but toxic doses <strong>of</strong> beta‐cyfluthrin pesticide. The pesticide, in combination with gill hyperplasia<br />

pathology caused by gill flukes and heavy metals was a significant stress to the fish. When high environmental<br />

temperatures occurred concurrent with pesticide spray drift, the chain <strong>of</strong> events produced a major fish kill at the<br />

hatchery pond <strong>of</strong> silver perch.<br />

The current laboratory and veterinary epidemiological data is supported through spray drift modeling conducted<br />

by the Australian Pesticides and <strong>Veterinary</strong> Medicines Authority (APVMA) AgDRIFT model. AgDRIFT<br />

demonstrated that all fish ponds on the hatchery would receive pesticides including beta‐cyfluthrin even when<br />

applied under current pesticide label conditions. The potential averaged initial concentrations <strong>of</strong> pesticides<br />

achieved in the fish hatchery water storages by spray drift were :<br />

o Without buffer<br />

o With buffer<br />

Cardendazim 0.013 – 0.162 µg/L<br />

Methidathion 0.027 – 0.323 µg/L<br />

beta‐cyfluthrin 0.00068 – 0.0082 µg/L<br />

Cardendazim 0.007 – 0.079 µg/L<br />

Methidathion 0.013 – 0.158 µg/L<br />

beta‐cyfluthrin 0.0006 – 0.004 µg/L<br />

By extrapolating from literature sources, the toxicity end points for silver perch when based on the Bluegill<br />

sunfish demonstrate a number <strong>of</strong> toxic exposure scenarios :<br />

1. The 10% lethal concentration <strong>of</strong> beta‐cyfluthrin has the potential to cause temperature<br />

stress effects at an exposure <strong>of</strong> 0.087 – 0.15 µg/L.<br />

2. Swimming abnormality in fish can be due to toxic effects at 0.7 – 5% <strong>of</strong> the lethal<br />

concentration at an exposure <strong>of</strong> 0.0006 – 0.0075 µg/L beta‐cyfluthrin.<br />

3. An estimated safe level for exposure to beta‐cyfluthrin for silver perch is up to 0.00087<br />

µg/L.<br />

From these, an estimated cyfluthrin exposure level <strong>of</strong> the order <strong>of</strong> 0.00087 – 0.15 µg/L (ppb) cyfluthrin could<br />

contaminate the pond sufficient to result in a sublethal toxic effect on silver perch resulting in fish temperature<br />

tolerance and swimming behaviour changes. Given that the AgDRIFT model exposure level is estimated to be<br />

0.0006 ‐ 0.0082 µg/L (ppb), this fitted within the range for sublethal toxicity.<br />

On its own this range <strong>of</strong> beta‐cyfluthrin exposure would not be expected to result in temperature stress effects<br />

or mortalities. However fish with pre‐existing pathology such as gill hyperplasia when linked with successive heat<br />

waves would stress the fish beyond the point <strong>of</strong> survival. By addressing the significant and additional stress<br />

factors in an epidemiological framework <strong>of</strong> cause and effect, the veterinary risk assessment arrived at a more<br />

realistic estimation <strong>of</strong> the toxic impact for the pesticide. Thus the veterinary risk assessment indicated that the<br />

AgDRIFT beta‐cyfluthrin exposure is between 4.6 and 9.4 times the approximate cyfluthrin No Observable Effect<br />

Concentration (NOEC) for silver perch. This translates to a significant health risk to the silver perch fish. The<br />

concept <strong>of</strong> a causal web involving multiple stressors on the fish and ecosystem health is a well recognised<br />

phenomenon by ecotoxicologists Carson (1962) and Heath (1998) because sublethal toxic effects at extremely<br />

low concentrations can have significant consequences in the aquatic environment particularly where species are<br />

exposed to many different stressors occurring concurrently.<br />

The available information from the veterinary investigation show that the silver perch have been exposed to a<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 6 <strong>of</strong> 27


toxic level <strong>of</strong> beta‐cyfluthrin which was undetectable with current laboratory test sensitivities, in the water<br />

samples or in fish tissue samples but yet significantly contributed to the eventual deaths <strong>of</strong> the fish .<br />

Australian Bass Deformity<br />

Histology has confirmed the lesions described by Sunland Hatchery in that fish formed twin bodies/heads. The<br />

early deformities appear to indicate interferance with the control mechanisms governing distribution <strong>of</strong> the cells<br />

in the embryo rather than causing the death <strong>of</strong> embryonic cells. This may involve abnormalities with the<br />

hormonal control mechanisms <strong>of</strong> the blastomere and if it is due to a chemical compound its source may need to<br />

be considered as originating in the yolk material (ie. broodstock source) or in the water source used for the<br />

spawning <strong>of</strong> these eggs. Given that broodstocks from a non‐Noosa River source produced normal fry using the<br />

same water as that used for the broodstocks producing defective fry, the Noosa broodstock may more likely be<br />

the source <strong>of</strong> the problem. If these deformity lesions exist in the Noosa River bass over several breeding seasons,<br />

the implication would be a significant decline in the recruitment rate <strong>of</strong> juvenile fish in the hatchery and an<br />

eventual loss <strong>of</strong> the population <strong>of</strong> bass in the river unless intervention through the stocking <strong>of</strong> viable fry occurs.<br />

There is a requirement to examine the role <strong>of</strong> pesticides as teratogens in aquatic species. For example, atrazine<br />

has been shown to cause embryonic teratogenic effects in catfish (Berge et.al. 1983). Non‐pesticide teratogens<br />

such as heavy metals also need to be considered in the context <strong>of</strong> the aquatic environment <strong>of</strong> teratogenic effects.<br />

In the context <strong>of</strong> the veterinary epidemiology the issue <strong>of</strong> discovery <strong>of</strong> deformed Australian Bass at Sunland<br />

Hatchery is not related to husbandry or hormonal issues because the hatchery succesfully spawned normal bass<br />

fry when broodstock from the wild other than from the Noosa River were used for breeding. This is a critical<br />

epidemiological pointer that should guide the investigation into potential issues with the Noosa River which may<br />

be impacting the recruitment and replenishment <strong>of</strong> fish stocks over a period <strong>of</strong> years. To this end, the spray drift<br />

modelling data on the hatchery and nut farm are not directly relevant to the risk assessment <strong>of</strong> embryonic<br />

deformities reported by the hatchery. The epidemiological evidence suggests that since beta‐cyfluthrin and<br />

methidathion are much more toxic than carbendazim and that the frequency <strong>of</strong> carbendazim application is<br />

product label restrained to a maximum <strong>of</strong> 2 applications, together with the spray record indication that<br />

carbendazim was only used in 2007 (and not prior in 2005 or 2006), the likelihood <strong>of</strong> carbendazim being a major<br />

cause <strong>of</strong> fish kills is low.<br />

Golden Perch Neurological Derangement<br />

A histological lesion <strong>of</strong> spinal inflexion and fracture is not in‐consistent with reports <strong>of</strong> partially atropine<br />

responsive treatment <strong>of</strong> neurological problems with fish and supports the real risk <strong>of</strong> exposure to<br />

organophosphate type pesticides. Spray log data confirmed that methidathion was used in the period associated<br />

with observation <strong>of</strong> spinning or convulsive symptoms in the fry particularly after water from ouside the hatchery<br />

building ie. from the blocked tanks that have been modelled by AgDRIFT to receive pesticides including levels <strong>of</strong><br />

methidathion in the range <strong>of</strong> 0.027 to 0.323 µg/L based on a reported 2008/09 application rate <strong>of</strong> 1030 L/ha.<br />

However the spray records showed that methidathion was not applied in that period. Rather methidahion was<br />

used in 2007 and the application rate from spray records indicated that up to 1396 L/ha was used at the time <strong>of</strong><br />

the neurological symptoms observed in the fish fry held in tanks inside the hatchery or from broodstocks which<br />

were in the ponds during the spray period. This would potentially result in a 35.5% increase <strong>of</strong> drift concentration<br />

<strong>of</strong> 0.0<strong>37</strong> – 0.438 µg/L. The LC50 95h for the most sensitive species <strong>of</strong> Bluegill sunfish is 0.9 – 5.1 µg/L (averaged<br />

2.2 µg/L). Given that the golden perch (and silver perch) fry did not suffer an acute fish kill but continued with<br />

neurological symptoms for several days and recovered in 72h with atropine therapy – the exposure pr<strong>of</strong>ile <strong>of</strong><br />

methidathion is up to 49% that <strong>of</strong> the acute mortality but still below. There is therefore a significant risk <strong>of</strong><br />

exposure leading to clinical signs consistent with acute toxicity without causing a mass fish kill.<br />

It is interesting to note from an epidemiological perspective that all 3 syndromes <strong>of</strong> fish at Sunland Hatchery can<br />

be explained by exposure to 3 classes <strong>of</strong> pesticides. This would be improbable if husbandry, water quality,<br />

nutritional, bacterial, viral, fungal or parasitic disease were a problem at the hatchery. For example, it would be<br />

highly improbably for a single pathogen to manifest the 3 different syndromes <strong>of</strong> acute fish kills, neurological<br />

symptoms and embryonic fish deformities as no such pathogen exists. Different pathogens would need to be<br />

present all together at a virulent level on the farm and this is not the case after the veterinary sampling and<br />

testing for viral, fungal, bacterial and parasitic agents. Further for husbandry to be an issue, it would have to be<br />

so far removed from industry standards as to be unsustainable. This is just not the case with Sunland Hatchery<br />

which has been for 26 years a reliable producer <strong>of</strong> quality fish for many stocking groups and including the<br />

Queensland Government. What the epidemiology consistently points to is an issue with pesticide use activity for<br />

the period 2005 onwards, this being the time <strong>of</strong> onset <strong>of</strong> a series <strong>of</strong> fish kills, losses and health problems.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 7 <strong>of</strong> 27


<strong>Report</strong> Recommendations<br />

1. The veterinary investigation recommends an adverse event report process for the APVMA to be<br />

initiated in relation to beta‐cyfluthrin. This signals the need to conduct structured research into<br />

pesticide exposure and toxicity to aquatic species such as commercial fish because existing label<br />

regulations do not appear to safe guard against spray drift in certain situations <strong>of</strong> pesticide use<br />

identified in this report. Options for this research are presented in this report.<br />

2. The veterinary investigation recommends on‐going structured surveillance into the Australian Bass<br />

deformity syndrome based on pathological confirmation that a significant early embryonic disorder is<br />

present with the potential to impact bass recruitment and replenishment in the Noosa River<br />

Catchment. Options for surveillance research are presented in this report.<br />

3. The veterinary investigation recommends the development <strong>of</strong> a risk mitigation plan for the Sunland<br />

Fish Hatchery which is able to ensure sustainable production <strong>of</strong> valuable native Australian fish species.<br />

This plan should contain in its core requirement specific strategies to protect fish culture from<br />

inadvertant spray drift with pesticide chemicals. Options for risk mitigation are presented in this report.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 8 <strong>of</strong> 27


Mullet Deformities Syndrome<br />

Mullet Deformities Syndrome (MDS)<br />

o Is a new and serious condition affecting the reproductive health <strong>of</strong> mullet fish in the Noosa River with a<br />

potential to alter the general mullet population recruitment rate. This is dependant on the prevalence<br />

<strong>of</strong> MDS in the mullet population.<br />

o Has significant similarites to the deformity syndrome described for Australian Bass from the Noosa<br />

River.<br />

o It would not be inconsistent to consider that the reason or risk factor for MDS to be the same as that<br />

for the deformities in Australian Bass fry <strong>of</strong> the Noosa River. The risk factor causes reproductive failure<br />

in both species.<br />

o Is caused by a non‐infectious agent(s) with potential genotoxic or mutagenic properties, being present<br />

in the ecosystem where mullet and bass co‐habitat. Exposure period(s) in the Noosa River may increase<br />

or decrease the risk <strong>of</strong> MDS in mullet.<br />

Case Definition – Mullet Deformities Syndrome (MDS)<br />

MDS is defined as a disorder <strong>of</strong> the reproductive health <strong>of</strong> Mugil cephalus currently detected in fish sourced from<br />

the Noosa River system. MDS is clinically presented as resulting in the failure <strong>of</strong> normal, full‐term development<br />

<strong>of</strong> fertilised mullet eggs from the stage <strong>of</strong> egg activation , through cell division, embryonic organogenesis and to<br />

hatch. The clinical signs appear to be more severe in mullet which commercial fishers consider to be Noosa River<br />

resident fish. Clinical signs and pathologies are variously presented as deformites <strong>of</strong> cell development (eccentric<br />

cells, halos, tophats) and deformities <strong>of</strong> organogenesis (axial duplication and axial triplication, dwarfs and snake<br />

forms) in the formed embryo. Clinical sign also appears to reflect an arrestment and/or an abortive effect on<br />

apparently fertilised eggs in the absence <strong>of</strong> visible deformities. The net result <strong>of</strong> MDS being a failure <strong>of</strong> effective<br />

reproduction from fish in normal spawning condition and in fish with no evidence <strong>of</strong> significant disease from<br />

viral, bacterial, fungal, parasitic or chlamydial pathogens. MDS appears to be independent <strong>of</strong> husbandry factors .<br />

The recommendations <strong>of</strong> this report are –<br />

A. Fish surveillance program to –<br />

o Monitor the impact <strong>of</strong> MDS to mullet and <strong>of</strong> two headed deformity to Australian Bass populations by<br />

comparing Noosa to non‐Noosa fish in fish breeding trials.<br />

o Surveillance <strong>of</strong> recruitment rates <strong>of</strong> mullet and bass in the Noosa river over a period <strong>of</strong> several years.<br />

B. Agrichemical exposure trials to ‐<br />

o Understand the genotoxic and mutagenic effects <strong>of</strong> agrichemicals detected in the Noosa catchment to<br />

fish reproductive performance.<br />

o Assess the toxicity levels <strong>of</strong> carbendazim and atrazine to reproductive performance <strong>of</strong> Australian Bass<br />

and mullet in controlled experimental conditions.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

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Bass Fry Kill Syndrome<br />

The incident <strong>of</strong> acute mortalities <strong>of</strong> Australian Bass at Sunland Hatchery was investigated and risk assessed with<br />

respect to spray activities at the adjacent macadamia plantation. The results <strong>of</strong> the investigation form the 3 rd<br />

<strong>Veterinary</strong> <strong>Report</strong> <strong>of</strong> the Noosa Fish Health Investigation Task Force. On the balance <strong>of</strong> the evidence at the<br />

epidemiological, pathological and toxicological levels, the risk <strong>of</strong> adverse effect in the bass fry points towards<br />

chemical toxicity with methoxifenozide based on :<br />

a. The pathology <strong>of</strong> the affected bass fry supports that <strong>of</strong> a toxicological process affecting both erythrocyte and<br />

hepatocellular functions. These changes have been reported for methoxyfenozide in animal species.<br />

b. There is temporal correlation between spray activity employing methoxyfenozide and urea potential for<br />

exposure to the chemicals via the route <strong>of</strong> ingestion <strong>of</strong> algae that was located outside the hatchery.<br />

c. Biotoxins from algal and bacterial sources have been assessed to be unlikely on the basis <strong>of</strong> clinical<br />

epidemiology.<br />

d. There is evidence <strong>of</strong> exposure to both chemicals reported used in macadamia spraying activities due to<br />

spray drift onto water storage locations on the hatchery.<br />

e. Available toxicological data for fish species does not indicate that the toxic concentration <strong>of</strong><br />

methoxyfenozide or urea has been reached for an acute lethal effect given a very low estimated toxicity risk<br />

ratio.<br />

f. The areas <strong>of</strong> uncertainty are :<br />

the concentrations <strong>of</strong> methoxyfenozide in affected fish<br />

the sensitivity <strong>of</strong> bass fry to methoxyfenozide<br />

mechanism <strong>of</strong> toxicity <strong>of</strong> methoxyfenozide in fish<br />

Elucidation <strong>of</strong> these issues on the basis <strong>of</strong> new research is likely to clarify the actual risk <strong>of</strong><br />

methoxyfenozide for Australian Bass in such a localised setting.<br />

The recommendations <strong>of</strong> this report are :<br />

A. Structured monitoring <strong>of</strong> spray drift and fish health indices to evaluate actual risks <strong>of</strong> spray practices <strong>of</strong> the<br />

macadamia plantation on hatchery operations.<br />

This should involve the use <strong>of</strong> sentinel fish to measure the actual contamination level <strong>of</strong> chemicals that may be<br />

applied through spray rigs at the macadamia plantation. It is important that the spraying practices reflect what is<br />

performed in the past and well as what is currently the routine. The monitoring should include collection <strong>of</strong><br />

environmental samples such as water, sediment and vegetation (for example leaves blown into ponds from the<br />

macadamia farm) for residue analyses <strong>of</strong> the specific chemicals used. This will provide more accurate data over<br />

time than that which is currently available either by ad‐hoc sampling or by spray drift modelling. Correlation <strong>of</strong><br />

results with wind speed and direction data as well as measurements <strong>of</strong> actual spray rates from the spray rigs are<br />

necessary for a robust assessment.<br />

This is necessary to understand the responses <strong>of</strong> native fish species <strong>of</strong> both larval, juvenile and adult life stages to<br />

the varied exposure scenarios. This information should include residue testing and histopathology with gross<br />

pathology as well as observations <strong>of</strong> clinical or sublethal behavioural changes. Information from this type <strong>of</strong><br />

surveillance would be useful to define the toxicity endpoints for the key pesticides and agri‐chemicals used for<br />

local species <strong>of</strong> fish.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 10 <strong>of</strong> 27


B. As the hatchery is a commercial operation, precautionary spray drift protection must be in place while<br />

structured studies are conducted. These include :<br />

e. Protection <strong>of</strong> all water sources within an enclosed structure<br />

f. Protection <strong>of</strong> all fish and algae production units with screens or covers to minimise drift <strong>of</strong><br />

pesticide and other agricultural chemicals<br />

g. Use <strong>of</strong> an alternate site for the sustainable production <strong>of</strong> grow out sized fish<br />

h. Use <strong>of</strong> an althernate site for the production <strong>of</strong> food items for larval fish eg. algal and<br />

zooplankton<br />

Refinement <strong>of</strong> the spray drift protection procedures currently adopted is needed to ensure that the<br />

additional costs <strong>of</strong> such measures are sustainable and appropropriate to the actual or defined spray drift<br />

risks. Without this refinement, it would be difficult to come to an agreeable basis for mediation that is<br />

required for the fish hatchery and macadamia plantation to co‐exist productively.<br />

C. An adverse reaction report should be compiled on the use <strong>of</strong> methoxyfenozide to the Australian Pesticides<br />

and <strong>Veterinary</strong> Authority for the purposes <strong>of</strong> :<br />

i. Conduct <strong>of</strong> a review <strong>of</strong> the active compound and label conditions<br />

ii. Conduct <strong>of</strong> research on the toxicity <strong>of</strong> methoxyfenozide to Australian Bass fry<br />

An adverse reaction report is the trigger to signal the need to conduct targeted research studies for a<br />

registered product used under label conditions but which still results in unintended effects in non‐target<br />

species. Information from the veterinary reports 1‐3 may be used to assist in the development <strong>of</strong> an adverse<br />

reaction report management strategy which specifically addresses the issues <strong>of</strong> information gaps for end‐<br />

point toxicity limits for local conditions and local species <strong>of</strong> fish.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 11 <strong>of</strong> 27


Golden Perch Loss Syndrome<br />

The Golden Perch Loss Syndrome was a replication <strong>of</strong> historical reports <strong>of</strong> fish health problems at Sunland<br />

Hatchery. This was the first instance when an adverse event in fish production had been observed from the<br />

commencement to the end <strong>of</strong> the reported spray period. It thus provided a much more complete opportunity<br />

than previously possible to identify the primary cause <strong>of</strong> the fish health problem.<br />

1. The primary cause <strong>of</strong> the Golden Perch Fish Loss Syndrome is the parasitic activity <strong>of</strong> large numbers <strong>of</strong> a<br />

protozoan ectoparasite – Costia sp.(or Ichthyobodo sp.) mainly infesting the skin <strong>of</strong> the very small fry<br />

stocked into the Barra pond. Costia sp. can result in acute mortalities <strong>of</strong> more susceptible fry. However fry<br />

can be rendered more susceptible when other concurrent tissue pathology is present. The likely source <strong>of</strong><br />

the parasite involved the use <strong>of</strong> water collected from a dam which has a connection to Cooloothin Creek.<br />

2. The Golden Perch Fish Loss Syndrome has a significant toxic component resulting in pathological injury to<br />

the gills, liver and erythrocytes <strong>of</strong> the fish. This cannot be explained by the presence <strong>of</strong> parasitic Costia sp..<br />

These toxic responses can increase the susceptibility <strong>of</strong> the injured fish to pathogens including Costia sp. by<br />

increasing the stressor factors active on the fish. The pathological changes <strong>of</strong> gill hypertrophy, eosinophilic<br />

cytoplasmic change and vacuolation, liver changes <strong>of</strong> hepatocellular eosinophilic microgranule<br />

accummulation, vacuolation and mild degeneration as well as increased immature erythrocyte response to a<br />

probable haemolytic disorder are consistent with exposure to toxin because mechanisms <strong>of</strong> toxicity to<br />

produce these changes are within the scope <strong>of</strong> action <strong>of</strong> several chemical toxins detected. Research work is<br />

required to define the respective roles <strong>of</strong> these chemical toxins.<br />

3. Carbendazim, nonylphenol, 4‐t‐octylphenol, and bisphenol A pesticide and urea residues were detected in<br />

samples from water storage locations on the Gilson Rd. hatchery. Dichlorvos was detected in the hatchery<br />

shed using air sampling filter paper. This constitutes clear evidence <strong>of</strong> contamination with pesticides and<br />

agrichemical pesticides. Of these, carbendazim and nonlylphenol containing products has been reportedly<br />

used by macadamia operations in the adjacent farm. Information from the spray record would need to be<br />

examined to assess the likelihood <strong>of</strong> these agrichemicals originating from the macadamia farm in terms <strong>of</strong><br />

temporal relationships to spray activity in question and the onset‐duration <strong>of</strong> the fish loss syndrome.<br />

4. There is clear evidence <strong>of</strong> a range <strong>of</strong> toxic effects resulting in the fish where specific protection from<br />

agrichemical spray activity has been removed by placing the fish in the Barra pond. Since toxic changes<br />

which may be attributable to one or more <strong>of</strong> these pesticides were observed in the affected fish, it is not<br />

conclusive that the contamination scenario observed in this case represents a ‘No Observable Effect Level’<br />

<strong>of</strong> exposure despite meeting the published criteria for toxicity endpoint assessments. That is, though<br />

published toxicity data support the notion that the fish should be safe, the observed field and laboratory<br />

data indicated that the fish were not safe. Safe meaning the absence <strong>of</strong> toxicological injury or responses in<br />

the tissues <strong>of</strong> the fish. As none <strong>of</strong> published acute lethal or chronic toxic concentrations had been reached<br />

and no detectable pesticide residue was found in the Barra pond where the affected fish were held, it was<br />

highly unlikely that pesticides directly killed the fish in this syndrome. If the assumption that these residue<br />

levels represent the actual exposure scenario in the field, then there should not be toxic pathological<br />

responses in the fish. This assumption needs to be tested. Given that these residue results were an averaged<br />

concentration <strong>of</strong> the samples, there is a potential issue with localised ‘hotspot’ effect where fish may be<br />

exposed to a higher concentration <strong>of</strong> chemical at the point should the spray drift droplets land on the<br />

surface <strong>of</strong> the water. The issue <strong>of</strong> increased risk to toxicity from mixture effects <strong>of</strong> pesticide exposure is<br />

possible because the existing toxicity endpoint references values are only based on individual chemical<br />

toxicities. These factors could potentially lead to an underestimation <strong>of</strong> the true exposure risk and toxicity<br />

end points. Again these issues need to be further researched because the field and laboratory data suggests<br />

an anomaly with the standard approach to toxicity end point assessment.<br />

5. Of particular interest is the liver pathology which suggests a role for endocrine disruptor compounds (EDCs).<br />

4‐t‐octylphenol, nonylphenol and bisphenol A are compounds with known EDC activity and their detection<br />

as residues in conjunction with liver changes suggestive <strong>of</strong> vitellogenic production warrants additional<br />

investigation to confirm. Nevertheless the current evidence is consistent with this assessment.<br />

6. Golden perch which were <strong>of</strong> similar age, spawning batch and time <strong>of</strong> stocking produced no toxic changes in<br />

the tissues when these fish were specifically protected from macadamia spray activity and drift by way <strong>of</strong><br />

stocking at a remote site several kilometres away from the Gilson Rd hatchery. This is clear evidence that<br />

spray drift occurs in conjunction with macadamia spray activity and that there are toxic effects in fish caused<br />

by agri‐chemicals contaminating the Gilson Rd hatchery.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 12 <strong>of</strong> 27


Summary Risk Assessment Statement<br />

The Golden Perch Fish Loss Syndrome at Sunland Fish Hatchery in September 2009 was caused primarily by a<br />

parasitic infection with a protozoan Costia sp. resulting in fish mortalities, with significant secondary toxic<br />

pathological effects in connection to contamination <strong>of</strong> the hatchery by agrichemicals including pesticides such as<br />

nonylphenol, 4‐t‐octylphenol, bisphenol A, carbendazim, and dichlorvos. Toxic pathology in the fish gills, liver<br />

cells and erythrocytes may be specifically attributable to the endocrine disruptor compounds nonylphenol, 4‐t‐<br />

octylphenol and bisphenol A.<br />

Fish that were protected from spray activity did not experience similar toxicological effects and a specific time<br />

relationship <strong>of</strong> the syndrome to the reported spraying activity at the adjacent macadamia plantation is clear<br />

evidence that spray activity and spray drift are the common factors resulting in contamination <strong>of</strong> the hatchery<br />

environment with agrichemicals including pesticides thus producing observable toxicological effects in<br />

unprotected fish.<br />

The recommendations <strong>of</strong> this report are :<br />

A. Provision <strong>of</strong> the spray record information to the veterinary investigation as it is vital to elucidate the exact<br />

sources <strong>of</strong> these agrichemicals with respect to macadamia farming activities.<br />

B. Review <strong>of</strong> the current standards for aquatic toxicity endpoint assessments with respect to delineation <strong>of</strong><br />

actual field exposure scenarios, influence <strong>of</strong> chemical mixtures and toxicity endpoints for native Australian<br />

fish species including the golden perch (Macquaria ambigua) so as to improve the sensitivity and thus<br />

reliability <strong>of</strong> risk assessment standards.<br />

C. Research into the toxicity pathways for nonylphenol, 4‐t‐octylphenol and bisphenol A endocrine disruptors<br />

in fish fry <strong>of</strong> Australian native fish species including M.ambigua, under actual field conditions is required to<br />

elucidate the responses <strong>of</strong> fish to varying conditions <strong>of</strong> exposure. This is necessary to support the<br />

development <strong>of</strong> effective safe practices with respect to agrichemical spray drift risks.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 13 <strong>of</strong> 27


Australian Bass Growth Retardation Syndrome<br />

1. The Australian Bass Growth Retardation Syndrome (ABGRS) is a significant fish health disorder<br />

impacting the productivity <strong>of</strong> the Sunland Fish Hatchery. ABGRS is now a verifiable condition under the<br />

terms <strong>of</strong> reference <strong>of</strong> the Noosa Fish Health Investigation Task Force (NFHITF).<br />

2. ABGRS manifests itself when fish are reared in a pond subjected to agrichemical spray drift risk during<br />

spray application events by the adjacent macadamia plantation. The period <strong>of</strong> potential exposure in<br />

this study was from 25.11.09 until the 10.2.2010, the period when fish were stocked into the Barra<br />

pond until the time <strong>of</strong> sampling and fish measurements. Evidence <strong>of</strong> contamination <strong>of</strong> the barra pond<br />

specifically and also the hatchery internal environment and other water storages at Sunland Hatchery<br />

(Gilson Rd.) with nonylphenol was established. As nonylphenol has been used by the adjacent<br />

macadamia plantation, the source <strong>of</strong> this agrichemical is likely to be the adjacent macadamia<br />

plantation unless, audited spray record information and environmental sampling and testing <strong>of</strong> the<br />

macadamia plantation show contrary evidence – ie absence <strong>of</strong> use and lack <strong>of</strong> detectable presence on<br />

soil, water or foliage <strong>of</strong> the plantation.<br />

3. ABGRS resulted in a statistically significant (P


The recommendations <strong>of</strong> this report are :<br />

A. To prevent the recurrence <strong>of</strong> Australian Bass Growth Retardation Syndrome (ABGRS), fish must be fully<br />

protected from proximity to all spray activity in time and distance during their entire grow‐out period.<br />

This may be achieved by relocating all grow‐out activities to several kilometres away from the Gilson<br />

road location.<br />

B. Published data on the toxicity <strong>of</strong> nonylphenol agrichemical is not currently available to native<br />

Australian fish species. This makes practical risk assessment currently unreliable and can result in<br />

occurences <strong>of</strong> adverse events such as ABGRS. As a priority, research into the toxicity threshold <strong>of</strong><br />

nonylphenol for native Australian fish species, including the Australian Bass is indicated. To achieve this<br />

end, an Adverse Event <strong>Report</strong> (AER) on nonylphenol to the APVMA is justifiable. Direct tank exposure<br />

trials with known dilutions to levels below current published toxicity endpoints would be useful to<br />

minimise setting no observable toxic effect levels that are too high. Tools for measuring toxic effects<br />

need to be more specific and sensitive, aimed at capturing mechanisms <strong>of</strong> toxicity at the cellular and<br />

sub‐cellular level. Tools such as biochemistry and cell‐line studies are relevant in this regard.<br />

C. Risk modelling <strong>of</strong> spray application scenarios that use the agrichemical nonylphenol as a surfactant or<br />

wetting agent based on actual operational situations <strong>of</strong> application is required to quantity more<br />

accurately the exposure concentrations to fish species. This should replace the current approach <strong>of</strong><br />

grab water samples to estimate exposure, primarily to minimise error <strong>of</strong> underestimation <strong>of</strong> exposure<br />

concentration.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 15 <strong>of</strong> 27


Silver Perch Larval Malformation,Discoordination and Acute Death Syndrome<br />

1. Silver Perch Larval Malformation, Discoordination and Acute Death (SPMDAD) Syndrome is a complex<br />

fish health disorder within the scope <strong>of</strong> syndromes described by the Noosa Fish Health Investigation<br />

Task Force. Although there is insufficient pathological data to study the development <strong>of</strong> SPMDAD in<br />

detail, this epidemiological and toxicological assessment provided a necessary starting point. It is a<br />

significant fish health disorder within the context <strong>of</strong> agrichemical spray drift risk assessment and<br />

mitigation.<br />

2. SPMDAD is a toxin related and acute condition. This is supported by the observation that activated<br />

charcoal filtration <strong>of</strong> spawning tank water improved the survival rate <strong>of</strong> affected fish larvae. SPMDAD<br />

causes severe morbidity and mortality <strong>of</strong> affected fish resulting in estimated rates <strong>of</strong> mortality in<br />

fertilised fish embryos <strong>of</strong> 99%, <strong>of</strong> malformation in embryos <strong>of</strong> 25% and <strong>of</strong> swimming discoordination in<br />

hatched fish larvae <strong>of</strong> 65%.<br />

3. Spray drift contamination occurred through a breach in the hatchery spray drift biosecurity program by<br />

the opening <strong>of</strong> the hatchery door in the evenings and through lack <strong>of</strong> covering over water storage<br />

tanks. This contributed to the contamination <strong>of</strong> the hatchery air environment and potentially water<br />

used for fish spawning with trichlorphon/dichlorvos and nonylphenol. Both agrichemicals have been<br />

reported to be used recently by the macadamia plantation. However, the actual exposure<br />

concentration to the affected fish eggs and larvae are not known due to lack <strong>of</strong> water samples from the<br />

hatchery tanks.<br />

4. Nonylphenol has been shown to cause lethal and non‐lethal fish embryonic deformities. Nonylphenol<br />

has been shown to cause hatching failures in Australian native fish. Nonylphenol exposure may explain<br />

the malformation and hatching failure observed. Trichlorphon/dichlorvos are agrichemicals with<br />

neurological toxicities which may explain the swimming discoordination observed. A combination <strong>of</strong><br />

toxicities by nonylphenol and trichlorphon/dichlorvos may result in acute death <strong>of</strong> fish embryos and<br />

larvae.<br />

5. Definitive studies on the toxicity <strong>of</strong> nonylphenol and trichlorphon/dichlorvos are indicated to provide<br />

risk mitigation information in relation to agrichemical spray drift scenarios for fish hatchery operations.<br />

Summary Risk Assessment Statement<br />

Silver Perch Larval Malformation, Discoordination and Acute Death (SPMDAD) Syndrome can be<br />

explained by agrichemical spray drift contamination into a hatchery environment involving nonylphenol<br />

and trichlorphon/dichlorvos.<br />

The issue <strong>of</strong> uncertainty is with respect to the actual exposure scenarios and the exposure<br />

concentrations at which silver perch fish eggs, embryos and fish larvae would not experience SPMDAD.<br />

The recommendations <strong>of</strong> this report are :<br />

A. Spray drift protection measures in a hatchery environment should consider the following risk factors :<br />

o Opening <strong>of</strong> the door <strong>of</strong> the hatchery at night time even in the absence <strong>of</strong> spray activities at night. Day<br />

time spray residue may still be present in the air for an undeterimined period depending on wind<br />

and temperature conditions as well as agrichemical behaviour. Therefore the hatchery door should<br />

be closed with only very short periods <strong>of</strong> opening for ventilation and other activities.<br />

o All water storage tanks inside the hatchery can be contaminated if the concentration in the air <strong>of</strong><br />

agrichemical spray droplets is high enough. Therefore tank covers may mitigate the risk <strong>of</strong><br />

contamination in this situation.<br />

o Use and replenishment <strong>of</strong> activated charcoal filtration <strong>of</strong> water used in spawning tanks should be a<br />

standard preventative procedure as long as it is applied to treat water prior to exposure <strong>of</strong> fish eggs<br />

to potentially contaminated water.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 16 <strong>of</strong> 27


B. Nonylphenol, though not a pesticide, is an agrichemical commonly used in the delivery <strong>of</strong> pesticides. It<br />

appears to have a potentially wide range <strong>of</strong> toxicities in fish including endocrine disruption, growth<br />

retardation, oxidative stress stimulation, embryonic malformations and acute death. Although published<br />

toxicity endpoints for various effects suggest a high tolerable concentration ( tens <strong>of</strong> g to several mg/L),<br />

whether the combined toxic mechanisms <strong>of</strong> this agrichemical when expressed in susceptible species <strong>of</strong> fish<br />

could result in endpoint toxicities several orders <strong>of</strong> magnitude less than the individual toxicity endpoints<br />

needs to be thoroughly researched and investigated<br />

C. Until such time when specific risk mitigation information from (B) is available, from a fish health protection<br />

point <strong>of</strong> view, avoidance <strong>of</strong> any exposure to nonylphenol is recommended.<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 17 <strong>of</strong> 27


Supporting Documents<br />

Date Title<br />

Content pr<strong>of</strong>ile<br />

14.11.08 Biosecurity Sciences Laboratory (BSL)<br />

Test results on silver perch, golden perch and<br />

Supplementary pathology report 08‐178975 Australian bass samples<br />

31.10.08 Chemical residue report 6134 Test results on silver perch, golden perch<br />

samples<br />

14.11.08 BSL pathology report 08‐180386 Test results on chicken samples<br />

13.11.08 Chemical residue report 6147 Test results on chicken samples<br />

13.11.08 BSL pathology report 08‐180<strong>37</strong>1 Test results on horse samples<br />

13.11.08 Chemical residue report 6148 Test results on horse samples<br />

BSL pathology report 08‐179890 Test results on silver perch samples<br />

16.12.08 Queensland Health Forensic and Scientific Services<br />

(QHFSS) analytical report 08NA12582‐08NA12583 :<br />

XY<br />

Test results on water samples<br />

14.1.09 Chemical residue report 6198 Test results on water sample<br />

21.1.09 Chemical residue report 6200 Test results on silver perch sample<br />

18.2.09 QHFSS anaysis report 08PE328‐330:UT Test results on silver perch samples<br />

21.1.09 Chemical residue report 6201 Test results on silver perch samples<br />

14.1.09 Chemical residue report 6199 Test results on water sample<br />

20.3.09 BSL pathology report 08‐182660 Test results on silver perch samples<br />

5.2.09 BSL pathology report 08‐184972 Test results on silver perch samples<br />

21.1.09 Chemical residue report 6203 Test results on silver perch samples<br />

20.3.09 BSL pathology report 08‐184980 Test results on silver perch samples<br />

21.1.09 Chemical residue report 6202 Test results on silver perch samples<br />

20.3.09 BSL pathology report 08‐185511 Test results on silver perch samples<br />

27.1.09 Chemical residue report 6204 Test results on silver perch sample<br />

20.3.09 BSL pathology report 08‐185511 Test results on silver perch samples<br />

20.3.09 BSL pathology report 09‐103042 Test results on silver perch, water lily and<br />

sediment samples<br />

20.3.09 BSL pathology report 09‐103050 Test results on silver perch samples<br />

20.3.09 BSL pathology report 09‐103692 Test results on feed and mosquito fish<br />

samples<br />

20.3.09 BSL pathology report 09‐10<strong>37</strong>03 Test results on tadpole samples<br />

20.3.09 BSL pathology report 09‐103951 Test results on silver perch samples<br />

20.3.09 BSL pathology report 09‐103966 Test results on golden perch samples<br />

20.3.09 BSL pathology report 09‐103943 Test results on Australian bass samples<br />

15.12.08 Sunland Fish Hatchery – Farm Inspection and Results <strong>of</strong> farm inspection and record <strong>of</strong><br />

Sampling 9.12.08 <strong>Report</strong><br />

sampling<br />

6.12.08 Sunland Fish Hatchery <strong>Veterinary</strong> Investigation<br />

Work Instruction Version 4/4<br />

<strong>Veterinary</strong> investigation work strategy<br />

20.3.09 Chemical residue report 6252 Cyfluthrin repeat at LOR 1ppb 08‐184980<br />

20.3.09 Chemical residue report 6253 Cyfluthrin at LOR 1ppb 09‐103042<br />

20.3.09 Chemical residue report 6254 Test results on sediment samples<br />

20.3.09 Chemical residue report 6255 Test results on mosquito fish and feed<br />

sample<br />

20.3.09 Chemical residue report 6256 Test results on cane toad tadpoles<br />

8.10.09 Spray Record Transcripts Appendix 1,13,14,16,18 Macadamia farm pesticide spray information<br />

15.7.09 BSL Pathology <strong>Report</strong> 09‐119795<br />

Mullet pathology<br />

29.7.09 BSL Pathology <strong>Report</strong> 09‐120470<br />

5.3.2010 Queensland Health Scientific and Forensic Services<br />

Analytic <strong>Report</strong> Nos.<br />

Residue results on mullet samples<br />

22.10.09<br />

SSP0021779,21797‐10KE1258‐1264,1328‐1330<br />

(09‐120470)<br />

SSP0021781‐10KE1277‐1279 (09‐121094)<br />

Biosecurity Sciences Pathology <strong>Report</strong> 09‐126853 Bass fry pathology<br />

19.10.09 Queensland Health Scientific and Forensic Services<br />

Analytic <strong>Report</strong> No. 09KE6807‐09KE6809 : PW1<br />

Residue results on water samples – Bass fry<br />

1.12.09 Biosecurity Sciences Pathology <strong>Report</strong>s Golden perch pathology<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 18 <strong>of</strong> 27


14.12.09<br />

10.2.2010<br />

6.1.2010<br />

09‐132811<br />

09‐132792<br />

09‐132776<br />

09‐132803<br />

09‐132784<br />

09‐132761<br />

10‐102971<br />

Queensland Health Scientific and Forensic Services<br />

Analytic <strong>Report</strong> Nos.<br />

09KN228‐09KE8072:SC2<br />

09KE8064‐8701:SBC SSP20561<br />

SSP0020561‐09KE8072<br />

2009 Sunland Fish Hatchery Spray Drift Protection<br />

Program<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 19 <strong>of</strong> 27<br />

Residue results on water and filter paper<br />

samples<br />

Hatchery spray protection procedures<br />

4.3.2010 Biosecurity Sciences Pathology <strong>Report</strong>s<br />

Bass pathology<br />

10 ‐ 102963<br />

Queensland Health Scientific and Forensic Services<br />

Analytic <strong>Report</strong> Nos.<br />

Residue results on water samples<br />

17.2.1010 09KE8830‐8834,09KE8836:SBC SSP21044<br />

5.3.2010<br />

09KE8835‐SSP0021044<br />

3.2010 Biosecurity Sciences Pathology <strong>Report</strong><br />

Silver perch larvae pathology<br />

10‐103510<br />

4.3.2010 Chemical Residue <strong>Report</strong> 6662 Soil sample residue results<br />

5.3.2010 Queensland Health Scientific and Forensic Services<br />

Analytic <strong>Report</strong> Nos.<br />

Residue result on filter paper sample<br />

SSP0021044 – 09KE8835<br />

20.3.09 1 st <strong>Veterinary</strong> <strong>Report</strong> – Silver Perch Kill, Bass<br />

Deformity and Neurologic Syndromes 1st Edition<br />

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12.5.09 1 st <strong>Veterinary</strong> <strong>Report</strong> – Silver Perch Kill, Bass <strong>Veterinary</strong> investigation report – Peer<br />

Deformity and Neurologic Syndromes 2nd Edition Reviewed<br />

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Deformity and Neurologic Syndromes 3 rd <strong>Veterinary</strong> investigation report –<br />

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29.7.09 2 nd <strong>Veterinary</strong> <strong>Report</strong> – Mullet Defprmities<br />

Syndrome 1 st Edition<br />

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7.4.2010 2 nd <strong>Veterinary</strong> <strong>Report</strong> – Mullet Defprmities<br />

Syndrome 2 nd <strong>Veterinary</strong> investigation report –<br />

Edition<br />

incorporating residue results, environmental<br />

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23.10.09 3 rd <strong>Veterinary</strong> <strong>Report</strong> ‐ Bass Fry Kill Syndrome <strong>Veterinary</strong> investigation report<br />

11.2.2010 4 th <strong>Veterinary</strong> <strong>Report</strong> ‐ Golden Perch Loss<br />

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6.3.2010 5 th <strong>Veterinary</strong> <strong>Report</strong> ‐ Australian Bass Growth<br />

Retardation Syndrome<br />

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6.3.2010 6 th <strong>Veterinary</strong> <strong>Report</strong> ‐ Silver Perch Larval<br />

Malformation,Discoordination and Acute Death<br />

Syndrome<br />

<strong>Veterinary</strong> investigation report


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Acknowledgements<br />

Acknowledgement for this work is due to :<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 25 <strong>of</strong> 27


o My LORD and Redeemer Jesus Christ whose strength and counsel has guided the field, laboratory and<br />

reporting components <strong>of</strong> this veterinary investigation.<br />

Contributor<br />

And the fish in the Nile died, and the Nile stank, so that the Egyptians could not drink water<br />

from the Nile. There was blood throughout all the land <strong>of</strong> Egypt.<br />

Exodus 7:21<br />

Jesus said to them, “Children, do you have any fish?” They answered him, “No.” He said to<br />

them, “Cast the net on the right side <strong>of</strong> the boat, and you will find some.” So they cast it, and<br />

now they were not able to haul it in, because <strong>of</strong> the quantity <strong>of</strong> fish.<br />

John 21:5<br />

“And wherever the river goes, every living creature that swarms will live, and there will be<br />

very many fish. For this water goes there, that the waters <strong>of</strong> the sea may become fresh; so<br />

everything will live where the river goes.”<br />

Ezekiel 47:9<br />

Position Role<br />

Max Wingfield Fisheries Biologist and Extension Sampling and hatchery inspection<br />

Stephen Were Principal Chemist Chemical residue testing and results<br />

assessment<br />

Patrick Seydel Residue Analyst Chemical residue testing and results<br />

assessment<br />

Alan McMannus Biochemistry – laboratory technician AChE analyses and results assessment<br />

Mo Amigh<br />

Howard Prior<br />

Histotechnologist – senior technician<br />

Histotechnologist<br />

Histology processing<br />

Special stains<br />

Paul Duffy Bacteriology – senior technician Bacterial culture and isolation<br />

Annette Thomas Principal microbiologist Bacteriology and mycology<br />

Dr. Ian Anderson Principal Fish Pathologist Peer review – fish histopathology<br />

Dr. Rachel Bowater Senior <strong>Veterinary</strong> Officer – Fish Diseases Peer review – fish histopathology<br />

Richard Watts Chemical Use and Food Safety – A/Principal<br />

Scientific Advisor<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 26 <strong>of</strong> 27<br />

Pesticides risk assessment<br />

Peer review – AChE<br />

Peer review – 1 st Vet <strong>Report</strong><br />

Preparation <strong>of</strong> Spray Log Transcripts<br />

Ujang Tinggi QHFSS – Senior Scientist Trace Elements Metals residues analysis – fish<br />

Xiaohong Yang QHFSS ‐ Chemist Metals residues analysis – water<br />

David Waltisbuhl Manager – Biosecurity Sciences Laboratory Staff support and laboratory funding<br />

Belinda Fraser Laboratory Technician – Necropsy and<br />

Specimen Receipt<br />

Dr. Ian Douglas<br />

Dr. Munro Mortimer<br />

(Chair <strong>of</strong> SCC), Manager, Animal and Chemical<br />

Biosecurity Sciences, Biosecurity Queensland,<br />

Queensland <strong>Primary</strong> <strong>Industries</strong> & Fisheries,<br />

<strong>Department</strong> <strong>of</strong> Employment, Economic<br />

Development and Innovation.<br />

Senior Principal Scientist ‐ Investigations ,<br />

Fish sampling and necropsy kits<br />

Specimen receipt<br />

Peer review – 1 st Vet <strong>Report</strong><br />

Peer review – 1 st Vet <strong>Report</strong>


Troy Ziesemer<br />

Roger Arbuckle<br />

Gwen Gilson<br />

Bernie<br />

Freshwater and Marine Sciences Unit ,<br />

Division <strong>of</strong> Environmental Sciences ,<br />

Queensland <strong>Department</strong> <strong>of</strong> Environment and<br />

Resource Management.<br />

Macadamia Producers<br />

Sunland Fish Hatchery Australian Native Fish<br />

Producers<br />

<strong>Report</strong> to Noosa Fish Health Investigation Task Force<br />

<strong>7th</strong> <strong>Veterinary</strong> <strong>Report</strong><br />

Executive Summary <strong>of</strong> <strong>Veterinary</strong> Investigations<br />

Page 27 <strong>of</strong> 27<br />

Spray Log Information<br />

Hatchery records<br />

APVMA<br />

Australian Pesticides and <strong>Veterinary</strong><br />

Medicines Authority<br />

AgDRIFT Spray Modelling <strong>Report</strong><br />

Pat Pepper Senior Principal Scientist (Biometry) Animal<br />

Science<br />

Statistical analysis <strong>of</strong> fish data<br />

Dr. Renee<br />

<strong>Veterinary</strong> Officer Collection <strong>of</strong> soil samples from Sunland<br />

Thompson<br />

Hatchery to Biosecurity Sciences<br />

Laboratory. Investigation <strong>of</strong> horse,<br />

chicken and duck health problems on<br />

Sunland Hatchery.<br />

Dr. Mary Hodge<br />

Simon Christen<br />

Scott Turner<br />

Stewart Carswell<br />

Peter White<br />

Queensland Health and Forensic Services<br />

Residue analytical services.<br />

Ron Glanville Chief <strong>Veterinary</strong> Officer Prioritisation and authorisation <strong>of</strong> the<br />

veterinary investigation.<br />

Jim Thompson Director Biosecurity Science Prioritisation and authorisation <strong>of</strong> the<br />

veterinary investigation.<br />

Ian Douglas Manager Animal Biosecurity Laboratories Prioritisation and authorisation <strong>of</strong> the<br />

veterinary investigation.<br />

Vijay Mareedy (Fisheries Research Biologist), Bribie Island<br />

Research Centre<br />

Eliza Smith (Zoologist, veterinary student) , University <strong>of</strong><br />

Queensland<br />

Russel Scholl Principal Policy Officer, Plant Biosecurity and<br />

Product Integrity<br />

Technical support and assistance in the<br />

egg deformity counts and hatchery<br />

observations<br />

Technical assistance on the hatchery.<br />

For provision <strong>of</strong> macadamia spray log<br />

information on methoxyfenozide

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