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

Report to Noosa Fish Health Investigation Task Force 

7th Veterinary Report 

Executive Summary of Veterinary Investigations 

Prepared on 7 March 2010 by : 

Dr. Roger SM CHONG BVSc MACVSc 

Principal Veterinary Officer (Aquatic Animal Biosecurity) 

Biosecurity Queensland 

Department of Employment, Economic Development and Innovation 




Page 1 of 27

Contents 

Veterinary Investigations Executive Summary ………………………………………………………………………………………..3 

Silver Perch Kill, Bass Deformity and Neurologic Syndromes …………………………………………………………………..6 

Mullet Deformities Syndrome …………………………………………………………………………………………………………………9 

Bass Fry Kill Syndrome ……………………………………………………………………………………………………………………………10 

Golden Perch Loss Syndrome ………………………………………………………………………………………………………………….12 

Australian Bass Growth Retardation Syndrome ……………………………………………………………………………………..14 

Silver Perch Larval Malformation,Discoordination and Acute Death Syndrome ……………………………………..16 

Supporting Documents ………………………………………………………………………………………………………………………….18 

Literature ………………………………………………………………………………………………………………………………………………20 

Acknowledgements ……………………………………………………………………………………………………………………………….26 

Photos cover page : 

Upper 1 st row ‐left – Silver perch deaths associated with spraying activity. 

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

Upper 2 nd row left – Mullet embryo with three tails from Noosa broodfish. 

Upper 2 nd row right – Noosa mullet broodfish which produced deformed progeny. 

Lower 1 st row left – Fish pond and macadamia trees. 

Lower 1 st row right – Australian bass fingerlings with retarded growth. 

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

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

(Photos with are Copyright 2010 Gwen Gilson.) 





Veterinary Investigations Executive Summary 

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

and effects of agrichemicals and pesticides on fish health. It was a complex investigation which utilised the 

strengths of veterinary science with its multidisciplines of epidemiology, pathology, parasitology and toxicology. 

As a result, a clearer understanding of the fish health syndromes was achieved in the past year. The interplay of 

the risk factors involved with agrichemical use and the responses of a highly sensitive group of animals – fish, has 

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

and apply effective solutions. It will ensure that the health of the horticultural, aquacultural and ecological assets 

of the Noosa river catchment are sustainably protected into the future from inadvertant agrichemical 

contamination. 

Silver Perch Kill, Bass Deformity and Neurologic Syndromes 

Silver Perch Kill 

The epidemiological evidence was consistent with the silver perch being at high risk of acute exposure to very 

low sublethal but toxic doses of beta‐cyfluthrin pesticide. The pesticide, in combination with gill hyperplasia 

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

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

combined interplay of risk factors produced a major fish kill at the hatchery pond of silver perch. The fish were 

normal right up till the week of beta‐cyfluthrin spraying by the macadamia plantation. 

Australian Bass Deformity 

Pathology confirmed the two headed deformity in fish embryos reported and this appeared to indicate 

interferance with the control mechanisms of the embryonic cells. The implication would be reproductive failure 

of the bass population in the Noosa river as fewer young fish are produced or survive. Normal bass fry were 

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

as being the source of potential chemical toxins with mutagenic and genotoxic properties. 

Golden Perch Neurological Derangement 

A pathological lesion of spinal inflexion and fracture was consisitent with reports of partially atropine responsive 

treatment of spinning problems with fish larvae at Sunland Hatchery. This supports the real risk of exposure to 

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

the period associated with observation of spinning or convulsive symptoms in the fry particularly after water 

from ouside the hatchery building was used in spawning tanks. 

Mullet Deformities Syndrome (MDS) 

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

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

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

development of fertilised mullet eggs. Carbendazim and atrazine agrichemicals were detected in the catchment 

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

common link. 

Bass Fry Kill Syndrome 

Evidence of liver and red blood cell pathology in affected fish pointed to potential methoxifenozide 

contamination of algal feeds held in uncovered tanks outside from spray drift of macadamia operations leading 

to acute deaths of hatched Australian Bass. Fish that were not fed the algae on the days of agrichemical spraying 

did not experience similar mortalities. 

Golden Perch Loss Syndrome 

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

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

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

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

evidence of contamination from macadamia spray drift for carbendazim, nonylphenol and 

trichlorphon/dichlorvos. 

Australian Bass Growth Retardation Syndrome (ABGRS) 





ABGRS resulted in a statistically significant (P

Develop effective tools for sensitive monitoring of river ecosystems from the potential risks of 

agrichemical run‐off. 

Where agrichemicals are found to have unacceptable toxicity risks to the ecosystem under practical 

conditions of use, withdrawal from market is an option. 

Until clear outcomes are in progress, the Sunland Hatchery will continue to manage the agrichemical 

contamination risks experienced whch resulted in the last five years of fish health and production failures 

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

Hatchery Spray Drift Protection Program. This program entails ‐ 

a. Protection of all water sources within an enclosed structure. 

b. Protection of all fish and algae production units with screens or covers to minimise drift of 

pesticide and other agricultural chemicals. 

c. Use of an alternate site for the sustainable production of grow out sized fish. 

d. Use of an alternate site for the production of food items for larval fish eg. algal and 

zooplankton. 

This program has successfully resulted in the production of healthy and fecund Australian Bass, silver perch and 

golden perch fingerlings for sale in late 2009 and early 2010. However, this mode of biosecurity adds 

considerable costs to the production of fish for restocking groups and aquaculturists because of increased labour 

inputs to carting clean water from the Ringtail ponds, transportation of normal fish to Ringtail, decontamination 

procedures for utensils and equipment of the hatchery at Gilson road and increased monitoring of macadamia 

plantation spray activity. 

Prepared on 7 March 2010 by : 

Dr. Roger SM CHONG BVSc MACVSc 

Principal Veterinary Officer (Aquatic Animal Biosecurity) 

Biosecurity Queensland 

Department of Employment, Economic Development and Innovation 

Profitable Primary Industries for Queensland 





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 





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 Recommendations 

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

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

pesticide exposure and toxicity to aquatic species such as commercial fish because existing label 

regulations do not appear to safe guard against spray drift in certain situations of pesticide use 

identified in this report. Options for this research are presented in this report. 

2. The veterinary investigation recommends on‐going structured surveillance into the Australian Bass 

deformity syndrome based on pathological confirmation that a significant early embryonic disorder is 

present with the potential to impact bass recruitment and replenishment in the Noosa River 

Catchment. Options for surveillance research are presented in this report. 

3. The veterinary investigation recommends the development of a risk mitigation plan for the Sunland 

Fish Hatchery which is able to ensure sustainable production of valuable native Australian fish species. 

This plan should contain in its core requirement specific strategies to protect fish culture from 

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





Mullet Deformities Syndrome 

Mullet Deformities Syndrome (MDS) 

o Is a new and serious condition affecting the reproductive health of mullet fish in the Noosa River with a 

potential to alter the general mullet population recruitment rate. This is dependant on the prevalence 

of MDS in the mullet population. 

o Has significant similarites to the deformity syndrome described for Australian Bass from the Noosa 

River. 

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

for the deformities in Australian Bass fry of the Noosa River. The risk factor causes reproductive failure 

in both species. 

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

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

or decrease the risk of MDS in mullet. 

Case Definition – Mullet Deformities Syndrome (MDS) 

MDS is defined as a disorder of the reproductive health of Mugil cephalus currently detected in fish sourced from 

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

of fertilised mullet eggs from the stage of egg activation , through cell division, embryonic organogenesis and to 

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

resident fish. Clinical signs and pathologies are variously presented as deformites of cell development (eccentric 

cells, halos, tophats) and deformities of organogenesis (axial duplication and axial triplication, dwarfs and snake 

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

apparently fertilised eggs in the absence of visible deformities. The net result of MDS being a failure of effective 

reproduction from fish in normal spawning condition and in fish with no evidence of significant disease from 

viral, bacterial, fungal, parasitic or chlamydial pathogens. MDS appears to be independent of husbandry factors . 

The recommendations of this report are – 

A. Fish surveillance program to – 

o Monitor the impact of MDS to mullet and of two headed deformity to Australian Bass populations by 

comparing Noosa to non‐Noosa fish in fish breeding trials. 

o Surveillance of recruitment rates of mullet and bass in the Noosa river over a period of several years. 

B. Agrichemical exposure trials to ‐ 

o Understand the genotoxic and mutagenic effects of agrichemicals detected in the Noosa catchment to 

fish reproductive performance. 

o Assess the toxicity levels of carbendazim and atrazine to reproductive performance of Australian Bass 

and mullet in controlled experimental conditions. 





Bass Fry Kill Syndrome 

The incident of acute mortalities of Australian Bass at Sunland Hatchery was investigated and risk assessed with 

respect to spray activities at the adjacent macadamia plantation. The results of the investigation form the 3 rd 

Veterinary Report of the Noosa Fish Health Investigation Task Force. On the balance of the evidence at the 

epidemiological, pathological and toxicological levels, the risk of adverse effect in the bass fry points towards 

chemical toxicity with methoxifenozide based on : 

a. The pathology of the affected bass fry supports that of a toxicological process affecting both erythrocyte and 

hepatocellular functions. These changes have been reported for methoxyfenozide in animal species. 

b. There is temporal correlation between spray activity employing methoxyfenozide and urea potential for 

exposure to the chemicals via the route of ingestion of algae that was located outside the hatchery. 

c. Biotoxins from algal and bacterial sources have been assessed to be unlikely on the basis of clinical 

epidemiology. 

d. There is evidence of exposure to both chemicals reported used in macadamia spraying activities due to 

spray drift onto water storage locations on the hatchery. 

e. Available toxicological data for fish species does not indicate that the toxic concentration of 

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

ratio. 

f. The areas of uncertainty are : 

the concentrations of methoxyfenozide in affected fish 

the sensitivity of bass fry to methoxyfenozide 

mechanism of toxicity of methoxyfenozide in fish 

Elucidation of these issues on the basis of new research is likely to clarify the actual risk of 

methoxyfenozide for Australian Bass in such a localised setting. 

The recommendations of this report are : 

A. Structured monitoring of spray drift and fish health indices to evaluate actual risks of spray practices of the 

macadamia plantation on hatchery operations. 

This should involve the use of sentinel fish to measure the actual contamination level of chemicals that may be 

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

performed in the past and well as what is currently the routine. The monitoring should include collection of 

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

macadamia farm) for residue analyses of the specific chemicals used. This will provide more accurate data over 

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

results with wind speed and direction data as well as measurements of actual spray rates from the spray rigs are 

necessary for a robust assessment. 

This is necessary to understand the responses of native fish species of both larval, juvenile and adult life stages to 

the varied exposure scenarios. This information should include residue testing and histopathology with gross 

pathology as well as observations of clinical or sublethal behavioural changes. Information from this type of 

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

local species of fish. 





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

structured studies are conducted. These include : 

e. Protection of all water sources within an enclosed structure 

f. Protection of all fish and algae production units with screens or covers to minimise drift of 

pesticide and other agricultural chemicals 

g. Use of an alternate site for the sustainable production of grow out sized fish 

h. Use of an althernate site for the production of food items for larval fish eg. algal and 

zooplankton 

Refinement of the spray drift protection procedures currently adopted is needed to ensure that the 

additional costs of such measures are sustainable and appropropriate to the actual or defined spray drift 

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

required for the fish hatchery and macadamia plantation to co‐exist productively. 

C. An adverse reaction report should be compiled on the use of methoxyfenozide to the Australian Pesticides 

and Veterinary Authority for the purposes of : 

i. Conduct of a review of the active compound and label conditions 

ii. Conduct of research on the toxicity of methoxyfenozide to Australian Bass fry 

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

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

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

reaction report management strategy which specifically addresses the issues of information gaps for end‐ 

point toxicity limits for local conditions and local species of fish. 





Golden Perch Loss Syndrome 

The Golden Perch Loss Syndrome was a replication of historical reports of fish health problems at Sunland 

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

commencement to the end of the reported spray period. It thus provided a much more complete opportunity 

than previously possible to identify the primary cause of the fish health problem. 

1. The primary cause of the Golden Perch Fish Loss Syndrome is the parasitic activity of large numbers of a 

protozoan ectoparasite – Costia sp.(or Ichthyobodo sp.) mainly infesting the skin of the very small fry 

stocked into the Barra pond. Costia sp. can result in acute mortalities of more susceptible fry. However fry 

can be rendered more susceptible when other concurrent tissue pathology is present. The likely source of 

the parasite involved the use of water collected from a dam which has a connection to Cooloothin Creek. 

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

the gills, liver and erythrocytes of the fish. This cannot be explained by the presence of parasitic Costia sp.. 

These toxic responses can increase the susceptibility of the injured fish to pathogens including Costia sp. by 

increasing the stressor factors active on the fish. The pathological changes of gill hypertrophy, eosinophilic 

cytoplasmic change and vacuolation, liver changes of hepatocellular eosinophilic microgranule 

accummulation, vacuolation and mild degeneration as well as increased immature erythrocyte response to a 

probable haemolytic disorder are consistent with exposure to toxin because mechanisms of toxicity to 

produce these changes are within the scope of action of several chemical toxins detected. Research work is 

required to define the respective roles of these chemical toxins. 

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

samples from water storage locations on the Gilson Rd. hatchery. Dichlorvos was detected in the hatchery 

shed using air sampling filter paper. This constitutes clear evidence of contamination with pesticides and 

agrichemical pesticides. Of these, carbendazim and nonlylphenol containing products has been reportedly 

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

examined to assess the likelihood of these agrichemicals originating from the macadamia farm in terms of 

temporal relationships to spray activity in question and the onset‐duration of the fish loss syndrome. 

4. There is clear evidence of a range of toxic effects resulting in the fish where specific protection from 

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

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

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

of exposure despite meeting the published criteria for toxicity endpoint assessments. That is, though 

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

data indicated that the fish were not safe. Safe meaning the absence of toxicological injury or responses in 

the tissues of the fish. As none of published acute lethal or chronic toxic concentrations had been reached 

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

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

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

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

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

exposed to a higher concentration of chemical at the point should the spray drift droplets land on the 

surface of the water. The issue of increased risk to toxicity from mixture effects of pesticide exposure is 

possible because the existing toxicity endpoint references values are only based on individual chemical 

toxicities. These factors could potentially lead to an underestimation of the true exposure risk and toxicity 

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

an anomaly with the standard approach to toxicity end point assessment. 

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

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

as residues in conjunction with liver changes suggestive of vitellogenic production warrants additional 

investigation to confirm. Nevertheless the current evidence is consistent with this assessment. 

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

the tissues when these fish were specifically protected from macadamia spray activity and drift by way of 

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

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

by agri‐chemicals contaminating the Gilson Rd hatchery. 





Summary Risk Assessment Statement 

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

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

pathological effects in connection to contamination of the hatchery by agrichemicals including pesticides such as 

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

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

octylphenol and bisphenol A. 

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

relationship of the syndrome to the reported spraying activity at the adjacent macadamia plantation is clear 

evidence that spray activity and spray drift are the common factors resulting in contamination of the hatchery 

environment with agrichemicals including pesticides thus producing observable toxicological effects in 

unprotected fish. 


A. Provision of the spray record information to the veterinary investigation as it is vital to elucidate the exact 

sources of these agrichemicals with respect to macadamia farming activities. 

B. Review of the current standards for aquatic toxicity endpoint assessments with respect to delineation of 

actual field exposure scenarios, influence of chemical mixtures and toxicity endpoints for native Australian 

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

reliability of risk assessment standards. 

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

in fish fry of Australian native fish species including M.ambigua, under actual field conditions is required to 

elucidate the responses of fish to varying conditions of exposure. This is necessary to support the 

development of effective safe practices with respect to agrichemical spray drift risks. 





Australian Bass Growth Retardation Syndrome 

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

impacting the productivity of the Sunland Fish Hatchery. ABGRS is now a verifiable condition under the 

terms of reference of the Noosa Fish Health Investigation Task Force (NFHITF). 

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

spray application events by the adjacent macadamia plantation. The period of potential exposure in 

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

pond until the time of sampling and fish measurements. Evidence of contamination of the barra pond 

specifically and also the hatchery internal environment and other water storages at Sunland Hatchery 

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

macadamia plantation, the source of this agrichemical is likely to be the adjacent macadamia 

plantation unless, audited spray record information and environmental sampling and testing of the 

macadamia plantation show contrary evidence – ie absence of use and lack of detectable presence on 

soil, water or foliage of the plantation. 

3. ABGRS resulted in a statistically significant (P


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

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

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

road location. 

B. Published data on the toxicity of nonylphenol agrichemical is not currently available to native 

Australian fish species. This makes practical risk assessment currently unreliable and can result in 

occurences of adverse events such as ABGRS. As a priority, research into the toxicity threshold of 

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

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

trials with known dilutions to levels below current published toxicity endpoints would be useful to 

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

need to be more specific and sensitive, aimed at capturing mechanisms of toxicity at the cellular and 

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

C. Risk modelling of spray application scenarios that use the agrichemical nonylphenol as a surfactant or 

wetting agent based on actual operational situations of application is required to quantity more 

accurately the exposure concentrations to fish species. This should replace the current approach of 

grab water samples to estimate exposure, primarily to minimise error of underestimation of exposure 

concentration. 





Silver Perch Larval Malformation,Discoordination and Acute Death Syndrome 

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

fish health disorder within the scope of syndromes described by the Noosa Fish Health Investigation 

Task Force. Although there is insufficient pathological data to study the development of SPMDAD in 

detail, this epidemiological and toxicological assessment provided a necessary starting point. It is a 

significant fish health disorder within the context of agrichemical spray drift risk assessment and 

mitigation. 

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

charcoal filtration of spawning tank water improved the survival rate of affected fish larvae. SPMDAD 

causes severe morbidity and mortality of affected fish resulting in estimated rates of mortality in 

fertilised fish embryos of 99%, of malformation in embryos of 25% and of swimming discoordination in 

hatched fish larvae of 65%. 

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

the opening of the hatchery door in the evenings and through lack of covering over water storage 

tanks. This contributed to the contamination of the hatchery air environment and potentially water 

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

reported to be used recently by the macadamia plantation. However, the actual exposure 

concentration to the affected fish eggs and larvae are not known due to lack of water samples from the 

hatchery tanks. 

4. Nonylphenol has been shown to cause lethal and non‐lethal fish embryonic deformities. Nonylphenol 

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

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

neurological toxicities which may explain the swimming discoordination observed. A combination of 

toxicities by nonylphenol and trichlorphon/dichlorvos may result in acute death of fish embryos and 

larvae. 

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

risk mitigation information in relation to agrichemical spray drift scenarios for fish hatchery operations. 

Summary Risk Assessment Statement 

Silver Perch Larval Malformation, Discoordination and Acute Death (SPMDAD) Syndrome can be 

explained by agrichemical spray drift contamination into a hatchery environment involving nonylphenol 

and trichlorphon/dichlorvos. 

The issue of uncertainty is with respect to the actual exposure scenarios and the exposure 

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


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

o Opening of the door of the hatchery at night time even in the absence of spray activities at night. Day 

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

and temperature conditions as well as agrichemical behaviour. Therefore the hatchery door should 

be closed with only very short periods of opening for ventilation and other activities. 

o All water storage tanks inside the hatchery can be contaminated if the concentration in the air of 

agrichemical spray droplets is high enough. Therefore tank covers may mitigate the risk of 

contamination in this situation. 

o Use and replenishment of activated charcoal filtration of water used in spawning tanks should be a 

standard preventative procedure as long as it is applied to treat water prior to exposure of fish eggs 

to potentially contaminated water. 





B. Nonylphenol, though not a pesticide, is an agrichemical commonly used in the delivery of pesticides. It 

appears to have a potentially wide range of toxicities in fish including endocrine disruption, growth 

retardation, oxidative stress stimulation, embryonic malformations and acute death. Although published 

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

whether the combined toxic mechanisms of this agrichemical when expressed in susceptible species of fish 

could result in endpoint toxicities several orders of magnitude less than the individual toxicity endpoints 

needs to be thoroughly researched and investigated 

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

point of view, avoidance of any exposure to nonylphenol is recommended. 





Supporting Documents 

Date Title 

Content profile 

14.11.08 Biosecurity Sciences Laboratory (BSL) 

Test results on silver perch, golden perch and 

Supplementary pathology report 08‐178975 Australian bass samples 

31.10.08 Chemical residue report 6134 Test results on silver perch, golden perch 

samples 

14.11.08 BSL pathology report 08‐180386 Test results on chicken samples 

13.11.08 Chemical residue report 6147 Test results on chicken samples 

13.11.08 BSL pathology report 08‐180371 Test results on horse samples 

13.11.08 Chemical residue report 6148 Test results on horse samples 

BSL pathology report 08‐179890 Test results on silver perch samples 

16.12.08 Queensland Health Forensic and Scientific Services 

(QHFSS) analytical report 08NA12582‐08NA12583 : 

XY 

Test results on water samples 

14.1.09 Chemical residue report 6198 Test results on water sample 

21.1.09 Chemical residue report 6200 Test results on silver perch sample 

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

21.1.09 Chemical residue report 6201 Test results on silver perch samples 

14.1.09 Chemical residue report 6199 Test results on water sample 

20.3.09 BSL pathology report 08‐182660 Test results on silver perch samples 






27.1.09 Chemical residue report 6204 Test results on silver perch sample 


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

sediment samples 


20.3.09 BSL pathology report 09‐103692 Test results on feed and mosquito fish 

samples 

20.3.09 BSL pathology report 09‐103703 Test results on tadpole samples 


20.3.09 BSL pathology report 09‐103966 Test results on golden perch samples 

20.3.09 BSL pathology report 09‐103943 Test results on Australian bass samples 

15.12.08 Sunland Fish Hatchery – Farm Inspection and Results of farm inspection and record of 

Sampling 9.12.08 Report 

sampling 

6.12.08 Sunland Fish Hatchery Veterinary Investigation 

Work Instruction Version 4/4 

Veterinary investigation work strategy 

20.3.09 Chemical residue report 6252 Cyfluthrin repeat at LOR 1ppb 08‐184980 

20.3.09 Chemical residue report 6253 Cyfluthrin at LOR 1ppb 09‐103042 

20.3.09 Chemical residue report 6254 Test results on sediment samples 

20.3.09 Chemical residue report 6255 Test results on mosquito fish and feed 

sample 

20.3.09 Chemical residue report 6256 Test results on cane toad tadpoles 

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

15.7.09 BSL Pathology Report 09‐119795 

Mullet pathology 

29.7.09 BSL Pathology Report 09‐120470 

5.3.2010 Queensland Health Scientific and Forensic Services 

Analytic Report Nos. 

Residue results on mullet samples 

22.10.09 

SSP0021779,21797‐10KE1258‐1264,1328‐1330 

(09‐120470) 

SSP0021781‐10KE1277‐1279 (09‐121094) 

Biosecurity Sciences Pathology Report 09‐126853 Bass fry pathology 


Analytic Report No. 09KE6807‐09KE6809 : PW1 

Residue results on water samples – Bass fry 

1.12.09 Biosecurity Sciences Pathology Reports Golden perch pathology 





14.12.09 

10.2.2010 

6.1.2010 

09‐132811 

09‐132792 

09‐132776 

09‐132803 

09‐132784 

09‐132761 

10‐102971 

Queensland Health Scientific and Forensic Services 


09KN228‐09KE8072:SC2 

09KE8064‐8701:SBC SSP20561 

SSP0020561‐09KE8072 

2009 Sunland Fish Hatchery Spray Drift Protection 

Program 




Page 19 of 27 

Residue results on water and filter paper 

samples 

Hatchery spray protection procedures 

4.3.2010 Biosecurity Sciences Pathology Reports 

Bass pathology 

10 ‐ 102963 

Queensland Health Scientific and Forensic Services 


Residue results on water samples 

17.2.1010 09KE8830‐8834,09KE8836:SBC SSP21044 

5.3.2010 

09KE8835‐SSP0021044 

3.2010 Biosecurity Sciences Pathology Report 

Silver perch larvae pathology 

10‐103510 

4.3.2010 Chemical Residue Report 6662 Soil sample residue results 



Residue result on filter paper sample 

SSP0021044 – 09KE8835 

20.3.09 1 st Veterinary Report – Silver Perch Kill, Bass 

Deformity and Neurologic Syndromes 1st Edition 

Veterinary investigation report 

12.5.09 1 st Veterinary Report – Silver Perch Kill, Bass Veterinary investigation report – Peer 

Deformity and Neurologic Syndromes 2nd Edition Reviewed 

16.10.09 1 st Veterinary Report – Silver Perch Kill, Bass 

Deformity and Neurologic Syndromes 3 rd Veterinary investigation report – 

Edition incorporating spray drift model and spray log 

information 

29.7.09 2 nd Veterinary Report – Mullet Defprmities 

Syndrome 1 st Edition 


7.4.2010 2 nd Veterinary Report – Mullet Defprmities 

Syndrome 2 nd Veterinary investigation report – 

Edition 

incorporating residue results, environmental 

data and statistical analysis 

23.10.09 3 rd Veterinary Report ‐ Bass Fry Kill Syndrome Veterinary investigation report 

11.2.2010 4 th Veterinary Report ‐ Golden Perch Loss 

Syndrome 


6.3.2010 5 th Veterinary Report ‐ Australian Bass Growth 

Retardation Syndrome 


6.3.2010 6 th Veterinary Report ‐ Silver Perch Larval 

Malformation,Discoordination and Acute Death 

Syndrome 

Veterinary investigation report

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Acknowledgements 

Acknowledgement for this work is due to : 





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

reporting components of this veterinary investigation. 

Contributor 

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

from the Nile. There was blood throughout all the land of Egypt. 

Exodus 7:21 

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

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

now they were not able to haul it in, because of the quantity of fish. 

John 21:5 

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

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

everything will live where the river goes.” 

Ezekiel 47:9 

Position Role 

Max Wingfield Fisheries Biologist and Extension Sampling and hatchery inspection 

Stephen Were Principal Chemist Chemical residue testing and results 

assessment 

Patrick Seydel Residue Analyst Chemical residue testing and results 

assessment 

Alan McMannus Biochemistry – laboratory technician AChE analyses and results assessment 

Mo Amigh 

Howard Prior 

Histotechnologist – senior technician 

Histotechnologist 

Histology processing 

Special stains 

Paul Duffy Bacteriology – senior technician Bacterial culture and isolation 

Annette Thomas Principal microbiologist Bacteriology and mycology 

Dr. Ian Anderson Principal Fish Pathologist Peer review – fish histopathology 

Dr. Rachel Bowater Senior Veterinary Officer – Fish Diseases Peer review – fish histopathology 

Richard Watts Chemical Use and Food Safety – A/Principal 

Scientific Advisor 





Pesticides risk assessment 

Peer review – AChE 

Peer review – 1 st Vet Report 

Preparation of Spray Log Transcripts 

Ujang Tinggi QHFSS – Senior Scientist Trace Elements Metals residues analysis – fish 

Xiaohong Yang QHFSS ‐ Chemist Metals residues analysis – water 

David Waltisbuhl Manager – Biosecurity Sciences Laboratory Staff support and laboratory funding 

Belinda Fraser Laboratory Technician – Necropsy and 

Specimen Receipt 

Dr. Ian Douglas 

Dr. Munro Mortimer 

(Chair of SCC), Manager, Animal and Chemical 

Biosecurity Sciences, Biosecurity Queensland, 

Queensland Primary Industries & Fisheries, 

Department of Employment, Economic 

Development and Innovation. 

Senior Principal Scientist ‐ Investigations , 

Fish sampling and necropsy kits 

Specimen receipt 

Peer review – 1 st Vet Report 

Peer review – 1 st Vet Report

Troy Ziesemer 

Roger Arbuckle 

Gwen Gilson 

Bernie 

Freshwater and Marine Sciences Unit , 

Division of Environmental Sciences , 

Queensland Department of Environment and 

Resource Management. 

Macadamia Producers 

Sunland Fish Hatchery Australian Native Fish 

Producers 





Spray Log Information 

Hatchery records 

APVMA 

Australian Pesticides and Veterinary 

Medicines Authority 

AgDRIFT Spray Modelling Report 

Pat Pepper Senior Principal Scientist (Biometry) Animal 

Science 

Statistical analysis of fish data 

Dr. Renee 

Veterinary Officer Collection of soil samples from Sunland 

Thompson 

Hatchery to Biosecurity Sciences 

Laboratory. Investigation of horse, 

chicken and duck health problems on 

Sunland Hatchery. 

Dr. Mary Hodge 

Simon Christen 

Scott Turner 

Stewart Carswell 

Peter White 

Queensland Health and Forensic Services 

Residue analytical services. 

Ron Glanville Chief Veterinary Officer Prioritisation and authorisation of the 

veterinary investigation. 

Jim Thompson Director Biosecurity Science Prioritisation and authorisation of the 


Ian Douglas Manager Animal Biosecurity Laboratories Prioritisation and authorisation of the 


Vijay Mareedy (Fisheries Research Biologist), Bribie Island 

Research Centre 

Eliza Smith (Zoologist, veterinary student) , University of 

Queensland 

Russel Scholl Principal Policy Officer, Plant Biosecurity and 

Product Integrity 

Technical support and assistance in the 

egg deformity counts and hatchery 

observations 

Technical assistance on the hatchery. 

For provision of macadamia spray log 

information on methoxyfenozide

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

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