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

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.
Report to Noosa Fish Health Investigation Task Force
7th Veterinary Report
Executive Summary of Veterinary Investigations
Page 12 of 27