Volume 40, no. 2, June 2013 - Biosecurity New Zealand

MINISTRY FOR PRIMARY INDUSTRIES REPORTING ON NEW ZEALAND’S BIOSECURITY HEALTH STATUS 

surveillance 

Volume 40, no.2, June 2013 

INSIDE: 

Southward extension of the Asian tiger mosquito 

Mycoplasma in a Fiordland crested penguin 

Ostreid herpesvirus type 1 in Pacific oysters 

Quarterly review of diagnostic cases: January to March 2013 

Quarterly report of investigations of suspected exotic diseases 

Plants and environment investigation report 

Quarterly report of investigations of suspected exotic marine and 

freshwater pests and diseases

2 

Surveillance 

ISSN 1176-5305 

Surveillance is published on behalf of the 

Director IDC and Response (Veronica Herrera). 

The articles in this quarterly report do not 

necessarily reflect government policy. 

Editor: Michael Bradstock 

Technical Editors: Jonathan Watts, Lora 

Peacock 

Correspondence and requests to receive 

Surveillance should be addressed to: 

Editor 

Surveillance 

Ministry for Primary Industries 

PO Box 2526 

Wellington, New Zealand 

email: surveillance@mpi.govt.nz 

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veterinary continuing education publications, 

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Photo credit (mussel farm photo): 

Aquaculture New Zealand 

SURVEILLANCE 40 (2) 2013 

Contents 

Editorial 

MPI one year down the track 3 

ANIMALS 

Reports 

First isolation in New Zealand of Mycoplasma lipofaciens, from 

the lung of a Fiordland crested penguin/tawaki with pneumonia 5 

Quarterly reports: October to December 2013 

Quarterly review of diagnostic cases: January to March 2013 8 

Quarterly report of investigations of suspected exotic diseases 14 

MARINE AND FRESHWATER 

Reports 

Investigation into the first diagnosis of ostreid herpesvirus 

type 1 in Pacific oysters 20 

Juvenile oyster mortality response: a laboratory perspective 25 

Quarterly reports: January to March 2013 

Quarterly report of investigations of suspected exotic marine and 

freshwater pests and diseases 28 

PLANTS AND ENVIRONMENT 

Reports 

Southward extension of the Asian tiger mosquito Aedes albopictus: 

is New Zealand at risk? 32 

Quarterly reports: January to March 2013 

Plants and environment investigation report 35 

PEST WATCH: 9 February – 15 May 2013 37 

Surveillance is published as the Ministry for Primary Industries’ authoritative source of information on 

the ongoing biosecurity surveillance activity and the health status of New Zealand’s animal and plant 

populations in both terrestrial and aquatic environments. It reports information of interest both locally and 

internationally and complements New Zealand’s international reporting.

EDITORIAL 

MPI one year down the track 

The new Ministry for Primary Industries (MPI) came 

into existence on 30 April 2012 and this month’s issue 

of Surveillance seems an appropriate time to reflect on 

that first year and some of the key developments in 

surveillance, preparedness and response during that 

first year. 

Much work has been underway setting the new 

Ministry’s strategic direction – growing and protecting 

New Zealand. Much of the work of my Directorate 

is focused on supporting the protective aspects of 

MPI’s strategy, with the surveillance, investigative and 

diagnostic and response functions of biosecurity 

in my sights. 

Looking first at what made the headlines, it’s hard to 

overlook the events of May last year when our response 

processes were well and truly tested with the discovery of 

a single male Queensland fruit fly in a surveillance trap 

in Auckland. 

A huge response operation swung into gear. A response 

team stood up and operations supplier AsureQuality 

and MPI’s laboratory teams set in place an enhanced 

network of traps and a programme of fruit sampling to 

see whether there were any more fruit flies out there. As 

a precautionary measure, an area within a 1.5 km radius 

from the site of the fly find was delineated as a controlled 

area and residents were asked not to move fresh fruit or 

vegetables outside of this zone. This meant that if any fruit 

fly populations were there, the controls in place would 

prevent any spread out of the area. 

It was a relief to everyone that no more flies were found 

and there was no evidence of a breeding population. 

As a result of this response MPI is satisfied that the 

existing operational plan for dealing with a fruit fly 

incursion is robust; the surveillance trapping system is 

adequate and the timing of trapping appropriate; and 

the biosecurity response structure is ready and able to 

manage a response on this scale. 

Another big news item was the release of an audit 

of MPI’s preparedness and response systems by the 

Office of the Auditor-General in March this year. The 

report, while identifying areas requiring improvement, 

also acknowledged that MPI and its predecessor 

organisations responsible for biosecurity have been, by 

and large, successful at responding to incursions, dealing 

with between 30 and 40 cases a year. The audit also 

acknowledged that MPI has developed generally hightrust 

relationships with partners. 

MPI has fully accepted the audit’s recommendations 

and made significant progress in areas such as the 

implementation of regular simulations and exercises, 

review of our capability network project with 

AsureQuality and review of response plans for 

high-risk organisms. 

Enhancing New Zealand’s ability to manage outbreaks of 

significant animal disease, in particular foot and mouth 

disease (FMD), is a high priority for the Ministry. It’s well 

understood that our prosperity is highly dependant on 

our current FMD-free status and our ability to manage an 

outbreak of FMD should it ever arrive here. 

Over the years, New Zealand’s government agriculture 

and biosecurity agencies (MPI and its predecessors) have 

invested significant time and resources into preparing for 

an FMD outbreak and MPI has a well developed level of 

response readiness. We recognise, however, that being 

ready to respond to disease outbreaks requires continuous 

effort and MPI is making timely and significant 

improvements through a new work programme. This 

will mean a change to the way MPI prepares for largescale 

events, in particular an FMD outbreak, with 

more emphasis on an integrated nationwide focus, 

and requiring a whole-of-government approach. The 

work will demand significant strategic planning in cooperation 

with New Zealand’s livestock industries, other 

government agencies and local government. 

A key component of preparation for a major disease 

outbreak is researching possible scenarios and conducting 

exercises, both here and overseas. Such collaboration 

is vital to ensure our preparation is in line with 

internationally recognised best practice. Earlier this 

month I visited the UK with Deputy Director-General 

Andrew Coleman and Manager of Surveillance and 

Incursion Investigation (Animals and Marine), Paul 

Bingham, to participate in a disease outbreak simulation 

that gave us first-hand experience of how our British 

counterparts manage disease outbreaks. While this 

particular simulation was about classical swine fever, the 

general principles are the same for any outbreak. We were 

especially interested in the focus on the traceability of 

animals, management of stock and disposal of carcasses. 

SURVEILLANCE 40 (2) 2013 3

We are also focusing our effort closer to home, with a 

recently announced trans-Tasman action plan that will 

see defences against the threat of FMD strengthened 

in New Zealand and Australia. Two members of MPI’s 

animal response team recently visited Australia to 

work with officials at the Department of Agriculture, 

Fisheries and Forestry on the groundwork for this plan. 

Additionally, in late June an exercise at Wallaceville will 

see us working closely with animal industries on the 

simulated first day of an FMD outbreak. 

In the last few months a project to replace the high-level 

biocontainment laboratory at Wallaceville has started. 

We’re now working to put an initial business case for the 

new laboratory to the government for consideration at 

the end of this year. The present facility, built in 1999, 

has become too small and is nearing the end of its design 

life. The laboratory conducts diagnostic testing of cases 

of suspect exotic animal diseases such as avian influenza 

and anthrax. It is also used by Environmental Science and 

Research for diagnosing high-risk human diseases such as 

pandemic influenza, polio and SARS. The new laboratory 

will ensure we can continue this essential work and keep 

pace with changing international regulations. 

Finally, the past year has seen much progress with 

the Government Industry Agreement on Biosecurity 

Readiness and Response (GIA). Under the GIA, primary 

industries will have the opportunity to become partners, 

co-investors and joint decision makers in managing and 

preparing for biosecurity risks of most concern to them. 

The process has been formalised this month with the 

release of the enabling GIA Deed, written and prepared 

by industry and government members of a joint working 

group that was established at the request of industry. 

The updated Deed responds to all feedback received on 

an earlier draft from industry and government. Once 

approved by Cabinet, it will be available for signing by 

industry organisations that have successfully obtained 

mandate from their sectors. 

The GIA represents a significant milestone in the 

development of a partnership approach to biosecurity that 

has been many years in the making. Working together, 

4 SURVEILLANCE 40 (2) 2013 

government and industry can and will do more to reduce 

and manage biosecurity risks to our businesses, and to 

our country, than either of us can do separately. 

Veronica Herrera 

Director, Investigation and Diagnostic Centres and Response

ANIMALS 

FIRST ISOLATION IN NEW ZEALAND OF MYCOPLASMA 

LIPOFACIENS, FROM THE LUNG OF A FIORDLAND 

CRESTED PENGUIN/TAWAKI WITH PNEUMONIA 

Case report 

The Fiordland crested penguin is an endemic species that 

typically lives in isolated areas from south Westland to 

Stewart Island. An adult male was found on a Wellington 

beach in poor condition with a healed eye injury and 

lens opacity (cataract). The penguin received eye surgery, 

recovered, and was kept at a rehabilitation centre but died 

suddenly following moult. A post-mortem examination at 

Massey University’s Wildbase Pathology Service found the 

cause of death was severe bronchopneumonia affecting 

both lungs. Microscopically the lungs had subacute 

lymphoplasmacytic and heterophilic bronchopneumonia, 

and filamentous bacteria were present within sites of 

inflammation. Identification of the filamentous organisms 

is pending, as they are not consistent with a Mycoplasma 

species and are likely to have been a co-infecting agent. 

Pneumonia is unusual in penguins, so the notifying 

pathologist sent a frozen sample of lung to the MPI 

Animal Health Laboratory for culture to rule out 

Mycoplasma, a known bacterial cause of pneumonia in 

birds. The laboratory identified M. lipofaciens from the 

lung sample using selective enrichment in Friis broth 

followed by PCR and sequencing of isolated Mycoplasma 

colonies. M. lipofaciens has not been previously reported 

in New Zealand, but this case most likely represents a 

baseline surveillance find rather than a new incursion, 

especially as no reports could be found of previous 

Mycoplasma cultures from New Zealand penguins. It is 

not known whether M. lipofaciens is capable of causing 

the pneumonia seen in this case, but the presence of 

filamentous bacteria indicates that a co-infection was 

probably present. 

Organism background 

Mycoplasma spp. are common bacteria of birds, with more 

than 20 named species isolated from avian hosts (Kleven, 

2008). M. gallisepticum and M. synoviae are considered 

to be the most pathogenic and important in birds, with 

a few more (e.g., M. meleagridis, M. iowae) considered 

to be pathogenic in certain bird species and many others 

considered to be non-pathogenic commensals (i.e., 

normal flora). Pathogenic species can cause a range of 

diseases including pneumonia, sinusitis, conjunctivitis 

and arthritis/synovitis. 

M. lipofaciens is a relatively little-known member of 

the Mycoplasma genus. It is thought to be uncommon 

In April 2013 Mycoplasma lipofaciens was isolated for 

the first time from the lung of a wild adult male Fiordland 

crested penguin (Eudyptes pachyrhynchus) with a severe 

bronchopneumonia. The penguin had been found in 

poor condition on a Wellington beach and died during 

rehabilitation. A veterinary pathologist from Wildbase 

Pathology at Massey University identified unusual lung 

lesions and notified the Ministry for Primary Industries 

(MPI). Mycoplasmas are commonly found in birds and 

mammals, and pathogenic species can cause pneumonia, 

conjunctivitis and arthritis/synovitis. M. lipofaciens 

has been isolated from healthy poultry worldwide, and 

from an infertile raptor egg, but has not previously been 

reported in New Zealand. This is also the first reported 

culture of a Mycoplasma species from an endemic 

New Zealand penguin, and represents an important 

baseline surveillance find. Further investigation may 

clarify whether M. lipofaciens is a primary pathogen 

of Fiordland crested penguins capable of causing the 

pneumonia seen in this case. 

and usually non-pathogenic in birds, acting either as 

a commensal or a pathogenic organism under specific 

conditions. Isolation was first reported in 1983 (Bradbury 

et al., 1983) from the sinus of a healthy chicken in the 

United Kingdom. Sampling of European (Benčina, 

1987) and Mexican (Priante et al., 2011) poultry isolated 

M. lipofaciens from the upper respiratory tract of 

healthy chickens. An isolate from an infertile northern 

goshawk (Accipiter gentilis) egg found in Europe was 

shown to cause mortality and disease in embryos and 

hatchlings when injected into the eggs of chickens (Lierz 

et al., 2007a, 2007c) and turkeys (Lierz et al., 2007b). 

Horizontal transmission of infection between infected 

and non-infected turkey poults was observed in these 

trials. The veterinarian in charge of the infected birds 

also developed a mild self-limiting upper respiratory 

infection (Lierz et al., 2008). However, it should be noted 

that M. lipofaciens has not been associated with disease in 

adult poultry. 

Pathology of Mycoplasma in the 

respiratory system 

The pathogenicity of Mycoplasma species lies in their 

ability to colonise the respiratory epithelium. Normal 

respiratory epithelial cells have cilia that are covered by 


5

a thin layer of mucus. The mucus layer traps inhaled 

particles such as dust and bacteria. Rhythmic beating of 

the cilia moves the mucus layer upward and out of the 

system, along with the trapped debris. When Mycoplasma 

organisms colonise respiratory epithelium they can reduce 

ciliary function and thus inhibit the expulsion of inhaled 

microbes. In this changed micro-environment some 

bacteria can penetrate more deeply into the lung, setting 

up infection. The net result is that, although Mycoplasma 

predisposes to pneumonia, there are often other bacterial 

species involved. 

Mycoplasmosis of wild birds 

Mycoplasma infection has been recognised as an 

important disease of wild birds since 1994, when an 

outbreak of conjunctivitis caused by M. gallisepticum 

spread across the house finch (Haemorhous mexicanus) 

population of North America (Luttrell, 2001). This 

outbreak was possibly due to initial spread from poultry, 

though the picture is unclear since other Mycoplasma spp. 

were found in similar conjunctivitis lesions where they 

did not always cause disease (Ley, 2010). 

Very little is known about mycoplasmas of penguins, 

although several species have recently been isolated 

from healthy Antarctic penguins (Banks et al., 2009; 

Dewar et al., 2013). To our knowledge this is the 

first reported isolation of a Mycoplasma sp. from a 

New Zealand penguin. 

Avian mycoplasmas present in 

New Zealand 

Pathogenic avian Mycoplasma spp. known from 

New Zealand include M. gallisepticum (chickens, turkeys), 

M. synoviae (chickens, turkeys) and M. meleagridis 

(turkeys only). They are important pathogens in the 

poultry industry. To our knowledge no wide-scale culture 

survey of commensal mycoplasmas has been carried out 

for New Zealand poultry. 

Conclusion 

We have little knowledge about common commensal 

and pathogenic bacteria of our native wildlife. A broader 

understanding of the roles that bacteria, including 

Mycoplasma, play in the health of our native wildlife can 

have positive outcomes for both wildlife management and 

biosecurity awareness in the poultry sector. The present 

6 


case represents an important baseline surveillance find. 

Further work may clarify whether M. lipofaciens is a 

primary pathogen of Fiordland crested penguins. 

ACKNOWLEDGEMENTS 

We would like to thank Massey University’s Wildbase 

veterinary hospital, Department of Conservation 

personnel in Wellington and the Otago Peninsula, and 

Penguin Place Conservation Reserve for their work on 

this case. 

REFERENCES 

Banks JC, Cary SC, Hogg ID (2009) The phylogeography of Adelie penguin 

faecal flora. Environmental microbiology 11(3): 577–588. 

Benčina D, Dorrer D, Tadina T (1987) Mycoplasma species isolated from six 

avian species. Avian Pathology 16(4): 653–664. 

Bradbury JM, Forrest M, Williams A (1983) Mycoplasma lipofaciens, 

a new species of avian origin. International Journal of Systematic 

Bacteriology 33(2): 329–335. 

Dewar ML, Arnould JP, Dann P, Trathan P, Groscolas R, Smith, S (2013) 

Interspecific variations in the gastrointestinal microbiota in penguins. 

MicrobiologyOpen 2(1): 195–204. 

Kleven SH (2008) Control of avian mycoplasma infections in commercial 

poultry. Avian diseases 52(3): 367–374. 

Ley DH, Anderson N, Dhondt KV, Dhondt AA (2010) Mycoplasma sturni 

from a California house finch with conjunctivitis did not cause disease in 

experimentally infected house finches. Journal of Wildlife Diseases 46(3): 

994–999. 

Lierz M, Stark R, Brokat S, Hafez HM (2007a) Pathogenicity of Mycoplasma 

lipofaciens strain ML64, isolated from an egg of a Northern Goshawk 

(Accipiter gentilis), for chicken embryos. Avian Pathology 36(2): 151–153. 

Lierz M, Deppenmeier S, Gruber AD, Brokat S, Hafez HM (2007b) 

Pathogenicity of Mycoplasma lipofaciens strain ML64 for turkey embryos. 

Avian Pathology 36(5): 389–393. 

Lierz M, Hagen N, Harcourt-Brown N, Hernandez-Divers SJ, Luschow D, 

Hafez HM (2007c) Prevalence of mycoplasmas in eggs from birds of prey 

using culture and a genus-specific mycoplasma polymerase chain reaction. 

Avian Pathology 36(2): 145–150. 

Lierz M, Jansen A, Hafez HM (2008) Avian Mycoplasma lipofaciens 

transmission to veterinarian. Emerging Infectious Diseases 14(7): 1161. 

Luttrell MP, Stallknecht DE, Kleven SH, Kavanaugh DM, Corn JL, Fischer JR 

(2001) Mycoplasma gallisepticum in house finches (Carpodacus mexicanus) 

and other wild birds associated with poultry production facilities. Avian 

Diseases 45(2): 321–329. 

Priante ES, Flores CL, Muniz AO (2011) First isolation and identification 

of Ureaplasma spp. and Mycoplasma lipofaciens in commercial hens in 

Mexico. Revista Mexicana de Ciencias Pecuarias 2(1): 85-92.

Kelly Buckle 

Incursion Investigator (Animals & Marine) 

Surveillance and Incursion Investigation 


Kelly.Buckle@mpi.govt.nz 

Jenny Draper 

Senior Scientist (Bacteriology & Aquatic Animal Diseases) 

Animal Health Laboratory 


Jenny.Draper@mpi.govt.nz 

Sharon Humphrey 

Scientist (Bacteriology & Aquatic Animal Diseases) 

Animal Health Laboratory 


Sharon.Humphrey@mpi.govt.nz 

Stuart Hunter 

Wildlife Pathologist 

Wildbase 

IVABS, Massey University 

S.hunter@massey.ac.nz 


QUARTERLY REPORT OF DIAGNOSTIC CASES: JANUARY TO 

MARCH 2013 

Gribbles Veterinary Pathology 

CATTLE 

Three milking cows were affected by yarr or spurrey 

(Spergula arvensis) toxicity on an Otago dairy farm. 

One cow died shortly after milking, another went down 

in the shed but responded to intravenous calcium, and a 

third was found down in the paddock after milking. This 

cow also eventually responded to intravenous calcium 

therapy. The calcium concentration in the eye fluid of 

the dead cow was 0.74 mmol/L (normal level >1.0) and 

pre-treatment serum calcium from one of the live affected 

cows was 1.16 mmol/L (normal range 2.0–2.27). Later 

questioning of the farmer revealed that the farm was 

heavily infested with yarr, a pasture weed that has been 

identified as inducing hypocalcaemia in dairy cows on a 

number of occasions. 

A mob of 150 well-grown five-month-old dairy calves 

had been pastured at a Southland grazier’s farm since 

weaning. In early February the grazier found two dead 

and a number coughing and off-colour with elevated 

rectal temperatures and nasal discharge. Necropsy of 

the most recently dead calf showed consolidation of the 

cranial areas of both lungs. The veterinarian noted at the 

time that the calves looked as though they had recently 

lost weight. Histopathological examination of a section 

of lung showed a severe oedema and bronchopneumonia 

most likely consistent with an acute Histophilus somni 

infection. Lung cultures unfortunately were not able to 

confirm this diagnosis as they were overgrown with postmortem 

invaders. The most likely stressor that initiated 

this outbreak was poor nutrition. These calves had been 

short of feed because they were pastured on a paddock 

of new grass that had not germinated very well. The 

outbreak started shortly after they were shifted to a lush 

clover-rich pasture. Mass treatment of all calves in the 

mob eventually brought the outbreak under control, but 

over its course 30 calves were found to be sick and nine of 

these died. 

There was a sudden onset of nervous signs in seven out of 

16 non-lactating cows on a Southland dairy farm in early 

March. They were in a small paddock with mainly dried 

grass. Affected cows were ataxic and hyperaesthetic but 

still alert. Several became recumbent but failed to respond 

to metabolic treatments. All but one eventually recovered 

after being shifted to another paddock. Other cows in 

other paddocks on the same farm were unaffected. This 

8 


was most likely a small outbreak of ryegrass staggers 

caused by exposure to the endophyte mycotoxin, 

lolitrem B. This is a rare finding in Southland but the 

summer had been very dry this year. 

Skin lesions from the feet of four cows in Taranaki were 

sent for histology. All four animals had infiltrates of 

inflammatory cells in the superficial layers of the stratum 

spinosum and lower stratum corneum. There were 

infiltrates of filamentous bacteria staining positively with 

silver stains. This was consistent with bovine digital 

dermatitis. 

Half of a mob of 60 Jersey heifers on a Taranaki property 

were noticed to have raised 1–2-mm lesions on the vulva 

and vagina around the clitoris while being checked for 

pregnancy. Biopsy of an affected heifer found the lesions 

were dense focal infiltrates of mostly lymphocytes, mixed 

with a few plasma cells and macrophages. It was felt that 

the lesions were healed and were probably formed in 

response to a case of infectious pustular vulvovaginitis 

virus infection. 

Three beef weaner cattle from Hastings died suddenly in 

a mob of 100. Three others were visibly lame and unwell. 

Post-mortem examination found blackened gassy skeletal 

muscle in the shoulder region of the dead animals. 

Culture of the muscle isolated Clostridium septicum, 

consistent with a diagnosis of malignant oedema. 

Samples were collected from a single 18-month-old 

Wagyu cross steer that was wandering aimlessly. When 

closely examined the steer had nystagmus, appeared blind 

with peripheral opacity in one eye, was pyrexic (rectal 

temperature 40.5 o C) and had diffuse muscle tension. 

Ovine herpes virus-2 was detected by PCR, confirming a 

diagnosis of malignant catarrhal fever. 

Ten calves from a herd of 80 five-month old Northland 

dairy cattle died suddenly over a period of one week. 

Tissues from a dead calf were submitted for 

histopathology, which revealed skeletal muscle oedema 

and emphysema, interstitial neutrophilic myositis, 

fibrinosuppurative pleuropneumonia and neutrophilic 

epicarditis, consistent with blackleg. Germination of 

dormant Clostridium chauvoei spores results in local 

tissue damage and toxaemia. This is thought to take place 

in the anaerobic environment of traumatised muscle, 

but the pathogenesis of cardiac and pleural lesions is 

uncertain.

Fifteen 2-year-old steers from a Northland sheep and 

beef farm were not doing as well as others. Serum 

concentrations of vitamin B12, copper, selenium and 

gamma-glutamyl transferase (GGT) were assessed, and a 

pooled serum sample was tested for liver fluke exposure 

by ELISA. The mean serum copper concentration was 

7.6 umol/L (reference range 7.5–20), but seven out of the 

15 calves were below the reference interval, resulting in a 

diagnosis of copper deficiency. Serum GGT, vitamin B12 

and selenium were within normal ranges, and the pooled 

liver fluke ELISA was negative. 

SHEEP 

One lamb in a mob of 490 stud ram lambs on a North 

Canterbury farm had developed extensive dorsal 

crusting and thickening of the skin from the neck to 

the rump. Histologically, the skin had infection with 

Dermatophilus congolensis. 

Two animals were found dead in a mob of 500 six-monthold 

lambs on Banks Peninsula. Another was recumbent 

and died soon afterwards. The lambs were grazing Pasja, 

a high-yielding brassica forage crop. The brain sample 

showed lesions of protein-rich perivascular oedema, 

typical of the lesions produced by the epsilon toxin of 

Clostridium perfringens type D (enterotoxaemia). 

Lightning strike killed 30 out of 180 Merino ewes in a 

large paddock on a Central Otago sheep farm in early 

January. The dead ewes were all found within an area 

25 metres in diameter. Other ewes in the paddock were 

unaffected. The ewes had been dead for two days before 

they were discovered, so there were significant postmortem 

changes. Two days before they were found, 

there had been a violent night-time electrical storm 

over this area. 

Six-month-old Romney cross lambs being fed grain in 

a feedlot in the Rangitikei were dying because of renal 

failure associated with urethral obstruction by calculi. 

Analysis of the calculi found they were smooth bladder 

stones composed of 60 percent calcium oxalate and 

5 percent phosphate. 

A mob of 430 six-month-old Romney lambs was grazing 

a brassica crop in the Rangitikei. Twenty-five lambs died 

over a two-week period and a further 25 lost weight. Postmortem 

examination of an affected lamb found swollen 

kidneys and the renal capsule expanded by gelatinous 

fluid. Histopathology confirmed severe renal nephrosis, 

consistent with a toxic insult. The most common cause in 

lambs grazing crops is consumption of a weed known as 

redroot (Amaranthus retroflexus). This plant contains a 

nephrotoxin leading to renal failure and typically causes 

perirenal oedema. 

CANINE AND FELINE 

An 18-month-old female Pomeranian dog had four 

seizures over a three-week period. A lead sinker was 

passed in the faeces five days before sample submission. 

Haematology revealed a moderate increase in nucleated 

red blood cells (7/100 leukocytes, reference range < 0) 

and basophilic stippling within red blood cells. Serum 

lead concentrations were 0.75 mg/L (toxic level > 0.5), 

confirming a diagnosis of lead poisoning. 

A nine-month-old male Staffordshire Bull Terrier cross 

dog had marked coprophagia and diarrhoea about once 

a week for a month, and vomiting for the week before 

sample submission. A species of Campylobacter was 

cultured but could not be identified to species level 

through routine tests. An ELISA for Giardia spp. was 

positive, yielding a diagnosis of intestinal giardiasis and 

campylobacteriosis. 

A 12-year-old female domestic Shorthaired cat had a 

lesion on the nasal planum. Histopathology showed focal 

epidermal hyperplasia overlying a mass composed of 

interweaving spindle cells. The epidermis extended long 

rete pegs into the spindle cells. A diagnosis of probable 

feline sarcoid was made. This is a lesion caused by 

feline sarcoid-associated papillomavirus, which is very 

similar to bovine papillomaviruses and probably related. 

These lesions are more common in young cats but other 

differential diagnoses for spindle-cell proliferation do not 

typically involve the epidermis. 

NON-POULTRY AVIAN 

An eight-week-old kiwi from South Westland presented 

with a solitary 10 mm nodule at the end of its bill. 

Histological examination revealed typical lesions of a 

poxvirus infection. This infection has previously been 

reported in brown kiwis (Ha et al., 2013). 

An immature female kiwi from an aviary in the Waikato 

was submitted for post-mortem examination. It weighed 

1484 g and was in very fat condition. There was no food in 

the crop or proventriculus and the gizzard contained only 

khaki-coloured fluid and stones. The spleen was enlarged 

(35 x 20 mm) and dark red. No other gross abnormalities 


were noted. Histology of the spleen revealed marked 

autolysis. It appeared hypercellular and had low numbers 

of aggregates of densely packed basophilic organisms 

about two microns in diameter with a small halo. 

Samples were sent to Massey University where it was 

confirmed as malaria positive and sequenced as 

Plasmodium elongatum. 

POULTRY 

Six male broiler chickens were lame or unable to stand; 

some were also dirty, lice-ridden and suffered pressure 

sores or had dermatitis on their ventrum. Post-mortem 

examination of two chickens identified poor body 

condition in one, and purulent material within various 

joints including stifle, hip, tarsometatarsal-phalangeal 

and carpal joints of the other. The femoral heads of the 

lighter chicken were also friable, fragmentary and yellowgreen 

on sectioning. Blackened and thickened skin was 

noted on their hocks. Smears from joint fluid showed 

heterophils, macrophages, synoviocytes, lymphocytes 

and extra- or intra-cellular cocci. A diagnosis of septic 

polyarthritis and osteomyelitis was made. Culture of the 

purulent material was declined, but Staphylococcus aureus 

is a common cause of such lesions in chickens. Disease 

may be subclinical, with aggravation in conditions of high 

environmental contamination, immunocompromise or 

damage to the beak during de-beaking allowing bacteria 

to enter. 

REPTILIAN 

A four-year-old female bearded dragon (Pogona vittiiceps) 

died suddenly. There had been a recent change in 

husbandry and feeding practices. On post-mortem the 

pericardial sac contained about a millilitre of clotted 

yellow exudate and the peritoneal cavity contained 

10 mL of dark red, malodorous fluid. The liver was 

large, yellow and soft with rounded edges, and samples 

floated in formalin. The oviducts were empty. A smear of 

pericardial exudate showed large numbers of heterophils 

and macrophages associated with extra- and intra-cellular 

coccobacilli. Culture of a swab from the pericardial sac 

produced a pure growth of Listeria monocytogenes. A 

diagnosis of listerial pericarditis and hepatic lipidosis 

was made, with probable peritonitis. The pericarditis was 

ascribed to septicaemia, perhaps secondary to nutritional 

stress. Fatty liver can be physiological in reproductively 

active females, but did not seem to be the case. 

10 


PRIMATE 

A pygmy marmoset (Cebuella pygmaea) in a zoological 

collection died suddenly. At post-mortem it was 

emaciated. Intestinal contents were cultured, producing 

a heavy growth of mixed organisms including clostridia 

and Listeria monocytogenes. The isolation of Listeria was 

regarded as significant, indicating a possible diagnosis of 

listerial septicaemia. 

EQUINE 

A 10-year-old male Appaloosa horse had a 4–5-month 

history of lethargy, depression and intermittent epistaxis, 

which was initially unilateral but had become bilateral 

for the two weeks before samples were submitted. The 

horse had received chloramphenicol, phenylbutazone and 

long-acting penicillin for a corneal ulcer. Phenylbutazone 

treatment had finished three weeks before sample 

submission. Clinical examination revealed oral mucosal 

petechiae and slightly pale mucous membranes. 

Haematology showed a marked anaemia: haematocrit 

0.18 (reference range 0.32–0.55), RBC 3.34 x 10 12 /L 

(reference range 7–11 x 10 12 ), haemoglobin 61 g/L 

(reference range 110–173) and MCHC 349 g/L (reference 

range 360–390). There was also macrocytosis (53 fL; 

reference range 36–48) and severe thrombocytopenia, 

assessed subjectively from the smear. These findings were 

consistent with a diagnosis of regenerative anaemia, likely 

reflecting haemorrhage caused by thrombocytopenia. 

This was characterised as idiopathic since no infectious 

or drug-related cause for the thrombocytopenia was 

confirmed. The horse also had mild neutrophilia 

(7.2 x 10 9 /L; reference range 3–7 x 10 9 ) and lymphopenia 

(0.2 x 10 9 /L; reference range 1.3–6.5 x 10 9 ), consistent 

with a stress leucogram; and low total protein (50 g/L; 

reference range 57–77) and albumin (24 g/L; reference 

range 27–39), consistent with haemorrhage. There were 

also minor alterations in serum chloride (111 mmol/L; 

reference range 92–104), phosphate (0.71 mmol/L; 

reference range 1–1.8) and CPK (374 IU/L; reference 

range 0–310). 

PORCINE 

A backyard piggery in South Canterbury was losing 

weaners aged eight to ten weeks through diarrhoea and 

wasting. Histological examination of one pig showed a 

superficial necrotising and suppurative colitis consistent 

with Brachyspira hyodysenteriae (swine dysentery).

Sudden post-weaning deaths occurred in young pigs in 

a small, well-run piggery with 12 breeding sows. Deaths 

began shortly after zinc oxide was added to the homemade 

ration (no other supplements were being fed.) 

This farmer had previously fed raw milk and a vitamin 

A, D and E supplement to his younger pigs but for some 

reason it was not given to this group. Necropsy of one 

dead pig showed a large amount of bloodstained fluid 

in the abdomen, and a mottled liver. Histopathological 

examination of the fixed liver showed massive hepatic 

necrosis with haemorrhage, consistent with hepatosis 

dietetica, a disease induced by vitamin E deficiency. 

Kidney zinc concentration was 260 umol/kg (toxic level 

> 2900), ruling out zinc toxicity. The zinc was removed 

from the ration, fresh milk was added and the deaths 

stopped. Hepatosis dietetica is rarely seen these days. 

CAPRINE 

A one-year-old milking doe in the Waikato had diarrhoea 

and then died. On post-mortem there was some 

consolidation of the lung and the mesenteric lymph nodes 

were enlarged. Histology of the liver showed frequent 

small globules of amorphous, faintly eosinophilic material 

scattered at random in the sinusoids. The kidneys had 

occasional clumps of amorphous, faintly eosinophilic 

material within the glomerular tufts and frequent 

larger deposits of this material in the interstitium of the 

medulla. The mesenteric lymph nodes were oedematous, 

with frequent macrophages in the sinusoids and frequent 

deposits of this eosinophilic material in the interstitium 

of the medulla. There were linear deposits of this 

eosinophilic material beneath the epithelium of the 

rumen and beneath the epithelium at the tips of the 

villi of the small intestine. This was consistent with 

systemic amyloidosis. 

DEER 

There was an outbreak of parapoxvirus infection in 

two-year-old stags on a large Southland deer farm. 

Unfortunately this outbreak occurred at the same time as 

velvet removal so much of the velvet had to be discarded. 

Clinically affected deer had masses of small uniform 

nodular scabby lesions all over the velvet antler and in 

the most severely affected there was a moderate amount 

of subcutaneous oedema over the head and below the 

jaw. These animals otherwise appeared clinically normal. 

Histopathological examination of fixed affected antler 

showed changes consistent with a parapox infection, 

but very few viral inclusions were found. However, a 

preparation of fresh affected antler was examined by 

direct electron microscopy and large numbers of poxlike 

virus particles were identified, confirming the 

provisional diagnosis. After about three weeks there was a 

spontaneous clearance of the infection and no new cases 

were seen. Parapoxvirus outbreaks of this magnitude are 

now rare on deer farms but were more common 10–20 

years ago, usually spread by contact with thistles. There 

were no thistles on this farm and the paddocks had been 

recently topped. 

Two hinds from a mob of 400 with fawns at foot were 

found dead on an Otago deer farm over a two-day period. 

The first hind to die was too decomposed for examination 

but a necropsy of the second hind showed expanded lungs 

that failed to collapse when the chest was opened. The 

airways were full of foam. Histopathological examination 

of fixed lung showed a severe diffuse interstitial 

pneumonia with hyaline membranes, type 2 pneumocyte 

hyperplasia and syncytia. These findings are consistent 

with atypical interstitial pneumonia caused by exposure 

to L-tryptophan in lush pasture. This condition has been 

reported in deer, both in this country and overseas, but is 

more commonly seen in beef cattle shifted rapidly from 

dry upland pastures to lush, often irrigated pastures. 

These deer were well fed and the farm was partly irrigated. 

New Zealand Veterinary Pathology 

CATTLE 

Two samples of mastitic milk were submitted from two 

cows in the Waikato. One cow had a milk somatic cell 

count of 14 500 000 and a pure growth of Prototheca sp. 

was obtained from a sample. The milk somatic cell count 

of the other cow was 1 500 000 and a heavy pure growth 

of Streptococcus uberis was obtained. Prototheca sp. is 

a type of green alga that lacks chlorophyll. Its natural 

habitat is the soil and it is an uncommon cause of mastitis. 

In the Waikato, a mob of six-month-old calves presented 

with weight loss and diarrhoea. Specimens from five 

calves were submitted. Faecal egg counts did not indicate 

parasitism but Yersinia paratuberculosis was cultured 

from all five faecal samples. The calves were all negative 

for BVD antigen. 


Three 9-month-old calves in the Auckland supercity 

developed oropharyngeal ulcers covered by a 

pseudomembrane. The lesions resembled the lesions 

of calf diphtheria. Parenteral treatment with an 

oxytetracycline preparation was clinically ineffective. 

Swabs were taken and submitted to the laboratory for 

culture. Mixed growths were obtained from each, but 

one calf yielded a heavy growth of Fusobacterium 

necrophorum. Calf diphtheria usually affects suckling 

calves. The occurrence of pseudomembranous 

pharyngitis in nine-month-old calves raises the 

possibility of drench-gun or bolus-gun injury. 

Dairy cows grazing a crop of turnips in the Bay of Plenty 

developed skin lesions consistent with photosensitisation. 

The serum gamma-glutamyl transferase (GGT) activity 

of three cows was determined. The range of GGT values 

was 298 to 1262 IU/L and the mean was 804 (reference 

range 0–36). These findings are consistent with biliary 

damage and secondary photosensitisation caused by 

turnip toxicosis. Turnip crops stressed by drought can 

accumulate high concentrations of glucosinolates in 

the foliage. The glucosinolates are converted to toxic 

metabolites in the rumen. As far as the author is aware, 

the toxic metabolite and mechanism of toxicity have not 

been elucidated. 

Two Friesian cows in the same Bay of Plenty herd each 

developed a mass on the perineum adjacent to the vulva. 

One cow was 11 years old and had an 800-mm-diameter 

mass. The other cow was 12 and had a 600-mm-diameter 

mass. Both masses were composed of neoplastic stratified 

squamous epithelium characteristic of squamous cell 

carcinoma. Squamous cell carcinoma is common on 

non-pigmented skin of the eyelids but it is not common 

elsewhere on the body. Interestingly, these two cows were 

both quite old. 

Two 6-month-old beef calves in Hawke’s Bay became 

recumbent after being moved onto a new break of grass. 

The calves were in poor body condition. Serum samples 

were negative for BVD antigen. A faecal sample from 

one calf contained 200 strongyle eggs per gram and a 

few coccidians. Culture of the faeces yielded Yersinia 

pseudotuberculosis. 

Twelve of 16 unweaned Hereford calves in Northland 

developed acute respiratory distress and four died. 

A specimen of consolidated lung was submitted to 

the laboratory. The histopathology findings were 

12 


characteristic of chronic verminous pneumonia 

caused by Dictyocaulus sp. and subacute suppurative 

bronchopneumonia. 

In the Auckland supercity 12 of 60 post-partum 

Hereford cows developed anaemia and jaundice, and 

two died. Whole blood was submitted from six affected 

cows for haematology. The haematocrits ranged from 

0.08 to 0.18 L/L, and the mean was 0.12 (reference 

range 0.24–0.4). Reticulocytes were 28–197 x10 9 /L 

with a mean of 142 x10 9 (reference 1 x10 9 ). Nucleated 

red blood cell counts were 0–59 per 100 leukocytes, 

with a mean of 25 (reference 0). There was marked 

anisocytosis, polychromasia and macrocytosis of 

erythrocytes. These findings indicate severe anaemia 

with strong regenerative responses. In addition, Theileria 

sp. organisms were seen infecting erythrocytes. The 

number of these organisms ranged from 2 to 81 per 

1000 erythrocytes, with a mean of 21. Heinz bodies 

were not seen. Serum biochemistry demonstrated that 

the magnesium, phosphate and copper concentrations 

and the gamma-glutamyl transferase activities were not 

abnormal. Tissue samples were submitted from one of 

the animals that died. Histopathology found severe acute 

centrilobular coagulative necrosis of the liver, which is 

the typical sequel of hypoxia and is consistent with severe 

anaemia. The liver copper and zinc concentrations of 

the dead animal sampled were within normal ranges. 

These findings do not support non-infectious causes 

of haemolytic anaemia such as copper poisoning, zinc 

toxicosis, acute sporidesmin poisoning, Heinz body 

anaemia and hypophosphataemia. The herd had been 

vaccinated against leptospirosis. Therefore the findings 

were interpreted as being consistent with haemolytic 

anaemia caused by infection of erythrocytes by Theileria 

sp. organisms. 

Two 5-month-old calves in the Waikato presented with 

deep red urine. They had been receiving zinc prophylaxis 

against facial eczema for four weeks. Their serum zinc 

concentrations were 430 and 480 mmol/L (reference 

range 11–20; therapeutic range up to 35). These findings 

are diagnostic for zinc toxicosis. 

GOATS 

Two 8-month-old Nubian billy goats failed to thrive 

after returning to their Waikato home property. A faecal 

sample was submitted from each. The worm eggs counts 

were 750 and 2600 eggs per gram and both goats were

shedding moderate numbers of coccidian oocysts. 

These findings indicate the goats had gastrointestinal 

nematode parasitism and coccidiosis. 

SHEEP 

Neoplasia in sheep is unusual. On the West Coast a 

50-mm-diameter pedunculated mass was discovered 

on an adult ewe during shearing. The mass arose from 

the skin cranial to the shoulder. A mucoid mass with a 

narrow stalk was submitted for laboratory examination. 

The mass comprised haphazardly arranged spindle cells 

that were widely separated by mucinous extracellular 

matrix. These findings are consistent with a diagnosis 

of benign myxoma. 

A mob of 450 two-year-old ewes was bought at a 

Northland sale yards in February 2012. Three months 

later some sheep became ill-thrifty, wasted away and 

developed diarrhoea. Fifty had died by January 2013. 

The sheep had been vaccinated against clostridial disease 

before lambing in the spring and had been drenched 

three times with mineralised anthelmintic. One ewe 

had a faecal egg count of 4550 eggs per gram (epg) and 

a positive Johne’s serum antibody ELISA result. The 

sheep were drenched again with a combination product 

containing abamectin, levamisole and oxfendazole. Seven 

days later the mean faecal egg count of ten lambs was 760 

epg, and the mean faecal egg count of ten ewes was 470. 

Larval culture of pooled lamb’s faeces demonstrated that 

14 percent of the larvae were Ostertagia (Teladorsagia) 

sp. and 86 percent were Trichostrongylus sp. These results 

indicate that drenching has been ineffective on this 

property, resulting in chronic severe gastrointestinal 

parasitism. In addition the positive Johne’s antibody 

ELISA result suggests that Johne’s disease could also be 

contributing to the ill-thrift and deaths. 

EQUINE 

Several Thoroughbred foals on a Waikato property 

presented with pruritis. There were circular areas of 

alopecia and hyperkeratosis on the head, which the 

handlers described as being like ash. A sample of 

plucked hair with adherent exudate was submitted and 

Trychophyton rubrum was obtained, which supported 

a diagnosis of dermatophytosis. Ringworm is not 

uncommon in young stock in mixed groups and is usually 

self-limiting. 

In the Auckland supercity a two-month-old Standardbred 

foal was treated for suspected Rhodococcus equi 

infection. The foal continued to deteriorate and died. 

Specimens were collected post-mortem and submitted for 

histopathology. In the duodenum there were numerous 

cross-sections of nematode parasites in the lamina 

propria. These had morphologic features consistent with 

Strongyloides sp. Heavy infection with Strongyloides 

westeri occasionally kills foals. 

AVIAN 

A five-year-old cockatiel in Auckland developed a 

mass on the upper eyelid of the right eye. A biopsy was 

performed and multiple fragments were submitted. 

The tissues were expanded by infiltrates of epithelioid 

macrophages and multinucleate giant cells. Ziehl-Nielsen 

stain demonstrated acid-fast bacilli within areas of 

necrotic debris and in the cytoplasm of macrophages. 

These findings are diagnostic for mycobacterial 

granulomatous blepharitis. 

REFERENCE 

Ha HJ, Alley M, Howe L, Castro I, Gartrell B (2013) Avipoxvirus infections 

in brown kiwi (Apteryx mantelli). New Zealand Veterinary Journal 6: 49–52. 


QUARTERLY REPORT OF INVESTIGATIONS OF SUSPECTED 

EXOTIC DISEASES 

Vesicular disease ruled out 

An MPI veterinarian at a meatworks called the exotic 

pest and disease hotline to report foot lesions in sheep. 

The veterinarian was concerned that the lesions could be 

caused by exotic vesicular disease. Six of 504 lambs were 

affected with mild focal to severe extensive coronary band 

ulceration. No vesicles were seen in the animals’ mouths 

but, owing to the distribution and lack of an obvious 

endemic rule-out, a vesicular investigation was initiated. 

An initial investigating veterinarian (IIV) dispatched by 

AsureQuality was able to exclude exotic vesicular disease 

based on the clinical appearance of the lesions (which 

were severely proliferative) and epidemiological signs. 

The IIV observed a high prevalence of small proliferative 

nose and lip lesions resembling orf (ovine parapox 

virus), an endemic disease in New Zealand. The IIV also 

discovered that these lambs had been run through fresh 

gravel multiple times during the week preceding this 

event. Gravel can cause coronary damage (excoriations), 

allowing viral entry and secondary bacterial infection. 

This pathogenesis explains the unusual and severe 

distribution of orf-like lesions on the coronary band 

and interdigital region. Histopathology to differentiate 

orf from simple bacterial infection was performed to 

confirm an endemic diagnosis. Lesions were confirmed as 

being consistent with ovine parapoxvirus and secondary 

bacterial infection. Foot and mouth disease in sheep can 

be subclinical or may present with mild lesions that may 

be overlooked, so a absence of systemic clinical illness in 

these sheep was not a helpful differentiating factor. 

Theileria investigation 

In late 2012 there was an increase in the number of 

reports of anaemia associated with Theileria infection in 

cattle. From late August 2012 to May 2013 there were 21 

reports from beef properties and 28 reports from dairy 

properties. These reports were largely clustered in the 

Northland, Auckland and Waikato districts of the North 

Island. 

MPI initiated an investigation which is still ongoing. The 

aims were to document and describe the recent outbreak; 

determine if there was an emerging disease issue 

associated with Theileria; confirm that reported outbreaks 

were not caused by exotic species of Theileria or a change 

in strain type; and to gain a greater understanding of the 

14 


Exotic disease investigations are managed and 

reported by MPI Investigation and Diagnostic Centre 

(IDC), Wallaceville. The following is a summary of 

investigations of suspected exotic disease during the 

period from January to March 2013. 

epidemiology of anaemia associated with Theileria in 

New Zealand. 

Molecular analysis of samples has indicated an association 

with type 2 (Ikeda) strains of T. orientalis, which was 

previously unknown in New Zealand. Ikeda and the 

strains of T. orientalis (Chitose and Buffeli) that are 

known to be present in New Zealand are generally 

regarded as benign. Highly pathogenic exotic species of 

Theileria have been ruled out. A full description of the 

MPI investigation will be published in a later edition of 

Surveillance. 

Anthrax ruled out 

A private veterinarian reported a mortality event affecting 

10 of 24 Hereford suckler cows with calves at foot near 

Lake Rotoma. The notifying veterinarian reported that 

only the cows were affected and that the dead cows had 

blood coming down their noses. The only animal of 

the 10 that were still alive at examination was pyrexic 

(42 o C) and inco-ordinated. This animal subsequently 

collapsed and was euthanased. The water tank supplying 

this paddock was observed by the veterinarian to be very 

slow to fill, but according to the owner this had not been 

an issue before. The exotic rule-out of concern in this 

case was anthrax, which can present as sudden death 

and bleeding. Anthrax was considered unlikely in this 

case given the history, and confirmed to be negative on 

direct blood smears examined at MPI’s Animal Health 

Laboratory. Tests on samples submitted to a private 

veterinary laboratory for biochemistry and histopathology 

were inconclusive. They did not support the diagnosis 

of a toxin but suggested that heat stroke brought on 

by water deprivation was most probable. Temperature 

records for Edgecumbe showed that it had been very hot 

the previous, weekend with just under 30 o C recorded 

on 3 and 4 March. The investigation was stood down 

following the exclusion of the exotic disease of interest 

and the identification of a more likely cause of death.

Haemorrhagic septicaemia excluded 

A Gribbles pathologist reported a disease outbreak in fivemonth-old 

calves where pleurisy and peritonitis were the 

primary gross pathology findings. Pasteurella multocida 

was cultured from tissues from affected calves by 

Gribbles Veterinary Pathology and the Investigation and 

Diagnostic Centre at Wallaceville. The outbreak occurred 

in calves born during early summer 2012. Three out of 35 

calves (9 percent) died acutely over a four-day period. A 

P. multocida capsular serogroup specific multiplex PCR 

amplified a capsular type B specific product from the 

P. multocida isolate. An HS-B PCR was negative for all 

samples tested. Hence, the species isolated from calves in 

the outbreak was a non-haemorrhagic septicaemia strain 

of P. multocida. 

Bovine herpes virus type 1 

(abortifacient strain) excluded 

An aborted foetus submitted to Gribbles Veterinary 

Pathology in Christchurch tested positive for infectious 

bovine rhinotracheitis (IBR) by ELISA performed on 

serum. The cow had aborted at eight months’ gestation 

and the farm had suffered six other abortions in the 

previous two weeks. PCR at MPI’s Animal Health 

Laboratory was negative for IBR, ruling out bovine herpes 

virus type 1 (abortifacient strain) as the cause. 

Mycoplasma haemolamae confirmed 

A veterinary laboratory informed the Investigation 

and Diagnostic Centre at Wallaceville that a client had 

requested testing for Mycoplasma haemolamae from a 

herd of alpaca that had been experiencing problems with 

anaemia. M. haemolamae is a haemotropic mycoplasma 

that adheres to the surface of the red blood cells of 

camelids. This organism can be associated with anaemia 

(Foster et al., 2009), depression, fever and weight loss 

(Kaufmann et al., 2011). Animals subjected to stress, 

immune suppression or concurrent disease conditions 

are more likely to have clinical signs. They are also more 

likely to have visible blood parasites in their blood smears. 

Treatment is typically with oxytetracyclines and it appears 

that animals remain chronically infected despite treatment 

(Torquist et al., 2009). Asymptomatic carriers are possible 

and seem to occur often. Prevalence estimates in nonclinically-affected 

populations vary from 18.7 percent in 

central Europe and 9 percent to 19 percent in Peru and 

Chile (Kaufmann et al., 2010; Forman, 2009). 

M. haemolamae was first identified in camelids in 1990 

(McLaughlin et al., 1990). The first alpacas were imported 

into New Zealand in 1986, four years before the first 

identification and 15 years before the development of a 

PCR test in 2001. M. haemolamae is not mentioned in 

the Import Health Standard for alpacas imported from 

the USA (where the parasite was first identified in 1990). 

The import risk assessment performed by MPI notes the 

organism is suspected to be present in New Zealand. 

This particular alpaca farming operation has been 

identified as being in an area at risk for cobalt deficiency. 

Cobalt is an essential building block of vitamin B12. 

Signs of vitamin B12 deficiency are listlessness, weight 

loss, anaemia and ketosis. Eight of 10 animals sampled 

from the herd had levels of vitamin B12 well below the 

reference range, and resistance to ivermectin was also 

identified by the attending veterinarian. Animals were 

found to have large numbers of Haemonchus contortus 

larvae still present post-drenching. This resistance along 

with the cobalt deficiency is considered to be the most 

likely cause of the anaemia in these animals. Also, no 

organisms were noted on blood smears from the property. 

Blood samples were collected from 10 animals that 

showed clinical signs of weight loss and depression. 

These samples were analysed for evidence of anaemia 

and sent to Oregon State University for subcontracted 

blood testing by PCR, which detected the organism in 

one sample. The animal that produced the positive result 

had no clinical signs of anaemia (PCV of 41 percent ). A 

stored blood sample from the same animal tested positive 

at IVABS at Massey University with a PCR that was more 

generic for haemotropic mycoplasmas. Sequencing of the 

PCR product for this animal was 100 percent homologous 

with M. haemolamae DNA held in Genebank. This 

finding, although significant as the first confirmed report 

of this organism in New Zealand, appears to be an 

incidental finding in this particular animal and confirms 

the position of the import risk assessment for alpacas 

and llamas published on the MPI (then Biosecurity 

New Zealand) website in 2010 (http://www.biosecurity. 

govt.nz/files/biosec/consult/final-import-risk-analysisllamas-alpacas.pdf.). 

An alpaca farm with about 300 animals experienced acute 

and chronic animal health issues in 2012 (including a 

5 percent mortality), associated with a variety of factors 

including mineral deficiencies and parasitism. The 


most common clinical presentation was weight loss and 

weakness. In addition these animals were often anaemic 

(HCT < 27 in adults). On pen-side blood testing a suspect 

organism with characteristics of Mycoplasma hemolamae 

was seen on red blood cells in several individuals in a 

cohort showing sub-optimal body condition. Testing for 

this blood parasite was performed by PCR in addition 

to further interpretation of the pen-side blood smears 

by pathologists. Despite evidence of the organism on 

blood smears, all PCR samples tested by two independent 

laboratories were negative. The entire herd has been 

placed on a revised protocol of mineral supplementation 

and de-worming and an improvement has been noted. 

The investigation was closed as inconclusive as there is 

not enough evidence to rule out M. hemolamae but no 

confirmatory evidence of infection in this herd. 

Q fever excluded 

During routine export testing of a shipment of 37 alpacas, 

two animals were identified as having serum reactivity to 

bovine Anaplasma sp. on ELISA testing and one animal 

showed serum reactivity to Coxiella burnetii (Q fever) on 

complement fixation testing. The three animals and their 

cohort were healthy, with no clinical signs suggestive of 

anaplasmosis or Q fever. On re-testing the three positive 

animals, about six weeks after the first test, two returned 

negative but Anaplasma serum reactivity remained in one. 

Anaplasma was excluded after a negative follow-up test 

of whole blood using PCR. The low prevalence in serum 

reactivity for Q fever and Anaplasma is consistent with 

the known test characteristics of the original tests used. 

Exotic causes of stomatitis in alpaca 

excluded 

An alpaca imported six weeks previously from Australia 

was reported to MPI as it had unusual chronic mouth 

lesions. The attending veterinarian had made a 

presumptive diagnosis of actinobacillosis and treated 

the animal with antibiotics without success. The lesions 

remained unchanged. The animal had concurrent heavy 

infestation with demodex mites, a common condition 

in alpacas. The animal was otherwise in good health. 

Biopsies of oral mucosa were collected and histopathogy 

revealed large numbers of eosinophils. The suspected 

aetiology of these lesions is demodicosis leading to a 

hyperimmune reaction in this animal. There was no 

16 


indication of infectious disease as a cause of the lesions 

in this case. The histopathology was reviewed by Massey 

University pathologists. Exotic disease was ruled out on 

histopathological and clinical grounds. The veterinarian 

will undertake a treatment trial with corticosteroid, which 

may improve the condition, and will keep MPI informed 

of the animal’s progress. 

EIA/EVA ruled out 

A pathologist reported a seven-year-old Thoroughbred 

horse with oedema, hyperglobulinaemia and 

hypoalbuminaemia via the MPI exotic disease and pest 

hotline. The horse had oedema of the legs which, over the 

past week, had frequently flared up then receded, but it 

was otherwise well. The horse had not left the property 

it lived on for years, though other horses it grazed with 

attended race meetings; however, none of these horses 

exhibited similar signs. Likely causes of the pathology 

were inflammation or hepatic disease, but antibodyproducing 

tumours were also a possibility. Testing to rule 

out exotic causes of oedema were conducted at MPI’s 

Animal Health Laboratory. The horse was serologically 

negative for equine infectious anaemia AGID, equine viral 

arteritis VNT, and Babesia caballi and B. equi ELISA. The 

horse made a full recovery the day after notification, and 

the oedema has not recurred. 

Gribbles Veterinary Pathology in Hamilton was asked 

by a private veterinarian to test a five-year-old mare for 

equine infectious anaemia (EIA). Clinical signs included 

mild anaemia, anorexia, pyrexia, shifting lameness, 

mild lower limb oedema, endocarditis and tachycardia. 

This was the second horse on the same property in the 

last 12 months to get oedema. The clinical signs were 

consistent with EIA, an exotic disease in New Zealand, 

but the other horse had tested negative for this. A serum 

sample forwarded to the IDC Animal Health Laboratory 

tested negative for EIA by AGID (Coggins test) and the 

investigation was stood down. 

Contageous equine metritis excluded 

A quarantine veterinarian reported that a mare 

had aborted while undergoing post-arrival import 

requirements with regard to Taylorella equigenitalis 

(contagious equine metritis). Two previous vaginal 

swabs had cultured negative for CEM. Histopathology of 

a broad range of tissues from the aborted fetus did not

suggest an infectious aetiology, as they tested negative by 

PCR for T. equigenitalis, equine viral arteritis virus and 

equine herpes virus 1. In addition, endometrial swabs 

from the aborted mare were negative by PCR and culture 

for T. equigenitalis. No organisms were isolated by virus 

isolation. The cause of the abortion was not determined 

but may have been environmental stressors caused by 

international transport. 

Actinobacillus pleuropneumoniae 

exotic serovars excluded 

A veterinary pathologist reported the isolation of 

Actinobacillus pleuropneumoniae serovar 15 from an 

outbreak of pneumonia in a commercial piggery. MPI 

records showed that this particular serovar had previously 

been isolated in New Zealand, in association with a 

pneumonia outbreak. The report had already been 

notified to the pig industry veterinarians. 

Brucella canis ruled out 

A Gribbles pathologist reported a five-year-old dog of 

mixed breed with unilateral orchitis and epididymitis. 

There was no history of movement or use as a breeding 

animal that would suggest Brucella canis. The dog 

had been returned to the Chatham Islands and was 

not available for further testing. As part of routine 

surveillance a portion of the fixed testis and epididymus 

were tested by PCR. The negative result confirmed 

absence of B. canis. 

Ehrlichia canis investigated 

A scientist from the Animal Health Laboratory at 

Wallaceville forwarded routine pre-export testing results 

for a New Zealand dog with a seropositive result for 

Ehrlichia canis (> 1:80) by the microscopic agglutination 

test. The five-year-old neutered male Border Collie had 

been bought from a pet shop in Auckland as a pup, but 

had not been registered with the Auckland City Council 

every year. It is therefore possible (although unlikely) 

that the dog could have been out of the country but this 

could not be confirmed. The owners of the dog have 

left New Zealand and now live in Australia. The present 

whereabouts of the dog is unknown and MPI Compliance 

and the dog’s veterinarian have been unable to locate the 

new owners. Without finding the dog, further testing to 

rule out E. canis is not possible. A border alert has been 

placed on the previous owner’s passport and when they 

next enter New Zealand they will be questioned as to 

the whereabouts of the dog, which will then be tested if 

it can be located. Given that the dog was New Zealandborn 

and-bred, the risk that it has contracted E. canis 

appears to be low. 

Myxomatosis ruled out 

A veterinarian phoned the MPI exotic pest and disease 

hotline to report bilateral purulent conjunctivitis in a 

domestic rabbit at the Marlborough SPCA. The possibility 

of exotic disease such as myxomatosis could not be ruled 

out based on the clinical signs. The rabbit responded to 

standard treatment for bacterial conjunctivitis and rhinitis 

and myxomatosis was was excluded by a negative agar-gel 

immunodiffusion antibody test at VLA, Weybridge, UK. 

Feline heartworm confirmed 

A veterinarian phoned MPI to report an imported cat 

with wasting and behavioural changes. Full blood counts 

had revealed marked eosinophilia. The cat had been 

imported from Singapore in August 2012 along with 

another cat that was clinically normal. The clinically ill cat 

was referred to a feline specialist for further investigation 

and testing. Treatment for a preliminary diagnosis of 

toxoplasmosis was pursued but the feline specialist could 

not rule out heartworm (infestation with Dirofilaria 

immitis). During examination the feline specialist found 

a crusted, non-healing lesion on the cat’s ear. Sera were 

sent to two overseas laboratories for D. immitis antigen 

and antibody testing by ELISA, and Leishmania PCR. 

These organisms both cause exotic diseases of companion 

animals in New Zealand and are known to occur in 

Singapore. Leishmania was ruled out and the clinically 

ill cat was negative for D. immitis antigen and antibody. 

The healthy in-contact cat tested positive for Dirofilaria 

antigen at both laboratories. The clinically ill cat 

responded well to treatment for toxoplasmosis and is still 

improving. The in-contact cat remains asymptomatic and 

clinically normal. Cats are considered a dead-end host for 

D. immitis so there is negligible risk associated with this 

detection (MPI Import Risk Analysis, 2009). The owner of 

the cats has been advised of the risks of treatment and the 

prognosis for the infected cat. 

Exotic tick ruled out 

A tick was reported to the MPI exotic pest and disease 

hotline by a pathologist who had been consulted by a 

Christchurch veterinarian who had found it on a dog. 


The concern of the notifier was that the dog had been 

around the Lyttelton port area the day before the tick 

was found, and that ticks are relatively uncommon in 

Christchurch, so there was a risk that it was an exotic 

species. The tick was identified at PHEL Tamaki as 

Haemaphysalis longicornis, the New Zealand cattle tick, 

which is widely distributed throughout the country. 

Exotic tick confirmed 

About 200 live ticks were found during routine veterinary 

examination of a Jack Russell Terrier in post-entry 

quarantine in Auckland after it had been imported from 

Australia. The dog had been inspected and treated for 

ticks before import and it was believed that the infestation 

had occurred between inspection and import. The dog 

owner’s household effects that had been imported in a 

container were inspected at the point of arrival and no 

evidence of ticks was found. The ticks were identified 

as the brown dog tick Rhipicephalus sanguineus, an 

exotic species. The dog was subsequently released after 

tick treatments were carried out, no further ticks were 

found, and a negative results were received for two 

Babesia gibsoni tests (by PCR at Acarus Laboratories, 

Bristol University Veterinary School, UK, and by IFAT 

(titre: 1:40)). 

Toxoplasmosis in kiwi confirmed 

The wildlife surveillance programme funds the testing 

of wildlife post-mortem specimens for endemic OIElisted 

diseases through a contract with Wildbase, 

Massey University. The contract aims to improve MPI’s 

monitoring for emerging diseases, and over time improve 

the quality and credibility of New Zealand’s OIE reports 

and our surveillance system in the wildlife area. A 

case of toxoplasmosis was identified in a dead kiwi by 

Wildbase staff. Toxoplasmosis is on the list of diseases 

that are included in the OIE annual wildlife reports. This 

result will change the status reported in wildlife from 

presumptive (?) to positive occurrence of clinical disease. 

Samples of extracted DNA material were submitted to 

the Friedrich-Loeffler-Institut in Reims, France, and 

Toxoplasma gondii was confirmed by PCR. 

Avian mortalities investigated 

A veterinarian phoned the MPI pest and disease hotline 

to report concurrent ill-thrift and mortality in a small 

backyard poultry flock and diminished sightings of a wild 

18 


in-contact weka population over a period of one month. 

The weka population is one of few remaining populations 

in the North Island. A sick chicken was euthanased and 

post-mortem examination carried out. Samples were 

taken for bacteriology, virology and histopathology. Egg 

yolk peritonitis was diagnosed and a known endemic 

strain of Salmonella isolated. Exotic disease was ruled 

out. The case was notified to DoC and after discussion 

between the property owner, the veterinarian and DoC, it 

was determined that monitoring and/or sampling of the 

in-contact weka population was not possible. 

Highly pathogenic avian influenza and 

Newcastle disease ruled out 

A commercial duck farmer in the Manawatu called 

his veterinarian to report an outbreak of sinusitis in 

28 percent of a pen of 50 animals. The outbreak was 

subsequently reported to the exotic pest and disease 

hotline. The animals were about four months old at 

the time of the outbreak. The farm has since been 

depopulated of all ducks as the farmer has started to 

produce chickens instead. Major exotic differentials were 

ruled out (avian influenza and Newcastle disease negative 

by PCR testing). Further PCR testing was performed 

for Pasteurella multocida (endemic), Ornithobacterium 

rhinotracheale (exotic) and Avibacterium paragallinarum 

(endemic), all with negative results. General bacterial 

culture and mycoplasma culture were performed 

to establish an endemic differential. No pathogenic 

bacteria were isolated but mycoplasma culture identified 

Mycoplasma anatis, a species not previously isolated in 

New Zealand (based on a literature review) but assumed 

to be present here. The MPI import risk analysis for duck 

meat states: “M. anatis is frequently reported in healthy 

wild and domestic ducks throughout the world … Wild 

mallards are commonly exposed to M. anatis without 

any evidence of disease and there is believed to be a 

high transmission rate among wild birds … M. anatis 

may be pathogenic to domestic ducks, causing reduced 

growth rates, respiratory and reproductive disorders … 

However, there are few reports of naturally-occurring 

disease in the field. A mycoplasma of unknown species 

has been isolated from a Peking duck in New Zealand … 

and given that M. anatis is the most commonly isolated 

mycoplasma species in ducks … it is reasonable to assume 

that it is present in New Zealand.” In addition there is one 

reference to the organism’s presence in New Zealand in

1988 in the Avian Veterinary Handbook but the isolation 

technique and method of diagnosis is not known. Based 

on this information the investigation was notified to the 

animals response team manager and stood down after 

it was agreed that there was no biosecurity issue in this 

particular instance. 

A poultry veterinarian submitted samples to MPI’s 

Animal Health Laboratory for PCR testing for avian 

paramyxovirus (Newcastle disease – ND), an exotic 

disease in New Zealand. The affected animals were a 

group of 55-week-old chickens with one month’s history 

of increased mortality (3–4 percent) and head-tilt in 

a single shed of 1000 birds. The submitter diagnosed 

intestinal parasitism with Davainia proglottina 

(microscopic tapeworm) as the most likely cause of 

mortality, based on post-mortem examination and 

mucosal scrapings. Serology for ND returned low positive 

titres (1:32) in two of three tested birds. Tissue samples 

(lung, spleen, brain, caecum, small intestine) from three 

birds tested negative for ND by PCR and the investigation 

was stood down. 

Starling circovirus confirmed 

A team of research scientists identified starling circovirus 

from mud snails (Amphibola crenata) sampled in 

the Avon-Heathcote estuary using next-generation 

sequencing (Illumina, HiSeq). The sequence was then 

verified by targeted PCR and Sanger sequencing. 

Worldwide, starling circovirus has only been isolated 

once before, from starlings in northeastern Spain (Johne 

et al., 2006). The pathogenicity of this virus was not 

established in that report, and the circovirus was found in 

both diseased and healthy starlings during an epidemic of 

salmonellosis. However, in many other species circovirus 

infection is linked to immunosuppression. The virus has 

not been isolated in New Zealand before and is unlikely to 

represent a new incursion. 

European foulbrood excluded 

An apiary advisory officer reported to MPI that larvae in 

a diseased hive had signs consistent with Melissococcus 

plutonius (European foulbrood). These signs included 

larvae with yellow discolouration and corkscrew larvae in 

the cell. Samples of affected larvae were collected and sent 

to the IDC Wallaceville for testing. M. plutonius was ruled 

out by a negative PCR. 

A hobbyist beekeeper called the exotic pest and disease 

hotline to report a five percent brood mortality in a 

single hive. An apiculturist from AsureQuality contacted 

the notifier/owner by telephone and after discussion 

established that the problem was almost certainly varroa 

mite (Varroa destructor) infestation. The owner was 

advised to keep the treatment strips in the hives for eight 

weeks and to reassess brood mortality after two weeks. 

A month later the notifier/owner requested a visit to 

examine the hive as they were still concerned about the 

mortality. Owing to the remote location an experienced 

local beekeeper was sent to examine the hive, and 

reported there was no sign of exotic disease. The varroa 

infestation was under control but there was evidence the 

queen was failing (a failing queen has irregular brood 

pattern, excessive pollen stores and the colony tries to 

replace her by raising queen cells.) The investigation was 

stood down following exclusion of exotic disease and 

confirmation of a known cause of mortality. 

REFERENCES 

Forman S (2009) Prevalence of Mycoplasma haemolamae infection in South 

American camelids in the Southeastern United States. Alpacas Magazine, 

ARF/MAF Research Update 278–281. 

Foster A, Bidewell C, Barnett J, Sayers R (2009) Haematology and 

biochemistry in alpacas and llamas. In Practice 31: 276–278. 

Johne R, Fernandez-de-Luco D, Hofle U, Muller H (2006) Genome of a 

novel circovirus of starlings, amplified by multiply primed rolling-circle 

amplification. Journal of General Virology 87: 1189–1195. 

Kaufmann C, Meli M, Hofmann-Lehmann R, Zanolari P (2010) First 

detection of “Candidatus Mycoplasma haemolamae” in South American 

camelids of Switzerland and evaluation of prevalence. Berl. Munch Tierarztl. 

Wochenschr. 11–12: 477–481. 

Kaufmann C, Meli M, Hofmann-Lehmann R, Riond B, Zanolari P (2011) 

Epidemiology of “Candidatus Mycoplasma haemolamae” infection in South 

American camelids in Central Europe. Journal of Camelid Science 4: 

23–29. 

McLaughlin BG, Evans CN, McLaughlin PS, Johnson LW, Smith AR, Zachary 

JF An Eperythrozoon-like parasite in llamas. Journal of the American 

Veterinary Medical Association 197(9):1170-1175 

Tornquist S, Boeder L, Cebra C, Messick J (2009) Use of a polymerase 

chain reaction assay to study response to oxytetracycline treatment in 

experimental Candidatus Mycoplasma haemolamae infection in alpacas. 

American Journal of Veterinary Research 70: 1102–1107. 

Paul Bingham 

Team Manager 

Surveillance and Incursion Investigation (Animals and Marine) 


paul.bingham@mpi.govt.nz 


MARINE AND FRESHWATER 

INVESTIGATION INTO THE FIRST DIAGNOSIS OF OSTREID 

HERPESVIRUS TYPE 1 IN PACIFIC OYSTERS 

Background 

The Pacific oyster (Crassostrea gigas Thunberg 1793) is 

one of the three main aquaculture species in New Zealand 

(along with king salmon and green mussels). Pacific 

oysters were introduced into NZ in the last century and 

have been farmed commercially since the 1990s. For the 

year ending 31 March 2011 their export value was $18 

million and domestic market value about $12 million 

(Anonymous, 2012). 

Oyster herpesvirosis is caused by a herpesvirus about 

120 nm in diameter. It is believed that the bivalve 

herpesviruses are a completely separate family of 

herpesviruses with extremely limited genetic homology 

to the herpesviruses of mammals, birds and reptiles, or 

to the herpesviruses of amphibians and teleosts (Davison 

et al., 2005). As a result the family Malacoherpesviridae 

now includes the new genus Ostreavirus, containing 

the species Ostreid herpesvirus 1 (OsHV-1) (Davison 

et al., 2009). 

Strain differences within OsHV-1 may be significant and 

associated with virulence. Since the summer of 2008 

increased mortality of young Pacific oysters on the French 

coast has been linked to a microvariant of the OsHV-1, 

named OsHV-1 μVar (Garcia et al., 2011; Martenot 

et al., 2012). 

OsHV-1 is not a notifiable or unwanted organism under 

the Biosecurity Act 1993, nor is it a listed disease with the 

World Organisation for Animal Health (OIE). 

Epidemiology 

The infectious dose of virus is unknown. The 

pathogenicity of the virus does vary with size of the host 

oyster (Burge, Griffin & Friedman, 2006). OsHV-1 DNA 

has been isolated from the water around infected Pacific 

oysters (Sauvage, Pépin, Lapègue, Boudry & Renault, 

2009) and the disease can be experimentally transmitted 

in water (Schikorski et al., 2011). Indirect spread between 

infected and healthy individuals via water, by excretion of 

virus particles and from tissue remnants, appears to be the 

main method of local spread. Local spread of pathogens 

also appears to be very rapid in marine environments 

(McCallum, Harvell & Dobson, 2003). 

Movement of infected animals is likely to be the main 

mechanism of long-distance spread (e.g., from harbour to 

harbour). Whether vertical spread occurs is inconclusive 

but the virus has been detected in adult oyster tissues 

20 


including gonad, and adult oysters could play the role of 

passive carriers (Barbosa-Solomieu et al., 2005). 

OsHV-1 is known to infect a number of different marine 

bivalve molluscs around the world (Hine & Thorne, 1997; 

Renault, Lipart & Arzul, 2001). In addition, the more 

intensive nature of commercial hatcheries, producing a 

number of bivalve species in recirculated water systems, 

could exacerbate this (Arzul, Renault, Lipart & Davison, 

2001). It seems unclear, however, whether these different 

species are truly infected or acting as mechanical carriers, 

given that they are filter-feeders. 

In the northern hemisphere several European countries 

experienced annual mortality events correlated with 

high prevalence of OsHV-1 and as a consequence 

developed long-term studies to understand the risk 

factors associated with the die-offs. Peeler et al. (2012) 

performed a comprehensive study of the risk factors of 

Irish and French oyster mortality events, including agent 

factors of OsHV-1, host factors, management factors and 

environmental factors. They placed particular emphasis 

on the types of temperature stresses, both water and 

ambient, that correlated with the location and time of 

mortality events. 

Pacific oyster mortalities are likely to be influenced 

by many factors, with OsHV-1 as a necessary but not 

sufficient cause. Figure 1 lists some of the possible risk 

factors. 

Farming method (depth, racks, long lines) 

Timing (spring/autumn) 

Travel factors (duration, conditions) 

Biosecurity practices 

Host 

Age/Size 

Genotype 

Plasticity/resilience 

Ploidy 

Agent 

Management 

OsHV-1 

Other pathogenic bacteria 

Environment 

Increases in temperature (sudden) 

Location 

Tidal effects 

Water column 

Phytoplankton blooms 

Affected/unaffected 

Figure 1: Possible risk factors for Pacific oyster mortality grouped around 

the epidemiological triangle of agent, host, and environment, with the 

addition of management factors.

First report in New Zealand 

On 17 November 2010 the Investigation and Diagnostic 

Centre (IDC) Wallaceville was notified by the oyster 

aquaculture industry of mortality events occurring in 

Pacific oyster farms in Northland and the Coromandel. 

A similar event had been reported the previous autumn 

(March–May 2009). An investigation was initiated, 

primarily to determine whether the mortalities described 

were associated with an infectious agent and secondarily 

to rule out OIE-listed diseases that could result in oyster 

mortalities. IDC epidemiologists also began work to 

describe the magnitude and pattern of the outbreaks. This 

report summarises the initial investigation work. 

Initial investigation 

An immediate field investigation was undertaken by a 

marine incursion investigator and aquatic scientist from 

the IDC. The clinical description was of acute mortality of 

Pacific oysters, particularly juvenile oysters (20–80 mm) 

and spat (free-swimming larvae less than 20 mm long) 

newly moved on to farms. Some animals displayed 

gaping (incomplete shell closure) on emersion and were 

slow to close when gently tapped while immersed. The 

most significant clinical findings, however, were large 

numbers of dead, gaping, empty shells or shells containing 

rapidly decomposing animals. From knowledge of animal 

movements onto properties an incubation period of less 

than seven days was evident. 

Samples were taken initially from five sites covering 

the far north, Bay of Islands, west coast and Auckland, 

amounting to about 250 oysters. Oysters selected for 

sampling were clinically unaffected owing to the difficulty 

of finding affected animals that were not already in a state 

of advanced decomposition. After laboratory testing at the 

IDC a presumptive identification of OsHV-1 was made 

by PCR on 27 November 2010 and this was confirmed on 

6 December 2010 by DNA sequencing. 

Testing limitations 

Operating characteristics of the real-time PCR were 

unknown as the test was developed during the response. 

The analytical sensitivity was unknown and as a result 

caution needed to be exercised when interpreting any 

negative results. This means that although surveys for 

freedom from disease can be justified, freedom from 

the organism in apparently disease-free areas cannot 

be validated. 

Histology was limited as a diagnostic tool because 

most of the samples obtained were healthy owing to 

the difficulty of finding affected oysters. As a result the 

samples obtained were not representative of the affected 

population. Possibly they represented latent infected, 

subclinical or recovered animals. 

Data collection, analysis and results 

Data on affected sites (numerator data) was collected 

opportunistically through industry assistance – initially 

from the minutes of industry meetings and, after the end 

of November, by voluntary weekly reporting. Estimates 

of the earliest time of onset and intra-farm prevalence 

by size-class were then made. The data is likely to be 

inaccurate and biased as it is based on visual inspection 

and recall, and limited by the numbers of farmers who 

participated. No baseline data was available to act as 

guidance as to the expected normal level of seasonal 

mortality. The data likely suffers from reporting biases, 

with most reports from the most severely affected or 

those with a greater frequency of observation. Caution 

is therefore necessary when making inferences from the 

data. This also limited analysis to being descriptive. 

Data on the overall population at risk (PAR) of being 

affected (denominator data) was extracted from the 

Aquaculture Readiness Data project (Brangenberg 

& Morrisey, 2010). Aggregate-level data (e.g., within 

growing area or geographic location) was good, as was 

knowledge of data sources and contacts available. The 

total number of oyster farm leases issued is 260 but there 

is no record of active leases, so the PAR was unknown at 

that level. No resources were available to perform active 

casing or surveillance. 

Owing to these limitations, the investigation was 

restricted to counting data largely collected after the event 

and it was not possible to determine the true prevalence, 

incidence, or incidence rates of disease within an 

aggregate level. 

Ideally the unit of interest would be at the lease or 

farm level, which would enable collection of intrinsic 

farm factors such as frequency of disease between and 

within farms and also management factors. Owing to 

the limitations of data collection described at both the 

numerator and denominator levels the reporting unit 

had to be confined to the harbour level. Also from the 

Aquaculture Readiness Data project, the defined dispersal 


areas of pathogens was shown to typically encompass all 

the farms in areas like harbours and inlets, making them 

epidemiological units. 

It was apparent, however, that 18 locations (harbours, 

bays and inlets) were in the affected area, which included 

260 farms. Of these, 15 locations were reported as 

affected. Seven locations were sampled (six affected, one 

unaffected), within which 14 different lease sites were 

sampled. Six of the seven locations sampled were positive 

for OsHV-1 and 11 of the 14 lease sites were positive 

(Table 1). No South Island farms were affected. 

TABLE 1: Reported, sampled and laboratory-tested status of harbours and growing areas 

during the oyster mortality event, from the first known occurrences to 18 January 2011. 

GROWING 

AREA (GA) 

22 

GEOGRAPHIC 

LOCATIONS 

201 Parengarenga 

Harbour 

202 Whangaroa 

Harbour 


REPORTED 

HARBOUR 

STATUS FROM 

1/11/10 TO 

18/1/11 

NUMBER 

OF 

FARMS 

SAMPLED 

NUMBER 

OF 

AT-RISK 

FARMS 

NUMBER OF 

OsHV-1 

CONFIRMED 

FARMS 

Affected 0 34 0 


204 Kerikeri Inlet Affected 0 12 0 

204A Kerikeri Inlet Affected 0 4 0 

205 Orongo Bay Affected 1 23 1 

206 Waikare Harbour Affected 3 29 3 

208 

(North) 

209 

(South) 

Kaipara Harbour Affected 0 36 0 

Kaipara Harbour Affected 1 1 1 

suspicious 

215 Houhora Harbour Unaffected 2 16 0 

218 Rangaunu Affected 1 7 1 

301 Mahurangi Harbour Affected 5 43 4 

412 Hauraki Gulf Affected 0 3 0 

413, 414 Hauraki Gulf Affected 0 3 0 

207 Whangarei Harbour Affected 0 1 0 

Hokianga Harbour Affected 

(unconfirmed) 

0 2 (spatcatching 

611, 612 Coromandel Affected 0 12 0 

6101, 

6102 

609 Whangapoua 

Harbour 

Coromandel Unaffected 0 6 


602 Whitianga Harbour Unaffected 0 1 0 

608 Kawhia Harbour Unaffected 0 1 0 

701 Ohiwa Harbour Affected 0 2 0 

502 Kauri Bay Affected 0 1 0 

0 

The earliest dates from the reports received for selected 

geographic locations and growing areas are shown in 

Figure 2, page 27. Most reports identified onset during 

the first three weeks of November. 

Disease frequency within individual 

farms 

During the voluntary weekly reporting periods in 

December 2010, 78 reports were received from 15 

farmers (Table 2). Mortality was significant on some 

farms and throughout all age-groups of oysters. From 

the average cumulative mortality figures there appears 

to be a gradient of effect by age (which equates to size) 

of oyster, with greater mortality in younger animals, but 

the normal mortality range by age is unknown. 

TABLE 2: Disease mortality presence and cumulative mortality by age, 

December 2010. 

MORTALITY* AVERAGE CUMULATIVE MORTALITY RANGE 

Spat 92% 50% 15–100% 

Small 78% 34% 0–80% 

Large 89% 14% 5–60% 

*Percentage of reports with mortality present in that size class 

Environmental risk factors 

Environmental risk factors (temperature, 

phytoplankton, salinity changes) were examined. Data 

to fully investigate these factors (matched to sites 

and times of interest and measuring the appropriate 

parameters) was very limited or in some cases not 

available. From the data available it appears sea 

temperatures at times preceding outbreaks of disease 

were higher in 2010 than in preceding years at some of 

the affected sites. This is probably not unexpected and 

due to the La Niña event, and supports other evidence 

that temperature is the environmental risk factor most 

often linked with oyster mortalities (Soletchnik et al., 

2007). No other conclusions about environmental risk 

factors could be drawn from the data. 

It is possible that the rate of temperature rise rather 

than the actual temperature reached is a risk factor. 

Figure 3 shows the trend in temperature over time at 

the Waiheke weather station.

Figure 2: Timeline of earliest observed oyster mortality 

Figure 3: Temperature readings for the Waiheke weather station, October–November 2010. Note 

the higher mean temperature from 26 October to 5 November in 2010, indicated by the solid red 

trendline when compared with the black trendline for preceding years. 

Industry movement patterns 

Movement data was collected before this outbreak 

through the Aquaculture Readiness Data project 

(Brangenberg & Morrissey, 2010). The industry appears 

to be very connected by movements that would lead to 

widespread dissemination of risk organisms. Organisms 

in one area are likely to be present 

in many or most other areas, though 

interestingly no disease has been 

reported in the South Island to date. 

Perhaps OsHV-1 is a necessary but 

insufficient cause of disease and other 

risk factors are required. 

Conclusions 

Evidence at the time that suggested 

OsHV-1 was directly associated 

with the mortality events described 

included: 

• the finding of OsHV-1 in oysters 

from all affected sites tested; 

• the massive increase in prevalence 

of OsHV-1 (detected by real- 

time PCR) by day 5 after transfer 

of susceptible animals into an 

affected growing area, with 

mortalities suddenly increasing on 

day 6; 

• evidence from overseas outbreaks 

that implicates OsHV-1 as a 

necessary cause of spat mortality 

and hatchery larval mortality; and 

• laboratory work at IDC that has 

revealed a close genetic association 

to the µ-var strain of OsHV-1, 

which has been linked to Pacific 

oyster mortalities in Europe since 

2008. 

Evidence that OsHV-1 was likely to be 

widespread throughout the industry 

included: 

1. The high prevalence of areas 

affected during this event as well as 

the autumn mortality. 

2. The high proportion of the affected 

farms sampled that tested positive for the virus in 

the spring event, together with the distribution of 

sampling. 

3. The fact that the compressed time period of first 

reported onset of mortality in affected farms (or 


24 

areas) is not consistent with a new introduction 

and propagating epidemic, but rather with an 

environmental trigger factor, or (less likely) a multiplepoint-source 

epidemic. 

4. Normal movement patterns and lack of biosecurity 

practices in the industry. 

5. Mortalities in C. gigas larvae were reported to have 

occurred in February 1991 in a New Zealand hatchery 

(Hine et al., 1992). This paper reported the detection 

of a herpes-like virus. 

6. Evidence from overseas outbreaks suggested that 

OsHV-1 can be present in the absence of disease, and 

that enabling factors (including environmental factors) 

are required to initiate an outbreak. 

REFERENCES 

Anon. (2012) Situation and outlook for primary industries, 50. http://tinyurl. 

com/lqcl88w. Accessed 20 June 2013 

Arzul I, Renault T, Lipart C, Davison AJ (2001) Evidence for interspecies 

transmission of oyster herpesvirus in marine bivalves. Journal of General 

Virology 82(4): 865–870. 

Barbosa-Solomieu V, Dégremont L, Vazquez-Juarez R, Ascencio-Valle F, 

Boudry P, Renault T (2005) Ostreid herpesvirus 1 (OsHV-1) detection 

among three successive generations of Pacific oysters (Crassostrea gigas). 

Virus Research 107(1): 47–56. 

Brangenberg N, Morrisey D (2010) Aquiculture readiness data project. 

Surveillance 37(4): 41–43. 

Burge CA, Griffin FJ, Friedman CS (2006) Mortality and herpesvirus 

infections of the Pacific oyster (Crassostrea gigas) in Tomales Bay, 

California, USA. Disease of Aquatic Organisms 72: 31–43. 

Davison A J., Eberle R., Ehlers B., Hayward G S., McGeoch D J., Minson A 

C., et al. (2009). The order herpesvirales. Archives of Virology; 2009.154: 

1, 171-177, 

Davison AJ, Trus BL, Cheng N, Steven AC, Watson MS, Cunningham C, 

et al. (2005) A novel class of herpesvirus with bivalve hosts. Journal of 

General Virology 86(1): 41–53. 

Hine P, Thorne T (1997) Replication of herpes-like viruses in haemocytes of 

adult flat oysters Ostrea angasi: an ultrastructural study. Diseases of Aquatic 

Organisms 29: 189–196. 

Keeling S E. New Zealand juvenile oyster mortality associated with ostreid 

herpesvirus - a longitudinal study. MPI internal document. 

McCallum H, Harvell D, Dobson A (2003) Rates of spread of marine 

pathogens. Ecology Letters 6(12): 1062–1067. 

Peeler E J, Allan Reese R, Cheslett DL, Geoghegan F, Power A, Thrush MA 

(2012) Investigation of mortality in Pacific oysters associated with ostreid 

herpesvirus- 1μVar in the Republic of Ireland in 2009. Preventive Veterinary 

Medicine, 105(1): 136–143 


Renault T, Lipart C, Arzul I (2001) A herpes-like virus infects a non-ostreid 

bivalve species: Virus replication in Ruditapes philippinarum larvae. 

Diseases of Aquatic Organisms 45(1) 1–7. 

Sauvage C, Pépin JF, Lapègue S, Boudry P, Renault T (2009) Ostreid 

herpesvirus 1 infection in families of the Pacific oyster, Crassostrea gigas, 

during a summer mortality outbreak: Differences in viral DNA detection and 

quantification using real-time PCR. Virus Research 142(1): 181–187. 

Schikorski D, Faury N, Pepin JF, Saulnier D, Tourbiez D, Renault T 

(2011) Experimental ostreid herpesvirus 1 infection of the Pacific oyster 

Crassostrea gigas: Kinetics of virus DNA detection by q-PCR in seawater and 

in oyster samples. Virus Research 155(1): 28–34. 

ACKNOWLEDGEMENTS 

The authors would like to thank members of the 

New Zealand oyster industry association who contributed 

to this article by providing data. Special thanks go to 

Colin Johnston, and Ministry for Primary Industries staff 

at the Animal Health Laboratory, Wallaceville and the 

animals response team at Pastoral House, Wellington. 

Paul Bingham 

Paul.bingham@mpi.govt.nz 

Naya Brangenberg 

Naya.brangenberg@mpi.govt.nz 

Rissa Williams 

Rissa.williams@mpi.govt.nz 

Mary Van Andel 

Mary.vanAndel@mpi.govt.nz 

Investigation and Diagnostic Centres and Response 


66 Ward Street 

Upper Hutt 

New Zealand

JUVENILE OYSTER MORTALITY RESPONSE: A LABORATORY 

PERSPECTIVE 

Field visit and initial testing 

Following notification of mortalities of juvenile 

Pacific oysters in the North Island, an immediate field 

investigation was undertaken by a marine incursion 

investigator and aquatic animal pathologist from the 

Ministry for Primary Industries’ (MPI) Investigation and 

Diagnostic Centre (IDC), Wallaceville. Samples from 

this investigation were brought back to the laboratory 

on 26 November 2010. The aquatic animal pathologist 

developed a list of differential diagnoses after the initial 

notification. During the initial field visit, the pathologist 

indicated that infection with ostreid herpesvirus 

(OsHV-1) should be considered to be a primary 

differential diagnosis associated with the mortalities. 

As part of preparedness planning, the IDC had previously 

ensured that reagents were immediately available on 

site for the molecular testing of OsHV-1. However, the 

nature of these initial diagnostic tests would not enable 

high-throughput processing so a review of published 

well-validated real-time PCR assays was conducted and 

reagents for a TaqMan assay (Martenot et al., 2010) were 

ordered from the USA through the supplier dnature on 

26 November. 

As part of the IDC protocol, initial samples submitted 

were subjected to a range of tests: 

• general aquatic animal bacteriology; 

• histopathology; 

• OsHV-1 conventional PCR; 

• Marteilia refringens PCR; 

• Perkinsus genus PCR; 

• Bonamia genus PCR; and 

• internal control PCR (mollusc 18S rRNA). 

TABLE 1: Summary of sample numbers tested and resources during response and 

longitudinal study. 

NUMBER HOURS PEOPLE 

INVOLVED 

Oysters processed 582 120 8 

Cockles processed 45 6 3 

Number of sites tested 10 n/a n/a 

PCR tests run 2820 120 4 

Histology slide examinations and 

interpretations 

1165 195 1 

Vibrio isolated >800 >270 3 

Vibrio speciated 40 80 2 

Laboratory reports produced 15 75 3 

Table 1 shows a summary of sample numbers tested 

during the response. 

Molecular testing 

The IDC had previously developed and validated 

protocols for high-throughput extraction of DNA from 

molluscs using the X-tractor gene (Qiagen, New Zealand). 

This work was done as part of an MPI operational 

research project whose outputs proved invaluable for the 

response work. 

Extracted DNA from the first samples received 

produced presumptive positives for the OsHV-1 nested 

conventional PCR (Arzul et al., 2001a,b) on 27 November. 

These presumptive positives were subsequently confirmed 

by sequencing. All other diagnostic differentials were 

negative for the first samples. 

Strain typing began on samples from the first DNA 

sequence-confirmed OsHV-1 positives by sequencing 

the genomic region C2:C6, a region used for strain 

characterisation. Samples were sent to Ecogene, Auckland, 

for DNA sequencing. Subsequent analysis by IDC 

scientists revealed a close genetic association (following 

the new EU regulation 175/2010) to the m-var strain 

of OsHV-1, which has been linked to Pacific oyster 

mortalities in France, the UK, Ireland and Spain since 

2008 (Garcia et al., 2011; Martenot et al., 2012). 

Samples that were positive for OsHV-1 were sent to 

another animal disease reference laboratory, Australian 

Animal Health Laboratory (AAHL) in Geelong, for 

confirmation in early December. On 24 December AAHL 

confirmed the identification of OsHV-1. 

Owing to limited resources it was decided to reduce the 

numbers of samples tested by PCR for protozoan parasites 

(Perkinsus genus, Bonamia genus and Marteilia refringens) 

and general aquatic bacteriology. About a third of samples 

were tested for these pathogens. 

Owing to courier delays, the laboratory was still awaiting 

the primers and probe for the TaqMan assay for OsHV-1. 

Because the nested conventional OsHV-1 PCR was very 

labour-intensive, about 25 percent of samples from each 

submission were tested by this method until the more 

efficient TaqMan assay was available. DNA extracts were 

held at -20⁰C until this assay became available for use. 

The primers and probe were received on 15 December 

and the real-time PCR was optimised for use with Ssofast 


probe mix (Bio-Rad) that day. Although purified virus 

was not available, infected oysters were used to implement 

and optimise the assay. Next day the backlog of samples 

was processed by real-time OsHV-1 PCR. In all, 1166 

tests plus controls were completed, demonstrating 

the efficiency of real-time PCR as a high-throughput 

testing method. All DNA was assessed for suitability for 

amplification using a mollusc internal control PCR that 

had been previously developed in-house. During the 

response, 112 samples were tested for Marteila refringens 

and Bonamia genus, and 132 for Perkinsus genus. All 

samples tested negative except one positive for Perkinsus 

genus. Further testing identified this as P. olseni, which is 

not exotic to New Zealand; it was reported to the OIE. 

In all, 376 oysters were tested for OsHV-1 from seven 

locations including affected and unaffected sites from 

both the North and South Islands. All unaffected sites 

tested negative and 62 percent of samples from the 

affected sites were positive. All South Island sites were 

unaffected and tested negative for OsHV-1. 

Bacteriology 

From the first 250 oyster samples, the total number of 

Vibrio isolated was over 800. Vibrio identification by 

biochemical methods is unreliable and complex, so all 

isolated Vibrio that were consistent across the samples 

received were stored until molecular methods were 

available. Previous work at the IDC had shown that 16S 

rRNA was not a suitable gene for speciation, so alternative 

published methods were reviewed. The method chosen 

was derived from Thompson et al. (2007) and targeted 

the atpA gene of Vibrio. Speciation was achieved through 

sequence analysis of the atpA gene. 

Histopathology 

Histopathology showed a generally consistent picture of 

interstitial haemocytosis associated with tissue necrosis, 

nuclear pyknosis and karyorrhexis. No evidence of 

protozoan pathogens or pathognomic indicators of other 

major molluscan diseases was found. Special stains were 

performed on some samples to rule out the presence of 

secondary fungal pathogens; these stains were negative. 

Longitudinal study 

During this response an opportunistic longitudinal study 

was carried out, taking advantage of pre-planned hatchery 

26 


spat movements. Healthy spat were moved to a location 

in the North Island that was experiencing mortalities and 

had previously tested positive by PCR for OsHV-1. 

The study design was streamlined as it was to be 

undertaken in parallel with sample processing as part 

of the response, so resources and staffing had to be 

considered. Following transfer of PCR-negative spat to the 

affected site, 30 spat were periodically tested over a 13day 

period. Testing ceased when animals were no longer 

suitable for testing owing to tissue degradation. 

The following tests were carried out on samples from each 

sampling day: 

• OsHV-1 by real-time PCR (n=30); 

• mollusc 18S real-time PCR (n=30); 

• culture for Vibrio species (n=10); and 

• histopathology (n=30). 

PCR positives peaked on day 7 and Vibrio splendidus 

was frequently seen, suggesting the possibility of a multifactorial 

event. This study, although small, provided 

useful insights into the behaviour of the virus in 

New Zealand waters. 

Work that followed the response 

Significant work continued in the aquatic animal 

diseases laboratory at the IDC to increase capability 

and knowledge of OsHV-1. In 2011, after extensive 

optimisation and validation work, the laboratory 

gained accreditation from International Accreditation 

New Zealand (IANZ) for the OsHV-1 real-time PCR. This 

gives clients confidence in the quality of results produced 

by the laboratory. 

The laboratory also increased its capability by extracting 

and amplifying DNA from formalin-fixed paraffinembedded 

tissue. This now enables the laboratory to go 

back to archived oyster samples submitted as far back as 

1999. Testing on these samples indicated the presence of 

OsHV-1 µVar-like in Crassostrea gigas samples from 1999 

in Northland. This technique has subsequently been used 

in other laboratories at the IDC and can be used on other 

archived material to test for other pathogens of interest. 

Another capability development to come out of the 

response was the in situ hybridisation (ISH) test for 

OsHV-1. This was developed using samples from 

the longitudinal study and enabled IDC scientists to

gain knowledge on how the virus moves through the 

oyster during infection and also to determine the most 

appropriate part of the oyster to target for molecular tests. 

To accommodate submitters and provide a fast 

turnaround for the real-time OsHV-1 PCR, the aquatic 

animal diseases laboratory validated a method that 

reduces sample preparation time from overnight to three 

hours. This ensures samples are processed and results 

reported to clients as soon as possible. 

The laboratory also undertook Next-generation 

sequencing of OsHV-1-infected larvae to further 

understand the complex aetiological picture associated 

with juvenile oyster mortalities. 

REFERENCES 

Arzul I, Nicolas JL, Davison AJ, Renault T (2001a) French scallops: A new 

host for Ostreid herpesvirus-1. Virology 290: 342–349. 

Arzul I, Renault T, Lipart C, Davison AJ (2001b) Evidence for interspecies 

transmission of oyster herpesvirus in marine bivalves. J. Gen. Virol. 82: 865. 

Garcia C, Thébault A, Dégremont L, Arzul I, Miossec L, Robert M et al. 

(2011) Ostreid herpesvirus 1 detection and relationship with Crassostrea 

gigas spat mortality in France between 1998 and 2006. Veterinary Research 

42(1): 73. 

Martenot C, Oden E, Travaillé E, Malas JP, Houssin M (2010) Comparison 

of two real-time PCR methods for detection of Ostreid herpesvirus 1 in the 

Pacific oyster, Crassostrea gigas. Virol. Methods (170): 86. 

Martenot C, Fourour S, Oden E, Jouaux A, Travaillé E, Malas J et al. (2012) 

Detection of the OsHV-1 μVar in the Pacific oyster Crassostrea gigas before 

2008 in France and description of two new microvariants of the ostreid 

herpesvirus 1 (OsHV-1). Aquaculture 338: 293. 

Thompson CC, Thompson FL, Vicente ACP, Swings J (2007) Phylogenetic 

analysis of vibrios and related species by means of atpA gene sequences. 

Int. J. Syst. Evol. Microbiol. 57: 2480. 

Cara Brosnahan 

cara.brosnahan@mpi.govt.nz 

Suzanne Keeling 

Suzanne.keeling@mpi.govt.nz 

Colin Johnston 

Colin.Johnston@aquaculture.org.nz 

Investigation and Diagnostic Centres and Response 



Upper Hutt 

New Zealand 


QUARTERLY REPORT OF INVESTIGATIONS OF SUSPECTED 

EXOTIC MARINE AND FRESHWATER PESTS AND DISEASES 

Fish kill investigated 

A Department of Conservation (DOC) staff member 

notified MPI of a fish kill involving upland bullies 

(Gobiomorphus breviceps) in Spider Lakes, Canterbury 

region. The kill was first observed at the end of November 

2012 and appeared to initially involve mostly larger 

fish. A subsequent visit the following week found that 

all sizes appeared to be affected. Only upland bullies 

were involved, though it is possible that no other fish 

species live in the Spider Lakes as water levels had 

dropped to levels which would not support salmonids 

and they have not been stocked with salmonids by Fish 

and Game since 1990. Vegetation around the lake edge 

appeared to be dying off, and a strong decomposing 

plant smell was noted. No dead fish were seen in nearby 

lakes. Seven whole fish were preserved and submitted 

to the Animal Health Laboratory for histopathology. 

Cysts of the digenean trematode Telogaster opisthorchis 

(Platyhelminthes: Trematoda) were found extensively 

throughout the organs of all fish, with minimal 

inflammatory response. Two digenean flukes identified as 

Coitocaecum parvum were also found in the intestine of 

one fish. Both these species have previously been found 

in New Zealand freshwater fish. In the opinion of the 

pathologist, while these parasites probably compromised 

the fishes’ health, they were unlikely to have been the 

cause of the mortality event. Given the isolation of the 

lake and the lack of any histological signs of infectious 

disease, the fish kill was thought to be most likely a 

natural event associated with the decomposition of 

plant material affecting water quality. The results were 

communicated to DOC and the investigation closed. 

Flavobacterium psychrophilum 

confirmed 

MPI investigated a chinook salmon (Oncorhynchus 

tshawytscha) hatchery that had been experiencing 

low levels of mortality (~0.03–0.06 percent/day). Fish 

were described as having ulcerated peduncles or were 

completely missing caudal fins, but were otherwise in 

normal body condition. Initial histopathology revealed 

acute deep tissue necrosis with little inflammatory 

response and the presence of green filamentous gramnegative 

organisms. The pathologist suggested this 

could be associated with peduncle disease caused by 

Flavobacterium psychrophilum, which had not been 

previously reported from New Zealand. More clinically 

28 


Exotic marine pest and aquatic disease investigations 

are managed and reported by MPI’s Investigation and 

Diagnostic Centre (IDC), Wallaceville. The following is 

a summary of investigations of suspected exotic marine 

diseases and pests during the period from January to 

March 2013. 

affected specimens were submitted to the MPI Animal 

Health Laboratory. PCR for Flavobacterium sp. was 

positive in 50 percent of fish submitted and sequencing 

indicated F. psychrophilum. Fry from two other chinook 

salmon hatcheries, one on the same river that was 

exhibiting fungal disease and one on a different river 

where fish were missing peduncles, also tested positive 

to F. psychrophilum by PCR, and these diagnoses were 

confirmed by sequencing. 

MPI initiated a response and worked collaboratively with 

the salmon industry (commercial hatcheries and their 

managers), Fish and Game, local iwi and Aquaculture 

New Zealand to find out more about this bacterium and 

its presence and significance in New Zealand. 

This disease typically affects salmonid fry (e.g., rainbow 

trout, brown trout and chinook salmon) and overseas it 

has also been reported from eels, lamprey and carp. It 

typically appears in fish farms and hatcheries, where large 

numbers of fish exist in confinement. In New Zealand it 

has only been reported from farmed chinook salmon fry. 

There were no reports of disease outbreaks occurring in 

wild fish in the rivers associated with the properties. 

F. psychrophilum is well established worldwide in 

countries that have cold fresh water. The resulting 

disease only appears in cold water (below 16 o C). Other 

environmental factors such as stress or poor water quality 

are often contributing factors. Simple husbandry and 

hygiene measures can be incorporated into hatchery 

management routines to minimise the risk of disease 

outbreaks from pathogens such as F. psychrophilum. 

There are no human health, food safety or trade concerns 

as a result of this identification. Flavobacteriums have 

been known from New Zealand for some years, and 

F. psychrophilum is known widely from around the world, 

including Australia. Genetic analysis has confirmed that 

the strain found in New Zealand is unique, and suggests 

that it is unlikely to be from a recent incursion. The 

reason it has not been detected sooner may be that it

co-occurs with other fish pathogens such as external 

parasites or fungal disease, making it difficult to 

recognise. Further, it is challenging to grow in bacterial 

culture, owing to its fastidiousness, and molecular tests 

for it have not previously been conducted. 

Overall, the risk F. psychrophilum poses to New Zealand 

was assessed as low, and owing to the likelihood that this 

species has been present for some time without appearing 

to cause severe outbreaks, the response was stood down. 

A fact sheet was produced and distributed to stakeholders 

to provide information including hygiene measures, 

hatchery maintenance to minimise the risk of disease 

outbreaks, how to recognise its effects on fish fry, and how 

to contact MPI. 

Caprellid shrimp confirmed 

On 14 October 2012 a scientist from the Cawthron 

Institute notified MPI that some biofouling specimens 

collected from a mussel farm off Opotiki could not be 

identified, and expressed concern that they might be 

exotic. The specimens had been collected as part of a 

project comparing biofouling between offshore and 

nearshore sites. Bryozoans, caprellid shrimps and a 

brittlestar were submitted to NIWA’s Marine Invasive 

Taxonomic Service (MITS). Most were identified as 

indigenous but the caprellid shrimps were identified as 

non-indigenous species, Caprella andreae. This is the first 

time that this species has been recorded in New Zealand. 

C. andreae is known from the northeastern Atlantic, 

Mediterranean Sea, Hawaii, Sea of Japan, Korean Strait, 

Atlantic coast of USA (including Key West, Florida and 

Ocean City, New Jersey) and Cuba (McCain 1968, Foster 

et al., 2004, Sezgin et al., 2009). There is also a single 

Australian record from South Solitary Island, New South 

Wales. The species is considered an obligate rafter on 

substrata such as driftwood, buoys, seaweed, and is also 

epibiotic on sea turtles (McCain 1968, Sezgin et al., 2009). 

Non-indigenous caprellids may also be transported 

in association with vessel biofouling (e.g., Boos 2009, 

Montelli 2010, Ros and Guerra-Garcia 2012). It is thought 

that C. andreae probably reached New Zealand by rafting, 

or by hitchhiking on a vessel as biofouling. It is the 

taxonomist’s opinion that although the Opotiki find is 

the first in New Zealand, this is unlikely to be the place 

it first arrived in the country. It probably was spread as a 

result of its preference for floating structures, by rafting 

or movements of aquaculture equipment, vessels, etc. 

C. andreae is typically found in shallow water (< 60 m) 

and has been associated with fish farms overseas. It is 

not surprising that in New Zealand it was first found 

associated with a mussel farm. While its environmental 

tolerances are not well understood, C. andreae has wide 

latitudinal range in the northern hemisphere (~19º to 

54ºN) and has been reported from a variety of habitats 

and substrata. It is therefore probably able to inhabit most 

coastal ecosystems around New Zealand. 

It is not known what impacts, if any, this species would 

have on the New Zealand environment. It does not have 

a history of becoming a pest like Caprella mutica, which 

was first found here in 2002 and is considered established. 

Caprellid amphipods are typically detritivores, although 

some species (mainly those that are widely distributed) 

are considered to be opportunistic or predatory (Guerra- 

Garcia & de Figueroa 2009; Alarcon-Ortega et al., 2012). 

Extrapolating from the work of Guerra-Garcia and de 

Figueroa (2009), the diet of C. andreae could overlap 

that of C. equilibra, but possibly not that of Caprellina 

longicollis (both species are widespread in New Zealand 

waters and are cosmopolitan.) Biosecurity response 

options to a small mobile crustacean like C. andreae are 

limited. The distribution of C. andreae is not known in 

New Zealand, but it is unlikely to be restricted to the 

mussel farm where it was first detected. It may have gone 

undetected in New Zealand for some time. 

Given the apparently low risks that C. andreae poses to 

New Zealand, the long time that the organism is believed 

to have been established, the likelihood that the mussel 

farm is not its first place of arrival, and the lack of tools 

for effective response, a response was not recommended 

and the investigation was closed. 

Biofouling investigated 

On 19 October 2012 MPI was notified by the Northland 

Regional Council (NRC) that a 17.5 m tug had arrived 

at Marsden Cove Marina with heavy biofouling. 

NRC arranged for divers to inspect the tug and take 

representative samples of its biofouling to assess any 

biosecurity risk. While the divers were underwater 

they noticed biofouling on three other vessels berthed 

nearby. These vessels included two 12 m yachts of Pacific 

Island origin and a 30 m centreboard yacht of domestic 

origin. The divers took samples from all the vessels 

and submitted them to the Marine Invasive Taxonomic 

Service for identification. 


Six adult specimens of a non-indigenous sabellid 

fanworm, Sabellestarte spectabilis, were identified from 

one of the 12 m yachts. The hull of this yacht had been 

fastidiously cleaned by its owners, who are commercial 

divers, and further to this, it was hauled out of the 

water for cleaning two weeks after the initial sampling 

event, effectively removing the source of infestation and 

mitigating any further biosecurity risk. The taxonomist 

who identified the Sabellestarte spectabilis reported that 

this species does have the potential to survive in northern 

New Zealand. However, unlike Sabella spallazanii, which 

is present in New Zealand, Sabellestarte spectabilis has 

not been reported as a pest fouling species overseas, and 

is not reported to grow in aggregations so it is unlikely to 

modify habitat or have significant impacts. 

The other 12 m yacht had reportedly arrived in November 

2011 and was laid up in Marsden Cove while its French 

owners returned home. Divers said it was heavily 

fouled with macrofouling consistent with its having 

been laid up for 12 months. One specimen of Sabella 

spallanzanii was collected from this vessel. From the 

size of the specimen, the taxonomist was of the opinion 

that it had settled on the vessel while it was in Marsden 

Cove. A cryptogenic ascidian, Styela plicata (known 

to be present in New Zealand), was also identified. 

While Sabella spallanzanii is established in some parts 

of New Zealand, NRC is actively seeking to prevent 

its establishment, and is backing ongoing activities to 

monitor Whangarei Harbour, including Marsden Cove 

Marina for infestations. Like the other 12 m yacht, this 

vessel was hauled out to be cleaned, removing this source 

of infestation and mitigating the future biosecurity risk. 

The 30 m domestic yacht had reportedly been in Marsden 

Cove Marina for 6–12 months and had heavy fouling 

on the bottom of its skeg and around the anodes and 

propeller shaft. Unusual anemones seen were identified 

as an undescribed native species of Epiactis. Ascidians 

and an oyster were respectively identified as the native 

species Corella eumyota and Ostrea chilensis. This vessel 

was not known to have travelled overseas recently, and 

therefore does not pose an immediate biosecurity risk, but 

the macrofouling already on its hull may provide habitat 

conducive to settlement of pest organisms. 

The tug had arrived from Brisbane, Australia, on 

6 October 2012. In the previous two years this vessel 

had moved between ports on the east coast of Australia 

as well as New Zealand. The divers described the hull 

30 


biofouling as typical of a working vessel that had been 

in the water for 12 months or more. Oysters, barnacles 

and other representative specimens were recovered from 

the screens, anodes, rope guard and other areas where 

antifouling paint typically fails. A damaged sabellid 

fanworm specimen of the genus Branchiomma could not 

be identified to species level. There are native species of 

this genus in New Zealand, but the taxonomist suspected 

this particular one was non-native. The indigenous 

sabellid fanworm Parasabella aberrans was also identified. 

A non-indigenous bryozoan, Scrupocellaria bertholletii, 

and a non-indigenous ascidian, Herdmania momus, were 

both identified; both have been previously found on vessel 

hulls in New Zealand but are not considered established. 

Specimens of S. bertholletii have previously been collected 

from vessel hulls in New Zealand in 2005 and 2008, but 

could not be identified until this most recent specimen 

was collected. The taxonomist reported that if this 

bryozoan were to become established here, it would likely 

occupy the same niche as the already-established alien 

species Tricellaria catalinensis. Because S. bertholleti is a 

small, turfing, hydroid-like species, it is the taxonomist’s 

opinion that ecological impact is likely to be relatively 

benign. 

The ascidian H. momus is predominantly a tropical 

species and is considered unlikely to be able to establish 

in New Zealand, except perhaps in the very far north. 

It has previously been found on visiting vessels, but no 

established populations have been found. This species 

is not noted as a pest overseas. Two other ascidians, 

Microcosmus squamiger (crytogenic, known to be 

present in New Zealand) and Cnemidocarpa hemprichi 

(indigenous) were also identified. Overall, the risk of 

the non-indigenous species establishing and causing 

significant ecological impacts was considered low. The 

results were communicated to NRC and the investigation 

was closed. 

This investigation reaffirms that biofouling on 

international vessels is an active pathway for marine pests 

to reach New Zealand, and that in turn domestic vessels 

can help spread these pests. 

Ascidian investigated 

A resident from Glen Bay, Akaroa, contacted 

Environment Canterbury (ECan) after finding a colonial 

ascidian that they did not recognise. ECan contacted 

NIWA for help with the identification, and a specimen

was submitted to the Marine Invasive Taxonomic Service. 

It could only be identified to the genus Didemnum as 

it was too degraded. To date, D. vexillum is the only 

recorded exotic didemnid species in New Zealand, and 

has been found at Tauranga, Lyttelton, Opua, Nelson, 

Picton, Wellington and Whangarei. There are also 

native didemnids including D. incanum from the South 

Island including Pelorus Sound, Bluff and Picton. The 

species reported from Glen Bay was thought likely to 

be one of those already recorded from New Zealand. 

NIWA communicated the results back to ECan and the 

investigation was stood down. 

Styela clava range extension confirmed 

Sampling of Wellington Harbour by the Marine High Risk 

Port Surveillance (MHRPPS) programme in February 

2013 found two solitary ascidians in Chaffers Marina, 

which were provisionally identified as Styela clava. They 

were sent to the Marine Invasive Taxonomic Service and 

subsequently confirmed as this species. The finding may 

represent a range extension for this species, as S. clava was 

previously found in Wellington at Clyde Quay Marina in 

2007 on the hulls of four vessels but has not been recorded 

since. These new specimens were collected by chance by 

MHRPPS divers on the marina seabed at a depth of 11 m 

(they were searching for some sunglasses lost overboard.) 

The ascidians were not attached to any substratum but 

appeared to be alive, which suggests they may have been 

scraped off a boat. It is of note that since these specimens 

may have come off a vessel hull, the species is possibly not 

yet established at this site. In the next port survey the area 

will be checked again. 

An ascidian suspected to be Styela clava was reported to 

the exotic pest and disease hotline by a Cawthron Institute 

scientist. It was found while examining some client 

samples from Pauatahanui, Porirua Harbour. Samples 

were submitted to the Marine Invasive Taxonomic Service 

and confirmed to be S. clava. A recent unconfirmed 

report of S. clava in this area has also been made. This 

identification serves as an official record of a range 

expansion for this invasive ascidian. No response will 

be initiated, as the species is known to be established in 

New Zealand. This investigation was closed after the range 

expansion was logged. 

New to New Zealand alga confirmed 

A NIWA scientist collected a sample of Schizymenia sp. 

(Rhodophyta: Nemastomatales) from the ferry terminal in 

Wellington in 2008. Sequencing data has just confirmed 

that it is S. apoda, a species exotic to New Zealand. The 

native range of this organism includes South Africa, the 

Azores, China and Korea. A publication documenting 

the finding is currently being written by the scientist, 

and further field sampling around the Wellington region 

has been carried out. Preliminary results indicate that 

this species is widespread in the harbour but not outside 

it. Another sample, from Otago, is suspected to be the 

same species. Since this appears to be well established 

in New Zealand and does not appear to pose a major 

biosecurity risk, this investigation was closed. 

REFERENCES 

Alarcon-Ortega LC, Guerra-Garcia JM, Sanchez-Moyano JE, Cupul-Magana 

FG (2012) Feeding habits of caprellids (Crustacea: Amphipoda) from the 

west coast of Mexico. Do they feed on their hosting substrates? Zoologica 

Baetica 23: 11–20. 

Boos K (2009) Mechanisms of a successful immigration from north-east 

Asia: population dynamics, life history traits and interspecific interactions 

in the caprellid amphipod Caprella mutica (Schurin, 1935) (Crustacea, 

Amphipoda) in European coastal waters. PhD thesis, Freie Universität 

Berlin. 

Foster JM, Thoma BP, Heard RW (2004) Range extensions and review of 

caprellid amphipods (Crustacea: Amphipoda) from the shallow, coastal 

waters from the Suwannee River, Florida, to Port Aransas, Texas, with an 

illustrated key. Gulf and Caribbean Research 16(2): 161–175. 

Guerra-Garcia JM, de Figueroa JMT (2009) What do caprellids (Crustacea: 

Amphipoda) feed on? Marine Biology 156: 1881–1890. 

McCain JC (1968) The Caprellidae (Crustacea: Amphipoda) of the Western 

North Atlantic. Bulletin of the United States National Museum 278: 1–147. 

Montelli, L. (2010) The recent geographical expansion of Caprella 

californica (Caprellidea:Caprellidae) around the coastline of Australia. 

Biological Invasions 12: 725–728. 

Ros M, Guerra-Garcia JM (2012) On the occurrence of the tropical caprellid 

Paracaprella pusilla Mayer, 1890 (Crustacea:Amphipoda) in Europe. 

Mediterranean Marine Science 13(1): 134–139. 

Sezgin M, Ates AS, Katagan T, Bakir K, Yalinozdilek S (2009) Notes on 

amphipods Caprella andreae Mayer, 1890 and Podocerus chelonophilus 

(Chevreux & Guerne, 1888) collected from the loggerhead sea turtle, Caretta 

caretta, off the Mediterranean and the Aegean coasts of Turkey. Turkish 

Journal of Zoology 33: 433–437. 

Paul Bingham 

Team Manager 

Surveillance and Incursion Investigation (Animals and Marine) 


paul.bingham@mpi.govt.nz 


PLANTS AND ENVIRONMENT 

SOUTHWARD EXTENSION OF THE ASIAN TIGER MOSQUITO 

AEDES ALBOPICTUS: IS NEW ZEALAND AT RISK? 

Introduction 

New Zealand has only 13 native mosquito species, 

including a recently discovered undescribed species from 

the Chatham Islands (Holder et al., 1999; Mark Disbury, 

Mosquito Consulting Ltd, pers. comm.). According 

to Laird (1995) our mosquito fauna is depauperate 

compared to other countries of similar size and latitude. 

New Zealand is particularly susceptible to invasion as 

larval habitats are largely underutilised, providing vacant 

niches in which new species could become established 

(Laird, 1995). Since the arrival of humans around the 

13th century, the environment has been invaded by a 

large number of exotic animal and plant species (Cook 

et al., 2002). Invasion continued at an unabated pace with 

the arrival of Europeans, who transformed the natural 

environment by large-scale pastoralism and horticulture, 

which coincided with the escalation of polyphagous insect 

pests (Cook et al., 2002). This expanded further with the 

rise of of global trade in the 19th century and tourism in 

the 20th century. 

Introduced species 

Four mosquito species have managed to become 

established despite the ongoing intensity of border 

interceptions. The first, the brown house mosquito 

(Culex (Culex) quinquefasciatus (Say)) is thought to 

have arrived on American whaling ships in the 

1830s and is found around North Island ports and 

as far south as Marlborough. There have also been 

finds in Christchurch and Queenstown but there is 

no evidence of establishment there (Mark Disbury, 

Mosquito Consulting Ltd, pers. comm.). Aedes 

(Finlaya) notoscriptus (Skuse), the striped mosquito, 

was first recorded in Auckland in 1916 and probably 

arrived from Australia. It is the mosquito most often 

seen in the North Island, while in the South Island 

it is thought to occur only in Nelson, Marlborough 

and Christchurch. The saltwater mosquito, Aedes 

(Halaedes) australis (Erichson), probably arrived at 

southern New Zealand ports on timber ships from 

Australia. It was first recorded at Stewart Island 

in 1961, and is found in Southland, Otago and 

Westland. The southern saltmarsh mosquito, Aedes 

(Ochlerotatus) camptorhynchus (Thomson) was 

first found in Napier in 1998, after complaints of its 

vicious daytime biting. It was progressively 

eradicated from ten other coastal locations around 

32 


Number of interceptions 1998-2012 

18 

12 

6 

0 

the North Island and from the Wairau River estuary, near 

Blenheim. The last adult southern saltmarsh mosquito 

was found at Wairau in October 2006 and the last larvae 

were found in June 2008. This species was officially 

declared to be eradicated from New Zealand 

in 2010. 

Disease risk 

At present there is no human disease transmission by 

mosquitoes within the country, but competent vectors 

do exist here (Mackereth et al., 2007) so New Zealand is 

at risk from disease introduction and subsequent vectorborne 

outbreaks (Kay, 1997). Also, there are many exotic 

mosquito species that present a risk of entry and could 

change our human-disease-free status. Immigration 

and tourism mean there is a regular influx of viraemic 

travellers. For example, most dengue cases come from the 

Pacific Islands (Kay, 1997). 

Asian tiger mosquito 

The Asian tiger mosquito Aedes (Stegomyia) albopictus 

(Skuse) is considered our most significant mosquito 

threat and is one of the most invasive mosquito species in 

the world (Holder et al., 2010). It is the most frequently 

intercepted species of mosquito associated with imported 

goods at our borders (Figure 1). 

Aedes polynesiensis 

Aedes aegypti 

Aedes albopictus 

Aedes camptorhynchus 

Aedes japonicus 

Aedes other 

Aedes vigilax 

Culex annulirostris 

Culex australicus 

Culex other 

Culex sitiens 

Figure 1: Interceptions of exotic mosquitoes of public health importance associated 

with imported goods, 1998–2012 (Ministry of Health, unpublished data provided by 

Sally Gilbert) 

Other

Most exotic mosquito interceptions have been on ships, 

and generally associated with used tyres and used 

machinery (Figure 2). The Ports of Auckland have 

been the most frequent site of interception (Derraik, 

2004). Climate modelling has shown that Auckland and 

Northland are the most suitable regions for establishment 

of Ae. albopictus (de Wit et al., 2001). 

Figure 2: sources of exotic mosquitoes of public health importance 

intercepted from 1998 to 2012 (Ministry of Health, unpublished data 

provided by Sally Gilbert) 

The Asian tiger mosquito, Ae. albopictus (Figure 3), has 

been one of the fastest-spreading animal species over the 

past two decades (Anon., 2013). From its native range 

in Asia, it has spread throughout the Americas, Europe 

and Africa, mainly through the international trade in 

used tyres (Guillaumot et al., 2012). Establishment at 

temperate latitudes has been facilitated by egg diapause, 

which confers cold-hardiness in the species but is absent 

in tropical populations (Benedict et al., 2007). The success 

of Ae. albopictus as an invader is partly due to its ability to 

use a wide variety of natural and artificial habitats. More 

importantly, it is found primarily in urban areas, where 

inspection and control can be logistically difficult. 

The Asian tiger mosquito can transmit a large number 

of arboviruses, but the vectorial status of its temperateclimate 

populations has been little investigated (Benedict 

et al., 2007). It is an important vector of dengue virus 

and more recently has become the primary vector of 

chikungunya virus, an arbovirus that causes a disease 

infecting more than a million people in India and 

islands of the Indian Ocean (Guillaumot et al., 2012). 

For example, it caused epidemics of chikungunya on the 

island of Réunion in 2005–2006, while in 2007 the first 

outbreak of the disease was reported in Italy and in 2010 

both chikungunya and dengue were reported in the south 

of France (Guillaumot et al., 2012). 

Figure 3: The Asian tiger mosquito Ae. albopictus, an aggressive daytime 

biter (Photo: James Gathany, Centres for Disease Control and Prevention 

USA / Global Invasive Species database) 

The distribution of Ae. albopictus across the Pacific 

Islands is patchy. Since the 1970s the species has been 

present in Papua New Guinea and the Solomon Islands, 

spreading south to Fiji in 1989 (Guillaumot et al., 2012). 

No further introduction was reported in any other Pacific 

Island country until 2011 when specimens were collected 

during a training workshop in Tonga’s capital, Nuku’alofa. 

Immature Ae. albopictus were found co-existing with 

Ae. aegypti (Linnaeus) in tyres on the waterfront, close 

to the main harbour (Guillaumot et al., 2012). This is 

its most southern reported distribution in the South 

Pacific. Establishment in Tonga is unsurprising owing to 

the proximity to Fiji and the extensive trade and travel 

between the two countries. 

It is noteworthy that the invasion into Tonga did not 

occur earlier as there was no evidence that Ae. albopictus 

was present before 2011 (Guillaumot et al., 2012). Given 

the intensive trade (both international and between 

islands of individual nations), Ae. albopictus is likely to 

have arrived in many Pacific Island countries on multiple 

occasions, especially since this species has many times 

been intercepted at New Zealand’s borders. While the 

reason Ae. albopictus has not established in some islands 

is not clear, it is thought that this species cannot co-exist 


with the local Stegomyia mosquitoes (Guillaumot et al., 

2012). 

Risk of introduction to New Zealand 

This new record of Asian tiger mosquito is of great 

concern as it may indicate a slow, inevitable trend 

of invasion through the Pacific region and towards 

New Zealand. Indeed, the recent southward extensions 

of its range will probably increase the numbers of these 

unwanted organisms arriving at the border. Routine 

surveillance for exotic mosquitoes is in place at air and 

sea ports around the country, carried out by local public 

health units under direction of the Ministry of Health. 

Carbon-dioxide-baited light traps, ovitraps and tyre 

traps are used, in addition to larval sampling and regular 

treatment of all suitable breeding habitats at the ports. 

Most mosquito interceptions have been made through the 

Ministry for Primary Industries during goods and cargo 

inspections. There have also been some very important 

finds through port surveillance in the past, with a more 

recent discovery of Ae. albopictus in a light trap at the 

Ports of Auckland in 2007 (Holder et al., 2010). A largescale 

biosecurity surveillance and control programme 

was undertaken but no further finds were made (Holder 

et al., 2010). The combination of border inspections and 

port surveillance helps prevent the establishment of exotic 

mosquitoes in New Zealand. 

REFERENCES 

Anon. Global Invasive Species Database. http://www.issg.org/database. 

Accessed June 2013 

Benedict MQ, Levine RS, Hawley WA, Lounibos L (2007) Spread of the 

Tiger: Global Risk of Invasion by the Mosquito Aedes albopictus. Vectorborne 

and Zoonotic Diseases 7(1): 76–85. 

Derraik JGB (2004) Exotic mosquitoes in New Zealand: a review of species 

intercepted, their pathways and ports of entry. Australian and New Zealand 

Journal of Public Health 28(5): 433–444. 

de Wet N, Wei Y, Hales S, Warrick R, Woodward A, Weinstein P ( 2001) 

Use of computer model to identify potential hotspots for dengue fever in 

New Zealand. New Zealand Medical Journal 114(1140): 420–422. 

Cook A, Weinstein P, Woodward A (2002) The impact of exotic insects 

in New Zealand. In Pimentel D, ed. Biological invasions economic and 

environmental costs of alien plant, animal and microbe species, pp. 217- 

239. CRC Pree LLC, Florida. 

Guillaumot L, Ofanoa R, Swillen L, Singh N, Bossin HC, Schaffner F (2012) 

Distribution of Aedes albopictus (Diptera, Culicidae) in southwestern Pacific 

countries, with a first report from the Kingdom of Tonga. Parasites and 

Vectors 5(247) http://www.parasitesandvectors.com/content/5/1/247. 

34 


Holder P, Brown G, Bullians M (1999) The mosquitoes of New Zealand and 

their animal disease significance. Surveillance 26(4): 12–15 

Holder P, George S, Disbury M, Singe M, Kean JM, McFadden A (2010) A 

biosecurity response to Aedes albopictus (Diptera: Culicidae) in Auckland, 

New Zealand. Journal of Medical Entomology 47(4): 600–609. 

Kay BH (1997) Review of New Zealand Programme for Exclusion and 

Surveillance of Exotic Mosquitoes of Public Health Significance. Wellington: 

Ministry of Health. Wellington, 35pp. 

Laird M (1995) Background findings of the 1993–94 New Zealand 

mosquito survey. New Zealand Entomologist 18: 77–90. 

Laird M, Easton JM (1994) Aedes notoscriptus (Diptera: Culicidae) in 

Wellington Province. New Zealand Entomologist 17: 14–17. 

Mackereth G, Cane RP, Snell-Wakefield A, Slaney D, Tompkins D, Jokob- 

Hoff R, Holder P, Cork S, Owen K, Heath A, Brady H, Thompson J (2007) 

Vectors and Vector borne disease: Ecological research and surveillance 

development for New Zealand: Risk Assessement. Cross department 

research project. MAF Biosecurity New Zealand, 64 pp. 

Lora Peacock 

Senior Adviser 



Lora.peacock@mpi.govt.nz

PLANTS AND ENVIRONMENT INVESTIGATION REPORT 

Metallic shield bug found on 

container, Bluff 

A metallic shield bug, Scutiphora pedicellata (Hemiptera: 

Scutelleridae), was found on the outside of an empty 

shipping container at Bluff, Southland, during a 

maintenance survey. Only one live specimen was found, 

although this species is known to aggregate. The shipping 

container and other containers in the area had recently 

been unloaded. Quarantine inspectors were alerted at the 

port of arrivals. No further bugs have been reported. 

Termites in fallen power pole in 

Wellington 

The New Zealand Fire Service notified MPI on 

2 January 2013 of suspect termites in a power pole 

blown over the previous night during high winds in 

Wellington. The fire service was first on site following a 

111 emergency call. A fire officer noticed the pole had 

broken at the base, exposing a termite colony, recognised 

a potential biosecurity risk and arranged for MPI to be 

contacted. The very old square Australian hardwood pole 

had originally been used to support trolley bus wires. 

The termite was identified as Glyptotermes tuberculatus, 

an Australian dampwood termite. Although this is not a 

species considered to be present in New Zealand, colonies 

are occasionally found in imported Australian hardwood 

poles and wharf timbers. The earliest such record was in 

1940, and the most recent in 1995. No G. tuberculatus 

termite colonies have ever been found other than in 

association with the original piece of timber they arrived 

in, and there is no evidence of their ever starting a new 

colony here. The species’ status as a termite with minimal 

impacts is consistent with its significance in Australia, 

where it is limited to small colonies in logs and has 

minimal economic impacts. In general, its importance to 

New Zealand is considered less than our native drywood 

termites, which themselves cause limited problems, 

especially to houses. Instructions were provided to the 

field team tasked with replacing the pole to wrap both 

the above-and below-ground sections of the pole before 

transport to their depot. The pole was then cut into 

sections, steam-sterilised and deeply buried. 

The Ministry for Primary Industries’ (MPI) Investigation 

and Diagnostic Centres & Response directorate (IDC & R) 

is accountable for the investigation and diagnosis of 

suspect exotic pests and diseases. In the plant and 

environment sectors IDC & R has investigators and 

scientists based in Auckland and Christchurch. The IDC 

& R provides field investigation, diagnostic testing and 

technical expertise with regard to new pests and diseases 

affecting plants and the environment. The IDC & R 

also conducts surveillance and response functions, and 

research and development to support surveillance and 

incursion response activities. 

Suspect termites on yacht from 

Australia in Nelson 

MPI Verification received advanced notification from 

the Australian Department of Agriculture, Fisheries 

and Forestry (DAFF) that a yacht with Cryptotermes 

spp. in its internal timbers had left Australia for Nelson 

without obtaining the required customs clearance. DAFF 

said its officers had found live termites in the vessel and 

that the pest controller in Newcastle had located dead 

alate termites. MPI Verification issued a Biosecurity 

Authority Clearance Certification (BACC) on 1 February 

allowing five days for seaworthy repairs, maintenance 

and provisioning, and for a Quarantine Inspector to 

apply a knock-down spray to areas on the yacht known 

to have had termite activity. MPI Verification negotiated 

the repairs with local businesses and warned the owner 

that if the deadline was not met the vessel would be 

seized, towed to Wellington and fumigated, and the 

costs recovered from the owner. Termite-damaged wood 

was disposed of in biosecurity waste. The vessel left 

New Zealand territorial waters as requested. 

Oriental wood borer in furniture 

ex Indonesia 

Fresh borer beetle emergence holes in wooden furniture 

manufactured in Java, Indonesia, were reported from a 

Blenheim house. Nelson-based MPI border clearance 

staff confirmed the presence of live borer activity but did 


not find any adults. They helped arrange for the infested 

items to be wrapped in plastic and transported to Nelson 

seaport for fumigation with methyl bromide. Treatment 

of these items is now complete but it was not possible to 

trace all goods from the original consignment. The goods 

were imported by a specialist Javanese furniture importer 

and retailer based in Blenheim, who typically imports 

up to five 20 ft (6 m) containers of household furniture 

a year from the same manufacturer in Java, via Nelson 

seaport. The importer confirmed that the goods were 

from a February 2012 consignment, with entry based on 

certified fumigation before shipping. Website information 

pertaining to the Australian Fumigation Accreditation 

Schemer (AFAS) was provided to the importer, and 

included a list of Indonesian AFAS-accredited fumigation 

providers. Subsequently, a single dead adult beetle was 

found in the house and identified as the Oriental wood 

borer Heterobostrychus aequalis. This species can live in 

low-moisture sawn timbers and has spread from its native 

range (India, China, Indonesia) to Africa, Australia, 

New Caledonia, North America and Venezuela. However, 

its ability to establish in New Zealand conditions is 

unknown. MPI records since 2000 show 46 detections 

of this species in wooden goods from Thailand, the 

Philippines, Vietnam, Malaysia, China, the United States, 

Australia, Taiwan, Burma and South Africa. 

Graham Burnip 

Incursion Investigator 



Graham.Burnip@mpi.govt.nz 

Heather Pearson 

Incursion Investigator 



Heather.Pearson@mpi.govt.nz 

36 

SURVEILLANCE 40 (2) 2013

PEST WATCH: 9 FEBRUARY – 15 MAY 2013 

Biosecurity is about managing risks: protecting New Zealand from exotic pests and diseases that could harm our natural resources and primary industries. MPI’s Investigation & 

Diagnostic Centres and Response directorate devote much of their time to ensuring that new organism records come to their attention, and to following up as appropriate. 

This information was collected from 9 February 2013 to 15 May 2013. The plant information is held in the MPI Plant Pest Information Network (PPIN) database. Wherever 

possible, common names have been included. Records in this format were previously published in the now discontinued magazine Biosecurity. 

To report suspect new pests and diseases to MPI phone 0800 80 99 66. 

Validated new to New Zealand reports 

Type Organism Host Location Submitted by Comments 

Chromist 

Insect 

Insect 

Virus 

Virus 

Pythium macrosporum 

(no common name) 

Amphaces sp. 

(shield bug) 

Paropsisterna beata 

(Eucalyptus leaf beetle) 

Rose cryptic virus-1 

(RCV-1) 

(syn. Rose multiflora cryptic virus) 

Rose yellow vein virus 

(RYVV) 

Inanimate host 

(soil) 

Eucalyptus nitens 

(shining gum) 

Eucalyptus nitens 

(shining gum) 

Wellington Scion (High-Risk Site Survey) 

Wellington IDC & R (General Surveillance) Possible undescribed species 

Wellington IDC & R (General Surveillance) A response has been initiated 

Rosa sp. 

(rose) Mid Canterbury IDC & R (General Surveillance) 

Rosa sp. 

(rose) 

If you have any enquiries regarding this information please contact surveillance@mpi.govt.nz 

Whanganui IDC & R (General Surveillance) 

Sample originally collected in 

2011 


To report suspected exotic land, freshwater and 

marine pests, or exotic diseases in plants or 

animals, call: 

0800 80 99 66 

Investigation and Diagnostic Centre – 

Wallaceville 


Upper Hutt 

Tel: 04 526 5600 


Tamaki 

231 Morrin Road 

St Johns 

Auckland 

Tel: 09 909 3568 


Christchurch 

14 Sir William Pickering Drive 

Christchurch 

Tel: 03 943 3209 

GRIBBLES VETERINARY PATHOLOGY 

• AUCKLAND 

Courier: 485 Great South Road, Penrose, Auckland 

Postal: PO Box 41, Auckland 

Tel: 09 526 4560 Fax: 09 526 4569 

• HAMILTON 

Courier: 57 Sunshine Ave, Hamilton 

Postal: PO Box 195, Hamilton 

Tel: 07 850 0777 Fax: 07 850 0770 

• PALMERSTON NORTH 

Courier: 840 Tremaine Avenue, Palmerston North 

Postal: PO Box 536, Palmerston North 

Tel: 06 356 7100 Fax: 06 357 1904 

• CHRISTCHURCH 

Courier: 7 Halkett Street, Christchurch 8015 

Postal: PO Box 3866, Christchurch 

Tel: 03 379 9484 Fax: 03 379 9485 

• DUNEDIN 

Courier: Invermay Campus, Block A, Puddle Alley, Mosgiel 

Postal: PO Box 371, Mosgiel 

Tel: 03 489 4600 Fax: 03 489 8576 

NEW ZEALAND VETERINARY PATHOLOGY 

• HAMILTON 

Courier: Cnr Anglesea and Knox Streets, Hamilton 

Postal: PO Box 944, Hamilton 

Tel: 07 839 1470 Fax: 07 839 1471 

• PALMERSTON NORTH 

Courier: IVABS Building, 1st Floor, 

Massey University, Tennant Drive, Palmerston North 

Postal: PO Box 325, Palmerston North 

Tel: 06 353 3983 Fax: 06 353 3986

Volume 40, no. 2, June 2013 - Biosecurity New Zealand

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