Import Risk Analysis: 
Hatching eggs of domestic 
ducks (Anas platyrhynchos domesticus  and Cairina 
moschata) from the European Union, Canada, the United States of America, and 
Australia 
 
May 2012  
 This page is intentionally blank
  
 
Ministry for Primary Industries  
Pastoral House 
25 The Terrace 
PO Box 2526 
Wellington 6011 
New Zealand 
Tel: 64 4 894 0100 
Fax: 64 4 894 0731 
 
 
 
Import Risk Analysis: Hatching eggs of domestic ducks ( Anas platyrhynchos domesticus  and Cairina 
moschata) from the European Union, Canada, the Un ited States of Amer ica, and Australia 
 
May 2012 
 
  This page is intentionally blank 
Contents 
 
1. Executive Summary 1  
2. Introduction 2 
3. Background 2  
4. Commodity Definition 2 
5. Risk Analysis Methodology 2 
6. Duck Virus Hepatitis Types 1, 2 and 3 8 
7. Anatid Herpesvirus 1 11 
8. Goose Parvovirus and Muscovy Duck Parvovirus 15 
9. Reovirus of Muscovy Ducks 20 
10. Duck Circovirus 24 
11. Avian Chlamydiosis 28 
 
i  
ii Contributors to this risk analysis 
1. Authors 
Kerry Mulqueen Veterinary Consultant  
Helen Smith Senior Adviser, Risk Analysis 
(Animals and Aquatic) MPI, Wellington 
Stephen Cobb Principal Adviser, Risk 
Analysis (Animals and 
Aquatic) MPI, Wellington 
   
2. Internal Peer Review 
 
Lucy Johnston Senior Adviser, Animal 
Imports Team MPI, Wellington 
Christine Reed Manager, Science and Risk 
Assessment MPI, Wellington 
Derek Belton Manage r, International 
Standards MPI, Wellington 
Howard Pharo Manager, Import and Export 
Animals MPI, Wellington 
   
3. External Scientific Review 
 
Neil Christensen Veterinary C onsultant Avivet Ltd.    
 
 
  
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 1 1. Executive Summary 
This import risk analysis supplements MAF’s Import Risk Analysis: Hatching eggs from 
chickens (Gallus gallus) from the European Union, Canada, the United States of America, 
and Australia , dated 28 January 20091.  The diseases considered to be a risk in chicken 
hatching eggs are assumed to be a risk in duc k hatching eggs and the risk mitigation steps 
previously outlined for chicken hatching eggs are considered appropriate for the importation 
of duck hatching eggs.  
This analysis outlines the additional biosecurity  risks associated with the importation of duck 
hatching eggs from the European Union, Canada, th e United States of Am erica, and Australia. 
As a result of further risk assessments of di seases found in ducks, it is concluded that the 
following organisms should be considered a ri sk in duck hatching eggs and options are 
presented for their effective management: 
 Duck virus enteritis virus (anatid herpesvirus 1) 
 Goose and Muscovy duck parvoviruses (Musco vy ducks and their hybrid breeds only) 
 Muscovy duck reovirus (Muscovy ducks and their hybrid breeds only) 
 Chlamydia psittaci 
                                                 
1See: http://www.biosecurity.govt.nz/files/ regs/imports/risk/hatching-eggs-eu-ra.pdf  
2 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries  2. Introduction 
The diseases previously determin ed to be a risk in chicken hatching eggs are assumed to be a 
risk in duck hatching eggs.  This  risk analysis is therefore limited to a consideration of the 
additional biosecurity risks that may be posed  by the importation of hatching eggs of Pekin 
ducks ( Anas platyrhynchos domesticus ) and their hybrids, or Muscovy ducks ( Cairina 
moschata) and their hybrids. 
3. Background 
A New Zealand poultry company wishes to im port duck hatching eggs from the European 
Union.  MAF has previously examined the risks associated with chicken hatching eggs from 
the European Union, Canada, the United States of America, and Australia2.  It is assumed that 
the diseases previously determined  to be a risk in chicken hatchi ng eggs are also a risk in duck 
hatching eggs.  To support the development of an import health standard for duck hatching 
eggs, this supplementary risk analysis specifica lly examines the additional risks that may be 
associated with duck hatching eggs.  
4. Commodity Definition 
The commodity considered by this risk analys is is hatching eggs of Pekin ducks, Muscovy 
ducks, and their hybrids, from the European Union, Canada, the United States of America, 
and Australia.  The eggs will be sourced from  duck breeding flocks compliant with the 
standards described in Chapter 6.4 of the OIE Code (or equivalent) and be clean (free of 
faeces) when collected, unwashed, and have intact  shells (uncracked).  Following collection, 
the eggs will be disinfected in accordance with Chapter 6.4 of the OIE Code (or equivalent). 
5. Risk Analysis Methodology 
The methodology used in this risk analysis  follows the guidelines as described in Biosecurity 
New Zealand Risk Analysis Procedures – Version 13 and in Section 2 of the OIE Code . 
The risk analysis process used by MPI is summarised in Figure 1. 
                                                 
2Import risk analysis: Hatching eggs from chickens (G allus gallus) from the Euro pean Union, Canada, the 
United States of America, and Australia . See: http://www.biosecurity.govt.nz/ files/regs/imports/risk/hatching-
eggs-eu-ra.pdf 
 
3 See www.biosecurity.govt.nz/files/pests-diseases /surveillance-review/risk-analysis-procedures.pdf.  
Figure 1. The risk analysis process 
 
 
Not considered to 
be a risk in the 
commodity 
Organism/disease is 
conside
red to be a risk 
in the commodity 
 
5.1. PRELIMINARY HAZARD LIST 
The hazard identification process begins with the collation of a list of organisms possibly 
associated with the commodity that were not co nsidered in MAF’s import risk analysis for 
chicken hatching eggs. Table 1 shows these or ganisms, together with some of the key 
information considered in determining whether each organism should be considered further. 
This list was compiled from the text Diseases of Poultry, 11th edition, ed. Saif, Y.M., and 
from a review of the scientific  literature of poultry diseases. 
 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 3  
Table 1. Preliminary hazards iden tified in duck hatching eggs  
Organism/Disease  New Zealand status# Infection in duck eggs?  Infection on duck 
eggs? Needs further 
consideration?  
Picornaviridae  
Duck virus hepatitis 
type 1 Exotic, notifiable No Yes Yes 
Astroviridae  
Duck virus hepatitis type 2 Exotic, unwanted No Yes Yes 
Duck virus hepatitis 
type 3 Not recognised No Yes Yes 
Herpesviridae 
Duck viral enteritis Exotic, notifiable Yes Yes Yes 
Goose herpesvirus Not recognised No No No 
Experimental transmission of goose herpesviru s was shown to cause mortality in Muscovy ducks (Gough and Hansen 2000) although n atural 
infection of either Muscovy ducks or Pekin ducks has not been decribed.  
Paramyxoviridae* 
Avian paramyxovirus 
type 4 Present (Stanislawek et al 
2002 ) N/A N/A No 
Avian paramyxovirus 
type 6 Present (Stanislawek et al 
2002) N/A N/A No 
Avian paramyxovirus types 8 and 9 Not recognised Unknown Unknown No 
APMV-8 and 9 have been reported from ducks but are usually identifi ed as incidental findings duri ng surveillance for avian infl uenza and 
reports suggesting pathogenicity have not been located.  (Shortridge et al 1980; Alexander and Senne 2008). 
Parvoviridae 
Muscovy duck virus Not recognised Yes Yes Yes 
Goose parvovirus Exotic, unwanted Yes Yes Yes 
Reoviridae 
Reovirus infection of Muscovy ducks   Not recognised Yes Yes Yes 
Circoviridae 
Duck circovirus Not recognised No Yes Yes 
Bacteria     
Chlamydia psittaci  Some serovars exotic Yes Yes Yes 
Available evidence suggests serovars A and B of C. psittaci  are present in the New Zealand avian pop ulation, whereas exotic serovars C and 
E are more commonly associated with ducks (MAF 2010). 
 
#Based on the information from the register of unwanted organisms at http://www.biosecurity.gov t.nz/pests/registers/uor  and from the 
Biosecurity (Notifiable Organisms) Order 2010 
http://www.legislation.govt.nz/regulation/pub lic/2010/0265/lates t/whole.html?search =ts_regulation_biosecurity _resel&p=1  
N/A. = Not applicable because assessment is not relevant to this process when the organism is recognised as present in New Zeal and. 
*Avian paramyxoviruses 4, 6, 8, and 9 were not considered to be potential hazards in the previous chicken hatching eggs risk an alysis as 
they are not associated with chickens 
4 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
 
5.2. HAZARD IDENTIFICATION 
For each organism identified as requiring furt her consideration in Table 1, the epidemiology 
is discussed, including a consideration of the following questions: 
1. Could the imported commodity act as a vehicle for the introduction of the 
organism? 
2. If the organism requires a vector, coul d competent vectors be present in New 
Zealand? 
3. Is the organism exotic to New Zealand? 
4. If it is present in New Zealand, 
i. is it "under official control" , which could be by government 
departments, by national or regional pest management strategies or by a 
small-scale programme, or 
ii. are more virulent strains known to exist in other countries? 
For any organism, if the answer to question on e is “yes” (and the answer to question 2 is 
“yes” in the cases of organisms requiring a vector ) and the answers to either questions 3 or 4 
are “yes”, it is classified as a poten tial hazard requiring risk assessment. 
Under this framework, organisms that are pres ent in New Zealand cannot be considered as 
potential hazards unless there is evidence that strains with higher pathogenicity are likely to 
be present in the commodity to be imported.  Therefore, although there may be potential for 
organisms to be present in the imported commod ity, the risks to human or animal health are 
no different from risks resulting from the presen ce of the organism already in this country. 
If importation of the commodity is considered likely to result  in an increased exposure of 
people to a potentially zoonotic organism already present in Ne w Zealand, then that organism 
is also considered to be a potential hazard.  However, consistent with Article 2 of the WTO 
Agreement on the Application of Sanitary and Phytosanitary Measures (the SPS Agreement), 
any sanitary measures applied to  a commodity to manage risk associated with such organisms 
must be no more restrictive th an our domestic requirements. 
5.3. RISK ASSESSMENT 
In line with the MPI and OIE risk analysis methodologies, for each potential hazard requiring risk assessment the following analysis is carried out: 
 a) Entry assessment -  the likelihood of the organism being imported in the 
commodity. 
 b) Exposure assessment - the likelihood of animals or humans in New 
Zealand being exposed to the potential hazard. 
 c) Consequence assessment - the consequences of entry, establishment or spread 
of the organism. 
 d) Risk estimation - a conclusion  on the risk posed by the organism 
based on the release, exposure and consequence 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 5  
assessments.  If the risk estimate is non-negligible, 
then the organism is classified as a risk. 
It is important to note that all of the above steps may not be nece ssary in all risk assessments.  
The MPI and OIE risk analysis methodologies make  it clear that if the likelihood of entry is 
negligible for a potential hazard, then the risk estimate is automatically negligible and the 
remaining steps of the risk assessment need not be carried out.  The same situation arises 
where the likelihood of entry is non-negligible but the exposure assessment concludes that the 
likelihood of exposure to susceptible species in the importing country is negligible, or where 
both entry and exposure are non-negligible but  the consequences of introduction are 
concluded to be negligible. 
5.4. RISK MANAGEMENT 
For each organism classified as a risk, a risk management step is carried out, which identifies 
the options available for managing the risk.  Where the Code  lists recommendations for the 
management of a risk, these are described along side options of similar, lesser, or greater 
stringency where available.  In addition to  the options presented, unrestricted entry or 
prohibition may also be considered for all ri sks.  Recommendations  for the appropriate 
sanitary measures to achieve the effective management of risks are not made in this 
document.  These will be determined when an import health standard (IHS) is drafted.  As 
obliged under Article 3.1 of the SPS Agreement the measures adopted in IHSs will be based on international standards, guidelines and recommendations where they exist, except as otherwise provided for under Article 3.3 (where measures providing a higher level of protection than intern ational standards can be ap plied if there is scientif ic justification, or if 
there is a level of protection th at the member country consider s is more appropriate following 
a risk assessment). 
5.5. RISK COMMUNICATION 
After an import risk analysis has been writte n, the Imports Standards Team of MPI analyses 
the options available and proposes draft measures  for the effective management of identified 
risks.  These are then presented in a draft IHS which is released together with a risk management proposal that summarises the optio ns analysis, the rationale for the proposed 
measures and a link to the draft risk analysis.  The package of documents is released for a six-
week period of stakeholder consultation.  Stakeholder subm issions in relation to these 
documents are reviewed befo re a final IHS is issued. 
References 
Alexander DJ, Senne DA (2008).  Newcastle disease, other avian paramyxoviruses, and pneumovirus 
infections.  In Diseases of Poultry  12th Edition. Ed Saif YM, Blackwell Publishing, 75-115. 
Gough RE, Hansen WR (2000).  Characterization of a herpesvirus isolat ed from domestic geese in Australia.  
Avian Pathology  29, 417-422. 
MAF (2010).  Import risk analysis: Psittacine hatching eggs .  MAF Biosecurity New Zealand, Wellington, New 
Zealand. 
Shortridge KF, Alexander DJ, Collins MS (1980).  Isolation and properties of viruses from poultry in Hong 
Kong which represent a new (sixth) distinct group of avian paramyxoviruses.  Journal of General Virology  49, 
255-262. 
Stanislawek WL, Wilks CR, Meers J, Horner GW, Alexander DJ, Manv ell RJ, Kattenbelt JA, Gould AR 
(2002).   Avian paramyxoviruses and influenza viruses isolated from mallard ducks ( Anas platyrhynchos ) in New 
Zealand .  Archives of Virology  147, 1287-1302.  
6 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 7  
6. Duck Virus Hepatitis Types 1, 2 and 3 
6.1. HAZARD IDENTIFICATION 
6.1.1. Aetiological agent 
Duck virus hepatitis (DVH) is caused by any one  of three different viruses (Duck hepatitis 
virus (DHV) types 1, 2, and 3). 
DHV-1 has been classified as an Avihepatovirus, a new genus in the P
icornaviridae  family 
(Tseng et al 2007).  Three distinct genot ypes have been identified, designated Duck Hepatitis 
A virus  (DHAV) types 1, 2, and 3 (Wang et al 2008). 
DHV-2 has been classified as an Avastrovirus species in the Astroviridae  family (Gough et al 
1985) and has been renamed Duck Astrovirus type 1 (DAstV-1). 
DHV-3 has also been classified as an Avastrovirus species (Kim et al 2008; Todd et al 2009) 
and has been renamed Duck Astrovirus type 2 (DAstV-2).  Sequence analysis has shown that 
DAstV-1 (DHV- 2) and DAstV-2 (DHV-3) are distinct isolates and may represent different 
species (Todd et al 2009). These duck hepatitis viruses are distinct from duck hepatitis B virus (DHBV), an 
Avihepadnavirus, which does not cause significant clinical disease in ducks (Yang et al 2008). 
6.1.2. OIE list 
Duck virus hepatitis is included in the OIE lis 
t of notifiable diseases. 
6.1.3. New Zealand status 
Duck hepatitis virus is listed as a notifiable exotic organism
 (MAF 2011). 
6.1.4. Epidemiology 
Duck virus hepatitis was first described in 1950,  causing severe losses in ducklings in Long 
Island, New York (Levine and Fabricant 1950).  DVH has su
bsequently been described in 
most duck-growing areas of the world although the viruses vary in their distributions.  
DHAV-1 is distributed widely and disease is usually ende mic where it is found (Gough and 
McNulty 2008a).  DHAV-2 and DHAV-3 have onl y been identified in Taiwan, South Korea 
and China (Kim et al 2009).  DAstV-1 (DHV-2)  has only been reported in the UK prior to 
1985, and DAstV-2 (DHV-3) has only been reported in the USA (Woolcock 2008a). 
Diagnosis of DVH is based on the characteristic disease pattern in th e flock.  Opisthotonus, 
ataxia, and mortality in duckli ngs are the most common presenti ng clinical signs.  The main 
lesions are in the liver, which is enlarged  with petechial and ecchymotic haemorrhages 
(Woolcock 2010). 
It is not possible to distin guish between DHV-1, DHV-2, or DHV- 3 on the basis of clinical 
findings and pathology alone.  Di stinctions can be made from  the responses of ducklings, 
embryonated eggs, and cell cultures to th e isolated viruses (Woolcock 2010). 
Duck hepatitis viruses may be isolated in duck embryos, day-old ducklings, and duck embryo 
liver cell cultures, or less easily in chicken embryos.  Immunologica l tests are not used 
extensively for the routine identification of  DHV-1, DHV-2, or DHV-3.  Serum neutralisation 
8 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
tests can be used to assay immune respons es to vaccination (Woolcock 2008b).  DHV-1 and 
DHV-3 viruses remain viable for many weeks in  faeces.  Ducklings become infected as a 
result of contact between live birds, moveme nt of people and/or fomites and insufficient 
cleaning of growing sheds (Woolcock 2008a). 
Natural transmission occurs by the faecal-oral route (Tripathy and Hanson 1986; MingShu et 
al 1997) and recovered ducks may excrete vi rus in their faeces for up to 8 weeks post 
infection (Woolcock 2008a).  Sp read occurs horizontally by cont act with infected ducklings 
or fomites (Gough and McNulty 2008a; 2008b).  Newly hatched ducklings produced by 
breeders on infected premises remained uninfect ed when taken to an area where no ducks 
were being kept (Asplin 1958). 
Vertical transmission is not  thought to occur (Gough and McNulty 2008a), although there 
may be a possibility of transmission on egg surfaces so newly hatched ducks could become 
infected from this source.  However, as noted  in the commodity definition, the eggs will be 
disinfected in accordance with Chapter 6.4 of the OIE Code (or equivalent) following 
collection, which would be expected to remove  any viral contamination on the egg surface. 
6.1.5. Hazard identification conclusion 
The aetio
logical agents of DVH are not transmitted in the egg and any surface contamination 
of imported eggs will be removed by disinfecti on of the commodity.  It is concluded that 
DHV-1, DHV-2, and DHV-3 are not considered to be potential hazards in the commodity. 
References 
Asplin FD (1958) . An attenuated strain of duck hepatitis virus. Veterinary Record 70, 1226-1230.  
Gough RE, Borland ED, Key mer IF, Stuart JC (1985).  An outbreak of duck hepatitis type II in commercial 
ducks.  Avian Pathology  14, 227–236. 
Gough RE, McNulty MS (2008a).  Astroviridae.  In Poultry Diseases , 6th Edition. Eds Pattison M, McMullin 
PF, Bradbury JM, Alexander DJ. Elsevier/Butterworth-Heinemann, 392-397.   
Gough RE, McNulty MS (2008b).  Picornaviridae. In Poultry Diseases , 6th Edition. Eds Pattison M, McMullin 
PF, Bradbury JM, Alexander DJ. Elsevier/Butterworth-Heinemann, 350-358. Kim MC, Kwon YK, Joh SJ, Kwon JH, Lindberg AM (2008).  Differential diagnosis between type-specific 
duck hepatitis virus type 1 (DHV-1) and recent Korean DHV-1-like isolates using a multiplex polymerase chain 
reaction.  Avian Pathology 37, 171-177. 
Kim MC, Kim MJ, Kwon YK, Lindberg AM, Joh SJ, Kwon HM, Lee YJ, Kwon JH (2009).  Development 
of duck hepatitis A virus type 3 vaccine and its use to protect ducklings against infections.  Vaccine 27, 6688-
6694. 
Levine PP, Fabricant J (1950) . A hitherto-undescribed virus dis ease of ducks in North America. Cornell 
Veterinarian  40, 71-86. 
MAF Biosecurity New Zealand (2011).  Unwanted Organisms.  Retrieved from 
http://www1.maf.govt.nz/uor/searchframe.htm on 15 September 2011. MingShu W, AnChun C, XiaoYue C (1997).  Study on duck viral hepatitis - distribution and excretion of 
virulent duck hepatitis virus in ducklings and adult ducks.  Chinese Journal of Veterinary Science  17, 254-257. 
Todd D, Smyth VJ, Ball NW, Donnelly BM, Wy lie M, Knowles NJ, Adair BM (2009).  Identification of 
chicken enterovirus-like viruses, duck hepatitis virus type 2 and duck hepatitis virus type 3 as Astroviruses.  
Avian Pathology 38, 21–30. 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 9  
Tripathy DN, Hanson LE (1986).  Impact of oral immunization against duck viral hepatitis in passively 
immune ducklings.  Preventive Veterinary Medicine 4, 355-360. 
Tseng CH, Knowles NJ, Tsai HJ (2007).  Molecular analysis of duck hepatitis virus type 1 indicates that it 
should be assigned to a new genus.  Virus Research  123, 190–203. 
Wang L, Pan M, Fu Y, Zhang D (2008).  Classification of duck hepatitis virus into three genotypes based on 
molecular evolutionary analysis .  Virus Genes  37, 52–59. 
Woolcock PR (2008a).   Duck hepatitis.  In Diseases of Poultry  12th Edition. Eds Saif YM, Fadly AM, Glisson 
JR, McDougald LR, Nolan LK, Swayne DE.  Blackwell Publishing, 373–384. 
Woolcock PR (2008b) . A Laboratory Manual for the Isolation, Identification and Characterization of Avian 
Pathogens. Fifth edition.(The American Association of Avian Pathologists), 175-178. 
Woolcock PR (2010) .  Duck Virus Hepatitis.  Manual of Diagnostic Tests and Va ccines for Terrestrial Animals.  
Chapter 2.3.8.  Retrieved 15 September 2011 from 
http://www.oie.int/fileadmin/Home/eng/He alth_standards/tahm/2.03.08_DVH.pdf 
Yang M, Cheng AC, Wang MS, Xing HY (2008).  Development and application of a one-step real-time 
TaqMan RT-PCR assay for detection of Duck hepatitis virus type1.  Journal of Virological Methods 153, 55-60. 
 
 
 
  
 
10 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
7. Anatid Herpesvirus 1 
7.1. HAZARD IDENTIFICATION 
7.1.1. Aetiological agent 
Duck virus e
nteritis (DVE) is also referred to as duck plague, anatid herpes, eendenpest and 
peste du canard.  The aetiological agent, a herpes virus, is a member of the alphaherpesvirinae 
subfamily of the Herpesviridae (Woolcock 2008). 
7.1.2. OIE list 
Not listed . 
7.1.3. New Zealand status 
Duck virus enteritis has not been reported in  New Zealand and
 is listed as an unwanted 
notifiable organism (MAF 2011). 
7.1.4. Epidemiology 
The disease was first described in the Nether lands in 1923 (Baudet 1923).  The specificity for 
ducks was substantiated and the disease term
ed “duck plague”, a distinct viral disease of 
ducks (Bos 1942).  DVE has been reported in th e USA, Canada, Europe, Asia, and Brazil but 
not Australia (Hansen and Gough 2007). 
Duck virus enteritis is reported in ducks, geese, and swans rangi ng in age from seven days to 
mature breeders.  In su sceptible flocks the first signs are often sudden high mortality with a 
significant drop in egg production.  In flocks of chronically infected pa rtially immune birds 
only occasional deaths occur (Sandhu and Metwally 2008).  Birds that do recover may be 
immune to reinfection and become  carriers, shedding virus in their faeces or on the surface of 
eggs for a prolonged period (Richter and Horzinek 1993; Shawky and Schat 2002).   
Natural susceptibility has been limited to member s of the family Anatidae (ducks, geese, coot, 
and swans) of the order Anseriformes. The infection has not been repo rted in other avian 
species, mammals, or humans (Jansen 1964; Sandhu and Metwally 2008).  DVE is considered 
a threat to wild and migratory wate rfowl populations (Shawky and Schat 2002). 
In commercial ducks, introduction of the virus is  usually associated with transmission from 
wild waterfowl.  The spring mi gration and onset of breeding s eason for waterfowl is noted as 
driving seasonal occurrences.  Some species  are highly susceptible (such as domestic 
Muscovy ducks) while others (such as ma llards) appear more resistant (Gough 2008). 
Horizontal spread is the principal mechanis m of transmission. In a susceptible host, the 
causative agent of DVE replicat es primarily in the mucosa of the digestive tract and then 
spreads to the bursa of Fabricius,  thymus, spleen, and liver.  The vi rus is shed in faeces and in 
oral-respiratory secretions, and is transmitted by direct contact between infected and susceptible birds, or indirectly by contact with a contaminated environment (Sandhu and 
Shawky 2003). 
Vertical transmission of herp esviruses has been recognised, including DVE, although more 
recent reports suggest that DVE virus may be excreted only on the surface of the egg from 
infected carriers (Burgess and Yuill 1983; Sandhu and Leibovitz 1997).  No DVE virus was 
recovered from eggs laid during a natural outbreak (Burgess and Yuill 1981a).  However, 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 11  
virus transmission through the egg has been repo rted in persistently infected ducks under 
experimental conditions (Burgess and Yuill 1981b; Gough 2008).  
Diagnosis can be confirmed by demonstration of th e virus in tissue samples, virus isolation, or 
PCR. Antibody develops in convalescent birds and may be detected by virus neutralisation, 
ELISA, or immunofluorescence (S andhu and Metwally 2008).  However, healthy birds may 
shed virus and show no detectable serum-neutralising antibody (Burgess and Yuill 1983). 
7.1.5. Hazard identification conclusion 
Duck virus enteritis occurs in m
any countries an d can cause serious dise ase in ducks and other 
Anseriformes.  Experimental studies have demons trated transmission in the eggs of infected 
birds so DVE virus is considered to be  a potential hazard in the commodity.  
7.2. RISK ASSESSMENT 
7.2.1. Entry assessment 
Vertical transm
ission of DVE th rough both transovarial and cloaca l contamination of eggs has 
been described in experimentally infected birds.   On that basis, the likelihood of entry for 
DVE in the commodity is assessed to be non-negligible. 
7.2.2. Exposure assessment 
If hatching eggs with DVE were im
ported, the most likely outcome woul d be the introduction 
of the virus into the hatchery.  From the ha tchery, exposure would be likely to occur by 
infected ducklings and mechanical spread by humans and fomites.  Exposure of wild and 
farmed ducks to the DVE-infected ducks would then disseminate the virus.  7.2.3. Consequence assessment 
The consequences of introduction of DVE into New Zealand could vary greatly.  Exposure of 
endem
ic and native duck populations would likely result in increased illness and mortality.  
DVE produces significant economic losses due to  mortality, condemnations, and decreased 
egg production (Sandhu and Metwally 2008).  If  DVE were established in New Zealand, 
commercial duck producers would need to c onsider improvements in biosecurity and 
vaccination.  
Because natural susceptibility to DVE is limite d to members of the family Anatidae of the 
order Anseriformes, there would be no consequences for other avian species, mammals, or 
humans. 
7.2.4. Risk estimation 
Since the entry, exposure and c onsequence assessm
ents are non-ne gligible, the risk estimation 
is non-negligible and DVE virus is classified as a risk in the commodity. Therefore, risk 
management measures are justified. 
7.3. RISK MANAGEMENT 
7.3.1. Options 
Diagnosis of DVE is based on a combinati on of clinical signs, gross pathology, and 
histopathology together with iden
tification of the agent e ither by virus isolation or by 
polymerase chain reaction (PCR).  Virus isolati on is best achieved from samples of liver, 
12 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
spleen, or kidney whilst PCR tests have been de veloped that can be used on various tissues 
including oesophagus, liver, and spleen (Woolcock 2008). 
The OIE Manual describes no specific test for DVE for international trade. As the humoral 
response to natural infection with DVE virus is often low and antibodies may be short-lived, it 
is assumed that cell-mediated immunity also plays a role in the infection.  Immunological 
tests have limited value, although detection of neutralising antibodies to  DVE virus in serum 
is possible and the Manual  describes virus neutra lisation assays performed in chicken or duck 
embryos using embryo-adapted virus, or in cell cultures (Woolcock 2008). The Australian import conditions for duck hatching eggs note the use of a serum 
neutralisation test and require that there should be no evidence of illness in the source flock 
from 90 days prior to egg collection (AQIS 2009) .  A number of othe r diagnostic tests to 
detect seroconversion have been describe d, including an agar gel diffusion test, 
immunochromatographic strip te sts, passive haemagglutinat ion assay, dot-enzyme-linked 
immunosorbent assay and a commer cial ELISA (Wu et al 2011). 
The disease, if present, would be likely detected shortly after hatching so imported eggs could 
be hatched in post arrival quara ntine (PAQ) and investigation of any mortality within PAQ 
could be required.  Vaccination of the source flock could be prohibited because the effects of vaccination on the 
reinfection of immunised birds, their carrier status, and vertical  transmission of the virus are 
unknown. 
One or more of the following options could ther efore be considered in order to effectively 
manage the risk: 
Option 1 
Eggs from flocks in countries where DVE has not been recognised could be imported without 
sanitary restrictions. 
Option 2 
Vaccination against DVE could be prohibite d in flocks supplying eggs for export. 
Option 3 
Eggs derived from flocks where virus isolati on or PCR has demonstrated flock freedom from 
DVE could be considered eligible for import. 
Option 4 
Imported eggs could be hatched under secure  quarantine conditions in New Zealand and 
material from embryos, dead-in-shell chicks, or hatchlings could be tested for DVE by virus 
isolation or PCR. 
References 
AQIS (2009).  Importation of Hatching (Fertile) Duck Eggs fr om Approved Countries Policy Review, July 2009. 
Baudet AERF (1923). Mortality in ducks in the Netherlands caused by a filtrable virus. Tijdschr Diergeneeskd  
50, 455- 459. 
Bos A (1942) . Some new diseases of duck plague. Tijdschr Diergeneeskd  69, 372-381. 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 13  
Burgess EC, Yuill TM (1981a). Persistent duck plague virus infection in mallard and black ducks. 
In: Wildlife Diseases of the Pacific Basin and Other Countries . Proceedings of the 4th International Conference 
of the Wildlife Disease Association. Sydney, Australia, August 25-28, 1981, 50-51. 
Burgess EC, Yuill TM (1981b).  Vertical transmission of duck plague virus (DPV) by apparently healthy DPV 
carrier waterfowl. Avian Diseases  25, 795-800. 
Burgess EC, Yuill TM (1983). The influence of seven environmental and physiological factors on duck plague 
virus shedding by carrier mallards, Journal of Wildlife Diseases 19, 77-81. 
Gough RE (2008). Duck virus enteritis. In:  Poultry Diseases Sixth edition. Eds Pattison M, McMullin P, 
Bradbury J, Alexander DJ. Saunders Elsevier, 272-273. 
Hansen WR, Gough RE (2007) . Duck plague (duck virus enteritis). In: Infectious Diseases of Wild Birds . Eds 
Thomas DL, Hunter DB, Atkinson CT . Blackwell, Ames, Iowa, 87-107. 
Jansen J (1964).   Duck plague: A concise survey. Indian Veterinary Journal 41, 309-316. 
MAF Biosecurity New Zealand (2011).  Unwanted Organisms.  Retrieved from 
http://www1.maf.govt.nz/uor/searchframe.htm on 15 September 2011. Richter JHM, Horzinek MC (1993). Duck Plague . In: Virus Infections of Birds . Eds McFerran JB, McNulty 
MS. Elsevier Sciences Publishers BV, Amsterdam, Netherlands, 77-90. Sandhu TS, Leibovitz L (1997). Duck viral enteritis. In:  Diseases of Poultry , 10
th edition. Eds Calnek BW, 
Barnes, HJ, Beard CW, McDougald LR, Saif YM. Mosby-Wolfe, London, 675- 684. Sandhu TS, Shawky SA (2003). Duck virus enteritis (duck plague). In: Diseases of Poultry, 11
th edition. Eds 
Saif YM, Barnes HJ, Glisson JR, Fadly AM, McDougald LR and Swayne DE. Iowa State Press, Ames, Iowa, 
354-363. Sandhu TS and Metwally SA (2008).  Duck virus enteritis (duck plague). In: Diseases of Poultry, 12
th edition. 
Eds Saif  YM, Fadly AM, Glisson JR, McDougald LR, Nolan LK, Swayne DE. Blackwell Publishing, 384-392. 
Shawky SA, Sandhu TS (1997).  Inactivated vaccine for protection against duck virus enteritis. Avian Diseases  
41, 461-468. Shawky SA, Schat KA (2002).  Latency sites and reactivation of duck enteritis virus. Avian Diseases 46, 308-
313. Woolcock PR (2008) .  Duck Virus Enteritis.  Manual of Diagnostic Tests and Va ccines for Terrestrial Animals.  
Chapter 2.3.7.  Retrieved 16 September 2011 from 
http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.03.07_DVE.pdf
. 
Wu Y, Cheng A, Wang M, Zhang S, Zhu D, Jia R, Luo Q, Chen Z, Chen X (2011).  Serologic detection of 
duck enteritis virus using an indirect ELISA based on recombinant UL55 protein. Avian Diseases  55, 626-632. 
14 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
8. Goose Parvovirus and Muscovy Duck Parvovirus 
8.1. HAZARD IDENTIFICATION 
8.1.1. Aetiological agent 
Fam
ily: Parvoviridae, Genus: Dependovirus , Species: Goose parvovirus  (GPV) (also called 
Derzsy’s disease virus (DDV)) and Duck parvovirus (also called Muscovy duck parvovirus 
(MDPV) or Barbary duck parvovirus (BDPV)) (Tattersall et al 2005). 
Other waterfowl parvoviruses can be categoris ed into GPV-related or MDPV-related groups 
based on their nucleotide se quences (Poonia et al 2006). 
8.1.2. OIE list 
Not listed. 
8.1.3. New Zealand status 
Waterfowl parvoviruses (GPV a nd MDPV) have never been r ecorded in New Zealand and 
Derzsy’s disease is listed on the unwante d exotic organism
s register (MAF 2011). 
8.1.4. Epidemiology 
Derzsy’s disease is a highly contagious disease affecting young goslings and Muscovy 
ducklings, and has been reported from m
ajor goose and Muscovy duck farming countries in 
many parts of the world, including Europe, Asia , and the USA.  Derzsy’s disease is known by 
many different names, including goose influenza,  goose plague, goose hepatitis, viral enteritis 
of goslings, infectious myocarditis, and hepatonephritis-ascites (Gough 2008). 
Domestic geese, wild geese, and Muscovy ducks (including some hybrids) are the only 
species in which natural clinical disease ha s been observed.  Other breeds of duck and 
domestic poultry appear refractor y to infection and the disease has not been reported in other 
avian species or mammals (Gough 2008).  The disease has no known public health 
significance (Irvine and Holmes 2010). 
GPV and MDPV differ in host ranges, antigenic ity, and nucleotide sequences but the clinical 
signs and pathological lesions cau sed by either virus are similar (Chang et al 2000).  GPV can 
cause severe disease is both goslings a nd Muscovy ducklings, whereas MDPV is not 
pathogenic for geese (Glavits et al 2005; Gough 2008).  Vaccinating Muscovy ducklings with 
GPV provides protection against both GPV and MDPV (Woolcock et al 2000). 
Derzsy’s disease is strictly age dependant, with birds building a pr ogressive resistance to 
infection with age.  100% mortality may occu r in goslings and Muscovy ducklings under 1 
week old, with negligible losse s in 4- to 5- week old bird s (Gough 2008; Irvine and Holmes 
2010).   
Older birds do not usually show clinical signs but can develop a subclinical infection, and 
latency may establish (Gough 2008; Irvine et al 2008; Irvine and Holmes 2010).  However, 
some older birds may show nervous, locomotor, and enteric signs (ascites and profuse white diarrhoea), abnormal feather development and stunting (Poonia et al 2006; Gough 2008).  
Survivors may suffer growth retardation, lo ss of feathering, and ascites (Gough 2008) and 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 15  
infection in older ducks result s in degenerative skeletal muscle myopathy (Woolcock et al 
2000; Glavits et al 2005;  Poonia et al 2006). 
Prominent pathological lesions in young birds in clude severe enteritis, hepatitis, myocarditis, 
and atrophy of the lymphoid organs (bursa of Fabr icius, thymus, spleen).  In less acute cases, 
perihepatitis, pericarditis, and ascites are frequent findings.  In addition to the lesions 
observed in the geese, degenerative skeletal muscle myopathy, sciatic neuritis, and polio-
encephalomyelitis are also frequently observed in Muscovy ducks infected  with either GPV or 
MDPV (Kisary 1993; Glavits et al 2005; Poonia et al 2006). 
Birds are infected either verti cally via the ova or the egg-shel l, or horizontally through the 
faecal-oral route (Schettler 1971).  After entering th e digestive tract, the virus replicates in the 
intestinal wall and then enters the blood stream  leading to viraemia and dissemination (Kisary 
1993; Gough 2008).  In the case of egg transmissi on, embryos either die during incubation or 
hatch out in an infected state.  The most  serious GPV outbreaks occur following vertical 
transmission of the virus (Irvine and Holmes 2010). 
The virus is distributed widely a nd has been detected in the small intestine, bursa of Fabricius, 
heart, liver, pancreas, spleen, bone marrow, thymus, blood, cardiac muscle, skeletal muscle, 
tongue, and brain of Muscovy ducklings from 2 days post-inoculation per os (Limn et al 
1996; Takehara et al 1998; Yu et al 2002; Zhu et al 2010). 
Infected birds excrete large amounts of virus in  their faeces resulting in a rapid spread of 
infection by direct and indirect contact (Gough 2008).  Infected bird s younger than 1 month 
shed the virus continuously, even if they do not develop clinical signs (Kisary 1993).  
Recovered birds and those which contract th e infection after the age of one month may 
become virus carriers.  The carrier state last s virtually lifelong (Kis ary 1993) and affected 
birds can transmit the virus vertically in their eggs and horizontally in their faeces (Gough 
2008; Irvine et al 2008; Irvine and Holmes  2010) although they do not shed the virus 
persistently (Gough 1987). 
GPV and MDPV are extremely resistant to chemical and physical c onditions and are not 
inactivated at temperatures of 65°C for 30 minutes or 56°C for 3 hours (Schettler 1971; 
Gough 2008).  This means the potential for inan imate objects to spread infection is high 
(Kisary 1993; Poonia et al 2006) , which has been demonstrated  in several field outbreaks 
(Irvine and Holmes 2010). 
Prophylaxis is based on vaccination of neonatal bi rds or breeding flocks, and elimination of 
carrier birds.  Live and inactivated GPV, MDPV , and bivalent vaccines are available in most 
countries where the disease is endemic (Gough 2008; Irvine and Holmes 2010). 
8.1.5. Hazard identification conclusion 
GPV and M
DPV may infect Muscovy ducks and their hybrids but not other species of duck. 
Since the viruses can be transmitted vertically by subclinically infected birds, they are 
considered to be potential hazards in the eggs  of Muscovy or Muscovy hybrids but not in the 
eggs of other duck species. 
16 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
8.2. RISK ASSESSMENT 
8.2.1. Entry assessment 
GPV and MDPV m
ay be transmitted in the eggs  of carrier Muscovy ducks. Therefore, the 
likelihood of introducing these viruses in Mu scovy duck eggs from countries where the 
disease occurs is assess ed to be non-negligible. 
8.2.2. Exposure assessment 
Introduction of the virus in hatching eggs would result in the hatching of infected ducklings 
that would b
e likely to transmit the disease when in contact with Muscovy ducks. Infected 
birds excrete large amounts of virus in their f aeces resulting in rapid spread by direct and 
indirect contact.  GPV and MDPV are extremely resistant to environmental conditions and 
inanimate objects can spread in fection widely.  Therefore, the likelihood of exposure is 
assessed to be non-negligible. 
8.2.3. Consequence assessment 
Derzsy’s disease is an acute, highly fatal,  rapidly spreading dis ease of young goslings and 
Muscovy ducklings.  Infection of backyard Musc ovy duck flocks, wild geese, or comm
ercial 
poultry would be associated with non-negligible consequences. 
Domestic geese, wild geese, and Muscovy ducks (including some hybrids) are the only 
species in which natural clin ical disease has been observe d (Gough 2008).  There would be 
negligible consequences for ot her commercial poultr y species, free-living avian species, or 
humans. 
8.2.4. Risk estimation 
Since entry, exposure, and consequence assessm
ents are non-negligible, the risk estimation is 
non-negligible and GPV and MDPV are classified as risks in th e commodity.  Therefore risk 
management measures can be justified. 
8.3. RISK MANAGEMENT 
8.3.1. Options 
Serological tests do not disti nguish between GPV a nd MDPV (Kisary 1977) .  Diagnostic tests 
for detection of antibodies include virus neutralisation, gel precipitation and ELISA tests. 
Virus can be detected by isola tion of virus, electron m
icrosco py on faeces or tissue sections, 
detection of viral antigen by immunofluorescence or by immu noperoxidase techniques, and 
PCR tests have been describe d to detect viral DNA (Gough 2008). 
One or more of the following options could ther efore be considered in order to effectively 
manage the risk: 
Option 1 
Eggs from duck species which are neither Mu scovy ducks nor their hybrids could be imported 
without sanitary measures 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 17  
Option 2 
Muscovy duck eggs could be imported without re strictions from countries known to be free 
from GPV or MDPV. 
Option 3 
Eggs could be imported from duck flocks that ar e maintained as closed flocks and in which 
the disease has not occurred for several ye ars (three to five years is suggested). 
Option 4 
Donor ducks could be kept isolat ed from other ducks for at leas t three weeks before eggs are 
collected, and the donors tested serologically before going into  isolation and again three 
weeks after the end of the collection period.  
Option 5 Imported eggs could be hatched under secure quarantine conditions in New Zealand and the 
hatchlings mixed with sen tinel sero-negative New Z ealand Muscovy ducklings.  A 
representative sample of imported and sentinel birds could be tested se rologically at the end 
of the quarantine period of at least three weeks.  
References 
Chang PC, Shien JH, Wang MS, Shieh HK (2000).  Phylogenetic analysis of parvoviruses isolated in Taiwan 
from ducks and geese.  Avian Pathology 29, 45-49. 
Glavits R, Zolnai A, Szabo E, Ivanics E, Zarka P, Mato T, Palya V (2005).  Comparative pathological 
studies on domestic geese ( Anser anser domestica ) and Muscovy ducks ( Cairina moschata ) experimentally 
infected with parvovirus strains of goose and Muscovy duck origin.  Acta Veterinaria Hungarica 53, 73-89.  
Abstract only. 
Gough RE (1987).  Persistence of parvovirus antibody in geese that have survived Derzsy’s Disease.  Avian 
Pathology 16, 327-330. 
Gough RE (2008).  .  Parvovirus Infections.  In  Diseases of Poultry  12th Edition. Eds Saif YM, Fadly AM, 
Glisson JR, McDougald LR, Nolan LK, Swayne DE.  Blackwell Publishing, 397–404. 
Irvine R, Ceeraz V, Cox B, Twomey F, Young S, Br adshaw J, Featherstone C, Holmes PJ, Ainsworth H, 
Jones R (2008).  Goose parvovirus in Great Britain.  Veterinary Record 11, 461. 
Irvine R, Homes P (2010).  Diagnosis and control of goose parvovirus.  In Practice 32, 382-386. 
Kisary J (1977). Immunological aspects of Derzsy's disease in goslings. Avian Pathology  6, 327-334. 
Kisary J (1993).  Derzsy’s disease of geese.  In Virus Infections of Birds Volume 4. Eds McFerran JB, McNulty 
MS. Elsevier Science Publishers B.V., 157-162. 
Limn CK, Yamada T, Nakamura M, Takehara K (1996).  Detection of Goose parvovirus genome by 
polymerase chain reaction: distribution of Goose parvovirus in Muscovy ducklings.  Virus Research 42, 167-
172. MAF Biosecurity New Zealand (2011).  Unwanted Organisms.  Accessed 20/05/2011 from 
http://www1.maf.govt.nz/uor/searchframe.htm Poonia B, Dunn PA, Huaguang L, Ja rosinski KW, Schat KA (2006).  Isolation and molecular 
characterisation of a new Muscovy duck parvovirus from Muscovy ducks in the USA.  Avian Pathology 35, 435-
441. 
Schettler CH (1971).  Virus hepatitis of geese 3 - Properties of the causal agent.  Avian Pathology 2 , 179-193. 
18 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
Takehara K, Saitoh M, Kiyono M, Nakamura M (1998).  Distribution of attenuated Goose parvoviruses in 
Muscovy ducklings.  Journal of Veterinary Medicine 60, 341-344. 
Tattersall P, Bergoin M, Bloom ME, Brown KE, Linden RM, Muzyczka N, Parish CR, Tjissen P (2005).  
Family Parvoviridae .  In Eighth Report of the International Committee on Taxonomy of VirusesI. Eds Fauquet 
CM, Mayo MA, Maniloff J, Desselberger U, Ball LA.  Elsevier Academic Press, Amsterdam, 353-69. 
Woolcock PR, Jestin V, Shivaprasad HL, Zwingelstein F, Arnauld C, McFarland MD, Pedersen JC, 
Senne DA (2000).  Evidence of Muscovy duck parvovirus in Muscovy ducklings in California.  Veterinary 
Record 146, 68-72. 
Yu B, Wang YK, Zhu GQ (2002).  Detection of goose parvovirus by nucleic acid dot-blotting assay.  Chinese 
Journal of Veterinary Science 22, 453-454.  Abstract only. 
Zhu LQ, Ding XY, Tao J, Wang JY, Zhang XJ, Wang XB, Hu Y, Li HF, Chen KW, Zhu GQ (2010).  Identification of target cells for Goose parvovir us infection in the immune system organs.  Acta Virologica 54, 
211-215. 
 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 19  
9. Reovirus of Muscovy Ducks 
9.1. HAZARD IDENTIFICATION 
9.1.1. Aetiological agent 
Fam
ily: Reoviridae , Genus: Orthoreovirus.  Five orthoreovirus species are recognised, with 
avian reoviruses classified in  group II (Fauquet et al 2005). 
9.1.2. OIE list 
Not listed. 
9.1.3. New Zealand status 
Muscovy duck reovirus (DRV) has not been r ecognised in New Zeal and although there has 
been no active surveillance for this pathogen.  DRV is not listed in the unwanted organism
s 
register. 9.1.4. Epidemiology 
Muscovy duck reovirus has been identified as the cause of a disease of Muscovy ducks and 
Barbary ducks (Robertson et al 1986). Infected ducklings show characteris tic necrotic foci in 
the liver and spleen (M alkinson et al 1981).  
Reovirus inf
ection of Muscovy ducks has been de scribed in South Africa,  France, Israel, and 
China (Malkinson et al 1981).  Chinese isolates have also been shown to infect Muscovy-
common duck hybrids (Huang et al 2004). 
Muscovy ducks and geese are affected between ten days and six weeks and present with 
malaise and diarrhoea.  Up to 20% mortality ha s been reported and individuals that recover 
are markedly stunted.  The hock and metatarsal jo ints, as well as the gastrocnemius and tarsal 
flexor tendons, and sometimes the synovial bu rsae are markedly swollen (Malkinson et al 
1981; Jones 2003). Transmission studies have shown that goslings, Pekin ducks, and chickens are resistant to 
infection with DRV when inoculated subc utaneously (Malkinson et al 1981).   
Reoviruses are recognised to be transmitted verti cally through the egg.  Virus may persist in 
breeding stock for long periods and Muscovy ducklings may be protected by maternal 
antibody (Malkinson et al 1981). 
Sequence analysis suggests that DRV should be considered a distinct genogroup from other 
avian reoviruses (Kuntz-Simon et al 2002; Zhang et al 2006a) and recombinant vaccines have 
been developed which have been shown to protect against DRV (Kuntz-Simon et al 2002). 
9.1.5. Hazard identification conclusion 
It is concluded that DRV is a prim 
ary pat hogen in Muscovy ducks and their hybrids and there 
is no evidence to support the pos ition that this disease is present in New Zealand.  As 
reoviruses are recognised to be transmitted in eggs, DRV is considered to be a potential 
hazard in the eggs of Muscovy ducks and their hybrids. 
 
 
20 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
9.2. RISK ASSESSMENT 
9.2.1. Entry assessment 
DRV may be transm
itted in the eggs of carrier Muscovy ducks or their hybrids.  Therefore, 
the likelihood of introducing the virus in the hatching eggs of Muscovy ducks or their hybrids 
from countries where the disease occurs  is assessed to be non-negligible. 
9.2.2. Exposure assessment 
Introduction of the virus in hatching eggs would result in the hatching of infected ducklings 
that would be highly contagious and transm
it the disease in contact with Muscovy ducks.  
Therefore, the likelihood of exposure is assessed to be non-negligible.  
9.2.3. Consequence assessment 
DRV causes m
alaise, diarrhoea, and mortality in  ducklings.  Infection of duck flocks would 
be associated with non-negligible consequen ces.  If DRV were introduced, commercial duck 
producers of Muscovy ducks and their hybrids w ould need to consider improvements in 
biosecurity and vaccination.  
Goslings, Pekin ducks, and chickens  are resistant to infection with  DRV.  It is assumed that 
there would be negligible consequences for other commercial poultry species, free-living 
avian species, or humans. 
9.2.4. Risk estimation 
Because the entry, exposure and consequence assessm
ents are non-negligible, the risk 
estimate is non-negligible and DRV is classified  as a risk in the eggs of Muscovy ducks or 
their hybrids. Therefore, risk mana gement measures can be justified. 
9.3. RISK MANAGEMENT 
9.3.1. Options 
Pekin ducks are resistant to infection with DRV (Malkinson et al 1981) so no risk 
m
anagement measures are required for the eggs of this species. 
DRV infection can be diagnosed serologically  using either a seru m neutralisation test 
(Giambrone 1980; Heffels-Redmann et al 1992),  agar gel immunodiffusion test (Olson and 
Weiss 1972; Adair et al 1987), or  an enzyme linked immunosorbent assay (Islam and Jones 
1988; Zhang et al 2007).  In addition to virus isolation, RT-PCR tests have been described to 
detect DRV in infected individuals (Zhang et al 2006b; Lin et al 2007). 
Options for the importation of duck eggs could apply only to Muscovy ducks or their hybrids.  
One or more of the following options could ther efore be considered in order to effectively 
manage the risk: 
Option 1 
Duck eggs could be imported without restricti ons from countries known to be free from DRV. 
 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 21  
Option 2 
Eggs could be imported from flocks that are ma intained as closed flocks and in which the 
disease has not occurred for seve ral years (three to five years). 
Option 3 
Donor ducks could be kept isolat ed from other ducks for at leas t three weeks before eggs are 
collected, and the donors tested serologically before going into  isolation and again three 
weeks after the end of the collect ion period, with negative results.  
Option 4 
Imported eggs could be hatched under secure quarantine conditions in New Zealand and the 
hatchlings mixed with sen tinel sero-negative New Z ealand Muscovy ducklings.  A 
representative sample of imported and sentinel birds could be tested se rologically at the end 
of the quarantine period of at least three weeks.  
References 
Adair BM, Burns K, McKillop FR (1987).  Serological studies with reoviruses  in chickens, turkeys and ducks. 
Journal of Comparative Pathology  97, 495-501. 
Barnes HJ (1997). Muscovy duck parvovirus . In: Diseases of Poultry  10th edition. Eds Calnek BW, Barnes HJ, 
Beard CW, McDougald LR, Saif YM. Mosby-Wolfe, London, 1032-1033.  
Giambrone JJ (1980).  Microculture neutralization test for serodiagnosis of three avian viral infection. Avian 
Diseases 24, 284-287.  
Heffels-Redmann U, Müller H, Kaleta EF (1992).  Structural and biological ch aracteristics of reoviruses 
isolated from Muscovy ducks ( Cairina moschata). Avian Pathology 21, 481-491. 
Huang Y, ShaoHua S, WenY ang L, LongFei C (2004).  The pathogenicity of the reovirus isolated from semi-
Muscovy ducklings, Chinese Journal of Veterinary Science 24, 326-328. (Abstract only). 
Islam MR, Jones RC (1988).  An enzyme-linked immunosorbent assa y for measuring antibody titre against 
avian reoviruses using a single dilution of serum. Avian Pathology  17, 411-425. 
Jones RC (2003).  Other reovirus infections. In: Diseases of Poultry 11th edition. Eds Saif YM, Barnes HJ, 
Glisson JR, Fadly AM, McDougald LR, Swayne DE. Io wa State University Press, Ames, Iowa, 293-298. 
Kuntz-Simon G, Le Gall-Reculé G, de Boisséson C, Jestin V (2002a). Muscovy duck reovirus σC protein is 
atypically encoded by the smallest genome segment. Journal of General Virology 83, 1189-1200. 
Kuntz-Simon G, Blanchard P, Cherbonnel M, Jestin A, Jestin V (2002b).  Baculovirus-expressed Muscovy 
duck reovirus σC protein induces serum-neutralising antibodies and protection against challenge. Vaccine 20, 
3113-3122. 
Lin FQ, Hu QL, Chen SY, Ouyang SD, Chen SL, Zhu XL, Cheng XX (2007).  Diagnosis of Muscovy duck 
reovirus disease by semi-nested RT-PCR. Journal of South China Agricultural University  2, 107-109. 
Malkinson M, Perk K, Weisman Y (1981). Reovirus infection in young Muscovy ducks ( Cairina moschata). 
Avian Pathology 10, 440-443. 
Olson NO, Weiss R (1972).  Similarity between arthritis virus and Fahey-Crawley virus. Avian Diseases  16, 
535-540. 
Robertson CL, Wilcox GE (1986).  Avian reovirus. Veterinary Bulletin 56, 155-174. 
Van der Heide L (1977). Viral arthritis/tenosynovitis: a review. Avian Pathology 6, 271-284. 
22 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
Zhang Y, Liu M, Hu Q, Ouyang S, Tong G (2006a).  Characterisation of the σC encoding gene from Muscovy 
duck reovirus. Virus Genes 32, 165-170. 
Zhang Y, Liu M, Shuidong O, Hu QL , Guo DC, Chen HY, Han Z (2006b) Detection and identification of 
avian, duck, and goose reoviruses  by RT-PCR: goose and duck reoviruses are part of the same genogroup in the 
genus Orthoreovirus . Archives of Virology  151, 1525-1538. 
Zhang Y, Guo D, Liu M, Geng H, Hu Q, Liu Y, Liu N (2007) Characterisation of the σ B-encoding genes of 
mucovy duck reovirus: σC-σB-ELISA for antibodies against duck reovirus in ducks. Veterinary Microbiology  
121, 231-241. 
 
 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 23  
10. Duck Circovirus  
10.1. HAZARD IDENTIFICATION 
10.1.1.  Aetiological agent 
Fam
ily: Circoviridae; Genus: Circovirus .  The Circovirus  genus includes the species Beak 
and Feather Disease Virus  (BFDV), Canary Circovirus  (CaCV), Goose Circovirus  (GoCV), 
Pigeon Circovirus  (PiCV), Porcine Circovirus – 1  (PCV-1), and Porcine Circovirus – 2  
(PCV-2). 
Sequencing and phylogenetic an alyses have confirmed Duck Circovirus (DuCV) as a novel 
and distinct circovirus (Fringuel li et al 2005) and a tentative speci es in this genus (Fauquet et 
al 2005), along with Finch Circovirus  (FiCV) and Gull Circovirus  (GuCV).  DuCV is closely 
related to GoCV (Hattermann et al 2003; Soike et al 2004). 
10.1.2.  OIE list 
Not listed. 10.1.3.  New Zealand status 
BFDV ( 
Ortiz-Catedral et al 2009), PiCV (MAF  2009), GuCV (Smyth et al 2006), PCV-1 and 
PCV-2 (Garkavenko et al 2005) are know n to be present in New Zealand. 
DuCV has not been recorded in the New Zeal and duck population.  However, it is recognised 
that many duck diseases may occur in New Zeal and despite them not having been detected 
(Hemsley 1996).  Surveillance programmes of asymptomatic waterfowl and commercial duck 
farms in New Zealand have been limited and no specific testing for DuCV has been 
performed.  DuCV is prevalent in many parts of  the world (Banda et al 2007) and, in the 
absence of any surveillance to demonstrate freed om, it is reasonable to conclude that DuCV 
may be present in New Zealand. 10.1.4.  Epidemiology 
The worldwide distribution of DuCV is unknown (Banda et al 2007).  It  is highly prevalent 
and widespread in Hungary (Fringuelli et al 2005), Taiwan an
d China (ShaoHua et al 2010a, 
2010b; Liu et al 2009, 2010), and has also been described in Germany (Hattermann et al 
2003; Soike et al 2004) and the Unite d States (Banda et al 2007). 
DuCV has been recovered from Muscovy, mulard  and Pekin ducks (Hattermann et al 2003; 
Soike et al 2004; Banda et al 2007) and cross- infection of other avian and mammalian species 
is considered unlikely (McNulty and Todd 2008) .  This host-specificity is supported by 
experimental work (Chen et al 2006; Woods and Latimer 2008) and there are no reports of 
natural infections in atypical hosts (Woods and Latimer 2008).   
The pathogenesis of DuCV, and avian circoviruse s in general, is not completely understood 
and current knowledge is based on field experien ce, since experimental inoculation in ducks 
has not been performed (Hattermann et al  2003; McNulty and Todd 2008).  However avian 
circovirus infections share ma ny characteristics (Soike et al 2004) and it is reasonable to 
extrapolate from studies of ot her avian circovirus species. 
24 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
Circoviral infection is typically reported in j uvenile birds but has been reported in adults 
without previous clinic al signs of disease (Banda et al  2007; Woods and Latimer 2008).  In 
one study, ducks aged 40-60 days demonstrated gr eater susceptibility to DuCV infection than 
those at other ages (ShaoHua et al 2010a).  Avian circoviruses are frequently detected in 
cloacal swabs several months following infection and it is known that ad ults may be carriers 
of the virus (McNulty and Todd 2008). 
Horizontal transmission, via the respiratory or faecal-oral route,  is thought to be the most 
common route of infection but ve rtical transmission may also o ccur, as with BFDV and PiCV 
(Fauquet et al 2005; Todd et al 2006; McNulty and Todd 2008). 
There is no evidence to support a pathogenic role for DuCV in ducks (Hattermann et al 2003).  
DuCV has a low prevalence in the United Stat es and the infection may not represent a 
significant problem for the duck industry (Banda  et al 2007).  However, in Hungary, Taiwan 
and China DuCV is associated with significant losses up to 70% (Soike et al 2004; Chen et al 
2006; Woods and Latimer 2008).  The factors that  dictate the course and outcome of the 
infection are unknown but may include virus strain, route of exposure, virus dose, levels of maternal antibody and presence of other pathogen s (Soike et al 2004; Fringuelli et al 2005; 
McNulty and Todd 2008; Woods and Latimer 2008).  DuCV replicates in healthy birds, with 
little or no apparent signs of infection, and no pathological significance has been proven (Hattermann et al 2003). 
Circoviruses are highly dependent on cellular enzymes for replication, which is typically 
intranuclear and occurs in targ eted rapidly dividing cells such as the basal feather follicular 
epithelium, lymphoreticular tissues and intes tinal crypt epithelium (Schmidt et al 2008; 
Woods and Latimer 2008).  An in situ  hybridisation (ISH) study of  geese showed that GoCV 
could be found in all tissue t ypes tested (bursa of Fabriciu s, spleen, thymus, bone marrow, 
liver, kidney, lung and heart) with the exception of brain, and was most abundant in the bursa, 
liver and small intestine (Smyth  et al 2005).  PiCV has additi onally been found in the brain 
and semen of pigeons (Duchatel et al 2009).  Du CV DNA has been isolated from extracts of 
liver, spleen, kidney, bursa, thymus, Harderia n gland, heart, blood, lung and pancreas of 
ducks (Li et al 2009), but the target cells and major sites of vi rus replication remain to be 
identified (McNulty and Todd 2008).  Intracyto plasmic globular or botryoid inclusions in 
these tissues are charac teristic of other circovirus infec tion (McNulty and Todd 2008) but are 
not a common feature of DuCV infe ction (Fringuelli et al 2005). 
Damage to lymphoreticular tissu e impairs both humoral and cellu lar immune functions.  This 
predisposes affected birds to  secondary pathogens (Soike et al 2004; McNulty and Todd 
2008) including Escherichia coli, Riemerella ana tipestifer, Pasteurella multocida,  duck 
hepatitis virus type 1 and reovirus (Liu et al 2010; ShaoHua et al 2010a).  DuCV infection is 
commonly associated with growth retardati on, feathering disorders and increased rearing 
losses (Soike et al 2004; Chen et al 2006; Woods and Latimer 2008) as well as signs of 
secondary infection, including mild arthritis and fibrinous pericarditis (Banda et al 2007).  
Many birds experience mild, subclinical infec tions (McNulty and Todd 2008; Liu et al 2010) 
and DuCV has been isolated in a healthy duck (S haoHua et al 2010b).  No  particular clinical 
syndrome can be specifically associated with DuCV infection (Sm
 yth et al 2005) and most 
mortalities result from secondary in fections (Woods and Latimer 2000). 
10.1.5.  Hazard identification conclusion 
Avian circoviruses closely re lated to DuCV are known to be  present in New Zealand and 
DuCV is wi
despread in many parts of the wo rld.  DuCV can be present in healthy ducks 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 25  
(ShaoHua et al 2010b) and there is no eviden ce to support a pathogenic role for DuCV in 
ducks (Hattermann et al 2003).  In the absence of surveillance for DuCV in New Zealand 
there is no evidence to suggest that it  should be considered exotic.  DuCV  is therefore 
assessed not to be a potential hazard. 
References 
Banda A, Galloway-Haskins R I, Sandhu T S, Schat K A (2007).  Genetic analysis of a duck circovirus 
detected in commercial Pekin ducks in New York.  Avian Diseases  51, 90-95. 
Chen C, Wan P, Lee M, Shien J, Shieh H K, Ou S, Chen C, Chang P (2006).  Development of a polymerase 
chain reaction procedure for detection and differentiation of duck and goose circovirus.  Avian Diseases 50, 92-
95. 
Duchatel JP, Todd D, Willeman C, Losson B (2009).  Quantification of pigeon circovirus in serum, blood, 
semen and different tissues of naturally infected pigeons using a real-time polymerase chain reaction.  Avian 
Pathology 38, 143-148. 
Fauquet CM, Mayo MA, Maniloff J, Desselberger U, Ball LA (Eds) (2005).  Virus taxonomy.  VIIIth Report 
of the International Committee on Taxonomy of Viruses .  Elsevier Academic Pr ess, California, 327-334 
Fringuelli E, Scott ANJ, Beckett A,  McKillen J, Smyth JA, Palya V, Gl avits R, Ivanics E, Mankertz A, 
Franciosini MP, Todd D (2005).  Diagnosis of duck circovirus infections by conventional and real-time 
polymerase chain reaction tests.  Avian Pathology 34, 495-500. 
Garkavenko O, Elliott RB, Croxson MC (2005).  Identification of pig circovirus type 2 in New Zealand pigs.  
Transplantation Proceedings 37, 506-509.  
Hattermann K, Schmitt C, Soike D, Mankertz A (2003).  Cloning and sequencing of duck circovirus (DuCV).  
Archives of Virology  148, 2471-2480. 
Hemsley LA (1996).  Duck Diseases in New Zealand.  Surveillance 23(4), 28. 
Li M, YanHua S, NaXiang W, Quan Z, Li Z, YongFeng S (2009).  PCR detection and sequence analysis of 
duck circovirus infection in Xinxing County of Guangdong Province.  Chinese Veterinary Science 39, 164-167. 
Liu S, Zhang X, Zhi C, JiMing G, XiuLi W, YiBo K, YanLi Z, ShiJin J (2009).  Epidemic investigation of 
duck circovirus in spontaneous diseased duck flocks in China.  Chinese Journal of Veterinary Science 29, 1402-
1405. 
Liu S, Zhang X, JinFeng Z, ZhiJing X, YanLi Z, Qin Z, EnMin Z, ShiJin J (2010).  Development of an 
indirect ELISA for the detection of duck circovirus infection in duck flocks.  Veterinary Microbiology 145, 41-
46. McNulty MS, Todd D (2008).  Circoviridae.  In .  In Poultry Diseases 6th Edition. Eds  Pattison M, McMullin 
PF, Bradbury JM, Alexander DJ. Elsevier/Butterworth-Heinemann, 398-404. 
MAF Biosecurity New Zealand (2009).  Import risk analysis:  Pigeons (Columba livia) from Australia. 
Biosecurity New Zealand, Ministry of Agricu lture and Forestry, We llington, New Zealand. 
http://www.biosecurity.gov t.nz/files/regs/imports/ri sk/pigeons-aus-ra.pdf.   
Ortiz-Catedral L, McInnes K, Hauber ME, Brunton DH (2009).  First report of beak and feather disease 
virus (BFDV) in wild red-fronted parakeets ( Cyanoramphus novaezelandiae ) in New Zealand.  Emu - Austral 
Ornithology 109, 244-247. 
Schmidt V, Schlomer J, Luken C, Johne R, Biere B, Muller H, Krautwald- Junghanns ME (2008).  
Experimental infection of domestic pigeons with pigeon circovirus.  Avian Diseases 52, 380-386. 
ShaoHua S, ChunHe W, Zhen C, Bin J, LongFei C, Ho ngMei C, ChunXiang X, Fang L, JianSheng L, Yu 
H (2010a).  Detection of duck circovirus infection.  China Poultry  32, 31-33. 
26 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
ShaoHua S, GuangHua F, LongFei C, HongMei C, Ch unHe W, Zhen C, ChunXiang P, Fang L, Yu H 
(2010b).  Sequencing and analysis of genome of duck circovirus PT07.  Chinese Journal of Preventive 
Veterinary Medicine 32, 235-237. 
Smyth J, Soike D, Moffett D, Weston J H, Todd D (2005).  Circovirus-infected geese studied by in situ 
hybridization.  Avian Pathology 34, 227-232. 
Smyth J, Todd D, Scott A, Becket t A, Twentyman CM, Bröjer C, Uhlh orn H, Gavier-Widen D (2006).  
Identification of circovirus infection in three species of gull.  Veterinary Record 159, 212-214. 
Soike D, Albrecht K, Hattermann K, Schmitt C, Mankertz A (2004).  Novel circovirus in mulard ducks with 
developmental and feathering disorders.  Veterinary Record  154, 792-793. 
Todd D, Duchatel JP, Bustin JC, Scullion FT, Scu llion MG, Scott ANJ, Curr y A, Ball NW, Smyth JA 
(2006).  Detection of pigeon cirovirus in cloacal swabs: implications for diagnosis, epidemiology and control.  
Veterinary Record 159, 314-317. 
Woods LW, Latimer KS (2008).  Circovirus infection of pigeons and other avian species.  In Diseases of 
Poultry 12th Edition. Eds Saif YM, Fadly AM, Glisson JR , McDougald LR, Nolan LK, Swayne DE. Blackwell 
Publishing, 236-249. 
 
 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 27  
11. Avian Chlamydiosis 
11.1. HAZARD IDENTIFICATION 
11.1.1.  Aetiological agent 
Obligate intracellular gram
-negative bacteria, Chlamydia psittaci (Andersen and Vanrompay 
2008). Eight serovars, distinguished  using monoclonal antibodies a nd with differences in their 
predominant host ranges, are rec ognised (Gilardi et al 1995).  
Six serovars (A to E) of Chlamydia psittaci are recognised in birds (Everett et al 1999) : 
 Serovar A is endemic in psittacines,  
 Serovar B in Columbiformes, with some presence in turkeys,  
 Serovar C has been isolated most frequently  from Anseriformes with reports also from 
turkey and partridge, 
 Serovar D is most common in  turkeys (Phasianiformes) with single isolates being 
identified from a seagull and a budgerigar, 
 Serovar E has been reported from ducks, pigeons, and ratites, 
 Serovar F has been reported only fr om a single psittacine (parakeet). 
11.1.2.  OIE list 
Listed. 
11.1.3.  New Zealand status 
Psittacosis was first des
cribed in 66 imported Australian parrots in 1954, with diarrhoea, 
listlessness, and death affecting at least 31 bi rds (Cairney 1954).  La boratory investigations 
between 1984 and 1985 identified C. psittaci  isolates from budgeriga rs, parakeets, pigeons, 
rosellas, and cockatiels (Bell and Schroeder 1986).  Psittacosis is consider ed to be prevalent in 
New Zealand wild pigeons, with a prevalence rate of between 9.5% and 25% (Motha et al 
1995). 
An unpublished survey of faecal samples from captive and wild endangered and threatened 
avian species was reported by Motha et al (1995) to have detected C. psittaci in a number of 
species, including kakapo, takahe, and kiwi.  However, a subsequent survey found no 
evidence of psittacosis in native psittacines w ith perhaps the exception of kakas and wekas on 
Kapiti Island and it was suggested that the ear lier unpublished findings were likely to have 
been false positive results due to th e choice of test (Motha et al 1995). 
Given the patterns of  host preference of C. psittaci  serotypes, the above evidence is consistent 
with the presence of serotypes B (Columbiformes) and possibly A (Psittaciformes) of C. 
psittaci  in the New Zealand avia n population (MAF 2010).  
11.1.4.  Epidemiology 
C. psittac
i serovars can be di stinguished in specialised labo ratories by a panel of serovar-
specific monoclonal antibodies (Andersen 1991; Andersen 1997).  Restriction fragment 
length polymorphism analysis and genotyping techniques are also  available to distinguish 
28 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
serovars (Vanrompay et al 1997; Geens et  al 2005).  Of the 8 known serovars of C. psittaci , 
serotypes C and E are associated with ducks. 
Chlamydiosis in ducks is usually a severe dis ease, with morbidity up to 80%, with up to 30% 
mortality (Andersen and Vanrompay 2008) although some outbreaks may be associated with 
few clinical signs (Arzey et al 1990; Newman et al  1992; Hinton et al 1993). 
Transmission of C. psittaci  occurs primarily through inhala tion of contaminated material, 
with large numbers of chlamydiae found in the re spiratory tract exudate and faeces of infected 
birds (Andersen 1996).   
Vertical transmission of C. psittaci  has been demonstrated in several avian species, including 
ducks, although the frequency of this appears to be fairly low (Wittenbrink et al 1993).  It has 
been suggested that C. psittaci may either penetrate the shell of freshly laid eggs or be present 
in the egg contents due to either sperm cont amination or transovarian haematogenous spread 
(Dickx and Vanrompay 2011).  Vert ical transmission is recognis ed as a possible route of 
introduction of C. psittaci into a poultry flock (Harkinezhad et al 2009). 
Serologic evidence of C. psittaci infection of ducks was descri bed in 1942 and within three 
years human infections due to contact with inf ected ducks had been reported (Harkinezhad et 
al 2009).  Human cases of severe respiratory di stress have been associated with zoonotic C. 
psittaci  infections acquired from infected duck farm s (Laroucau et al 2009).  Transmission to 
humans typically involves inhala tion of infectious aerosols during the handling of infected 
material.  The symptoms of human infection rang e from severe systemic disease to a complete 
absence of clinical signs (Andersen and Vanrompay 2000). 
11.1.5.  Hazard identification conclusion 
It is not known which serovars of C. psitta
ci are present in New Z ealand although there is no 
evidence to indicate the presence of serova r C in the New Zealand duck population.  Although 
transmission of C. psittaci primarily occurs horizontally from  one infected bird to another 
susceptible bird in close proxi mity, vertical transmission is described and recognised as a 
possible route of introduc tion into a poultry flock. 
Reflecting this, exotic stra ins (serovars C and E) of C. psittaci are considered to be a risk in 
the commodity. 
11.2. RISK ASSESSMENT 
11.2.1.  Entry assessment 
C. psittac
i may be transmitted in the eggs of infected ducks.  Therefore, the likelihood of 
introducing the organism in duck hatching eggs  imported from countries where serovars C 
and E of C. psittaci  have been described in ducks is assessed to be non-negligible. 
11.2.2.  Exposure assessment 
Although the occurrence of vertical transm
ission of C. psittaci  appears to be fairly low, an 
outbreak of disease in a flock can be started from a single infected chick (Andersen and 
Vanrompay 2000). 
Air-sampling of a hatchery for C. psittaci found high titres of live organisms following 
hatching of fumigated eggs whose shells were found to be negative for C. psittaci  by both 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 29  
PCR and culture (Dickx and Vanrompay 2011).  The hatching of infected chicks is therefore 
highly likely to result in dissemina tion of infection to other chicks 
Therefore, the likelihood of exposure is assessed to be non-negligible.  
11.2.3.  Consequence assessment 
In ducks, serovar C of C. psitta
ci has a morbidity rate of 10-80% and a mortality rate of 0-
30%, with some duck farms being infected with few or no clinical  signs.  Concurrent 
infections or stress increase the severity of the di sease (OIE 2009). 
Serovar E of C. psittaci  has a diverse host range, and has b een isolated from cases of fatal 
chlamydiosis in ratites, from outbreaks in duc ks and turkeys, and occasionally from humans 
(Harkinezhad et al 2009). 
Humans can become infected after inhaling contaminated dust, feathers or aerosolized 
secretions and excretions.  Direct  contact with infected birds can  also spread disease.  Human 
symptoms vary from mild, flu-like illness to  severe atypical pneumonia with dyspnoea.  
Illness usually lasts for 7 to 10 days a lthough complications including miscarriage, 
endocarditis, myocarditis, renal disease, he patitis, anaemia and neurological signs are 
described (OIE 2009). 
Considering the above, the consequences of introducing serovars C and E of C. psittaci  are 
considered to be non-negligible. 
11.2.4.  Risk estimation 
Because the entry, exposure and consequence assessm
ents are non-negligible, the risk 
estimate is non-negligible and serovars C and E of C. psittaci  are classified as a risk in 
imported duck eggs. Therefore, risk ma nagement measures can be justified. 
11.3. RISK MANAGEMENT 
11.3.1.  Options 
Because iso
lates of C. psittaci associated with ducks are limited to serovars C and E, there is 
no need for laboratory tests to dist inguish between any serovars of C. psittaci  isolated from 
breeding flocks or hatched ducklings. 
The OIE Code contains no recommended measures to manage the risk of C. psittaci  in 
imported hatching eggs. Pharyngeal or nasal swabs are the preferred samples for isolating C. psittaci  from live birds 
using cell culture techniques or embryonated eggs (Andersen 1996).  Intestinal content, 
cloacal swabs, conjunctival scrapings and peritoneal exudate may also be  used (OIE 2008). 
Histochemical straining of impression smears of liver and spleen can be used to demonstrate 
the presence of C. psittaci using Giemsa, Gimenez, Ziehl-Neelsen and Macchiavello’s stains.  
Immunohistochemical techniques are also de scribed which are more sensitive than 
histochemistry although these require greater expe rience to ensure correct interpretation (OIE 
2008). A modified direct complement fixation test to detect serol ogical evidence of exposure to C. 
psittaci  is widely used (OIE 2008).  Other serolo gical tests available include the agar gel 
immunodiffusion test (Page 1974), the latex agglutination test, the elementary body 
30 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries   
agglutination test (Grimes et al 1994; Grimes and Arizmendi 1996) and the micro-
immunofluorescence test (OIE 2008). 
One or more of the following options could ther efore be considered in order to effectively 
manage the risk: 
Option 1 
Duck eggs could be imported without restricti ons from countries where chlamydiosis has not 
been reported in commercial ducks. 
Option 2 
Eggs could be imported from flocks that are maintained as closed flocks and in which 
ongoing surveillance has demonstrated freedom from C. psittaci . 
Option 3 Donor ducks could be kept isolat ed from other ducks for at leas t three weeks before eggs are 
collected, and the donors tested serologically for exposure to C. psittaci  before going into 
isolation and again three weeks after the end of the collect ion period, with negative results.  
Option 4 
Imported eggs could be hatched in isolation in  New Zealand and a representative sample of 
chicks could be tested serologically.  Any dead  hatchlings or dead-in-shell chicks could be 
examined to detect the presence of C. psittaci using histochemical staining of liver and spleen 
impression smears. 
References 
Andersen AA (1991).  Serotyping of Chlamydia psittaci  isolates using serovar-specific monoclonal antibodies 
with the microimmunofluorescence test.  Journal of Clinical Microbiology  29, 707-711. 
Andersen AA (1996).  Comparison of pharyngeal, faecal, and cloacal samples for the isolation of Chlamydia 
psittaci  from experimentally infected  cockatiels and turkeys.  Journal of Veterinary Diagnostic Investigation  8, 
448-450. 
Andersen AA (1997).  Two new serovars of Chlamydia psittaci  from North American birds.  Journal of 
Veterinary Diagnostic Investigation  9, 159-164. 
Andersen AA, Vanrompay D (2000).  Avian chlamydiosis .  Revue Scientifique et Technique  19, 396-404. 
Andersen AA, Vanrompay D (2008).  Avian chlamydiosis (psittacosis, ornithosis).  In Diseases of Poultry  12th 
Edition, Ed Saif YM, Blackwell Publishing, 971-986. Arzey KE, Arzey GG, Reece RL (1990).  Chlamydiosis in commercial ducks.  Australian Veterinary Journal 
67, 333-334. 
Bell CW, Schroeder BA (1986).  Isolation and identification of Chlamydia psittaci in New Zealand.  New 
Zealand Veterinary Journal  34, 15-16. 
Cairney IM (1954).  Psittacosis in New Zealand.  New Zealand Veterinary Journal  2, 59. 
Dickx V and Vanrompay D (2011).  Zoonotic transmission of Chlamydia psittaci  in a chicken and turkey 
hatchery. Journal of Medical Microbiology  60, 775-779. 
Ministry for Primary Industries   Import risk analysis: Duck hatching eggs ● 31  
32 ● Import risk analysis: Duck hatching eggs Ministry for Primary Industries  Everett KDE, Bush RM, Andersen AA (1999). Emended description of the order Chlamydiales, proposal of 
Parachlamydiaceae fam. Nov. and Simk aniaceae fam. Nov., each containing  one monotypic genus, revised 
taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the 
identification of organisms.  International journal of Systematic Bacteriology  49, 415-440. 
Geens T, Desplanques A, Van Loock M, Bönner BM, Ka leta EF, Magnino S, Andersen AA, Everett KDE, 
Vanrompay D (2005).  Sequencing of the Chlamydophila psittaci ompA reveals a new genotype, E/B, and the 
need for a rapid discriminatory genotyping method.  Journal of Clinical Microbiology  43, 2456-2461. 
Gilardi KVK, Lowenstine LJ, Gilardi JD, Munn CA (1995).  A survey for selected viral, chlamydial, and 
parasitic diseases in wild dusky-headed parakeets (Aratinga weddellii) and Tui parakeets (Brotogeris 
sanctithomae) in Peru. Journal of Wildlife Diseases  31, 523-528. 
 
Grimes JE, Tully Jr TN, Arizmendi F, Phalen DN (1994).   Elementary body agglutination for rapidly 
demonstrating Chlamydial agglutinins in avian serum with emphasis on testing cockatiels. Avian Diseases  38, 
822-831. 
 Grimes JE, Arizmendi F (1996).  Usefulness and limitations of three serologic methods for diagnosing or 
excluding chlamydiosis in birds. Journal of the American Veterinary Medical Association  209, 747-750. 
Harkinezhad T, Geens T, Vanrompay D (2009). Chlamydia psittaci  infections in birds: A review with 
emphasis on zoonotic consequences. Veterinary Microbiology  135, 68-77. 
Hinton DG, Shipley A, Galvin JW, Harkin JT, Brunton RA (1993).  Chlamydiosis in workers at a duck farm 
and processing plant.  Australian Veterinary Journal  70, 174-176. 
Laroucau K, Barbeyrac B de, Vorimore F, Clerc M, Bertin C, Harkinezha d T, Verminnen K, Obeniche F, 
Capek I, Bébéar C, Durand B, Zanella G, Va nrompay D, Garin-Bastuji B, Sachse K (2009)  Chlamydial 
infections in duck farms associated w ith humahn cases of psittacosis in France. Veterinary Microbiology  135, 
82-89. 
MAF (2010).  Import risk analysis: Psittacine hatching eggs .  MAF Biosecurity New Zealand, Wellington, New 
Zealand. 
Motha J, Reed C, Gibbons A (1995).  The prevalence of Chlamydia psittaci  in feral pigeons and native 
psittacines.  Surveillance 22(4), 20-22. 
Newman CPStJ, Palmer SR, Ki rby FD, Caul EO (1992).  A prolonged outbreak of ornithosis in duck 
processors.  Epidemiology and Infection  108, 203-210. 
OIE (2008).  Chapter 2.3.1 Avian chlamydiosis.  In OIE Terrestrial Manual. OIE Paris. 
OIE (2009).  Avian chlamydiosis. http://www.cfsph.iastate.edu/Factsh eets/p
 dfs/chlamydiosis_avian.pdf .  Last 
accessed 20th February 2012. 
Page LA (1974).  Application of an agar gel precipitin test to the serodiagnosis of avian chlamydiosis. 
Proceedings of the American Association of Veterinary Laboratory Diagnosticians . 17. 51-61. 
 
Vanrompay D, Butaye P, Sayada C, Ducatelle R, Haesebrouck F (1997).  Characterisation of avian 
Chlamydia psittaci  strains using omp1 restriction mapping and serovar-specific monoclonal antibodies.  
Research in Microbiology  148, 327-333. 
Wittenbrink MM, Mrozek M, Bisping W (1993). Isolation of Chlamydia psittaci  from a chicken egg: 
Evidence of egg transmission. Journal fo Veterinary Medicine Series B  40, 451-452.