Supplementary import risk 
analysis : Sausage casings of 
bovine and porcine origin  
 
 
 
March 2015 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  
 
 
 
Biosecurity Science, Food  Science  and Risk Assessment , 
Ministry for Primary Industries  
 
 
 
 
 
Supplementary  Import risk a nalysis: Sausage casings of bovine and porcine origin  
DRAFT  for Public Consultation  
 
 
March 2015  
 
 
 
 
 
 
 
 
Approved for Public Consultation  
 
 
 
 
 
Christine Reed  
Manager, Biosecurity Science, Food Science and Risk Assessment ,  
Ministry for Primary Industries  
 This page is intentionally blank 
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 1 Contents   
 
1. Executive summary  3 
2. Introduction  5 
3. Scope and commodity definition  5 
4. Risk analysis methodology  6 
5. Preliminary list of hazards  9 
6. Bacillus anthracis  16 
7. Echinococcus granulosus  18 
8. Foot and mouth disease virus  20 
9. Exotic Salmonella  spp.  23 
10. African swine fever virus  26 
11. Aujeszky’s disease  virus  29 
12. Classical swine fever virus  32 
13. Porcine reproductive and respiratory syndrome virus  37 
14. Swine vesicular disease virus  40 
15. The agent of bovine spongiform encephalopathy  43 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
2 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Contributors to this risk analysis  
 
1. Author  
 
Abraham Growcott  
 Adviser, Animal and A quatics,  Biosecurity  Science, Food Science and 
Risk Assessment,  Ministry for Primary Industries,  
Wellington  
 
2. Internal peer r eview  
 
Stephen Cobb  Manager, Animal and A quatics,  Biosecurity  Science , Food Science 
and Risk Assessment, Ministry for Primary Industries,  
Wellington  
 
Lincoln Broad  
 
 
 Senior A dvise r, Animal  and A quatics,  Biosecurity  Science , Food 
Science and Risk Assessment,  Ministry for Primary Industries,  
Wellington   
Lou Gallagher  Senior Adviser, Animal Imports, Animal and Animal Products,  
Ministry for Primary Industries,  Wellington  
  
Stuart MacDiarmid  
 Principal Adviser, Risk Analysis, International Policy, Ministry for 
Primary Industries, Wellington | Adjunct Professor in Veterinary 
Biosecurity, Massey University  
  
3. External peer r eview  
 
Dr. Joris Wijnker  Consultant, Veterinary Public Health (VPH) Consultancy.  
 
  
 
 
 
 
   
 
 
 
 
 
 
 
 
 
 
 
 
   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 3 1. Executive summary  
This import risk analysis examines the biosecurity risks associated with the  international  trade 
in natural sausage casings of bovine and porcine origin, tha t have been prepared by methods  
which are standard operating procedure s in much of the international casing industry.  
Natural s ausage casings are made  from the intestines of cattle and pigs that have passed ante - 
and post -mortem inspection. The intestines are subject to a numbe r of processing  steps that 
remove  gut contents and differen t tissue layers and the casings are subsequently stored at 
room temperature for  a minimum of  30 days in dry salt or saturated brine.  
Hog casings  produced from the small intestine consist of  the submucosa tissue layer , with 
complete removal of all  lymphoid tissue (Peyer’s patches) . Hog casing s made from the  large 
intestine contain at least some of the major intestinal tissue layers.  
Beef casings  also contain most  of the intestinal tissue laye rs as only part of the mucosa and 
lymphoid tissue is removed during processing.  From a technological viewpoint the only part 
of the intestinal tract that is not utilised is the ileum1 due to its aberrant  shape .  
Disease -causing organisms associated with b ovine and porcine intestines were identified from 
previously peer -reviewed Ministry for Primary Industries risk analyses.  Of the 1 0 disease -
causing organisms examined in this risk analysis, 9 were identified from a risk analysis of 
cattle and pig meat, with the other organism identified from a single species risk analysis of 
pig meat.  
The 10 disease -causing organism s examined  in this risk analysis  are: 
 African swine fever virus  
 Aujeszky’s disease virus  
 Classical swine fever virus  
 Foot and mouth disease virus  
 Porcine reproductive and respiratory syndrome virus  
 Swine vesicular disease virus  
 Bacillus anthracis  
 Salmonella spp. 
 Echinococcus granulosu s 
 The agent of bovine spongiform encephalopathy  
Of these 1 0 organisms, one is assessed to be a risk; classical swine fever virus (hog casings) 
and risk management options are presented.  
 
 
                                                
 
1 In addition to the technological exclusion of the bovine ileum for beef casing production, the OIE recommends not to trade 
the ileum if derived from animals originating from countries with a BSE controlled or undetermined risk. This is because the 
ileum c ould contain BSE prions that if consumed by humans may cause variant Creutzfeld -Jakob disease.  
See OIE Article 11.4.14, http://www.oie.int/index.php?id=169&L=0&htmfile=chapitr e_bse.htm    
4 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI The following measures could be considered to effectively manage the risk  in imported hog 
casings . 
 
Option 1  
 
Hog casings  could be imported on ly from countries, zones or compartments recognised by 
New Zealand as free from CSFV.  
 
Option 2  
 
For the inactivation of CSFV in casings of pigs, the following procedures could  be used: 
salting for at least 30 days either with phosphate supplemented dry salt or saturated brine (Aw 
< 0.80) containing 86.5% NaCl, 10.7% Na 2HPO 4 and 2.8% Na 3PO 4 (weight/weight/weight), 
and kept at a temperature of greater than 20  °C during this entir e period.   
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 5 2. Introduction  
This import risk analysis examines the biosecurity  risks associated with imports of  sausage 
casings prepared from the inte stines of cattle and pigs. Disease -causing organisms  are identified 
from previously  peer-reviewed Ministry for Primary Industries (MPI) risk analyses of cattle and 
pig meat (MPI 2006; MPI 2014).  Only those disease -causing organisms requiring risk 
management measures  are considered further.   This risk analysis supplements MPI’s previous 
risk analysis for small ruminant sausage casings (MPI 2010).  
3. Scope and commodity definition  
This document  assesses the biosecuri ty risks associated with natural sausage casings of 
porcine and bovine origin, prepared by methods  which  are standard operating procedures in 
much of the international casings industry.  
The commodities  under consideration  are hog casings  consisting of  the submucosal  tissue  
layer of the  small intestine and  casing s made  from the large intestine which contain  all tissue 
layers . For beef casings  this consists of all intestinal layer s of the entire intestinal tract with 
the exc lusion  of the ileum.  Casings are produced from animals  that have passed ante - and 
post-mortem inspection according to the OIE’s Terrestrial  Animal Health Co de (here after 
referred to as the Code ) chapter 6.2 (OIE 2013) . After cleaning and scraping, the casings have 
been stored at room temperature in either dry salt or saturated brine . As an alternative 
treatment  the dry salt or saturated brine  may be supplemented with  sodium phosphate s 
(E339)  for a minimum of 30 days. The pH of  casing stored in  dry salt and saturated brine is 
between 7.5 and 8, and  if supplemented with  phosphate the pH increases to approximately  10 
(Wijnker  et al.  2009 ). 
The e ntire intestinal tract of pigs is used fo r the production of casings. With the small 
intestines (duodenum, jejunum, ileum), bung (caecum), large intestines (colon ascendens and 
transversum), after end (colon descendens) and fat end (rectum) being especially utilised 
(Wijnker 2009).  
The intestinal tract of cattle is also use d entirely for the production of beef casings with the 
exception of the ileum . Its shape differs too much from the jejunum to produce the classic 
beef rounds and is therefore removed prior to the cleaning process and destroyed. Beef 
casings are produced fr om the small intestines including the duodenum and jejunum (beef 
rounds) and the caecum and from the large intestines, including the entire colon (beef 
middles). Beef casings are also produced from the urinary bladder and the oesophagus  
(weasand) ( Ockerman  and Hansen, 2000 ; Wijnker et al. 2008 ; European Natural S ausage 
Casings Association 2013 ). 
The basic anatomy and function of the intestinal tract is very similar across  the species  used 
for casing manufactur e (Wijnker 2009) . The intestinal wall is compose d of four main layers 
(Figure 1). The outermost layer is the tunica serosa. The next layer, the tunica muscularis, 
consists of two layers of smooth muscle. Beneath these layers is the tunica submucosa, which  
is comprised of a network of collagen fibres, el astin and blood vessels. The innermost layer, 
which lines the lumen of the intestine,  is the tunica mucosa. Lymphoid tissue is embedded in 
the mucosa. This lymphoid tissue is most prominent in the ileum, where it is aggregated into 
Peyer’s patches (Wijnker  2009).  
Once pulled from the abdominal cavity the intestines have their gut contents removed. The 
intestines are then processed through a number of steps, which  involves equipment such as;   
6 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI conveyor belts, holding (soak) tanks, water sprinklers, rollers an d scrapers, which  facilitate 
the removal of unwanted tissue. Water in the holding tanks is usually heated to a temperature 
of 40  °C to assist cleaning. After processing,  the casings are placed in cold water or a salt 
brine tank to wash away any residual bl ood and prevent the growth of bacteria ( European 
Natural Sausage Casing s Association  2013).  
 
 
 
Figure 1: Schematic diagram of a small intestine showing (a) mesentery and serosa; (b) inner and outer 
muscle layers; (c) submucosal blood vessels; (d) muscularis mucosae; (e) submucosa; (f) lymphoid 
nodule (Peyer’s patch); (g) tunica mucosa (villus and crypt layers). In hog casings the tunica mucosa, 
the muscularis, the serosa and Peyer’s patches are removed during processing, so the natural casing 
consi sts of only the submucosa. In beef casings,  all intestinal  layers remain after cleaning (a dapted from 
Koolmees et al. 2004).  
 
4. Risk analysis methodology  
The methodology used in this risk analysis follows the guidelines as described in Biosecurity 
New Zealand Risk Analysis Procedures – Version 1  (MPI 2006 b) and in Section 2 of the Code  
(OIE 2013 ). The risk analysis process used by the Code  and adopted by the Ministry for 
Primary Industries  is summarised in Figure 2 (overleaf).  
 
 
 
 
  
 
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 7 Figure 2 . The risk analysis process.   
 
4.1. PRELIMINARY LIST  OF HAZARDS  (ORGANISMS OF POTENT IAL 
CONCERN)  
The first step in the risk analysis process is to compile  a list of pathogens known to infect cattle 
and pigs . This list is subjected to the application of specific criteria to eliminate those that are 
not organ isms of concern . The remaining organisms are then subjected to the process of hazard 
identification.  
4.2. HAZARD IDENTIFICATIO N 
Hazard identification  includes formal identification o f the organism, whether it is associated 
with an  OIE listed disease, its New Zealand status, and a discussion on the relevant aspects of 
the epidemiology and characteristics of the organism. The hazard identification section is 
concluded by an assessment of whether or not the organism is identified as a  hazard.  
 
8 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI  All hazards are subjected to risk assessment.  
4.3. RISK ASSESSMENT  
Risk assessment consists of:  
a) Entry assessment : The likelihood of a hazard (pathogenic organism) be ing imported 
with the commodity . 
b) Exposure assessment : Describes the biological pathwa y(s) necessary for exposure of 
susceptible animals or humans in New Zealand to the hazard. Further, a qualitative 
estimation of the probability of the exposure occurring is made.  
c) Consequence assessment : Describes the likely potential consequences of entry,  
exposure and establishment or spread of an imported hazard.  
d) Risk estimation : An estimation of the risk posed by the hazard associated with 
importing sausage casings . This is based on the entry, exposure and consequence 
assessments. If the risk estimate is  assessed to be non-negligible, then the  hazard is 
assessed to be a risk , and risk management measures may be justified to reduce the 
level of risk to an acceptable level.  
Not all of the above steps may be necessary in all risk assessments. The OIE methodo logy 
makes it clear that if the likelihood of entry is neg ligible for a 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 when the likelihood of entr y is non -negligible but the exposure 
assessment concludes that the likelihood of susceptible species being exposed is negligible, or 
when both entry and exposure are non -negligible but the consequences of introduction are 
assessed to be negligible.  
4.4. RISK MA NAGEMENT  OPTIONS  
For each organism assessed to be a risk  the op tions available for managing that  risk are 
presented . Where the Code  lists recommendations for the management of a risk , these are 
described alongside options of similar, lesser  or greater stri ngency , where available.  In addition 
to the options presented, unrestricted entry or prohibition may al so be considered . 
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 o f the World Trade Organization’s Agreement on the Application 
of Sanitary and Ph ytosanitary (SPS) measures,  the measures adopted in this IHS  will be based 
on international standards, guidelines and r ecommendations where they exist e xcept as 
otherwise provided for under Article 3.3 . That is,  measures providing a higher level of 
protection than international standards can be applied if there is scientific justification, or if 
there is a level of protection that the member country considers is more  appropriate.  
4.5. RISK COMMUNICATION  
In drafting  an IHS, MPI analyse s the options available and proposes measures for the effective 
management of identifie d risks. These are then presented in a draft IHS that is released together 
with a risk management proposal that summarises the options analysis, the rationale for the 
proposed measures and a link to the risk analysis. The package of documents is released f or a 
six-week period of stakeholder consultation. Stakeholder submissions in relation to these 
documents are reviewed before a final IHS is issued.    
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 9 5. Preliminary list of hazards  
The first step in the risk analysis  process  is the  identification of agents of  concern and the 
collation of these into a list of pathogens  that m ay be associated with the commodity under 
consideration.  
Following  the completion of the Import risk analysis: Meat and meat products from 
ruminants and pigs  (MPI 2014) , only  disease -causi ng organisms  associated with cattle  and 
pigs that require d risk management  measures are to be assessed . This is because  the 
commodity definition of meat used in this  previous  risk analysis  was “all edible parts of an 
animal ”. Therefore , the identification of disease -causing agents  associated with intestinal  
tissues has been  completed . In addition  to these  identified pathogens , porcine reproductive 
and respiratory syndrome virus will  also be in cluded in the  list, as it was assessed  in a 
separate  single species  risk analysis (MPI 2006).   
Organisms in Table 1  are classified as requiring further assessment  if they are:  
 Exotic to New Zealand ; and,  
 Require risk management measures as described in MPI (2006; 2014).  
Organisms  listed in Table 1  do not require further assessment  if they are:  
 Not assessed as requiring risk management measures as described in MPI (2014) ; or, 
 The organism is not associated with the intestinal tract.  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  
10 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Table 1: Exotic organisms  of concern that may be present in beef and hog casings  (adapted 
from MPI 201 4). 
 
Organism  OIE 
List Zoonotic  Relevant 
species 
infected  Transmission  Assessed to 
be a risk in 
edible 
tissue2 Requires 
further 
assessment  
Viruses        
Akabane and related 
simbu viruses  No No Cattle  Vector -borne  No No 
Adenovirus  No No Pigs Direct contact  No No 
African swine fever virus  Yes No Pigs Direct contact, 
ingestion, vector -
borne  Yes Yes 
Alcelaphine herpesvirus 
1 (malignant catarrhal 
fever)  No No Cattle  Close contact  No No 
Aujeszky’s disease virus  Yes No Pigs and cattle  Direct oral -nasal 
contact, ingestion  Yes Yes 
Blue eye disease virus  No No Pigs Direct contact  No No 
Bluetongue virus  Yes No Cattle  Vector -borne  No No 
Borna disease virus  No Yes Exceptionally 
cattle  Direct contact  No No 
Bovine ephemeral fever 
virus  No No Cattle  Vector -borne  No No 
Bovine herpesvirus 5, 
1.1 and 1.2a strains 
(IBR/IPV)  Yes No Cattle  Direct contact  No No 
Bovine parvovirus  No No Cattle  Faecal -oral No No 
Bovine rhinovirus  No No Cattle  Direct contact  No No 
Bovine viral diarrhoea 
virus 
 Yes No Cattle, pigs  Direct contact, 
ingestion (pigs)  No No 
Bungowannah virus  No No Pigs Direct contact, 
ingestion?  No No 
Classical swine fever 
virus ( hog cholera)  Yes No Pigs Direct contact, 
ingestion  Yes Yes 
Epizootic haemorrhagic 
disease (EHD) virus 
(including Ibaraki virus)  Yes No Cattle  Vector -borne  No No 
Equine encephalitis 
viruses ( eastern, 
western, Venezuelan)  Yes Yes Pigs Vector -borne  No No 
Foot and mouth disease 
virus  Yes No Pigs Close contact, 
aerosol, ingestion  Yes Yes 
                                                
 
2 See MPI’s 2014 Import risk analysis : Meat and meat products from ruminants and pigs. Draft for public consultation. 
[Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/meat -and-meat -products -from-ruminants -and-
pigs-feb-2014.pdf  [Accessed 3t h March 2014].   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 11 Table 1 (continued)        
Organism  OIE 
List Zoonotic  Species 
infected  Transmission  Assessed to 
be a risk in 
edible 
tissue  Requires 
further 
assessment  
Viruses (continued)        
Hendra virus  No Yes Pigs 
(experimentally)  Direct contact with 
fruit bats  No No 
Influenza viruses  No No Pigs Close contact  No No 
Japanese encephalitis 
virus  Yes Yes Pigs Vector -borne  No No 
Jembrana disease virus  No  No Cattle  Mechanical by biting 
insects  No No 
Kunjin virus  No Yes Pigs Vector -borne  No No 
Louping ill and related 
viruses (tick borne 
encephalitis)  No Yes Cattle and pigs   Vector -borne  No No 
Lumpy skin disease 
virus  Yes No Cattle  Mechanical by biting 
insects  No No 
Menangle virus  No Yes Pigs Contact with fruit 
bats No No 
Murray Valley 
encephalitis virus  No Yes Pigs Vector -borne  No No 
Nipah virus  
 Yes Yes Pigs Exposure to fruit 
bats, direct contact, 
ingestion  No No 
Porcine 
haemagglutinating 
encephalomyelitis virus  No No Pigs Direct contact  No No 
Porcine epidemic  
diarrhoea virus  No No Pigs Faecal -oral No No 
Porcine respiratory 
coronavirus  No No Pigs Direct contact, 
ingestion?  No No 
Porcine reproductive 
and respiratory 
syndrome virus  Yes No Pigs Direct contact, 
ingestion 
(experimentally)  Yes3 Yes 
Rabies virus  Yes Yes Cattle and pigs  Direct contact (bite), 
ingestion?  No No 
Rift Valley fever virus  Yes Yes  Cattle  Vector -borne  No No 
Ross River and Barmah 
Forest viruses  No Yes Cattle and pigs  Vector -borne  No No 
Swine pox virus  No No Pigs Mechanical 
arthropod vectors  No No 
Swine vesicular disease 
virus  No No Pigs Close contact, 
ingestion  Yes Yes 
                                                
 
3See MPI (2006). Import risk analysis : Porcine reproductive and respiratory syndrome (PRRS) virus in pig meat. [Online] 
Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/prrs -risk-analysis.pdf  [Accessed 4th December 2013].   
  
12 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Teschovirus serotype 1  No No Pigs Ingestion , aerosol  No No 
Table 1 (continued)        
Organism  OIE 
List Zoonotic  Species 
infected  Transmission  Assessed to 
be a risk  in 
edible 
tissue  Requires 
further 
assessment  
Viruses (continued)        
Transmissible 
gastroenteritis virus  Yes No Pigs Ingestion  No No 
Vesicular exanthema of 
swine virus  No No Pigs Ingestion  No No 
Vesicular stomatitis virus  Yes Yes Cattle and pigs  Vector -borne, direct 
contact  No No 
West Nile fever virus  Yes Yes Cattle and pigs  Vector -borne  No No 
Bacteria including 
Mycoplasma spp.        
Bacillus anthracis  Yes Yes Cattle and pigs  Ingestion of spores  Yes Yes 
Borrelia burgdorferi  No Yes Cattle  Vector -borne  No No 
Borrelia theileri  No No Cattle  Vector -borne  No No 
Brucella melitensis, B. 
abortus, B. suis  Yes Yes Cattle and pigs  Direct contact, 
ingestion  Yes No4 
Burkholderia 
pseudomallei  No Yes Cattle and pigs  Contact with 
contaminated 
environment  No No 
Exotic Salmonella spp. 
e.g. Salmonella abortus 
ovis, S. Dublin, S. 
Typhimurium DT 104  No Yes Cattle  Faecal -oral Yes Yes 
Francisella tularensis  Yes Yes Cattle and pigs  Vector -borne, 
ingestion  No No 
Leptospira spp. No Yes Cattle  Ingestion, cut skin   No No 
Mycobacterium bovis   Yes Yes Cattle  Direct contact, 
ingestion  No No 
Mycoplasma 
hyosynoviae  No No Pigs Direct contact  No No 
Mycoplasma mycoides 
Subsp.  mycoides SC  Yes No Cattle  Direct contact, 
ingestion of lung 
tissue?  No No 
Mycoplasma bovis  (and 
other exotic Mollicutes of 
cattle)  No Various  Cattle  Direct contact, 
ingestion (milk)  No No 
Pasteurella multocida B 
and E  Yes No Cattle and pigs  Close contact  No No 
Protozoal parasites        
Babesia bovis, B. 
bigemina  Yes No Cattle  Tick-borne  No No 
                                                
 
4 See OIE Article 8.4.2. Which lists the digestive tract as a safe commodity with regard to Brucella spp. 
http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_bovine_brucellosis.htm    
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 13 Besnoitia besnoiti, B. 
caprae  No No Cattle  Haematophagous 
insects, ingestion  No No 
Table 1 (continued)        
Organism  OIE 
List Zoonotic  Species 
infected  Transmission  Assessed to 
be a risk in 
edible 
tissue  Requires 
further 
assessment  
Protozoal parasites  
(continued)        
Theileria spp. (sheep, 
deer and cattle species)  No No Cattle  Tick-borne  No No 
Sarcocystis hominis  No  Yes Cattle  Ingestion  No No 
Sarcocystis suihominis  No  Yes Cattle  Ingestion  No  No 
Trypanosoma spp. 
(Tsetse transmitted)  Yes No Cattle  Vector -borne  No No 
Trypanosoma evansi  Yes No Cattle  Haematophagous 
insects  No No 
Rickettsial and 
Chlamydial organisms        
Anaplasma marginale, 
A. centrale, A. caudatum  Yes No Cattle  Tick-borne  No No 
Chlamydophila abortus  Yes Yes Cattle  Ingestion (foetal 
membranes and 
fluid)  No No 
Coxiella burnetii  Yes Yes Cattle  Aerosol, vector -
borne, ingestion  No No 
Ehrlichia ruminantum  Yes No Cattle  Vector -borne  No No 
Other Ehrlichia spp. e.g. 
E. chaffeensis  No Yes Cattle  Vector -borne  No No 
Arthropods        
Warble fly  No No Cattle  Fly  No No 
Internal parasites        
Echinococcus 
granulosus  Yes Yes Cattle, pigs  Ingestion  Yes Yes 
Exotic Trichinella  
species  No Yes Cattle, pigs  Ingestion  Yes No5 
Cysticercus cellulosae  Yes Yes Pigs Ingestion  No No 
Cysticercus bovis  No Yes Cattle  Ingestion  No No 
Coenurus cerebralis  No Yes Cattle, pigs  Ingestion of viable 
cyst Yes  No6 
Prions        
                                                
 
5 Infectious larvae only develop in striated muscle of infected animals (Gottstein et al. 2009).  The infectious stage of this 
organism’s lifecycle is not associated with the commodity.  
 
6 The infectious cysts (coenurus) can only develop and survive in the brain and spinal cord of cattle and pigs (Radostits et al. 
2007). The infectious stage of this o rganism’s lifecycle is not associated with the commodity.   
14 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Bovine spongiform 
encephalopathy  Yes Yes Cattle  Ingestion  Yes Yes 
 
 
Based on the above, the following organisms  are identified as requiring further assessment . 
Viruses  
African swine fever virus  
Aujeszky’s disease virus  
Classical swine fever virus  
Foot and mouth disease virus  
Porcine reproductive and respiratory syndrome virus   
Swine vesicular  disease virus  
Bacteria  
Bacillus anthracis  
Salmonella spp. 
Internal parasites  
Echinococcus granulosus  
Prions  
The agent of bovine spongiform encephalopathy  
The listed disease -causing organism s will be assessed in groups determined by the species they 
infec t. Those that infect both pigs and cattle will be assessed first, followed by those that 
infected only pigs and then only cattle.  
 
References   
 
European Natural Sausage Casing s Association  (2013).  Community guide to good practise  for Hygiene and 
the application of the HACCP principles in the production of natural sausage casi ngs. Wijnker J J (eds .). [Online] 
Available from: 
http://ec.europa.eu/food/food/biosafety/hygienelegislation/guidelines_good_practice_haccp_en.pdf . [Accessed 
4th December 2013].  
 
Gottstein B, Pozio E, Nöckler K (2009). Epidemiology, diagnosis, treatment, and control of trichinellosis. 
Clinical Microb iology Reviews , 22 (1), 127-145. 
 
Koolmees PA, Tersteeg MH G, Keizer G, van den Broek J, Bradley R (2004). Comparative histological 
studies of mechanically versus manually processed sheep intestines used to make natural sausage casings. 
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MPI (2006).  Import risk analysis : Porcine reproductive and respiratory syndrome (PRRS) virus in pig meat. 
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4th December 2013].   
 
MPI (2006b).  Risk analysis procedures. Version 1. [O nline] Available from: 
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December 2013] . 
 
MPI (2010). Import risk analysis : Sausage casings from small ruminants . [Online] Available from:  
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MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 15 MPI (201 4). Import risk analysis : Meat and meat products  from ruminants and pigs . Draft for public 
consultation.  [Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/meat -and-meat -
products -from -ruminants -and-pigs-feb-2014.pdf  [Accessed 6t h December 2013].  
 
Ockerman HW, Hansen CL (ed.) (2000).  Sausage containers. In: Animal by -product processing and         
utilization . CRC Press, Boca Raton, Fla, pp. 285 –323 
 
OIE (20 13). Terrestrial Animal Health Code . [Online] Available from:  http://www.oie.int/en/international -
standard -setting/terrestrial -code/ . [Accessed 6th December 2013 ].  
 
Radostits OM, Gay CC, Hinchcliff KW, Constable PD (2007). Coenurosis. In: Veterinary Medicine A 
textbook of the diseases of cattle, horses, sheep, pigs, and goats.  Saunders Elsevier, Edinburgh, pp. 607.  
 
Wijnker JJ, Tersteeg MHG, Berends BR, Vernooij JCM, Koolmees PA (2008). Quantitative histological 
analysis of bovine small intestines before and after processing into natural sausage casings. Journal of Food 
Protection , 71 (6), 1199 -1204.  
 
Wijnker J J (2009). Aspects of Quality Assurance in Processing Natural Sausage Casings . PhD Thesis, Utrecht 
University: Pp 114.  [Online] Available from:  Http:// igitur -archive.library.uu.nl/dissertatio ns/2009 -0108 -
201005/wijnker.pdf [Accessed 3rd December 2013 ]. 
 
Wijnker J J, Tjeerdsma -van Bokhoven  JLM, Veldhuizen EJA  (2009 ). Phosphate analysis of natural sausage  
casings preserved in brines with phosphate additives as inactivating agent – Method validation. Meat Science , 81 
(1), 245 -248. 
   
16 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 6. Bacillus anthracis   
6.1. HAZARD IDENTIFICATIO N 
6.1.1. Aetiological agent  
Bacillus anthracis  is a bacterium belonging to the family Bacillaceae  and genus Bacillus  (De 
Vos and Turnbull 2004).  
6.1.2. OIE list  
Anthrax is an OIE listed disease of multiple species . 
6.1.3. New Zealand status  
Anthrax is listed as an exotic notifiable disease ( Unwanted Organisms Register  2014). The first 
reported case of Anthrax in New Zealand was in 1895 and it  was last diagnosed in 1954 (Gill 
1993).  
6.1.4. Epidemiology  
Anthrax is a bacterial disease primarily of herbivores , although all mammals, including humans 
and some avian species are susceptible  (OIE 2012). Domest icated animals have varying 
susceptibility to disease with sheep being the most susceptible followed by cattle, goats, horses, 
pigs, dogs and cats (MacDiarmid and Thompson 1997).  
Natural infection of animals usually occurs by the ingestion of spores in me at or soil and other 
routes of infection include spores entering the body through cutaneous lesions, insect bites and , 
rarely, inhalation (De Vos and Turnbull 2004).  
Once within the body the most common c ourse of disease is septicaemia followed by death  
(MacDiarmid and Thompson 1997). Vegetative cells of B. anthracis  do not survi ve well outside 
their host. I n contrast , spores that form following exposure to oxygen are very resistant and can 
survive for a considerable time in the environment (De Vos and Tur nbull 2004).   
Pigs are more  resistant to anthrax  compared to herbivores  and large quantities of infected meat 
need to be consumed to initiate infection . Although, because of the feeding behaviour of pigs, 
they can be exposed to much higher levels of anthra x compared to herbivores and mass 
mortalities have been recorded (De Vos and Turnbull 2004) . 
The OIE  (2014)  considers that  “there is no evidence that anthrax is transmitted by animals 
before the onset of cli nical and pathological signs”.  
6.1.5. Hazard identifica tion conclusion  
Anthrax is a zoonotic disease that is present in a number of countries. It is capable of causing 
severe disease and can be transmitted to susceptible mammal species through the ingestion of 
contaminated animal products. As anthrax is capabl e of forming spores, and as other spore 
forming bacteria have been shown to survive commercial processing (Wijnker et al. 2006), the 
disease is  identified as a hazard in beef and hog casings.   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 17 6.2. RISK ASSESSMENT  
6.2.1. Entry assessment  
Cattle or pigs infected with anthrax and displaying clinical signs will not pass ante - and post -
mortem inspections and casings will not be made from these animals. The likelihood of entry is 
assessed as negligible.  
6.2.2. Risk estimation  
Since the likelihood of entry is assessed to be  negli gible,  the risk is assessed to be negligible.  
 
References   
 
De Vos V, Turnbull PCB (2004).  Anthrax. In: Coetzer JAW, Tustin RC (eds). Infectious Diseases of Livestock , 
2nd edition. Oxford University Press, 1788 -1818.  
 
Gill J (1993).  Anthrax - still history after all these years. Surveillance , 20 (1), 21 -22. 
 
MacDiarmid SC, Thompson EJ (1997).  The potential risks to animal health from imported sheep and goat 
meat. Revue Scientifique et Technique de l`office International des Epizooties , 16 (1), 45 -56. 
 
OIE (2012).  Antrax. Chapter 2.1.1. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals . [Online] 
Available from: http://www.oie.int /fileadmin/Home/fr/Health_standards/tahm/2.01.01_ANTHRAX.pdf  
[Accessed 29th March 2014].  
 
OIE (2014). Anthrax. Terrestrial Animal Health Code. Chapter 8.1. [Online] Available from: 
http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_anthrax.htm  [Accessed 13th August 2014].  
 
Unwanted Organisms Register (2014).  Anthrax. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 28th March 2014].  
 
Wijnker JJ, Koop G, Lipman LJA (2006).  Antimicrobial properties of salt (NaCl) used for the preservation of 
natural casings.  Food Microbiology , 23 (7), 657 -662. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
18 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 7. Echinococcus granulosus  
7.1. HAZARD IDENTIFICATIO N 
7.1.1. Aetiological agent  
Echinococcus granulosus is a cestode parasite within the family Taeniidae . Ten genotypes are 
recognised (G1 -G10) within this species complex (Youssefi et al. 2013).  
7.1.2. OIE list  
The OIE lists infection with Echinococcus granulosus  and E. multilocularis  as disease s of 
multiple species.  
7.1.3. New Zealand status  
In 2002, New Zealand was declared provisionally free from hydatid s infection (Pharo 2002) and 
no new cases have been identified s ince then. Echinococcus spp. are listed as unwanted 
notifiable organisms (Unwanted Organism Register 2014).  
7.1.4. Epidemiology  
E. granulosus  has a worldwide distribution and only a small number of mainly  island countries 
are free from  this orga nism (World Anima l Health Database 2014).  
Echinococcosis is a parasitic tapeworm infection occurring in dogs (and some species of wild 
canids) which are the primary host and several species of herbivores, and pigs are intermediate 
hosts (MacDiarmid and Thompson 1997; W orld Health Organisation  2001). Dogs become 
infected by consuming raw infected tissue (predominately lungs and liver) that contains viable 
cysts. Once a cyst is ingested, a tapeworm may develop within the  dog’s  intestine and once 
mature it will produce eggs th at are passed in faeces. Intermediate hosts can then 
opportunistically consume these  eggs and the resultant larvae migrate primarily  to the lungs, but 
also the liver, and develop into a fluid filled cyst. Other sites of infection may include the 
central ne rvous system, skeletal muscles and the marrow cavity of bones  (World Health 
Organisation  2001).  
Human ingestion of eggs excreted in dog faeces can cause infection leading to  death in extreme 
cases. Humans do not perpetuate the lifecycle of this parasite a nd are considered accidental 
hosts (W orld Health Organisation  2001).  
Cysts are rarely viable in cattle, except in countries where the cattle genotype (G5) is present 
(World Health Organisation  2001).  
The majority of cysts are located in offal (lungs and liver) (MacDiarmid and Thompson 1997), 
although there is a small likelihood of cysts being found in other body tissue (i.e. intestines). If 
this were to occur, the cysts would not remain associated with casings due to commercial 
processing  (MPI 2010) . Acco rdingly, the Code lists casings as a safe commodity that requires 
no risk management measures.  
7.1.5. Hazard identification conclusion  
The commercial processing of casings will eliminate any cysts associated with bovine or 
porcine intestinal tissue. Hence , E. granulosus is not identified as a hazard  in beef and hog 
casings.  
 
  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 19 References  
 
MacDiarmid SC, Thompson EJ (1997).  The potential risks to animal health from imported sheep and goat 
meat. Revue Scientifique et Technique de l`office International des Epi zooties , 16 (1), 45 -56. 
 
MPI (2010). Import risk analysis : Sausage casings from small ruminants. [Online] Available from:   
http://www.biosecurity.govt.nz/files/regs/imports/risk/sausage -casings -eu-ra.pdf  [Accessed 3rd April  2014].    
 
Pharo H (2002). New Zealand declares 'provisional freedom' from hydatids. Surveillance , 29 (3), 3 -7. 
 
Unwanted Organisms Register (2014).  Echinococcus spp. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 04th July 2014].      
 
World Animal Health Database (2014).  World Animal Health Infor mation Database Interface. [Online] 
Available from: http://www.oie.int/wahis_2/public/wahid.php/Diseaseinformation/statuslist  [Accessed 04th July 
2014].  
 
World Health  Organisation  (2001).  WHO/OIE manual on echinococcosis in humans and animals: a public 
health problem of global concern. [Online] Available from: 
http://whqlibdoc.who.int/publication s/2001/929044522X.pdf   [Accessed 04th July 2014].  
 
Youssefi MR, Tabaripour R, Omrani VF, Spotin A, Esfandiari B (2013).  Genotypic characterization of  
Echinococcus granulosus  in Iranian goats. Asian Pacific Journal of Tropical Disease , 3 (5), 362 -366. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
20 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 8. Foot and mouth disease virus   
8.1. HAZARD IDENTIFICATIO N 
8.1.1. Aetiological agent  
Foot and mouth disease virus (FMDV) is a member of the family Picornaviridae  and genus 
Aphthovirus . There are seven distinct serotypes ; A, O, C, SAT1, SAT2, SAT3, and Asia1 (OIE 
2012).  
8.1.2. OIE list  
Foot and mouth disease  (FMD)  is an OIE listed  disease.  
8.1.3. New Zealand status  
This virus has never been found in New Zealand  (Pharo 2002)  and is listed as an exotic 
notifiable organism  (Unwanted Organi sms Register 2014) .  
8.1.4. Epidemiology  
FMD is a highly contagious, economically significant disease of cloven -hoofed animals, 
including pigs and cattle (OIE 2012).  
FMD is distributed widely across the world and is endemic in large areas of Africa, Asia, the 
Middle East and South America (World Animal Health Information Database Interface  2014).   
All secretions and excretions from an infected individual can contain infectious virus and viral 
shedding can occur for up to four days before the onset of clinical sig ns (OIE 2009). The pattern 
of excretion is similar for pigs and cattle with a sharp decline occurring at approximately 4 -5 
days after signs of clinical disease and all secretions and excretions being  free from  detectable 
virus 10 -14 days post -infection (Al exandersen et al. 2012). Transmission to susceptible species 
can occur by a variety of routes, including direct contact, indirect contact via infected fomites, 
airborne infection caused by the inhalation of aerosols, and by the consumption of contaminated 
meat ( Thomson and Bastos 2004 ).  
Cattle can become carriers of FMD V for up to 3 years , whereas  pigs do not become carriers and 
do not harbour infectious virus for more than 28 days (OIE 2012). Cattle  that are in a carrier 
state may be able to transmit FMD V if they come into close contact with other susceptible 
species . However, the importance of this route for transmission is controversial ( Thomson and 
Bastos 2004 ). 
The severity of clinical signs is dependent on the strain of virus, exposure dose, age and b reed 
of animal, host species, and degree of host immunity. Mortality is lower in older animals (1 -
5%) and is generally higher in young calves and piglets ( ≥20%). Clinical signs in cattle include  
vesicles in the mouth and on the feet, pyrexia, anorexia, shi vering, and a reduction in milk 
production for 2 -3 days.  Clinical disease is usually severe in pigs and can include pyrexia, 
development of vesicles at pressure points on limbs, and severe foot lesions, which can cause 
lameness (OIE 2009 ; Alexandersen et al. 2012).  
Recen t outbreaks of FMD in countries  considered free from  the disease have probably been 
caused by contaminated untreated food waste that has been feed to livestock. The economic cost 
of such an outbreak was estimated at $US 15 billion for the United Kingdom incursion which 
occurred in 2001 (Alexandersen et al. 2012).   
  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 21 FMDV  has been isolated from the intestine s of experimentally infected cattle  and pigs ( Wijnker 
et al. 2007; 2012). McKercher et al. (1978) state in their paper that FMDV can sur vive in  
processed casings for 250 days, although Wijnker et al (2007) highlights that no experimental 
data is available to support this  suggestion . 
8.1.5. Hazard identification conclusion  
FMD V is a highly contagious, economically devastating disease, which can be transmitted  to 
susceptible species through the consumption of infected animal products . 
As FMDV  has been i solated from intestinal tissue, it  is identified  as a hazard in hog and beef 
casings.  
8.2. RISK ASSESSMENT  
8.2.1. Entry assessment  
FMDV can be present in both cattle and pig intestines.  
Clinical disease is usually severe in pigs and they do not become carriers as they only harbour 
infectious virus for up to 28 days. H ence, there is a lower likelihood that  infected  pigs would 
pass ante - and post -mortem inspections. Cattle, however, can be carriers of this virus for up to 
3.5 years and some breeds of cattle (for example Zebu ( Bos indicus )) often exhibit less severe 
or no  clinical signs compared to European bre eds of cattle ( Bos taurus ) (Alexandersen et al. 
2012).  FMDV persists in carrier cattle in the mucosa of the soft palate, pharynx and cranial 
oesophagus (Thompson and Bastos 2004) and is unlikely to be present in the intestines.  
Infected cattle that are carriers of FMDV are more likely to pass ante - and post -mortem 
inspections compared to pigs.  
FMDV has been shown to be inactivated in pig and cattle  intestines that were stored in dry 
salt or dry phosphate supplemented  salt for 30 days at 20 °C (Wijnker et al. 2007 ; Wijnker et 
al. 2012 ). Another study exposed FMDV within a 3D collagen matrix model to a salt solution 
or a phosphate supplemented salt solution and found that inactivation occurred after 30 days 
at all  tested temperatures (Wieringa -Jelsma et al. 2011).  
For the inactivation of FMDV in casings of ruminants and pigs , the Code  (Article 8.6.41)  
recommends that the following procedure should be used ; salting for at least 30  days either 
with dry salt (NaCl) or with saturated brine ( water activity; aw < 0.80), or with phosphate 
supplemented dry salt (containing 86.5  percent NaCl, 10.7  percent Na 2HPO 4 and 2.8  percent 
Na3PO 4, weight/weight/weight), and kept at a temperature of greater than 12  °C during this 
entire period (OIE 2013).  
The standard manufacturing procedure for the  international casings industry includes salting 
for 30 days at room temperature (see commodity definition Section 3).  
For beef and hog casings complying with the commodity definition, the like lihood that FMD V 
would enter New Zealand is assessed to be  negligible .  
8.2.2. Risk estimation  
Since the likelihood of entry is assessed to be negligible , the risk is estimated to be negligible.   
 
 
 
 
  
22 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI References   
 
Alexandersen S, Knowles NJ, Dekker A, Belsham GJ,  Zhang Z, Koenen F (2012).  Foot and mouth disease. 
In: Zimmerman JJ, Karrier LA, Ramirez A, Schwartz KJ, Stevenson GW (eds.) Diseases of Swine , 10th edition. 
John Wiley and Sons, pp. 590 -602.       
 
McKercher PD, Hess WR, Hamdy F (1978) . Residual viruses in Pork Products. Applied and Environmental 
Microbiology , 35, 142 -145.  
 
OIE (2009).  Foot and mouth disease. Technical disease card . Online] Available from: 
http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/FOOT_AND_MOUTH_DISEA
SE_FINAL.pdf  [Accessed 14th January 2014] . 
 
OIE (2012).  Foot and mouth disease. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals . Chapter 
2.1.5. [Online] Available from:  
http://www.oie.int/ fileadmin/Home/eng/Health_standards/tahm/2.01.05_FMD.pdf  [Accessed 14th January 
2014].  
 
OIE (2013).  Foot and mouth disease. Chapter 8.6. Terrestrial Animal Health Code . Online] Available from:  
http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_1.8.6.htm  [Accessed 14th January 2014].  
 
Pharo (2002).  Foot-and-mouth disease: an assessment of the risks facing New Zealand. New Zealand Veterinary 
Journal , 50 (2), 46 -55.   
 
Thomson GR, Bastos ADS (2004).  Foot-and-mouth disease. In: Coetzer JAW, Tustin RC (eds). Infectious 
Diseases of Livestock , 2nd edition. Oxford University Press, 1324 -1365.  
 
Unwanted Organisms Register (2014).  Foot and Mouth disease. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 23rd January 2014].      
 
Wieringa -Jelsma T, Wijnker JJ, Zijlstra -Willems EM, Dekker A, Stockhofe -Zurwieden N, Maas R, 
Wisselink , HJ (2011).  Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen 
matrix model for natural sausage casings . International Journal of Food Microbiology , 148 (2), 128 -134. 
 
Wijnker JJ, Haas B, Berends BR (2007).  Removal of foot -and-mouth disease virus infectivity in salted natural 
casings by minor adaptation of standardized industrial procedures. International Journal of Food Microbiology , 
115, 214 -219.  
 
Wijnker JJ, Haas B, Berends BR (2012). Inactivation of foot -and-mouth disease virus in various bovine 
tissues used for the production of natural sausage casings. International Journal of Food Microbiology , 153, 
237-240.  
 
World Animal Healt h Information Database Interface (2014). Foot and mouth disease . [Online] Available  
from : http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home  [Accessed 30th September  2014].  
 
 
 
 
 
   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 23 9. Exotic Salmonella  spp. 
9.1. HAZARD IDENTIFICATIO N 
9.1.1. Aetiological agent  
Salmonella spp. are Gram -negative bacteria which belong to the family Enterobacteriaceae . 
There are approximately 2500 serovars in the Salmonella genus and most of these belong to the 
species enteric a and subspecies enteric . For simplicity, only the genus name followed by the 
serovar will be written e.g. Salmonella Dublin.  
Multiple different strains are present in each serovar, which can be differentiated by phage 
typing and identified by the notation DT and a number.  The strain  Salmonella Typhimurium 
DT104  is important  as it has developed resistance to multiple types of antibiotics and is widely 
distributed around the world (MPI 2010).  
9.1.2. OIE list  
Salmonellosis of sheep and goats associated with Salmonella Abortusovis is an OIE listed  
disease . In poultry, fowl  typhoid and pullorum disease ( Salmonella Gallinarum -Pullorum ) are 
listed by the OIE.    
9.1.3. New Zealand status  
Salmonella Dublin  is listed as  an unwanted notifiable organisms and was first isolated from a 
sheep in 1966 and since then no new isolates have been reported (Clark 1999). Salmonella 
Typhimurium  is endemic in New Zealand , although, S. Typhimurium  DT 104 has been rarely 
isolated from humans and, in New Zealand, it has only  been recorded once in three dogs in a 
household in which  the owner was suffering from diarrhoea after returning from overseas 
(Julian 2002). It is classified in the category of “other exotic organism” and is unwanted 
(Unwanted Organisms Register  2014).      
9.1.4. Epidemiology  
Salmonella spp. have been isolated from virtually all species of v ertebrate s that have been tested 
and this genus of bacteria can contaminate the environment for a considerable period of time 
(Penrith et al. 2004).  
Transmission of Salmonella spp. occurs mainly by the faecal oral route. Oral infection results in 
the mult iplication of the organism in the intestine and invasion of the intestinal mucosa, 
followed by replication in the intestinal lymphatic tissue. Bacterial replication may also occur in 
the lungs if the organism is introduced intranasally (Penrith et al. 2004 ).  
The course of infection is dependent on the infectious dose, serovar virulence and the host’s 
immune response. Clinical signs of disease may appear 38 to 48 hours after infection and 
intesti nal salmonellosis usually lasts 2 to 7 days (Penrith et al. 2004).  
If the infection is restricted to the intestinal tract clinical signs may present as watery diarrhoea 
and may progress to enterocolitis. Infection in the intestinal tract may also spread to other 
organs causing septicaemia or bacteraemia (Fenwick and  Collet 2004).  
Salmonellosis is a zoonosis and can be easily transmitted from animals to humans by ingestion 
or inhalation. Animal products especially raw milk, meat and eggs are the most common cause 
of infection in humans (Fenwick and Collet 2004).   
24 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI In outbreaks of bovine salmonellosis, the morbidity may reach 50 per cent and the fatality rate 
in untreated animals can be 100 per cent (Fenwick and Collet 2004). In pigs that display clinical 
signs of disease mortality can also be high (Penrith et al. 2004) .  
Clinically infected animals excrete large numbers of bacteria, especially in faeces and adult 
animals can become carriers, which may  then sporadically shed bacteria (Penrith et al. 2004).  
Casings  are cleaned  in batches in water heated to 40  °C (see commodity definition section 3)  
and bacterial cross -contamination between casings may occur ( Wijnker 2009).   
9.1.5. Hazard identification conclusion  
Salmonella spp. are associated with bovine  and porcine  intestines  and faecal cross -
contamination occur s during processing  into casings . Exotic Salmonella spp. are identified  as a 
hazard in beef and hog casings .   
9.2. RISK ASSESSMENT  
9.2.1. Entry assessment  
Casings are stored for 30 days in either a dry salt which has a water activity (a w) of 0.75, or in 
saturated brine (a w 0.75-0.80). Most bacterial species cannot survive a water activity of less than 
0.91 (Wijnker et al. 2006 ). Houben (2005) sampled 214 consignments of internationally traded 
casings and found that none tested positive for Salmonella  spp. This provides evi dence that the 
commercial manufacturing process inactivates vegetative bacteria .  
As the aw level in commercially processed casings is below that at  which vegetative  bacteria can 
remain viable, the likelihood of entry for all exotic Salmonella  spp. is assessed as negligible.  
9.2.2. Risk estimation  
Since the likelihood of entry is assessed as negligible, the risk is estimated to be negligible.  
 
References   
 
Clark  G (1999 ). Salmonella isolates in New Zealand s heep. Surveillance , 26 (3), 6 -7.  
 
Fenwick SG, Collett M G (2004) . Bovine salmonellosis. In:  Coetzer JAW, Tustin RC (eds) . Infectious Diseases 
of Livestock , 2nd edition. Oxford Unive rsity Press, Oxford, 1582 -1593.  
 
Houben J H (2005) . A survey of dry -salted natural casings for the presence of Salmonella spp . Listeria 
monocytogenes  and sulphite -reducing Clostridium spores. Food M icrobiology , 22 (2), 221-225. 
 
Julian A (2002). Quarterly review of diagnostic cases: Gribbles Veterinary Pathology: Dogs. Surveillance , 29 
(3), 28. 
 
MPI (2010). Import risk analysis : Sausage casings from small ruminants. [Online] Available from:   
http://www.biosecurity.govt.nz/files/regs/imports/risk/sausage -casings -eu-ra.pdf  [Accessed 3rd April  2014].    
 
Penrith ML, Neser JA, Henton MM (2004).  Porcine salmonellosis. In:  Coetzer JAW, Tustin RC (eds) . 
Infectious Diseases of Livestock , 2nd edition . Oxford University Press, Oxford,  1601 -1607.  
 
Unwanted Organisms R egister (2014) . Salmonella . [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 3rd April 2014].  
 
Wijnker JJ, Koop G, Lipman LJA (2006).  Antimicrobial properties of salt ( NaCl) used for the preservation of 
natural casings.  Food Microbiology , 23 (7), 657-662. 
  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 25 Wijnker JJ (2009). Aspects of Quality Assurance in Processing Natural Sausage Casings . PhD Thesis, Utrecht 
University: Pp 114. [Online] Available from:  Http:// igitur -archive.library.uu.nl/dissertations/2009 -0108 -
201005/wijnker.pdf  [Accessed 3rd December 2013].  
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
   
26 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 10. African swine fever virus  
10.1. HAZARD IDENTIFICATIO N 
10.1.1.  Aetiological agent  
African swine fever virus  (ASFV) is the sole member of the family Asfarviridae and genus 
Asfivirus  (International Committee on Taxonomy of Viruses  2012).   
10.1.2.  OIE list  
African swine fever (ASF)  is listed by the OIE as a disease of swine.  
10.1.3.  New Zealand status  
ASFV has not been describe d in New Zealand and is listed as an unwanted notifiable organism  
(Unwanted Organisms R egister 2014) .  
10.1.4.  Epidemiology  
ASF is a highly contagious viral disease of pigs, which is endemic in many countries in sub -
Saharan Africa (OIE 2013). Within Europe ASFV ha s been eradicated from the Iberian 
Peninsula but is endemic in  feral pigs in Sardinia, Italy.  In 2007 ASFV was isolated from pigs 
in Georgia (ProMed 2007) and since then the virus has spread eastwards and northwest and is 
currently present in western Russi a, Armenia, Azerbaijan, Ukraine, Belarus, Lithuania, Lativa, 
Poland and the latest country to report the disease as of the 29th of September 2014 is Estonia 
(ProMed 2014). The virus is maintained mostly in the wild boar population and they are the 
main sou rce of infection for domestic pigs (ProMed 2014).  
ASFV affects members of the pig family (Suidae). Domesticated and feral pigs and European 
wild boars are susceptible to this virus (Sanchez -Vizcaino and Neira 2012).  Three African suid 
species are subclini cal carriers and act as reservoirs: warthogs ( Phacochoerus africanus ), giant 
forest hogs ( Hylochoerus meinertzhageni ) and bush pigs (Potamochoerus porcus ) (Sanchez -
Vizcaino and Neira 2012).  
The spread of ASFV can occur by direct contact with infected pigs, contact with contaminated 
fomites and through tick vectors (genus Ornthidoros ). This virus has often spread to new areas 
by pigs consuming uncooked infected pork. Waste food from internatio nal tr ansport carriers 
(e.g. aircraft ) have been shown to be an important source of ASFV (European Food Safety 
Authority 2010).  ASFV strains vary in virulence and the incubation period for this disease is 4 -
19 days. Virulent  strains can cause death within 4-10 days and mortality rates within the herd 
can reach 100%. These virulent strains are characterised by high fever, loss of appetite, and 
haemorrhages in the skin and internal organs (OIE 2012).  After the onset of clinical signs, 
ASFV is shed at high lev els in all secretions and excretions (Sanchez -Vizcaino and Neira 2012).     
Less virulent strains are characterised by a slight fever, reduced appetite and depression, and 
these general signs can lead to the misidentification of the disease. Low virulence s trains can 
cause seroconversion and on occasion subclinical non -haemorrhagic infection (OIE 2012).  
ASFV can remain viable for up to 140 days in salted dried hams (Mebus et al. 1993; Mebus et 
al. 1997) and for up to 30 days in smoked pepperoni and salami s ausage (McKercher et al.  
1978). McKercher et al. (1980) also reported ASFV surviving in natural hog casings that were 
stored for 97 days, although no data is provided in the paper to support this claim.   
  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 27 10.1.5.  Hazard identification conclusion  
ASFV is an environ mentally stable, highly contagious OIE listed disease and is found 
throughout all tissues and body fluids of infected pigs.  
ASFV is identified as  a hazard in hog casings .  
ASFV is not identified as a hazard in b eef casings.  
10.2. RISK ASSESSMENT  
10.2.1.  Entry assessment  
Pigs that are infected with low virulen ce strains  of ASFV  and those that have recovered from 
infection , but are chronic carriers , are most likely to be infectious at slaughter (MPI 2014) . 
Ante - and post -mortem inspections may not exclude these infected pigs from slaughter due to 
the absence of  observable clinical signs . 
There have been no  studies conducted on the inactivation of ASFV in swine casings,  although 
a study by Wieringa -Jelsma et al. (2011 ) found that ASFV in a 3D collagen matrix model , 
developed to simulate the situation in natural casings,  was inactivated in 21 days at all tested 
temperatures when stored in a saturated salt solution.   
Due to the manufacturing steps used to produce casings it is likely that the titre of any ASFV 
presen t would be significantly reduced . AFSV  in cell culture  has been  inactivated when 
heated to 56 °C for 70 minutes or 60 °C for 20 minutes  (Plowright and Parker 1967 ) and it has 
been inactivated in pig slurry when heated to 65 °C for 1 minute ( Turner and Williams 1999 ). 
During processing casings are placed in heated water  (approximately 40  °C) for an 
unspecified period to assist with cleaning. This may reduce the titre  of virus . Additionally,  the 
storage conditions that are a part of the standard operating  procedure used by the international 
casing industry  (see commodity definition  section 3)  would be expected to inactive any 
residual virus , as shown by Wierenga -Jelsma et al. (2011), especially when the salting process 
is supplemented by the addition of phosphate .  
The likelihood that ASFV would enter New Zealand in this commodity is assessed as 
negligible.   
10.2.2.  Risk estimation  
Since the likelihood of entry is assessed to be negligible, the risk is estimated to be negligible.  
 
References  
 
European Food Safety Authority (2010). Scientific opinion on African swine fever. European Food Safety 
Journal ,  8 (3) , 11556. [Online] Available from: http://www.efsa.europa.eu/en/efsajournal/doc/1556.pdf    
[Accessed 30th September 2014].  
 
International Committee on Taxonomy of Viruses (2012).  Virus taxonomy: 2012 release. [Online] Avail able 
from: http://www.ictvonline.org/virusTaxonomy.asp  [Accessed 17th December 2013].  
 
McKercher PD, Hess WR, Hamdy F (1978).  Residual viruses in pork products. Applied and environmental 
microbiol ogy, 35 (1), 142 -145. 
 
McKercher PD, Morgan O, McVicar JW, Shuot NJ (1980).  Thermal processing to inactivate viruses in meat 
products. In: Proceedings of the 84th Annual Meeting of the United States Animal Health Association, 
Louisville, Ky. U.S. Animal Health Association, Richmond, Va, pp. 320 -328. 
  
28 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Mebus CA, House C, Gonzalvo FR, Pineda JM, Tapiador J, Pire JJ, Bergada J, Yedloutschnig RJ, Sahu 
S, Becerra V, Sanchez -Vizcaino JM (1993).  Survival of foot -and-mouth disease, African swine fever, and hog 
cholera viruses in Spanish serrano cured hams and Iberian cured hams, shoulders and loins. Food microbiology , 
10 (2), 133 -143. 
 
Mebus C, Arias M, Pineda JM, Tapiador J, House C, Sanchez -Vizcaino JM (1997).  Survival of several 
porcine viruses in different Spanish dry -cured meat products. Food Chemistry , 59 (4), 555 -559. 
 
MPI (2014). Import risk analysis : Meat and meat products from ruminants and pigs. Draft for public 
consultation. [Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/meat -and-meat -
products -from -ruminants -and-pigs-feb-2014.pdf  [Accessed 6 th December 2013].  
 
OIE (2012).  African swine fever.  Manual of Diagnostic Tests and Vaccines for Terrestrial Animals . Chapter 
2.8.1. [Online] Available from:  www.oie.int/fileadmin/Home/eng/Health_standards/.../2.08.01_ASF.pdf  
[Accessed 17th December 2013].  
 
OIE (2013).  African swine fever. Technical disease card . [Online] Available from: 
http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/Disease_cards/AFRICAN_SWI
NE_FEVER.pdf  [Accessed 22nd July 2014].  
 
Plowright W, Parker J (1967).  The stability of African swine fever virus with particular reference to heat and 
pH inactivation. Archiv für die gesamte Virusforschung , 21(3), 383 -402. 
 
ProMed (2007). African Swine Fever – Georgia: OIE. Archive number: 20070607.1845. [Online] Available  
from: http://www.promedmail.org/direct.php?id=20070607.1845  [Accessed 29th September 2014].   
 
ProMed (2014). African Swine Fever -Europe (14): Estonia (Valga) Porcine, Boar, First case,  OIE. Archive 
number: 20140908.2757737. [Online] Available from: 
http://www.promedmail.org/direct.php?id=20140908.2757737  [Accessed 29th September 2014].   
 
Sanchez -Vizcaino JM, Neria  MA (2012). African Swine Fever Virus . In Zimmerman J, Karriker LA, Ramirez A, 
Schwartz KJ, Stevenson GW (eds.)  Diseases of Swine , 10th edition, John Wiley & Sons publishing, pp. 396-404.  
 
Turner C, Williams S M (1999).  Laboratory -scale inactivation of African swine fever virus and swine vesicular 
disease virus in pig slurry. Journal of Applied Microbiology, 87, 148 -157. 
 
Unwant ed Organisms R egister (2014).  African swine fever. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 21st January 2014].      
 
Wieringa -Jelsma T, Wijnker JJ, Zijlstra -Willems E M, Dekker A, Stockhofe -Zurwieden N, Maas R,  
Wisselink, H J (2011).  Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen 
matrix model for natural sausage casings. International Journal of Food M icrobiology , 148 (2), 128-134. 
    
 
 
 
 
 
 
 
 
 
 
 
 
 
 
    
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 29 11. Aujeszky ’s disease virus  
11.1. HAZARD IDENTIFICATIO N 
11.1.1.  Aetiological agent  
The causative agent of Aujesky’s disease (also known as pseudorabies) is suid herpesvirus type 
1, a member of the Varicellovirus genus within the subfamily Alphaherpesvirinae and family 
Herpesviridae  (International Committee on Taxonomy of Viruses 2012).  
11.1.2.  OIE list  
Aujesky’s disease (AD) is an OIE listed disease.  
11.1.3.  New Zealand status  
AD was first identified in domestic pigs in New Zealand in 1976. The source of the introduction 
is unknown but is suspect ed to have been by the importation of new pig breeds from Britain. 
Disease surveillance began in 1988 and all individuals that were serologically positive were 
culled. The last domestic pig that tested seropositive was in 1995 and New Zealand is now 
regard ed as being free from this disease in both domestic and feral pig populations (Motha  
1998; MacDiarmid 2000).  
Aujesky’s disease virus  (ADV) is an unwanted  notifiable organism (Unwanted Organisms 
Register 2014).  
11.1.4.  Epidemiology  
AD is widespread throughout the  world and is especially prevalent in areas that farm pigs at 
high densities. Several countries have successfully eradicated AD from their domestic herds and 
are now regarded as  free from  the disease. This includes a number of countries in Europe, and 
the United States. Feral pigs in these countries still harbour the disease and present a constant 
threat of reintroduction into AD free herds (Mettenleiter et al.  2012).  
ADV  is shed in pig secretions, excretions and aerosols and the incubation period is 
appro ximately 1 -8 days. Virus shedding commences 1 -2 days post infection but before the onset 
of viremia and clinical signs. Shedding peaks 2 -5 days post infection  and lasts for up to 17 days 
(Mettenleiter et al.  2012).  
Pigs are the only natural host for AD , being the only species which can survive infection . 
However, cattle, sheep, cats, dogs and rats can also be naturally infected resulting in fatal 
disease (Mettenleiter et al.  2012). Cattle do not survive infection and the incubation period is 
usually a co uple of days before the onset of severe neurological signs (Van Oirschot 2004 ). 
Humans are not susceptible to infection and all susceptible species except pigs are considered 
dead-end hosts (MPI 2014) .  
Clinical signs of disease are variable and are depend ent on the age of the pig and strain of virus. 
In neonatal pigs the disease may result in sudden death with few, if any clinical signs. In 1 -2 
week old pigs, signs may include trembling, incoordination, convulsion, tremor, ataxia and 
paralysis and mortalit y can be 100%. Older animals aged between 3 -6 weeks may exhibit 
similar signs and as they age the mortality rate decreases to less than 5% in pigs aged 5 months. 
Individuals who survive infection become latently infected and reactivation of the virus can 
occur if animals are stressed (Mettenleiter et al.  2012).  
ADV  is relatively resistant to environmental conditions and is stable at pH 4 -12. At extreme pH 
values , below  2 or above  13.5 viral inactivation takes  2-4 hours. With regards to thermal  
30 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI stability , ADV was found to survive at 25  °C, 15  °C, and  4 °C for approximately 6, 9 and 20 
weeks respectively. At a temperature of 60  °C, inactivation takes about 60 minutes and at 100  
°C about 1 minute (Mettenleiter et al.  2012). ADV is most stable  at pH 7  and wh en stored in 
water heated to 25 °C inact ivation of 99.99% of the virus  occurred after 4 days  (Van Oirschot 
2004). Further , ADV has been found to be inactivated by ultraviolet light and dry conditions 
(Animal Health  Australia 2012; Mettenleiter et al.  2012) .  
ADV is not very contagious ; for example an infectious dose (ID) of >1  × 104 tissue culture 
infective dose ( TCID 50)7  is needed to cause infection in animals . However, piglets are more 
susceptible to infection with an ID of 1 × 102 TCID 50 initiating infection. Larger doses of virus 
are needed to cause infection by the oral route compared to intranasal infection (Mettenleiter et 
al. 2012).    
Transmission of ADV  is primarily through the respiratory route from direct nose -to-nose 
contact and b y contact with contaminated  fomites, with the nasal and oral cavities being the 
main entry points for infection (Mettenleiter et al.  2012). Under favourable atmospheric 
conditions, when virus loads are high ADV may be disseminated short distances  by the ai rborne 
route , although long distance airborne spread is disputed. Exposure to semen and vaginal 
mucosa can also transmit infection and AD appears to be predominantly transmitted by the 
venereal route in feral swine (Mettenleiter et al.  2012). Regarding the  consumption of infective 
tissue, the Code does not consider meat or meat products that contain no offal to pose a risk to  
the importing country (OIE 2014 ). Offal containing head, thoracic or abdominal viscera, 
however, require risk management measures.  
ADV has been isolated from Meissner’s plexuses within submucosa tissue in both 
experimentally and naturally infected pigs (Narita et al. 1984; Ezura et al. 1995; Zhao 1996; 
Narita et al.  1998). There have been no studies on the inactivation of ADV virus in c asings.   
11.1.5.  Hazard identification conclusion  
ADV has been isolated from intestinal tissue from infected pigs. It is relatively  stable , has been 
isolated from the submucosa,  and the OIE has made recommendations for the trade in swine 
viscera.  For these reasons, ADV is identified as a hazard in hog casings.  
In cattle this disease is rapidly fatal so infected individuals are not likely to pass ante - and post -
mortem inspe ctions. ADV is not identified as a hazard in beef casings.  
11.2. RISK ASSESSMENT  
11.2.1.  Entry assessment  
Pigs are the only species that can remain latently infected after recovering from this disease. 
Clinical signs may be minor or not apparent when animals are either incubating the virus or are 
latent carriers. Ante - and post -mortem inspect ions may subsequently not detect these animals. 
ADV in latently infected animals has been shown to be reactivated by stress , and handling and 
transport prior to slaughter may contribute to this reactivation.  
Even though no studies have been conducted on A DV survival in swine casings there are 
factors that will likely lead to a  substantial  reductio n in virus titre. Storage of ADV in water for 
four days at 25 °C resulted in a 99.99% reduction in virus titre ( Van Oirschot 2004 ). During 
processing casings are placed in heated water (approximatel y 40 °C; see commodity definition 
                                                
 
7 Tissue culture infective dose (TCID 50): The dose of virus that will produce pathological changes in 50% of cell cultures 
inoculated.   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 31 section 3 ) and t his will reduce the titre  of virus . The standard operating procedure of  storing 
casings in dry  salt or saturated brine for a minimum of 30 days would be expected to  further  
reduce the titre of virus.  
The lik elihood of entry is assessed as negligible .  
11.2.2.  Risk estimation  
Since the likelihood of entry is assessed to be negligible, the risk estimate for ADV is 
negligible.  
 
References  
 
Animal Health Australia (2012) . Disease strategy: Aujeszky’s disease (Version 3.1). Australian Veterinary 
Emergency Plan (AUSVETPLAN), Edition 3, Standing Council on Primary Industries, Canberra, ACT. [Online] 
Available from: http://www.animalhealthaustralia.com.au/wp -content/uploads/2011/04/AUJ3.1 -
10FINAL20Sep12.pdf   [Accessed 28th January 2014].      
 
Ezura K, Usami Y, Tajima K, Komaniwa H, Nagai S, Narita M, Kawashima K (1995) . Gastrointestinal and 
skin lesions in piglets naturally infected with pseudorabies virus. Journal of Veterinary Diagnostic Investigation , 
7 (4), 451-455. 
 
International Committee on Taxonomy of Viruses (2012) . Virus taxonomy: 2012 release. International 
Committee on the Taxonomy of Viruses. [Online] Available from: 
http://www.ictvonline.org/virusTaxonomy.asp  [Accessed 18th December 2013].  
 
MacDiarmid S  (2000).  Aujeszky’s disease eradication in New Zealand. Australian Veterinary Journal , 78 (7),  
470-471.  
 
Mettenleiter T C, Ehlers B, Muller  T, Yong K, Teifke J P (2012). Herpesvirus es. In Zimmerman J, Karriker LA, 
Ramirez A, Schwartz KJ, Stevenson G W (eds .) Diseases of Swine , 10th edition , John Wiley & Sons publishing, pp.  
421-434.  
 
Motha MX J (1998).  Aujeszky’s disease status of feral pigs in the North Island. Surveillance , 25 (3),  13-14. 
 
MPI (201 4). Import risk analysis : Meat and meat products  from ruminants and pigs . Draft for public 
consultation.  [Online] Available from : http://www.biosecurity.govt.nz/files/regs/i mports/risk/meat -and-meat -
products -from -ruminants -and-pigs-feb-2014.pdf  [Accessed 6th December 2013].  
 
Narita M, Kubo M, Fukusho A, Haritani M, Moriwaki M (1984) . Necrotizing enteritis in piglets associated 
with Aujeszky's disease virus infection. Veterina ry pathology , 21 (4), 450-452. 
 
Narita M, Zhao Y M, Kawashima K, Arai S, Hirose H, Yamada S, Ezura K (1998) . Enteric lesions induced 
by different pseudorabies (Aujeszky's disease) virus strains inoculated into closed intestinal loops of pigs. 
Journal of Veterinary Diagnostic Investigation , 10 (1), 36-42. 
 
OIE (2014). Infection with Aujesky’s disease virus. Terrestrial Animal Health Code. Chapter 8.2. [Online] 
Available from: http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_aujeszky.htm  [Accessed 13th 
August 2014] . 
 
Unwanted Organisms Register (2014) . Aujeszky’s disease. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 28th January 2014].    
 
Van Oirschot J T (2004).  Pseudorabies. In: Coetzer JAW, Tustin RC (eds). Infectious diseases of livestock , 2nd 
edition.  Oxford University Press , 909-917. 
 
Zhao Y, Narita M,  Kawashima K (1996) . Pathologic changes in closed porcine intestinal loops inoculated with 
Aujeszky's disease virus. The Journal of Veterinary M edical science/the Japanese Society of Veterinary Science . 
58 (8), 809-810.   
32 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 12. Classical swine fever virus  
12.1. HAZARD  IDENTIFICATION  
12.1.1.  Aetiological agent  
Classical swine fever virus (CSFV) is a member of the Pestivirus genus within the family 
Flaviviridae (International Committee on Taxonomy of Viruses 2012) . 
12.1.2.  OIE list  
Classical swine fever (CSF) is an OIE listed disease.  
12.1.3.  New Zealand status  
New Zealand has been free from CSF since 1953 (Davidson 2002) and it is listed as an exotic 
notifiable organism.  
12.1.4.  Epidemiology  
CSF is a highly contagious and economically important disease of swine, which includes all 
breeds of the speci es Sus scrofa  that are the only natural host for this virus (OIE 2009).  
In the last 15 years, more than 60 countries have notified the OIE of at least one outbreak of 
CSF. Presently,  it is found in much of Asia, some African countries, Central and S outh 
America, and Russia and Latvia in Europe (United States Department of Agriculture 2013; 
World Animal Health Information Database Interface 2014) .  
There have been two CSF outbreaks in New Zealand (Wellington 1930, Auckland 1953). 
Eradication of the disease was achieved by culling infected herds (Anonymous 1991).  
Transmission of CSF is mainly by the oral and oronasal routes, via direct and indirect contact. 
All bodily fluids of an infected individual can contain infectious virus and the most common 
pathways of introductio n into new countries is by pigs  being fed insufficiently cooked pork  in 
food waste . Once  CSF is  present in a country , wild pigs can harbour the virus and reintroduce it 
to domestic populations.  Shedding of the virus can occur for months from  infected individuals 
(OIE 2009).  
The incubation period for CSF is 2 -14 days. Shedding of the virus may occur before the onset 
of clinical signs and the amount excreted within body fluids is dependent on the virulence of the 
strain with more virulent stra ins resulting in a higher concentration of virus (United States 
Department of Agriculture 2013).  
Clinical signs of disease are variable and depend on the virus strain, the age,  the health status  
and breed of the pigs ( Kirkland et al. 2012 ). Acute  CSF is ca used by virulent strains and is the 
most devastating form of the disease , usually causing  death within 1 -3 weeks. Signs  of acute 
disease  include high fever, huddling, weakness, drowsiness, anorexia, conjunctivitis and 
constipation followed by diarrhoea.  Mortality in young pigs may reach 100% (OIE 2009).  In 
the chronic form of the disease,  the same clinical signs may be observed and pigs usually 
survive for 2 -3 months before dying ( Kirkland et al. 2012).    
McKercher et al. (1980) demonstrated that CSFV may survive in processed casings for up to  
147 days when stored in saturated brine and held at a temperature of 4 °C, as pigs inoculated 
intramuscularly with these infected casings produced clinical signs of disease and died. 
Further, Depner et al. (1998) show ed that CSFV can survive in casings that have been stored 
in saturated brine (pH 6.3) at 4 °C for 20 days. The mean half -life of CSFV has been shown to  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 33 be 50 hours when held in suspension and stored at a pH of 7 and tempe rature of 21 °C 
(Dep ner et al. 1992 ). 
Recently, Wijnker et al. (2008)  inoculated a pig with a  highly virulent strain of CSFV 
(“Koslov”) . The intestines from this animal were used to make casings and these casings were 
treated with phosphate -supplemented salt or citrate -supplemented salt and  stored for 30 days 
at 4 or 20 °C . After the 30 -day storage period, the casings were fed to susceptible pigs and 
disease occurred in those pigs which consumed casings that were stored in citrate -
supplemented salted and held at a temperature of 4 °C. All ot her pigs did not become infected.  
Reflecting these findings , the Code  recommends that casings be stored in phosphate 
supplemented salt or brine for a minimum of 30 days at a temperature above 20 °C to enable 
the safe trade in hog casings.  
12.1.5.  Hazard identifi cation conclusion  
As the standard manufacturing procedure for casings does not include the addition of 
phosphate -supplemented salt there is the potential for CSFV to be present in hog casings and, 
therefore, CSFV is identified as a hazard.  
CSFV is not  identified as  a hazard in b eef casings.  
12.2. RISK ASSESSMENT  
12.2.1.  Entry assessment  
Pigs infected with less virulent strains of CSFV may pass a nte- and post -mortem inspection  and 
hence infected intestines from such animals may be used for the production of casings.  
The standard processing procedure for hog casings is to apply salt for a minimum  of 30 days 
and this treatment may not inactive CSFV, especially if the temperature is less than 20  °C 
(Wijnker et al. 2008; Wieringa -Jelsma et al.  2011). Viable virus may remain and the likelihood  
of entry of CSF in the commodity is assessed as non -negligible.  
12.2.2.  Exposure assessment  
Historically the main pathway of entry of CSF into countries has been attributed to the 
importation of contaminated meat  that has been fed  to pigs in food waste (Anonymous 1991).  
In New Zealand the feeding of untreated meat or food waste is prohibited by legislation           
(Biosecurity Meat and Food Waste for Pigs Regulations 2005). Compliance with this regulation 
is tho ught to vary across the pig farming community, and is likely to be high in commercial 
operations but lower in small -scale  backyard pig farms (MPI 2006 ).   
If pigs were illegally fed with contaminated casings,  infection could spread to other pigs and 
contaminate the environment.  
The likelihood of exposure  is assessed as non -negligible.  
12.2.3.  Consequence  assessment  
The consequence s of introduction would be dependent on the strain of CSFV and its 
pathogenicity (MPI 201 4). High mortalities (90 -100%) could occur due to the naivety of New 
Zealand herds to this disease  (Anonymous 1991). If the disease was allowed to spread, the 
economic cost could be high. Furthermore, feral pigs could become infected and be a persistent 
source of infection for domestic herds.   
34 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Control measures to limit the spread of CSF would likely consist of  the quarantine of infected 
premises, trace back of pigs that could have been exposed, the slaughter of all pigs on the farm 
and th orough cleaning and disinfection of all the exposed premises with carcasses being 
disposed by burning or deep burial (MPI 2014) .  
Pigs are the only host for this virus so there are no consequences for human  health  or for other 
animals.  
12.2.4.  Risk estimation  
Since the likelihood of entry and  exposure, and  the consequence s are all assess ed to be  non-
negligible, the risk estimation is also non -negligible . CSFV is assessed to be a risk in hog 
casings . 
12.3. RISK MANAGEMENT  
12.3.1.  Options  
The Code  chapter for CSF states that the s tatus of a country, zone or compartment can be 
determined after considering the criteria listed in Article 15.2.2. These criteria include that the 
disease should be notifiable in the whole territory  (OIE 2014 ).  
The Code  sets out recommendat ions that allow  for a country,  zone  or compartment  to be 
considered free from CSF if there has been no outbreak of CSF and no vaccination has been 
carried out in the last 12 months, unless there are means, validated according to Chapter 2.8.3 
of the  OIE Manual , to distin guish between vaccinated and unvaccinated pigs. 
Recommendations on how to recover a free status after an outbreak has occurred in a 
previously free country or zone are provided in Article 15.2.6. Furthermore, Article 15.2.4 
provides recommendations on the bilateral recognition of CSF free compartments and Article 
15.2.5 details how a containment zone can be established in a previously CSF free country or 
zone. In May 2013, CSF was added to the list of diseases f or which official OIE recognition 
of disease free status can be obtained. No countries, zones or compartments  have been  
recognised as officially disease free and applications for freedom will start to be evaluated 
from May 2014 to May 2015.   
The Code  gives recommendations for the importation of  swine  casings that may originate 
from C SF infected countries or zone.  
The relevant  Code  article is reproduced below:  
Article 15.2.24. Procedures for the inactivation of the CSFV in casings of pigs  
For the inactivat ion of CSFV in casings of pigs, the following procedures should be used: 
salting for at least 30 days either with phosphate supplemented dry salt or saturated brine (Aw 
< 0.80) containing 86.5% NaCl, 10.7% Na 2HPO 4 and 2.8% Na 3PO 4 (weight/weight/weight), 
and kept at a temperature of greater than 20  °C during this entire period.  
CSFV is not identified as a hazard in b eef casings so no risk management measures are 
justified for this commodity.  
The following measures could be considered to effectively manage th e risk  in imported hog 
casings . 
Option 1  
 
Hog casings  could be imported only from countries, zones or compartments recognised  by 
New Zealand  as free from CSFV.   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 35 Option 2  
 
For the inactivation of CSFV in casings of pigs, the following procedures could  be used: 
salting for at least 30 days either with phosphate supplemented dry salt or saturated brine (Aw 
< 0.80) containing 86.5% NaCl, 10.7% Na 2HPO 4 and 2.8% Na 3PO 4 (weight/weight/weight), 
and kept at a temperature of greater than 20  °C during this entir e period.   
 
References   
 
Anonymous (1991). Hog cholera (Classical swine fever). Surveillance , 18 (3),  16-27.  
 
Biosecurity meat and food waste for pigs regulations (2005).  [Online] Available from: 
www.legislation.govt.nz/pdflink.aspx?id=DLM332616  [Accessed 6th December 2013].   
 
Davidson R M (2002).  Control and eradication of animal diseases in New Zealand. New Zealand Veterinary 
Journal , 50 (3), 6-12.  
 
Depner K, Bauer T, Liess B (1992).  Thermal and pH stability of pestiviruses. Revue Scientifique et Technique 
de l`office International des Epizooties , 11 (3), 885 -893. 
 
Depner KR, Lange E, Strebelow G, Kaden V (1998).  Nachweis von Schweinepestvirus im behandelten 
Schweinedarm nach 30 -tägiger Lagerung in Salzlake. Bundesforschungsanstalt für Viruskrankheiten der Tiere, 
Nationales Referenzlaboratorium für klassische Schweinepest, Insel Riems, Germany. In: Wijnker JJ, Dep ner 
KR, Berends BR (2008). Inactivation of classical swine fever virus in porcine casing preserved in salt. 
International journal of food microbiology , 128 (2), 411 -413. 
 
International Committee on Taxonomy of Viruses (2012).  Virus taxonomy: 2012 release. International 
Committee on Taxonomy of Viruses. [Online] Available from: http://www.ictvonline.org/virusTaxonomy.asp  
[Accessed 19th December 2013].  
 
Kirkland PD, Le Potier MF, Vannier P, Finlasion  D (2012) . Pestiviruses . In Zimmerman J, Karriker LA, 
Ramirez A, Schwartz KJ, Stevenson GW (eds.)  Diseases of Swine , 10th edition, John Wiley & Sons publishing, pp. 
538-546.  
 
McKercher PD, Morgan O, McVicar JW, Shuot NJ (1980).  Thermal processing to inactivate viruses in meat 
products. In: Proceedings of the 84th Annual Meeting of the United States Animal Health Association, 
Louisville, Ky. U.S. Animal Health Association, Richmond, Va, pp. 320 -328. 
 
MPI (2006). Import risk analy sis: Porcine reproductive and respiratory syndrome (PRRS) virus in pig meat. 
[Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/prrs -risk-analysis.pdf  [Accessed 
21st January 2014].  
 
MPI (2014). Import risk analysis : Meat and meat products from ruminants and pigs. Draft for public 
consultation. [Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/meat -and-meat -
products -from -ruminants -and-pigs-feb-2014.pdf  [Accessed 6t h December 2013].  
 
OIE (2009).  Classical swine fever. Technical Disease C ard. [Online] Available from: 
http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/CLASSICAL_SWINE_FEVER
_FINAL.pdf   [Accessed 21th December 2013].  
 
OIE (2014 ). Classical  swine fever. Terrestrial Animal Health Code. Chapter 15.2. [Online] Available from: 
http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_csf.htm   [Accessed 20th August  2014]. 
 
United States Department of Agriculture (2013).  Classical swine fever, standard operating procedure: 1. 
Overview of etiology and ecology. Foreign animal disease preparedness and response plan. United States 
Department of Agriculture. [Online] Available from: 
www.aphis.usda.gov/animal_health/emergency.../sop/sop_csf_e -e.pdf  [Accessed 20th December 2013].  
  
36 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI World Animal Health Information Database Interface (2014). Classical swine fever. [Online] Available  
from:  http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home  [Accessed 21st January 2014].  
 
Wieringa -Jelsma T, Wijnker JJ, Zijlstra -Willems E M, Dekker A, Stockhofe -Zurwieden N, Maas R,  
Wisselink, H J (2011). Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen 
matrix model for natural sausage casings. International Journal of Food M icrobiology , 148 (2), 128-134. 
 
Wijnker JJ, Depner KR, Berends BR (2008).  Inactivation of classical swine fever virus in porcine casing 
preserved in salt. International journal of food microbiology , 128 (2), 411 -413. 
   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 37 13. Porcine reproductive and respiratory syndrome virus  
13.1. HAZARD IDENTIFICATIO N 
13.1.1.  Aetiological agent  
Porcine reproduc tive and respiratory syndrome virus (PRRSV) is a member of the family 
Arteriviridae within the genus Arterivirus  (International Committee on Taxonomy of Viruses 
2012).  
13.1.2.  OIE list  
Porcine reproductive and respiratory syndrome (PRRS) is listed as a disease notifiable to the 
OIE.  
13.1.3.  New Zealand status  
PRRS has not been described in New Zealand and is listed as an unwanted notifiable organism 
(Unwanted Organisms R egister 2014).  
13.1.4.  Epidemio logy 
PRRS was first recognised in 1987 in the USA and  within a few years  it had been described in a 
number of pig producing countries (OIE 2010). Currently, it is found in many countries in 
Europe, the Americas, and Asia (World Animal Health Information Da tabase Interface 2014). 
Pigs are the only host for this virus.  
Arterviruses  are characterised as having a high rate of mutation because of their mechanism of 
RNA replication. This makes PRRS V genetically unstable and isolates vary in both nucleic 
sequence  and pathogenicity (MPI 2006). Differences in virulence between strains also exist and 
the basis for this is not yet fully understood (College of Veterinary Medicine 2013).  
Clinical signs of disease are variable and influenced by a number of factors inclu ding the 
virulence of the virus, whether the virus is infecting a naïve population, the age at which the 
onset of infection occurs, whether other diseases are present in the populat ion, the size of the 
herd, and farm management practi ces. Some herds may ex perience reproductive failure , with 
sows aborting or farrowing pre -term, the birth of stillborn or mummified piglets, sow deaths 
and pre -weaning mortality of piglets. Respiratory disease and death can also occur in weaners 
and fattening pigs. In contrast, due to the differences in virulence between strains , some herds 
may be relatively unaffected (MPI 2006; College of Veterinary Medicine 2013).   
Previous studies have found that the highest titre of virus is located in macrophages, particularly 
those in the  lungs and lymph nodes (MPI 2006). In addition, PRRSV has been isolated from the 
small and large intestine of experimentally infected pigs. The virus was mainly observed in the 
mucous membrane epithelium or glandular epithelium, located within the mucosa l ayer of the 
intestine (Li et al.  2012). In hog casings only a residual amount of mucosa tissue remains after 
processing (see commodity definition section 3).  
Transmission can occur by a variety of routes including direct contact with an infected pig, 
conta minated semen, infected fomites, consumption of infected meat and aerosol s (European 
Food Safety Authority 2005, MPI 2006).  Several studies have shown that PRRS can be 
transmitted by the consumption of raw infected pig meat . However, no study has exposed m eat 
to normal handling and commercial processing conditions before feeding to pigs and this would 
be expected to have a significant effect on the titre of virus in meat (Pharo and Cobb 2011).        
38 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Several studies have found that a high percentage of pigs presented for slaughter in countries 
where PRRS is established have tested seropositive ( MPI 2006 ).  
PRRSV persists relatively poorly in the external environment and this is due to the 
characteristics of the  lipid envelope, which is susceptible to heat, pH , desiccation and time since 
slaughter (MPI 2006; Zimmerman et al.  2012). This virus has been shown to persist for 1 -6 
days at 20 -21 °C, 2 -24 hours at 37  °C and 6 -20 minutes at 56  °C. At refrigeration temperature 
(4 °C), approximately 90% of PRRSV infectivity is lost within a week (Benfield et al.  1999). A 
study measuring the survival time of four PRRSV isolates held at ambient temperatures and a 
pH of 7.5 found that the mean half -life was 155.5 hours at 4  °C; 84.8 ho urs at 10  °C; 27.4 hours  
at 20  °C; and 1.6 hours at 30  °C (Jacobs et al.  2010) . PRRSV is stable when the pH is 6.5 - 7.5 
and infectivity is rapidly reduced when the pH is below 6 or above 7.5 (Zimmerman et al. 
2006 ).  
13.1.5.  Hazard identification conclusion  
PRRSV  has been identified in the small and large intestines of experimentally infected swine 
and is identified as a hazard in hog casings.  
PRRSV is not identified as a hazard in beef casings.  
13.2. RISK ASSESSMENT  
13.2.1.  Entry assessment  
PRRSV strains vary in pathogenicit y and for some strains infection can remain inapparent in 
many herds ( European Food Safety Authority  2005). Ante - and post -mortem inspections may 
not exclude these infected pigs from slaughter.  
Viral persistence in pig tissue is influenced by the interact ion between time since slaughter, 
storage temperature and pH .  
PRRSV is heat liable and placing intestines  into heated water (approximately 40  °C; see 
commodity definition section 3 ) which assists with their cleaning would reduce the titre of 
virus in infected mucosa tissue.  
 
After cleaning, casings are stored for  at least  30 days at room temperature (approximately 20 
°C; European Food Safety Authority  2012 ). Jacobs et al.  (2010) pred ict the half -life of 
PRRSV to be 27. 4 hours at 20 °C. Storage of casin gs for 30 days  at room temperature would, 
therefore, be associated with a reduction in viral titre equivalent to 26 half -lives ; that is, a 
reduction of >99.99 99% of the original virus titre will occur over this period . 
As PRRSV is only found in mucosa tiss ue which is present in  hog casings in residual amounts, 
and there would be a significant inactivation  of virus during the 30 day storage period, the 
likelihood of entry  is assessed as negligible.  
13.2.2.  Risk estimation  
Since the likelihood of entry is assessed to be negligible, the risk is estimated to be negligible.  
 
References   
 
Benfield DA, Collins JE, Dee SA, Halbur PG, Joo HS, Lager KM, Mengeling WL, Murtaugh MP, Rossow 
KD, Stevenson GW, Zimmerman J J (1999). Porcin e Reproductive and Respiratory Syndrome . In: Straw E S,  
D’Allaire S, Mengeling W L, Taylor D J (eds .) Disease of Swine , 8th edition,  Iowa State University  Press, 201 -
232.  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 39  
College of Veterinary Medicine (2013) . Porcine reproductive and respiratory syndrome (PRRS). Iowa State 
University. [Online] Available from:   http://v etmed.iastate.edu/vdpam/new -vdpam -employees/food -supply -
veterinary -medicine/swine/swine -diseases/porcine -reproductive - [Accessed 19th December 2013].  
 
European Food Safety Authority (2005 ). The probability of transmission of porcine reproductive and 
respir atory syndrome virus (PRRSv) to naïve pigs via fresh meat. European Food Safety Journal , 239, 1-85. 
[Online] Available from: http://www.efsa.europa.eu/en/efsajournal/doc/239.pdf  [Accessed  14th January 2014].  
 
European Food Safety Authority (2012) . Scientific opinion on animal health risk mitigation treatments as 
regards imports of animal casings. European Food Safety Journal , 10 (7), 2820. [Online] Available from: 
www.efsa.europa.eu/efsajournal  [Accessed 23rd July 2014].  
 
International Committee on the Taxonomy of Viruses (2012) . Virus taxonomy: 2012 release. [Online] 
Available from: http://www.ictvonline.org/virusTaxonomy.asp  [Accessed 19th December 2013].  
 
Jacobs AC, Hermann J R, Muñoz -Zanzi C, Prick ett JR, Roof MB, Yoon KJ, Zimmerman J J (2010 ). 
Stability of porcine reproductiv e and respiratory syndrome virus at ambient temperatures. Journal of Veterinary 
Diagnostic Investigation , 22 (2), 257-260. 
 
Li  L, Zhao Q, Xinna G, Teng K, Kuang Y, Chen Y, Guo X, Yang H (2012 ). Chinese highly pathogenic 
porcine reproductive and respirator y syndrome virus exhibits more ex tensive tissue tropism for pigs.  Virology 
Journal , 9 (1), 203. [Online] Available from: http://www.biomedcentral.com/content/pdf/1743 -422X -9-203.pdf   
[Accessed 19th December 2013].  
 
MPI (2006). Import risk analysis : Porcine reproductive and respiratory syndrome (PRRS) virus in pig meat. 
[Online] Available from: http://www.biosecurity.govt.nz/files/regs/imports/risk/prrs -risk-analysis.pdf  [Accessed 
6th January 2014].  
 
OIE (2010). Porcine reproductive and respiratory syndrome.  Manual of Diagnostic Tests  and Vaccines for 
Terrestrial Animals . Chapter 2.8.7. [Online] Available from:  
http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.08.07_PRRS.pdf  [Accessed 14th January 
2014].  
 
Pharo H, Cobb S P (2011) . The spread of pathogens through trade in pig meat: overview and recent 
developments . Revue Scientifique et Technique de l`office International des E pizooties , 30 (1), 139-148.   
 
Unwanted Organisms R egister (2014) . Porcine reproductive and respiratory syndrome. [Online] Available 
from: http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 21st January 2014].      
 
World Animal H ealth Information Database Interface (2014). Porcine reproductive and respiratory 
syndrome. [Online] Available  from : http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home  [Acce ssed 
21st January 2014].  
 
Zimmerman JJ, Benfield D A, Murtaugh MP, Osoria F, Stevenson GW, Torremorell M (2006). Porcine 
reproductive and respiratory syndrome virus (porcine arterivirus). In Straw BE, Zimmerman JJ, D’Allaire, 
Taylor DJ (eds.) Diseases of Sw ine, 9th edition. Blackwell Publishing, 387 -417. 
 
Zimmerman JJ, Benfield D A, De e SA, Murtaugh MP, Stadejek T, Stevenson G W, Torremorell M (2012) . 
Porcine reproductive and respiratory syndrome virus (Porci ne arterivirus). In Zimmerman JJ, Karrier LA, 
Ramire z A, Schwartz KJ, Stevenson G W (eds.) Diseases of Swine , 10th edition . John Wiley and Sons, 461 -486. 
   
40 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI 14. Swine vesicular disease virus   
14.1. HAZARD IDENTIFICATIO N 
14.1.1.  Aetiological agent  
Swine vesicular disease virus (SVDV) is a variant of Enterovirus B that is a member of family 
Picornaviridae and genus Enterovirus (International Committee on Taxonomy of Viruses 
2012). There is only one serotype with strain variation between isolates (OIE  2009).   
14.1.2.  OIE list  
Swine vesicular disease (SVD) is  not listed  by the OIE .  
14.1.3.  New Zealand status  
SVD has never been reported in  New Zealand and is an exotic notifiable organism ( Unwanted 
Organisms Register  2014).  
14.1.4.  Epidemiology  
SVD was once found  throughout Eu rope but has since been eradicated from many countries 
with recent outbreaks occurring in Portugal (2007) and Italy (2009) (Alexandersen et al.  2012). 
The disease is also likely to be present in some Asian countries and the last documented 
outbreak was in Taiwan in 2000 (European Food Safety Authority 2012).  
Swine are the only host for SVDV and it is not a zoonotic disease (European Food Safety 
Authority 2012).  
The result of infection with SVDV is variable and strain dependant. Vesicles may develop on 
the c oronary band, at the junction with the heel, and interdigital spaces of the feet, and less often 
on the snout, tongue and lips (OIE 2009). Mortality does not usually occur, but morbidity may 
reach 100%. Recent outbreaks have been notable for displaying les s severe or no clinical signs 
and infection has only been found when animals are tested in serosurveillance programmes or  
for export certification (OIE 2009). The clinical signs of SVD can be wrongly attributed to foot 
and mouth disease or vesicular stomat itis and any outbreak must  be confirmed by enzyme -
linked immunosorbent assay (OIE 2009; European Food Safety Authority 2012).  
The most common way of introducing this disease to new areas is through the movement of 
subclinically infected animals. The incub ation period for this virus is between 2 -7 days although 
for trade purposes  the Code  consider s it to be 28 days  (OIE 2009). The virus can be excreted 
from the nose and mouth and in faeces for up to 48 hours before  the onset of  clinical signs. 
Virus sheddi ng continues for up to 2 weeks from the nose and mouth, up to 3 months in faeces, 
and at least 7 days from vesicles, with the highest titre of virus being shed in the first 7 days 
post infection  (PI) (OIE 2009; Alexandersen et al.  2012). All tissues also contain virus during 
the viraemic period, which can occur within 1 day PI, and lasts for approximately 2 -3 days (OIE 
2009; Alexandersen et al.  2012; European Food Safety Authority 2012). Not all infected 
animals develop viraemia (E uropean Food Safety Authority 2012). Transmission occurs by 
exposure to contaminated excretions, faeces, fomites, direct contact and consumption of 
infected meat.  
SVDV can survive for a prolonged period in the environment  (Alexandersen et al. 2012) . It is 
preserved by refrigeration , can withstand a wide range of pH (2.5 -12) and is inactivated when 
heated to 56 °C for 1 hour  (OIE 2009) .  It can also  survive the commercial curing process for 
Serrano hams (Mebus 1993; Mebus et al. 1997) .  
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 41 A recent study has fo und that SVDV titre is reduced significantly  when exposed to the 
conditions applied  in the commercial production  of casings (Wieringa -Jelsma et al.  2011).   
The European Food Safety Authority (2012) has assessed  that animal products are unlikely to 
contrib ute to the spread of SVDV.  
14.1.5.  Hazard identification conclusion  
SVD V is an environmentally stable virus that has never been reported as occurring in  New 
Zealand. SVD V is identified as a hazard in hog casings.  
SVD V is not identified as a hazard in b eef casings.  
14.2. RISK ASSESSMENT  
14.2.1.  Entry assessment  
As pigs may be subclinically infected with SVD and viraemic at the time of slaughter, ante - and 
post-mortem inspections may not always detect these infections, especially as recent SVD 
outbreaks have exhibited le ss severe or no clinical signs (OIE 2009). Casings derived from such 
animals may subsequently contain infectious virus.  
Several steps used in the manufacturing  process of casings will reduce the survival of SVDV. 
During processing casings are placed in he ated water (approximately 40  °C; see commodity 
definition  section 3 ) to assist with clean ing. T his process may reduce th e titre  of any SVDV 
that might be present in casing s, as it has been shown  that a heat treatment of 56 °C one hour 
inactiv ates this virus (OIE 2009 ). After cleaning the casings are stored in dry salt or saturated 
brine for a minimum of 30 days  and this  has been ex perimentally shown to reduce the titre of  
SVDV  in a 3D collagen matrix model  (Wieringa -Jelsma et al.  2011). Moreover , experience 
from international trade has shown that SVDV does not appear to be a risk in hog casings.  
The combination of the se two processing steps will reduce the likelihood of entry of SVDV to a 
negligible level.  
14.2.2.  Risk estimation  
Since the likelihood of entry is assessed to be negligible, the risk estimate for SVD V is 
negligible.  SVDV is assessed  not to be a risk  in hog casings . 
 
References   
 
Alexandersen S, Knowles N J, Dekker A,  Belsham G J, Zhang Z, Koenen F (2012) . Swine vesicular disease . 
In: Zimmerman  JJ, Karrier LA, Ramirez A, Schwartz KJ, Stevenson G W (eds.) Diseases of Swine , 10th edition. 
John Wiley and Sons , 602 -606.       
 
European Food Safety Authority (2012) . Scientific Opinion on Swine Vesicular Disease and Vesicular 
Stomatitis . European Food Safety Authority,  10 (4), 2631. [Online] Available from: 
http://www.efsa.europa.eu/en/efsajournal/doc/2631.pdf  [Accessed 16th January 2014].      
 
International Committee on the Taxonomy  of Viruses (2013) . Virus taxonomy: 2012 release. [Online] 
Available from: http://www.ictvonline.org/proposals/2011.018a,bV.A.v2.Enterovirus -Sp,Ren.pdf   [Accessed 
15th January 2014].  
 
Mebus CA, House C, Gonzalvo FR, Pineda JM, Tapiador J, Pire JJ, Bergada J, Yedloutschnig RJ, Sahu 
S, Becerra V, Sanchez -Vizcaino JM (1993).  Survival of foot -and-mouth disease, African swine fever, and hog 
cholera viruses in Spanish ser rano cured hams and Iberian cured hams, shoulders and loins. Food microbiology , 
10 (2), 133 -143. 
  
42 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI Mebus C, Arias M, Pineda JM, Tapiador J, House C, Sanchez -Vizcaino JM (1997).  Survival of several 
porcine viruses in different Spanish dry -cured meat products . Food Chemistry , 59 (4), 555 -559. 
 
OIE (2009) . Swine vesicular disease. Technical disease card . [Online] Available from: 
http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/SWINE_VESICULAR_DISEA
SE_FINAL.pdf  [Accessed 15th January 2014].  
 
Unwanted Organisms R egister (2014) . Swine vesicular disease virus. [Online] Available from: 
http://www.biosecurity.govt.nz/pests/registers/uor  [Accessed 15th January 2014].      
 
Wieringa -Jelsma T, Wijnker J J, Zijlstra -Willem s EM, Dekker A, Stockhofe -Zurwieden N, Maas R , 
Wisselink, H J (2011).  Virus inacti vation by salt (NaCl) and phosphate supplemented salt in a 3D collagen 
matrix model for natural sausage casings. International Journal of Food M icrobiology , 148 (2), 128-134. 
   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 43 15. The agent of b ovine spongiform encephalopathy   
15.1. HAZARD IDENTIFICATIO N 
15.1.1.  Aetiological agent  
Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy 
(TSE) or prion disease (OIE 20 10). 
15.1.2.  OIE list  
BSE is an OIE listed disease of cattle.  
15.1.3.  New Zealand status  
New Zealand is free from  BSE and the OIE categorises  New Zealand ’s risk status for this 
disease as negligible.  
Variant Creutzfeldt -Jacob disease is the human manifestation of BSE  and it  has never been 
identified in New Zealand (Environmental Science and Research 2013).  
15.1.4.  Epidemiology  
BSE is an inva riably fatal disease of cattle that was first identified in the United Kingdom 
(UK)  in 1986.  Since then it has been reported in 27 other countries, the majority of which are 
within Europe (OIE 2014). In the UK  the outbreak peaked in 1992 when 37  280 cases were 
recorded (MPI 2014)  and in 2013 there were  three cases. Outside of the UK  in 2013, there 
were four cases, all of which occurred within Europe (2 in Franc e, 1 in Ireland and 1 in 
Poland)  (OIE 2014).  Globally, BSE is disappearing rapidly.  
BSE was spread by feeding cat tle infected meat and bone meal of bovine origin. The disease 
originally spread from the UK  most likely due to the export of infected cattle and infected 
meat and bone meal. There is no evidence for horizontal transmission of this disease and 
vertical transmission does not play a role in perpetuating epidemics (Radostits et al. 2007; 
OIE 20 10). In July 1988, the UK enacted a ban prohibiting the feeding of ruminant proteins to 
ruminants and in 1994, this ban was extended to all forms  of mammalian protein as cross 
contamination in feed mills was occurring resulting in further cases of BSE (Radostits et al. 
2007; Scottish Government 2012). The result of these control measures is that the number of 
infected animals has significantly decr eased  and BSE has now become rare .   
Pigs have been experimentally  infect ed with BSE when inoculated simultaneously by the 
intracranial, intravenous and intraperitoneal routes. Infection by oral exposure to BSE, 
however, has not been demonstrated and no cases of TSE in pigs were found during the BSE 
epidemic  in cattle in the UK (Wells et al. 2003). TSEs  have also been found in eight species 
of ungulates in zoos  or wildlife parks in the UK and it is likely that these animals we re 
exposed to contaminated feed  (Kirkwood and Cunningham 1994). Feline spongiform 
encephalopathy (FSE) was also identified in domestic cats and zoo felines in the UK , with 
this outbreak coinciding with the BSE outbreak in cattle . The infectious agent in these cases 
was shown to be the same in these species. Up to 2003, 89 cases of FSE had been identified 
(Radostits et al. 2007) but no cases have  been reported since 2007, which suggest s that the 
disease has disappeared (MPI 2014) .  
The incubation period for BSE is long, ranging from 2.5 t o over 8 years and it could persist 
for the entire lifespan of cattle. Because of this, it is a disease that manifests predominately in 
adult animals. The risk of infection is highest in the first 6 months of life and adult cattle are  
44 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI at a lower risk of acquiring  infection. Infected animals display clinical signs which are 
variable but which include changes in temperament, posture, sensorium and movement. These  
clinical  signs become progressively worse , with the course of the disease ranging from 1  to 6 
months. There is no cure for BSE and clinical infection always results in mortality (Radostits 
et al. 2007).  
BSE infection in humans causes  a syndrome  called variant Creutzfeldt -Jakob disease (vCJD). 
As of the 7th of July 2014, 177 cases (definite or probab le) of vCJD had been identified in the 
UK of which all have resulted in death (National CJD Research and Surveillance Unit 2014). 
The most important route of transmission to humans is through the consumption of food 
products that contain infectious tissue.  The number of  infectious tissues in cattle is small and 
the majority is located within the central nervous system, with 60% of BSE infectivity in the 
brain, followed by 24% in the spinal cord, 9.6% in the ileum, 3.6% in the dorsal root ganglia 
and <0.1% in the tonsils (New Zealand Food Safety Authority 20 06).  
Initially it was uncertain how humans were becoming infected with the BSE agent until 
mechanically recovered meat (MRM) was investigated. MRM was processed from the 
vertebral column of cattle using high-pressure techniques. The spinal cord was removed 
before processing, however, residual spinal tissue and the two dorsal root ganglia that are 
attached to the spinal cord were incorporated into a meat paste, which was used as an 
ingredient in a number o f foods, such as burgers, sausages, pies and baby food.  Up to 2% of 
the meat paste could contain central nervous system tissue. For example, a sausage weighing 
100 grams could have contained up to two grams of infectious tissue and in sheep it has been 
shown that the infectious oral dose is only 0.5 grams (MacDiarmid 2004).  Cooper and Bird 
(2002) concluded that about 90% of the MRM paste was used in burgers and it is the 
consumption of this product that drove the dietary exposure to BSE. So, while it is tr ue that 
BSE infectivity is found in the intestines it was not a significant  route of exposure for the  
people in the UK who acquired the disease.  
In response to this outbreak t he European Union has classified the entire intestinal tract of 
cattle from the duodenum to the rectum as ‘specified risk material’ ( Regulation EC,  No 
999/2001 of the European Parliament), which is excluded from processing, and must be 
destroyed (Wijnker et al. 2008). The Code , on the other hand, recommends the exclusion of 
the ileum only (OIE 2014).  
The European Food Safety Authority (2014) has developed a  BSE infectivity model  of cattle 
intestines and mesenteries from the  European Union. This model showed that the distribution 
of infectious tissue within the intestines and the titre of the BSE agent vary by age. In cattle 
aged 18 months or less the jejunum, ileum and caecum contain the majority  of infectious  
tissue , which peaks at approximately 15 bovine oral infectious doses (BoID 50)8 per animal. 
Infectivity declines as cattle age and in animals aged 60 months or more, less than one BoID 50 
is present  in intestines and mesenteries. The majority of  infectious tissue in these  older  
animals is present not within  the intestine  but in the mesenteric nerves and  celiac and 
mesenteric gangli on complex, with t he ileum  and jejunum contain ing only a residual amount 
of the total  infectivity  (1% and 6% respectively).  
After processing cattle intestines into casings it has been estimated that there is on average a 
25% reduction in infectivity in the  duodenum, jejunum, caecum and colon tissues. The 
greatest reduction in infectivity (approximately 3 BoID 50) for processed casings occurs in 
cattle slaughtered before 18 months of age and in cattle older than 120 months the mean 
reduction in infectivity is  only 0.01 BoID 50 (European Food Safety Authority  2014a) .  
                                                
 
8 Bovine oral infectious dose (BoID 50): The oral dose that infe cts 50% of bovine animals following experimental inoculation.   
MPI  Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  ● 45 In addition , the European F ood Safety A uthority (2014a) has concluded that for any given 
situation the exclusion of the last 4 metres of the small intestine  (which includes the ileum)  
and of the ca ecum from the food and animal feed pathway will decrease the infectivity 
associated with intestinal tissue  by more than 90% in cattle aged 36 months old and below.  
It has been estimated that the outbreak of BSE in the United Kingdom has cost 600 billion 
pounds. In response, many countries have developed active surveillance programmes to 
provide evidence of freedom from this disease. The detection of only a single case of BSE can 
result in export bans and significant economic losses (Radostits et al. 2007).  
15.1.5.  Hazard identification conclusion  
BSE has never occurred in New Zealand. Cattle intestines have been found to harbour BSE 
and this pathogen is identified as a hazard in beef casings.  
BSE is not identified as a hazard in hog casings.  
15.2. RISK ASSESSMENT  
15.2.1.  Entry assessment  
In 2013, the total number of cattle identified as infected worldwide  with BSE was 7 (OIE 
2014 ). In 2014 (up to the 1st of May) , two cattle have been found infected in Germany (OIE 
2014 b). The number of cases  worldwide  has steadily declin ed and because BSE is now so 
rare, the likelihood of casings being prepared from an infected cow is extremely low.  
The OIE categorises  the BSE risk status of countries as “negligible ”, “controlled ” or 
“undetermined ”. The likelihood of BSE entering in any commodity  from a c ountr y with a 
negligible BSE risk status would  be negligible.  
BSE infected animals will pass ante - and post -mortem inspection as there are no gross 
patholog ical changes detectable in  an infected animal , and there are no preclinical tests 
available  to diagnose infection . For countries with a controlled risk or undetermined risk 
status, the Code  (Article 11.4.14) recommends that the ileum should not be traded. The 
likelihood that BSE would enter New Zealand in beef casings from countries with a 
contr olled or undetermined risk status that  are certified to  comply with the commodity 
definition (exclusion of the ileum from international trade) is assessed as negligible.  
15.2.2.  Risk estimation  
Since the likelihood of entry, is assessed to be negligible, the risk is assessed as negligible. 
BSE is assessed not to be a risk .  
 
References   
 
Cooper JD, Bird SM (2002). UK dietary exposure to BSE in mechanically recovered meat by birth cohort and 
gender. Journal of Cancer Epidemiology and Prevention , 7, 59 -70. 
 
Environmental Science and Research (2013). Notifiable and other diseases in New Zealand: Annual 
surveillance report 2012. The Institute of Environmental Science and Research Ltd. Porirua, New Zealand. 
[Online] Available from: 
https://surv.esr.cri.nz/PDF_surveillance/AnnualRpt/AnnualSurv/2012/2012AnnualSurvRpt.pdf   [Accessed 1st 
May 2014].  
 
European Food Safety Authority (2014).  TSE infectivity model (TSEi) in animal tissues: Bovine intestines 
and mesenteries. [Online] Available from: http://www.efsa.europa.eu/en/supporting/pub/559e.htm  [Accessed 1st 
May 2014 ].  
46 ● Supplementary Import risk analysis : Sausage casings of bovine and porcine origin  MPI  
European Food Safety Authority (2014a). Scientific opinion on BSE risk in bovine intestines and mesentery . 
[Online] Available from: http://www.efsa.europa.eu/en/efsajournal/pub/3554.htm  [Accessed 1st May 2014 ]. 
 
Kirkwood JK, Cunningham AA (1994).  Epidemiological observations on spongiform encephalopathies in 
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