D5650.PDF

Conf. OIE 1998, 289-302
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STRATEGIES FOR THE CONTROL OF CLASSICAL SWINE FEVER,
INCLUDING THE APPLICATION OF MODERN VACCINES
V. Moennig
Institute of Virology, School of Veterinary Medicine, Buenteweg 17, D-30559 Hannover, Germany
Original: English
Summary: Classical swine fever (CSF) is an infectious viral disease which has severe economic impact
on the pig industry of several European countries. Whereas European Union (EU) Member States and
other Western European countries are almost free of the disease in domestic pigs, the CSF situation in
many Central and Eastern European countries remains unclear. The number of outbreaks in domestic
pigs decreased in the EU in the 1990s, but financial losses increased greatly due to changes in the
structure of the pig industry and control policy. The concentration of pigs and farms in some regions of
Europe and long distance trade increased the risk of spreading the disease and the number of pigs
affected by control measures. Primary CSF outbreaks are mostly due to (illegal) swill feeding.
In some areas of Europe, CSF has become endemic in the wild boar population. This poses a constant
risk for domestic pigs. Knowledge about the epidemiological situation of CSF in wild boar is insufficient
in many countries.
Laboratory diagnosis has improved markedly during the last decade. Most European countries are
equipped for CSF diagnosis and participate in international inter-laboratory comparison tests in order to
standardise CSF diagnosis. Molecular typing of CSF virus isolates has become a valuable tool for
epidemiology. Diagnostic capacities for emergency situations must be considered in national
contingency plans.
Since the prevalence of infected animals has decreased, the EU pursues a non-vaccination policy to
control CSF. This facilitates the internal market and fulfils the requirements of the international market.
Several other European countries have adopted this policy.
Although this control strategy is widely accepted today, legislation needs some amendment based on the
scientific evaluation of the recent CSF epidemics in Europe. Currently, two subunit marker vaccines are
undergoing the licencing procedure. These vaccines might be a future option for restricted use in
emergency situations.
Essentially, the success of control programmes depends on education and awareness of all parties
involved, i.e. farmers, practitioners and Veterinary Services.
1. INTRODUCTION
Classical Swine Fever (CSF) is one of the most economically important viral infectious diseases of domestic and wild
pigs and is classified as an OIE List A disease. After implementation of consequent control measures, several countries,
including Australia, Canada, New Zealand, United States of America (USA), and some Member States of the European
Union (EU), succeeded in eradicating the virus. In most other parts of the world the CSF virus is present, causing
considerable economical damage. The manifestation of the infection may vary greatly depending on the age of the
animal and the virus virulence. Young animals often display the acute classical form, with high fever, haemorrhages
and high mortality. Alternatively, the chronic and ultimately fatal form may obscure the characteristic classical picture
in young animals. Older animals often show only mild clinical symptoms. Like all pestiviruses, CSF virus may pass
through the placenta of pregnant animals, infecting foetuses and leading incidentally to the birth of persistently viremic
piglets. The latter develop late onset CSF later in life and die from CSF. The multitude of possible clinical signs very
often hampers prompt diagnosis of primary outbreaks (photo 1).

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In order to compile information about occurrence, diagnosis and eradication in OIE Member Countries, a questionnaire
was prepared and sent to each country. Out of 50 countries, 33 provided the requested information to OIE. Seventeen
countries did not respond.
The following countries made information available: Andorra, Armenia, Austria, Belarus, Croatia, Cyprus, Czech
Republic, Denmark, Estonia, Finland, France, Germany, Greece, Iceland, Ireland, Italy, Latvia, Lithuania,
Luxembourg, Malta, Moldavia, Netherlands, Norway, Portugal, Romania, Slovakia, Slovenia, Spain, Sweden,
Switzerland, Ukraine, United Kingdom and Uzbekistan.
2. ETIOLOGY
The causative agent of CSF is a small (40-60 nm) enveloped ribonucleic acid (RNA) virus with a single stranded RNA
genome with positive polarity. CSF virus belongs to the pestivirus genus of the Flaviviridae family (29). It is related to
the bovine viral diarrhoea (BVD) virus and the border disease (BD) virus of sheep. The genomic sequence of about
12,000 bases is known and infectious copy deoxyribonucleic acid (cDNAs) have been produced in several laboratories
(16, 19, 20). The viral RNA codes for four structural and seven nonstructural proteins (17, 18). The virus is relatively
stable in moist excretions and fresh meat products, including ham and salami type sausages (22). However, it is readily
inactivated by detergents, lipid solvents, proteases and common disinfectants.
3. CLINICAL SIGNS
The incubation period is seven to ten days. The clinical signs of CSF are extremely variable (18, 26). Infected pigs
develop pyrexia and leukopenia. Petechial haemorrhages of the outer skin and mucosae are the most typical sign
although they are not seen consistently (photos 2 & 3). Central nervous system disorders and obstipation followed by
diarrhoea may also be characteristic clinical findings.
The severity of clinical signs largely depends on the age of the animal and viral virulence. Usually young animals are
affected more severely than older animals. In older breeding pigs the course of the infection is often mild or even
subclinic.
Acute and chronic courses of CSF are known. All courses of the infection have in common that the animals are viremic
at least as long as they show clinical signs. Deaths occurs two to three weeks after infection (acute course) or after up to
three months (chronic course).
The outcome of transplacental infection of foetuses depends largely on the time of gestation (26) and may result in
abortions and stillbirths, mummifications, malformations or the birth of weak or persistently viremic piglets (15) (photo
4). Although persistently infected offspring may be clinically normal at birth, they invariably die from CSF. Survival
periods of 11 months after birth have been observed. This course of infection is referred to as 'late onset CSF' (25).
4. PATHOLOGY AND PATHOGENESIS
Under natural conditions the most frequent route by which the CSF virus enters its host is oronasal. Major target cells
for the virus are endothelial cells, lymphoreticular cells, macrophages, and some kinds of epithelial cells. Pathological
findings vary according to clinical signs (18, 25).
Prenatally, at the early phases of ontogenesis, the virus affects organ differentiation and leads to malformations.
In postnatal infections, lesions are generally caused by widespread thrombosis and/or endothelial damage, inducing
haemorrhagic diathesis and petechiation. Bronchopneumonia is another regular feature. In a high proportion of fatal
cases, histopathology of the brain shows a non-suppurative encephalitis with severe vasculitis. Severe
thrombocytopenia is a consistent finding. The terminal stage of acute infection is associated with a marked depletion of
B lymphocytes in the circulatory system as well as in lymphoid tissues (24).

Conf. OIE 1998
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Photo 1: Pox-like skin lesions
Lésions cutanées varioliformes
Оспоподобные кожные поражения
Photo 2: Skin haemorrhages and necroses on the ear edges
Hémorragies et nécroses cutanées au bord des oreilles
Кожные геморрагии и некрозы по краям уха

Conf. OIE 1998
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5. IMMUNOLOGY
Like all pestiviruses, the CSF virus is immuno-suppressive during acute infection. Pigs that have recovered are
protected against CSF for several years or even for their lifetime. Neutralising antibodies are detectable two weeks after
infection at the earliest. In pigs with chronic CSF, neutralising antibodies are detectable at the end of the first month
postinfection for a few days and disappear afterwards. Persistently viremic, in utero infected pigs seldom produce
specific antibodies.
Maternal antibodies have a half-life of approximately 14 days. Passive immunity generally protects piglets against
mortality during the first five weeks of life, but not against virus replication and shedding. Little is known about cell-
mediated immunity against CSF.
6. DIAGNOSIS OF CSF AND LABORATORY FACILITIES
Clinical diagnosis is of prime importance for the detection of CSF. However, it may prove difficult and many primary
outbreaks are initially not recognised as CSF, because clinical signs are often variable and non specific. This applies
especially for older animals in breeding herds. In general, CSF should be considered whenever a disease with high
body temperature that does not react to treatment is diagnosed. This is especially relevant in regions where CSF has
occurred during the last 12 months in domestic pigs or wild boar. Veterinarians, farmers and hunters should be highly
aware of the risk.
A modern and efficient laboratory diagnosis is an essential tool for CSF control. Monitoring of the status of the pig
population in 'peace time' and early detection of CSF depend on reliable diagnostic methods and adequate laboratory
facilities.
In order to discover CSF infected herds at an early stage, it is important to identify the right animals for laboratory
investigation. These are clinically sick animals and should be tested virologically. Random sampling is not suitable for
CSF diagnosis. It may be used for epidemiological purposes, such as monitoring and serological prevalence studies.
6.1. Virology
The 'gold standard' for CSF diagnosis is virus isolation. CSF virus can be isolated from buffy coat cells or organ
suspensions of viremic animals. Suitable organs are spleen, tonsils, lymphnodes, parotid glands and kidneys
(1, 3).
The samples are incubated on susceptible cell cultures of porcine origin. As the CSF virus is
non-cytopathogenic, CSF specific antibodies are a prerequisite for detection of the virus in cell culture.
Differentiation of the CSF virus from ruminant pestiviruses can be achieved using monoclonal antibodies (1, 3,
6). The virus isolation protocol requires at least three days and is labour intensive. A rapid diagnostic test for
CSF is based on the demonstration of viral antigen in organ tissue sections using conjugated antibodies for direct
immunofluorescence (fluorescent antibody test, FAT). To screen large numbers of animals in herds suspect of
being recently infected by CSF, virus antigen capture enzyme-linked immunosorbent assays (AgC-ELISAs) can
be used for the detection of viral antigen in blood samples. However, the latter tests are less sensitive than virus
isolation.
Recently, detection of viral RNA has become an additional option for laboratory diagnosis. In particular, the
5'-nontranslated region of the genome has been used for amplification by the reverse transcriptase polymerase
chain reaction (RT-PCR). Subsequent nucleotide sequencing of the respective region allows discrimination
between different CSF virus isolates (9, 14). The OIE Reference Laboratory for CSF in Hannover, Germany,
keeps an extensive computer data base on CSF virus isolates including epidemiological and virus type
information data.
The 'molecular epidemiology' based on the above technique has become a useful tool and may well support
epidemiological investigations (tracing on/back). Typing of CSF virus isolates of at least each primary outbreak
in domestic pigs and isolates originating from wild boar is desirable. OIE Member Countries are encouraged to
send respective materials to the above-mentioned OIE Reference Laboratory.

Conf. OIE 1998
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Photo 3: Multiple petechial haemorrhages on different wild boar organs (acute CSF)
Pétéchies multiples de différents organes chez un sanglier (peste porcine aiguë)
Множественные петехии в различных органах дикого кабана (острая чума свиней)
Photo 4: Aborted and mumified fetuses
Avortons momifiés
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