CLASSICAL SWINE FEVER
VOLKER MOENNIG
Institute of Virology, Department of Infectious Diseases, University of Veterinary Medicine, Hannover, Germany
Classical swine fever (CSF) is a highly contagious, febrile, viral disease of pigs.
It was first described in the early 19th century in the USA and was termed ‘hog cholera’. Later, a condition in Europe named ‘swine fever’ was recognized to be the same disease. Both names continue to be in use. In general the disease is now called CSF to distinguish it from African swine fever (ASF), which is clinically indistinguishable but caused by an unrelated virus. CSF affects domestic pigs and wild boar (Sus scrofa). Owing to their severe economical impact, outbreaks of CSF in domestic and wildlife populations are notifiable to the OIE.AETIOLOGY
CSF is caused by a small, enveloped RNA virus in the genus Pestivirus of the family Flaviviridae. Classical swine fever virus (CSFV) is antigenically related to the other Pestiviruses, namely Bovine viral diarrhea virus of cattle and Border disease virus of sheep. The latter two viruses are widespread in domestic as well as wild ruminants and can occasionally infect pigs. Usually, ruminant pestiviruses do not cause disease in pigs, and they are eliminated after a few days. However, these infections have diagnostic consequences because serological cross-reactions with CSF virus do occur and may lead to false- positive laboratory results. In these cases additional tests are required to differentiate CSF antibodies from antibodies induced by ruminant pestiviruses.
Under natural conditions CSFV infects only Suidae, i.e. domestic pigs and wild boar, although the virus can be transmitted experimentally to other species. It will grow in porcine cell cultures but does not generally cause a visible cytopathic effect. The virus has only one serotype, and only some limited antigenic variability between strains can be shown.
Strain typing for epidemiologic mapping purposes had been done by sequencing of the viral RNA combined with phylogenetic analysis. A large database of CSF viral sequences is available at the Community Reference Laboratory for CSF at the University of Veterinary Medicine in Hannover(77).The virus is moderately fragile and does not persist in the environment or spread long distances by the airborne route. It can survive for prolonged periods in moist excretions of infected pigs and also in fresh meat products, including ham and salami- type sausages. Low temperatures extend viral survival times, and the virus has been shown to remain viable after several years in frozen pig meat, or months in chilled or cured meat. However, it is readily inactivated by detergents, lipid solvents, proteases and common disinfectants.
EPIDEMIOLOGY
CSF has worldwide distribution. It is endemic in parts of Latin America, some Caribbean islands and pig-producing countries of Asia. In 2005 South Africa reported to the OIE the first occurrence of CSF in mainland Africa since 1918. Australia, New Zealand, Canada and the USA are free of CSF, as is most of Western and Central Europe, although sporadic outbreaks occur in some countries.
Data on the geographic distribution of CSF in Europe is incomplete. The World Animal Health Information Database (WAHID) of the OIE indicates that the countries of the EU are CSF-free and that outbreaks have been reported in the Russian Federation, although some other non-EU countries have not supplied information to OIE. It is known that in some western Balkan countries CSF occurs in domestic pigs. The epidemiological situation in wild boar in these countries is not known.
CSF virus readily infects European wild boar, and direct and indirect transmission of the virus is comparable to that in domestic pigs. In countries that are free of CSF in domestic pigs, epidemics in wild boar are typically initiated by deliberate or accidental feeding of contaminated pork in garbage at rest sites or landfills.
Although the feeding of swill is prohibited in EU countries, knowledge of this and awareness of the risks is often inadequate among farmers, hunters and tourists. In countries with CSF in domestic pigs, wild boar may become infected largely through indirect contact with infected pigs (e.g. manure). Once introduced in this way, the virus can spread within wild boar populations by direct contact and contact with contaminated excretions and carcasses. PI piglets can contribute to virus circulation in wild boar populations. Transmission to domestic pigs may arise as a result of direct or indirect contact with wild boar. Contamination of hunting equipment, livestock feed, swill and shared environments with wild boar excretions or carcasses provide opportunities for the transmission of CSF virus. There are no known animal vectors.The first indication of an outbreak of CSF in a wild boar population is usually a mortality event. Effective spread of the virus within wild boar populations requires transmission both within and among social groups. Within social groups, the virus is transmitted relatively rapidly by direct and indirect contact, particularly between piglets. By contrast, rates of direct contact among boar from different social groups are lower, and hence transmission occurs mainly by contact with contaminated excretions and carcasses. Direct transmission between groups may be enhanced during the rutting season through dispersing males, and when new social groups are being established. The outcome of CSF infection in individual boar resembles that in domestic pigs, in that a high percentage of young pigs succumb to the infection, but older animals survive. Convalescent pigs mount a sufficiently strong immune response to protect them from future CSF virus infection. There are two possible courses for an epidemic of CSF in wild boar: either the epidemic is self-limiting or it becomes endemic. For some time historical experience of CSF outbreaks suggested that epidemics of CSF in wild boar are always self-limiting.
Typically, acquired immunity in a proportion of the population in combination with reduced host density arising from disease-induced mortality, decreased the number of susceptible animals and the infection died out. However, during the last two decades epidemics in some regions have been observed to become endemic with CSF virus persisting in wild boar populations for prolonged periods without signs of self-limitation. Possible reasons for the emergence of endemicity are the increasing density and size of wild boar populations and the involvement of viral strains of low virulence(78). The principal reason is most likely to be the recent increase in the abundance and distribution of wild boar populations throughout Europe(79). This is at least in part the result of improvements in nutrition due to intensified agriculture and the effects of climate change, which have led to prolonged breeding seasons. Changes in hunting practices are also likely to have contributed. The increase in wild boar abundance allows the establishment of endemic CSF, because there are at any time sufficient susceptible animals to sustain the chain of infection, i.e. viraemic animals are always able to transmit the virus to at least one other susceptible wild boar (and so the basic reproductive rate of the pathogen is R0 ≥ 1). The more susceptible animals belong to a wild boar population and the higher the animal density in a certain area is, the higher is the probability that R0 > 1 will persist for a prolonged time. During initial outbreaks and epidemics all animals are susceptible, whereas in endemic situations it is mainly young animals that are susceptible. Due to the high reproductive rate of wild boar, there is a constant supply of young animals that become susceptible after the waning of maternal immunity. This young age class constitutes a reservoir for the virus and maintains the infection in the population. By contrast, CSF outbreaks in smaller populations are likely to be selflimiting. For example, in populations of about 1500 to 2000 animals, the virus may disappear within 1 year(80).Epidemiological links between CSF virus infections in wild boar and domestic pigs have been reported repeatedly. Between 1993 and 1997 80% of the 92 primary outbreaks of CSF in domestic pigs in Germany were located in geographic regions where CSF was endemic in wild boar. In 60% of these cases a direct or indirect contact with infected wild boar or wild boar meat was established1-81).
PATHOGENESIS, PATHOLOGY AND IMMUNITY
CSF in wild boar has not been studied as extensively as in domestic pigs. Therefore most of the theoretical and practical considerations regarding the disease in wild boar are mainly based on knowledge of CSF in domestic pigs. However, a few experimental studies conducted on wild boar indicate that the clinical course of CSF is similar to that in domestic pigs(82,83).
Infection with virulent CSFV results in an acute haemorrhagic disease of pigs, characterized by disseminated intravascular coagulation, thrombocytopenia and immunosuppression. CSFV replicates in macrophages and vascular endothelial cells of pigs and it is able to suppress interferon production and apoptosis of infected cells.
The course of CSFV infection may follow two different pathways, depending on the time of infection: the animal either gets infected prenatally as a fetus when the immune system is not fully developed; or the infection takes place postnatally when the immune system is already developed (for review see (84)). The two courses differ in their patho- mechanisms and have different consequences for the clinical disease, as well as for the perpetuation of the virus within a population of susceptible hosts.
Prenatal Infection
Like all other pestiviruses, CSFV has the ability to cross the placental barrier and infect the fetus in utero. This happens if a pregnant sow, which is not protected by CSF- specific antibodies, undergoes a transient infection with CSFV (see the section on postnatal infection, below).
Early infections of susceptible pregnant sows (within the first 6 weeks of gestation) usually result in abortions and stillbirths, whereas later infections yield persistently virae- mic piglets. Stillborn and/or mummified animals may be present along with viraemic and non- infected piglets in one litter. PI piglets shed virus permanently until they die. These PI animals can play an important role in the spread of CSF virus in the domestic pig or wild boar population. Although PI piglets are weaker than non- viraemic ones, some of them may survive for several weeks or even months. In domestic pigs the longest period of persistent viraemia reported so far was 11 months and for wild boar piglets 39 days(83). PI piglets develop the so- called late- onset form of CSF.Postnatal Infection
The postnatal infection is the common, or ‘classical’ form of CSF. This can be acute or chronic. The acute course lasts less than 4 weeks and the infected animals either recover completely (transient infection) or die (lethal infection). The mortality rate may be as high as 90%, depending on a number of factors. The chronic form has been defined as lethal disease with a duration of 30 days or more. Under field conditions different forms of CSF occur simultaneously.
The outcome of postnatal CSF has often been related solely to the virulence of the particular virus causing the infection. However, virulence on its own is a confusing and misleading parameter. The age of the pig at the time of exposure, its immunological status, the dose of the infecting virus and the breed are other factors of importance for the outcome of the infection. In adult animals CSFV often induces only transient infections with few mild clinical signs and lesions and low mortality. In pregnant sows reproductive failure frequently occurs (see also the prenatal infection section, above). By contrast, the disease in young animals is generally more serious, leading to high mortality rates. These observations are also valid for wild boar(85). In wild boar only the acute course of disease has been described so far, and no experimental or field data are available for the chronic course. It may be assumed that the chronic form occurs in wild boar; however, survival time of chronically sick animals might be shorter than in domestic pigs owing to harsher environmental conditions.
Under natural conditions, the mode of entry of CSFV into the animal is the oronasal route. The tonsils are primary sites of virus replication, and CSFV can be found in the tonsils as early as 7 hours post-exposure. Interestingly, also after intramuscular and subcutaneous inoculation CSFV was found most consistently and in high concentration in the tonsils. From the tonsils, CSFV is transported via the lymphatic circulation to the regional lymph nodes. After replication in regional lymph nodes the virus reaches all other organs of the body via the blood. High titres of virus have been demonstrated in spleen, bone marrow, visceral lymph nodes and lymphoid structures lining the small intestine. The virus probably does not invade parenchymatous organs until late in the virae- mic phase. Virus spread is usually completed within 5—6 days.
Post mortem examination of pigs that have succumbed to acute CSF often show pathological changes in lymph nodes, tonsils, spleen and kidneys. Lymph nodes may be swollen, oedematous and haemorrhagic. Haemorrhages of the kidney may vary in size from hardly visible petechiae to ecchymotic haemorrhages. Similar haemorrhages can also be observed in the urinary bladder, larynx, epiglottis and heart and sometimes widespread over the serosae of the abdomen and chest. A non- purulent encephalitis is often present. Lesions due to secondary infections may also be seen, which may mislead the pathologist. Pathological lesions induced by chronic CSF are less typical, especially concerning the lesser extent of haemorrhages on organs and serosae. In animals showing chronic diarrhoea, necrotic lesions in the ileum, the ileo-caecal valve and the rectum are common. As clinical signs of chronic CSF are rather non-specific, many other diseases must be considered as differential diagnoses.
Prenatally, at the early phases of ontogenesis, the virus affects organ differentiation, which may lead to malformations. However, this may not be detectable under field conditions in wild boar.
In general the acute form of ASF leads to a very similar clinical and pathological picture. When present, haemorrhages on the skin and ears are easy to detect and lead to suspicions of acute ASF or CSF. The predominant post mortem findings consist of haemorrhagic diathesis and swollen, haemorrhagic lymph nodes. However, the severity of pathological lesions can vary widely. Both diseases can be clearly differentiated by laboratory diagnosis.
In the field the most visible signs of CSF (and ASF) are the lesions described above. However, it takes experience and the awareness of the persons handling wild boar, e.g. hunters and gamekeepers, to recognize the typical signs and to interpret them properly.
The immune response of wild boar against CSFV is analogous to the immune response of domestic pigs. Like all pestiviruses, CSFV affects the immune system, causing transient immunosuppression during acute infection. The CSFV has a distinct affinity to cells of lympho- reticular organs and causes severe depletion of lymphocytes, affecting both B and T cells. Thymus and bone marrow atrophy, as well as generalized lymphocytopenia have been recorded with a prominent B- lymphocyte deficiency. Generalized leucocytopenia, which is usually seen before the onset of fever, is considered a primary characteristic of CSF. Little is known about cell-mediated immunity against CSF. In transient acute CSF, neutralizing antibodies do not appear in blood until the animal has recovered from the leucocy- topenia, 2 weeks post-infection at the earliest. Pigs that have recovered are protected against CSF at least for 6 months or even for their lifetime. Likewise, pigs that have been vaccinated with modified live vaccines develop a solid and long-lasting immunity. In wild boar, oral vaccination using the live C-strain vaccine, has been demonstrated to be fully protective at the individual level1-86’87).
Maternal antibodies have a half-life of about 11 days and last until the piglets are 3 to 4 months old. Passive immunity generally protects piglets against mortality during the first weeks of life, but not necessarily against virus replication and shedding(88). In PI piglets colostrum- derived antibodies can only be detected for a short time after birth (less than 1 week) compared with non-viraemic littermates(83).
CLINICAL SIGNS
Clinical manifestation of CSF may vary greatly depending on the age of the animal and viral virulence. In domestic pigs, after an incubation period of approximately 4—7 days, animals become febrile and may develop symptoms typical for CSF. Three clinical courses can be distinguished, i.e. acute infection, chronic infection and late-onset CSF.
I n acute cases of CSF, the first signs, e.g. high body temperature (>41°C), inappetence and apathy can be seen after the incubation period. The progression of the disease is marked by conjunctivitis, nasal discharge, intermittent diarrhoea, swollen lymph nodes and muscle tremor. The terminal stage in domestic pigs is often characterized by skin cyanosis, mainly on ears, nose, tail and abdomen, and skin haemorrhages of different grades, predominantly over bone protuberances. In wild boar skin lesions are less evident and may be masked by skin bristles. Sick animals show hind-limb weakness and a staggering gait which is often followed by a posterior paresis. Leucocytopenia and thrombocytopenia are common findings. In addition, wild boar exhibit behavioural changes, becoming seemingly tame and roaming during daylight hours(89).
Animals that do not die within 4 weeks post-infection either recover, developing high titres of neutralizing antibodies, or become chronically ill and remain virus shed- ders until death. Wasting and diarrhoea are the most evident signs in chronic CSF in domestic pigs. Such pigs have skin lesions, and frequently stand with arched backs. Pigs with chronic CSF may survive for more than 100 days. Secondary bacterial and parasitic infections are frequently present. Thus the clinical picture may often be atypical, variable and misleading.
The late-onset form of the disease is seen in piglets that have been infected in utero and that have been born as PI piglets. After a period without clinical signs, they may develop mild anorexia and depression, conjunctivitis, dermatitis, diarrhoea and locomotive disturbances leading to posterior paresis. CSF characteristic lesions, particularly petechial haemorrhages, are not present. Retarded growth is the most common finding. Although the prenatal intrauterine infection leading to PI offspring is a rather rare event, it is regarded as one possible mechanism contributing to the persistence of CSFV within a population. In wild boar the prenatal form of CSF has only been demonstrated experimentally1-83). Field data on the occurrence of PI wild boar manifesting the late-onset form of disease are not available.
I n summary it must be emphasized that the clinical signs of CSF in wild boar — as in domestic pigs — can be extremely variable, depending on different factors. This may impede early recognition in the field.
DIAGNOSIS
Hunters, veterinarians and farmers should always be highly aware of the risk of CSFV introduction. Close observation of wild boar populations is important for the early suspicion and detection of outbreaks. Abnormal mortality, particularly in young animals and sometimes obviously sick wild boar, are early signs of a CSFV outbreak in a population. A tentative diagnosis of CSF can also be made based on gross pathological lesions found in shot animals, e.g. petechial bleedings and/or haemorrhages. Any suspicion must be confirmed by laboratory diagnosis. Suitable samples for virological investigation can be retrieved from animals found dead or clinically sick wild boar that have been shot. Random sampling of shot animals is the method of choice for epidemiological investigations, such as monitoring and serological prevalence studies.
Laboratory diagnosis
All laboratory techniques for diagnosing CSF have been compiled in the Classical Swine Fever Diagnostic Manual of the European Commission1-90) and in the OIE Manual of Diagnostic Test and Vaccines for Terrestrial Animals(91). However, unlike laboratory diagnosis in domestic pigs, the diagnosis in wild boar is often hampered by the poor quality of samples. This makes inter-laboratory comparison tests difficult, if not impossible, and error rates might be higher compared with routine diagnosis of samples from domestic pigs.
The laboratory diagnosis of CSF is based on detection of viral antigen, isolation of virus, detection of viral RNA and demonstration of virus-specific antibodies. Tonsils, mandibular lymph nodes and spleen are the most appropriate tissues for virus detection in wild boar. Blood (if available) and homogenized lymphatic tissues are the materials of choice for virus isolation. For antigen detection the direct immunofluorescence test (FAT) is widely used. The test is both rapid and reliable and is applied to detect CSFV in cryostat sections.
Isolation of CSFV in cell cultures is regarded as a very sensitive method; however, it takes a minimum of 3—5 days. Virus isolation can provide confirmation in cases in which the FAT is inconclusive.
For large-scale screening, antigen-capture ELISA have been developed. These tests require less specialized facilities and can be performed much more rapidly than virus isolation. However, their sensitivity and specificity is inferior to FAT or virus isolation on cell culture. Reliable results are obtained only with samples from animals already displaying clinical signs. Therefore the use of antigen ELISA has to be linked with the clinical or pathological examination of the animal. RT-PCR has become a standard method for CSF diagnosis1-92’93). The sensitivity and specificity of RT-PCR is comparable to that of virus isolation, or is even superior to it. The molecular epidemiology based on the above technique has become a useful tool and may support epidemiological investigations. Typing of CSFV isolates of at least each primary outbreak in wild boar could provide useful information on the origin of the virus.
Serological diagnosis of CSF is important for the detection of the infection in wild boar populations, where acute clinical signs are absent. In addition, it is a tool for the monitoring of epidemic and endemic disease situations. Several tests are available for the detection of CSF antibodies. The fluorescent antibody virus neutralization test and the neutralizing peroxidase-linked assay are commonly used techniques. Although the neutralization tests are considered to be the most sensitive and specific tests, they are time- consuming and not suitable for automated systems and large-scale screening. To achieve these purposes, several ELISA techniques using specific monoclonal antibodies have been developed and are commercially available. However, the sensitivity of the ELISA is regarded to be inferior to the sensitivity of the neutralization tests. The ELISA technique requires less specialized facilities and can be performed much more rapidly than the neutralization test due to automated systems. Large numbers of sera can be examined within a short time. As ELISA systems are subject to occasional difficulties in interpretation, it is essential to have access to a neutralization test for investigation of sera that give inconclusive ELISA results.
In areas where oral vaccination of free-ranging wild boar is carried out, it is not possible to distinguish between vaccinated or naturally immunized individuals.
MANAGEMENT, CONTROL AND REGULATIONS
Awareness and vigilance are essential so that outbreaks in domestic pigs and wild boar are detected early and control measures are instituted rapidly to prevent further spread.
CSF-eradication programmes in recent decades have been successful in North America, Australia and in most European countries. CSF is notifiable to the OIE and to the competent veterinary authorities in member states of the EU. Prevention of CSF in wild boar is regarded as a crucial element for the protection of domestic pigs from infection.
Control and eradication of CSF in wild boar cannot be managed as in domestic pigs (i.e. by systematic culling and movement restrictions). Once CSFV is established in a wild boar population the primary goal of all control measures must be to reduce the number of susceptible animals in the affected area. The threshold level of susceptible hosts must drop to a level where the basic rate of infection R0 is reduced to below 1 (R0 < 1). The number of susceptible animals in an area will be influenced by many factors including the size of the infected population, disease- induced mortality rates, acquired immunity, hunting pressure, feeding (movement ofanimals) and other management interventions (e.g. oral vaccination). Furthermore, the response of the population to management interventions is likely to be influenced by population density and structure. Strategy and methods applied for the control of CSF in wild boar populations must take such factors into account(94).
Depending on the size and structure of the affected wild boar population, this goal can be achieved either by ‘doing nothing’, i.e. banning hunting and limiting all disturbances of the affected population in the case of small and isolated populations. Hunting, oral vaccination or a combination of both are possible strategies in large populations. Feeding should be avoided, as artificial feeding is a potential source of infection, if meat products or kitchen waste are (illegally) included. As feeding encourages boar to aggregate, it may contribute to further spread and perpetuation of the virus in the population. Feeding sites may be visited by animals whose normal home range is far away, thus intensifying direct and indirect contact between wild boar from different groups(95). The consequence is to enlarge the population at risk. An additional effect of artificial feeding might be increased fertility arising from improved nutritional condition of the females(96).
For several reasons indiscriminate hunting is not an effective control option. It fails to reduce the wild boar population to the threshold level required for transmission to cease because populations that are substantially reduced by hunting exhibit compensatory reproduction. Consequently, wild boar density tends to return quickly to the carrying capacity of the environment. One consequence of this process is that a large number of young susceptible animals are recruited into the population. Furthermore, immune adult animals in endemic areas will be among those shot, and their removal therefore reduces the proportion of immunes in the population1-97). The removal of older animals by hunting also leads to a dispersion of social groups and increased movement of individuals, thus enhancing opportunities for disease transmission.
Theoretically hunting could have a positive effect if only, or predominantly, young wild boar were removed, as this would reduce the number of susceptible animals in the population without disrupting social groups and increasing dispersal. In practice, however, hunting is often neither efficient nor sustainable, mainly due to the inherent difficulties in mounting sufficiently high hunting pressure, particularly in the face of compensatory reproduction in reduced populations. Hunting also requires the compliance of hunters, whose ethics may not necessarily be compatible with the objectives of CSF control. Financial incentives have been used to overcome the reluctance of hunters to shoot young animals. However, despite these limitations, hunting is useful and necessary for collecting samples for laboratory diagnosis(94). Trapping of young wild boar using cage traps is an efficient method, which could be applied as an alternative or in addition to hunting.
Oral immunization of wild boar is an effective control option and a key tool for the eradication of CSF in dense wild boar populations. However, in member states of the EU, where prophylactic vaccination against CSF is prohibited, emergency vaccination measures in wild boar must be notified to the Commission1-98). After an outbreak of CSF and during the progression of the epidemic, an increasing number of adult animals survive the infection and become immune, thereby reducing the number of susceptible animals. In this situation oral vaccination using baits containing live modified CSFV can be used to further reduce the number of susceptible animals below a critical threshold, where R0 drops below 1 (R0 < 1).
Areas to be vaccinated should be designed according to the spatial distribution of wild boar populations, and the ecological characteristics of the landscape (i.e. natural and artificial borders such as motorways, rivers, lakes, mountains, etc.)(98). Vaccination strategies have also to strictly define the epidemiological and sampling units. The success of oral vaccination campaigns largely depends on the strategy of bait delivery. CSF vaccine baits are distributed by hand at pre-defined feeding areas. The number of baits depends on the population density and typically ranges between 30 to 40 per km2. Vaccination is repeated 2 weeks later and thereafter this ‘double’ vaccination is repeated every 4—5 months(99). This vaccination procedure increases population immunity progressively, and the maximum population immunity is usually reached after three double campaigns per year. The high reproductive rate of wild boar requires that vaccination continues for at least 2 years after the last virus-positive boar had been detected in order to maintain a sufficiently high level of immunity in the population and so to eliminate the CSFV.
In animals older than 1 year immunity reaches 75—90% after 1 year of vaccination (i.e. three campaigns). In contrast often less than 30—50% of young wild boar are immune even after several years of vaccination. One explanation for the significantly lower seroconversion in young wild boar is insufficient bait consumption. Piglets younger than 6 months do not consume the vaccine baits, because:
i) animals higher up in the hierarchy eat most of the baits;
ii) the baits in current use are too large; and iii) piglets of that age prefer food of a different texture. Despite these limitations, in combination with natural immunity induced by circulating field virus, vaccination was shown to repeatedly reduce R0 (R0 < 1) sufficiently to successfully clear CSFV from wild boar populations(85,87,99,100).
CSF does not persist in smaller wild boar populations, as subsequent to virus introduction most of the surviving animals become immune, leaving too few susceptible pigs to maintain the chain of infection. CSFV can only persist in a wild boar population in the presence of viraemic animals, which transmit the virus to enough susceptible wild boar to ensure R0 > 1. However, monitoring and understanding demographic processes and the epidemiology of disease in wildlife populations is challenging, and several parameters of interest (e.g. population structure and dynamics, population size or herd immunity) remain unknown or can only be roughly estimated.
In addition to control measures aimed at the elimination of CSF from the wild boar population, strict measures must also be taken to avoid the transmission of virus to domestic pigs. Therefore wild boar and domestic pigs must be separated effectively, by fencing of holdings, strict hygiene measures, movement restrictions for wild boar (no trade of live wild boar) and trade restrictions for wild boar meat (i.e. wild boar carcasses must remain in the affected zone). For domestic pigs, movement restrictions should also be in place and animals should undergo clinical investigation before they leave a zone where wild boar are affected by CSF. In cases of clinical suspicion a virological investigation should be performed immediately. Pigs in outdoor holdings are at greatest risk, and therefore existing outdoor holdings in the affected zone should be reported to the veterinary authorities. These establishments should be organized and managed in such a manner as to reduce the likelihood of direct contact between wild boar and domestic pigs. In particular, outdoor holdings should be enclosed within a double fence with a gap of at least 1 metre. In addition, these farmers should provide sheds in order to be able to move domestic pigs into closed facilities when there is a high risk of CSFV infection (e.g. when virologically positive wild boar are detected in the vicinity of the holding). In times of CSF epidemics in wild boar the establishment of new outdoor holdings for domestic pigs should be forbidden.
Recent CSF epidemics/endemics in wild boar have made it clear that effective control requires a holistic approach that takes into account the characteristics of the disease, the biology of wild boar populations and human activities. Measures to increase public awareness of the disease are also essential for the success of control.
PUBLIC HEALTH CONCERN
CSF, like all other known pestiviruses, is not transmissible to humans or commonly kept pets such as dogs, cats and avian species. Therefore there is no public health concern in the strict sense.
SIGNIFICANCE AND IMPLICATIONS IN ANIMAL HEALTH
CSF can cause devastating epidemics in domestic pigs, particularly in countries that are free of the disease but have a fully susceptible pig population. In these countries, vaccination is generally only permitted in emergencies. In the event of an outbreak, strict measures (e.g. culling of infected and suspect pigs and movement restrictions) are enforced in order to control the spread of the disease. This can have severe consequences for the pig industry, especially in densely populated livestock areas. Several outbreaks in member states of the EU in recent years have caused very high economic losses. For example, a CSF epidemic in the Netherlands in 1997—1998 cost about 2 billion euros and more than 11 million pigs had to be destroyed1-101). The mass culling of pigs creates an ethical problem, and the economic losses mean that CSF is one of the most important diseases of domestic animals in Europe.
As CSF may become endemic in wild boar populations, they threaten domestic pig holdings as a possible source of infection, with considerable economic consequences. Therefore the main aims of controlling CSF in wild boar are to reduce the risk of transmission of the disease to domestic pigs, to prevent it becoming endemic, or to reduce the duration of the endemic phase, and finally to eradicate the disease in wild boar.
ACKNOWLEDGEMENT
The author is greatly indebted to Dr Klaus Depner, Friedrich-Loeffler- I nstitute, who has contributed greatly to the manuscript with his great experience in the field and his stimulating discussions.
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