Difference between revisions of "Classical Swine Fever"

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Also known as: '''''CSF — Hog Cholera — Pig Plague — CSFV
+
{{unfinished}}
  
−
==Introduction==
+
==Description==
−
Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a [[:Category:Pestiviruses|Pestivirus]] from the family Flaviviridae. Presentation may be acute, sub-acute, chronic or persistent, and the disease is indistinguishable in the field from [[African Swine Fever]]. Acutely, classical swine fever is characterised by severe depression, high fever and superficial and internal haemorrhages, with many cases resulting in death. Depression, anorexia and pyrexia are seen in chronic classical swine fever. Transplacental infection is also possible and results in persistently infected piglets.
+
 
 +
Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a Togavirus. Presentation may be actue, sub-acute, chronic or persistent, and the disease is indistinguishable in the field from African Swine Fever. Acutely, classical swine fever is characterised by severe depression, high fever and superficial and internal haemorrhages, with many cases resulting in death. Depression, anorexia and pyrexia are seen in chronic classical swine fever. Transplacental infection is also possible and results in persistently infected piglets.
  
 
==Aetiology==
 
==Aetiology==
−
The causative agent of classical swine fever is a small, enveloped virus of around 40nm diameter. The genome is comprised of single stranded positive sense RNA and contains about 12,300 bases. The sequence of the genome is known, and codes four structural and seven non-structural proteins. The classical swine fever virus is relatively stable in excretions and in fresh meat products including ham, salami and other similar sausages. It is, however, easily inactivated by detergents, common disinfectants and heat.
 
  
−
Classical swine fever virus is closely related to the [[Bovine Viral Diarrhoea Virus|bovine viral diarrhoea (BVD)]] virus of cattle, and the [[Border Disease Virus|border disease virus]] of sheep.
+
The causative agent of classical swine fever is a small, enveloped virus of around 40nm diameter. The genome is comprised of single stranded RNA, which is positive sense and contains about 12,300 bases. The sequence of the genome is known, and codes four structural and seven non-structural proteins. The classical swine fever virus is relatively stable in excretions and in fresh meat products including ham, salami and other similar sausages. It is, however, easily inactivated by detergents, common disinfectants and heat.
 +
 
 +
Classical swine fever virus is a Togavirus within the Pestivirus genus of the Flaviviridae. As such, it is closely related to the bovine viral diarrhoea (BVD) virus of cattle, and the border disease virus of sheep.
  
 
==Signalment==
 
==Signalment==
−
Domestic pigs and other swine of any age may become infected with classical swine fever virus.
+
Domestic pigs and other swine of any age may become infected with classical swine fever.
  
 
==Transmission and Pathogenesis==
 
==Transmission and Pathogenesis==
−
In field cases of CSFV, transmission is mainly oronasal by direct or indirect contact with infected pigs. Infected feed or pork products may also cause spread of disease, and transmission in semen can occur. Once the virus gains entry to the host an incubation period of around 7 days occurs prior to the onset of clinical signs, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, the virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to other tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also induces a [[thrombocytopenia]] which contributes to haemorrhage by impairing primary [[Normal_Mechanisms_of_Haemostatic_Control#Introduction|haemostasis]]. In acute CSF this angiopathy, in association with shock and pyrexia, leads to death. Surviving swine go on to develop a chronic form of the disease where tissue infarction results in joint and enteric lesions.
+
In field cases of CSFV, transmission is mainly oronasal by direct or indirect contact with infected pigs. Infected feed or pork products may also cause spread of disease, and transmission in semen can occur. Once the virus gains entry to the host an incubation period of around 7 days ensues, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, classical swine fever virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to further tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also causes a thrombocytopenia which contributes to haemorrhage by impairing primary haemostasis. In acute CSF this angiopathy causes pig death in association with shock and the febrile response. Surviving swine go on to develop a chronic form of the disease where joint and enteric lesions are seen resulting from tissue infarction.
  
−
The outcome of transplacental infection depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die eventually from full blown CSF.
+
The outcome of transplacental infection of foetuses depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die from CSF.
  
 
==Diagnosis==
 
==Diagnosis==
−
Diagnosis is made on the basis of history, clinical signs and gross pathological lesions. In Britain, classical swine fever is '''notifiable''' to the local Animal Health Office. Following notification, the State Veterinary Service is responsible for visiting the suspect premises to confirm the diagnosis by laboratory testing.
 
−
 
 
 
===Clinical Signs===
 
===Clinical Signs===
−
Although the incubation period for classical swine fever is generally less than ten days, in the field it may take up to four weeks for clinical signs to become apparent in a population. Disease severity varies with virulence, immune status and the age of the animal: this means that although acute, chronic and congenital forms of the disease can be appreciated, there is no "classic" disease presentation.
+
T
−
 
+
et al., 2000). The incubation period in individual
−
In the '''acute form''', animals are almost always pyrexic. In piglets the fever may exceed 40<sup>0</sup>C, but in adults temperatures may be no higher than 39.5<sup>0</sup>C. Lethargy, conjunctivitis and lymphomegaly may be seen, as well as respiratory signs and diarrhoea. Neurological signs such as gait abnormalities, incoordination and convulsions are also common. The most telling sign of classical swine fever is haemorrhage of the skin. Haemorrhages arise in the second or third week post-infection on the ear, tail, abdomen and medial aspect of the limbs and persist until death. CSF virus also causes severe leukopenia and immunosuppression, leading to secondary enteric or respiratory infections which may cause confusion by masking or overlapping the more typical signs of CSF. The clinical signs of acute CSF become less specific and diagnosis more difficult as the age of onset increases. Also, acute classical swine fever is clinically indistinguishable from African swine fever and so care must be taken when formulating a diagnosis. Other differential diagnoses for acute CSF are [[Erysipelas - Pig|erysipelas]], [[Porcine Reproductive and Respiratory Syndrome|PRRS]], [[Haemorrhage#Purpura|purpura haemorragica]], [[Porcine Circoviruses|PMWS, PDNS]], [[Salmonellosis]] and [[Pasteurellosis - Pigs|Pasteurellosis]]. Classical swine fever should also be considered in any pyrexic enteric or respiratory disease case that is not responsive to antibiotics.  
+
animals is about one week to 10 days. Under field
−
 
+
conditions, symptoms may only become evident in a
−
The '''chronic form''' of classical swine fever develops when pigs fail to mount an effective immune response to viral infection. Initially, the signs are similar to the acute form of the disease, but symptoms become less specific as the course progresses. For example, pigs may display chronic enteritis, loss of condition, lameness or intermittent pyrexia. In a herd, mortality may be increased or there may be large numbers of runty pigs. Although animals may survive some months after contracting chronic CSF, the disease is always eventually fatal and animals continue to shed virus until death.
+
holding 2–4 weeks after virus introduction, or even
−
 
+
later (Laevens et al., 1999). The severity of clinical
−
The course of infection in older, breeding-age animals is often initially subclinical; however, CSFV is able to cross the placenta at any stage of pregnancy. The outcome of transplacental infection is highly dependent on the stage of gestation, and also viral virulence. During early pregnancy, transplacental CSFV infection may cause abortions, mummifications, congenital malformations or stillbirths. Infection occurring after 50-70 days gestation can lead to the birth of persistently viraemic piglets. These may appear clinically normal at birth, but grow poorly and occasionally show congenital tremor. Persistently infected piglets shed virus and act as a reservoir for the virus, making a major contribution to the persistence of infection in the population. It is therefore important to consider classical swine fever as a differential diagnosis of reduced fertility in addition to [[Porcine Parvovirus|parvovirus]], [[Porcine Reproductive and Respiratory Syndrome|PRRS]], [[Leptospirosis - Pigs|leptospirosis]] and [[Suid Herpesvirus 1|Aujeszky's disease]].
+
signs mainly depends on the age of the animal and
 +
the virulence of the virus, and in older breeding pigs
 +
the course of the infection is often mild or subclinical.
 +
The virulence of a CSF virus isolate is difficult
 +
to determine on a rational basis (Mittelholzer
 +
et al., 2000), as the same CSF virus isolate can cause
 +
different forms of CSF depending on age, breed and
 +
immune status of the host animal (Floegel-Niesmann
 +
et al., unpublished observation).
 +
Acute, chronic and prenatal forms of CSF can be
 +
distinguished, and there is no array of classical
 +
symptoms that is invariably associated with the disease.
 +
Piglets up to 12 weeks of age most often display
 +
the acute form. A constant finding is pyrexia, usually
 +
higher than 40 �C, but in adults the temperature
 +
may not exceed 39.5 �C. Initial signs are anorexia,
 +
lethargy, conjunctivitis, enlarged and discoloured
 +
lymph nodes, respiratory signs and constipation
 +
followed by diarrhoea. Neurological signs are frequently
 +
seen, such as a staggering gait with weakness
 +
of hind legs, incoordination of movement, and
 +
convulsions (Fig. 1). The typical haemorrhages of
 +
the skin are usually observed on the ear, tail, abdomen
 +
and the inner side of the limbs during the
 +
second and third week after infection until death.
 +
The virus is shed from the infected animal by saliva,
 +
urine and faeces (Depner et al., 1994; Laevens et al.,
 +
1999).
 +
Pathological changes visible on post mortem examination
 +
are observed most often in lymph nodes,
 +
spleen and kidneys. The lymph nodes become swollen,
 +
oedematous and haemorrhagic (Fig. 2). Haemorrhages
 +
of the kidney may vary in size from petechiae
 +
to ecchymotic haemorrhages. Petechiae can also be
 +
observed in the urinary bladder, larynx, epiglottis and
 +
heart, and may be widespread over the serosae of the
 +
abdomen and chest. A non-purulent encephalitis is
 +
often present (Gruber et al., 1995).
 +
CSF virus causes severe leukopenia and immunosuppression,
 +
which often leads to secondary
 +
Fig. 1. Neurological signs of CSF. The back is hunched
 +
up and the hind legs are pushed under the abdomen.
 +
Wasting and haemorrhages on ears and hind legs are
 +
visible.
 +
Fig. 2. Swollen lymph nodes of the small intestine and
 +
necrosis of the ileocaecal valve (centre).
 +
12 THE VETERINARY JOURNAL, 165, 1
 +
enteric or respiratory infections. The signs of these
 +
secondary infections can mask or overlap the most
 +
typical signs of CSF and may mislead the veterinarian
 +
(Depner et al., 1999).
 +
In general, the acute form of African swine fever
 +
leads to a very similar clinical and pathological picture.
 +
CSF must also be considered in the differential
 +
diagnosis of erysipelas, porcine reproductive and
 +
respiratory syndrome (PRRS), cumarin poisoning,
 +
purpura haemorragica, post-weaning multisystemic
 +
wasting syndrome (PWMS), porcine dermatitis and
 +
nephropathy syndrome (PDNS), Salmonella or
 +
Pasteurella infections or any enteric or respiratory
 +
syndrome with fever not responding to antibiotic
 +
treatment.
 +
With increasing age of the infected pigs (fattening
 +
and breeding animals) the clinical signs are less
 +
specific and recovery with production of antibodies
 +
can occur. Antibodies against CSF virus become
 +
detectable 2–3 weeks postexposure to CSF virus
 +
(Laevens et al., 1998).
 +
CHRONIC COURSE OF CLASSICAL SWINE
 +
FEVER VIRUS INFECTION
 +
The chronic form of CSF is always fatal. It develops
 +
when pigs are not able to mount an effective immune
 +
response against the infection. Initial signs
 +
are similar to die acute infection. Later, predominantly
 +
non-specific signs are observed, e.g. intermittent
 +
fever, chronic enteritis and wasting. Animals
 +
may survive for 2–3 months before they die. CSF
 +
virus is shed from the onset of clinical signs constantly
 +
until death. Antibodies may be temporarily
 +
detected in serum samples, as the immune system
 +
starts to produce antibodies although they are not
 +
able to eliminate the virus from the host. Consequently
 +
the antibodies are neutralised by the virus
 +
and cease to be detectable (Depner et al., 1996).
 +
Pathological changes are less typical, especially the
 +
lack of haemorrhages on organs and serosae. In
 +
animals displaying chronic diarrhoea, necrotic and
 +
ulcerative lesions on the ileum, the ileocaecal valve
 +
and the rectum are common. Since clinical signs of
 +
chronic CSF are rather non-specific, a broad range
 +
of other diseases must be considered as part of any
 +
differential diagnosis.
 +
PRENATAL COURSE OF INFECTION AND
 +
LATE ONSET OF DISEASE
 +
Although the course of infection in the sow is often
 +
subclinical, CSF virus is able to cross the placenta of
 +
pregnant animals, thereby infecting fetuses during
 +
all stages of pregnancy. The outcome of transplacental
 +
infection of fetuses mainly depends on the
 +
time of gestation and viral virulence, respectively.
 +
Infection during early pregnancy may result in
 +
abortions and stillbirths, mummification and malformations.
 +
All of this will lead to a reduction in the
 +
fertility index in the holding.
 +
Infection of sows from about 50–70 days of pregnancy
 +
can lead to the birth of persistently viraemic
 +
piglets, which may be clinically normal at birth and
 +
survive for several months. After birth, theymay show
 +
poor growth, wasting or occasionally congenital tremor.
 +
This course of infection is referred to as �late
 +
onset CSF�. These piglets constantly shed large
 +
amounts of virus and are a dangerous virus reservoir,
 +
spreading the disease and maintaining the infection
 +
within the pig population (Van Oirschot and Terpstra,
 +
1977). This situation is comparable to cattle
 +
persistendy infected with BVD virus.
 +
CSF must be considered in the differential diagnosis
 +
of reduced fertility due to parvovirus infection,
 +
PRRS, leptospirosis and Aujeszky�s disease.
  
 +
===Laboratory Tests===
 
===Pathology===
 
===Pathology===
−
In acute classical swine fever, the major pathological change is multiple haemorrhages. This is seen as many purple blotches in the skin, and as sub-capsular bleeding in association with swelling and oedema in all lymph nodes. A "turkey egg" appearance to the kidneys is displayed, with haemorrhage varying from petechiae to ecchymoses. Haemorrhage may also be seen on any mucosal or serosal surface, including the urinary bladder and the larynx and epiglottis. The heart can be affected, and haemorrhage between other muscles is possible. The lungs are congested and haemorrhagic and often show bronchopneumonia, and straw-coloured fluid accumulates in the thoracic and abdominal cavities and the pericardial sac. A non-suppurative encephalitis can also feature.
+
==Treatment==
−
 
+
====Control====
−
The pathological changes of chronic classical swine fever are generally less typical, and organs and serosae usually lack haemorrhages. Necrotic, ulcerative lesions known as "button ulcers" are commonly seen in the ileum and rectum and at the ileocaecal junction in animals suffering chronic diarrhoea. Joint pathology is another frequent finding. The clinical signs of chronic CSF are non-specific, however and may vary according to secondary infections; this is reflected in the pathological presentation of the disease.
+
*'''NOTIFIABLE''' disease
−
 
+
*'''Vaccination''' (live attenuated) in endemic countries:
−
The most common finding in cases of congenital classical swine fever is CNS pathology, particularly cerebellar hypoplasia.
+
**Parts of EU are using vaccinated bait to control spread in wild boar population
−
 
+
**Vaccination does not curtail spread: marker vaccine needed to distinguish virus exposure from vaccine-induced antibody
−
===Laboratory Tests===
 
−
 
 
−
Laboratory testing is required to confirm a diagnosis of classical swine fever. As well as collection of tissues for histopathology, samples of tonsils, spleen, lymph nodes, kidney and distal ileum are taken for virus detection. Virus may be detected by fluorescent antibody detection, ''in situ'' hybridisation, PCR, immunoperoxidase staining or virus isolation. Several of these methods are reviewed by Moennig<sup>1</sup>, and are briefly summarised here.
 
−
 
 
−
The gold standard laboratory test for CSFV is '''virus isolation in cell culture'''. In viraemic animals, virus may be isolated both from buffy coat cells and from suspensions of spleen, lymph node, tonsil, kidney or parotid salivary glands. Samples are incubated on cultures of porcine cells, and since classical swine fever virus is non-cytopathogenic, anti-CSFV antibodies are used to detect virus. Despite good specificity and sensitivity, the virus isolation process takes around three days and is labour intensive and therefore costly. [[Immunofluorescence|'''Fluorescent antibody testing''']] is less sensitive but more rapid than virus isolation, and involves the used of fluoresecently-labelled anti-CSFV antibodies to demonstrate the presence of virus antigen in tissue. A virus antigen capture [[ELISA testing|'''ELISA''']] also establishes the presence of antigen through the use of specific antibodies, and is useful for screening large numbers of animals.  In the last ten years, it has become possible to detect CSF virus RNA by '''RT-PCR''', usually of the 5' untranslated region. As well as confirming infection, this allows subsequent genetic sequencing and differentiation between isolates.
 
−
 
 
−
Although antigen detection methods have largely replaced serology in the diagnosis of acute classical swine fever outbreaks, CSFV '''serology''' is important for disease surveillance, particularly in wild boar. A virus neutralisation test is the most sensitive and specific form of CSFV serology, and involves incubation of test sera with a CSFV to neutralise any anti-CSFV antibodies present. The virus neutralisation test takes several days, and so an ELISA test may be used when large numbers of samples must be processed urgently.
 
−
 
 
−
==Treatment==
 
−
 
 
−
Classical swine fever is '''controlled rather than treated'''. The policy for control depends on the prevalence of infection in the pig population of a particular country: where CSF is endemic vaccination strategies are commonly used, but outbreaks in the normally CSF-free countries of the EU are controlled by a slaughter policy. This policy aims for eradication of CSFV by "stamping out" infected and neighbouring herds and contacts, imposing movement restrictions and investigating the source and spread of the outbreak. Equipment, footwear and other fomites must be disinfected, and once a herd is depopulated farm buildings and other areas are thoroughly cleaned and disinfected. Effective disinfectants include sodium hydroxide, formalin and washing soda.
 
−
 
 
−
[[Vaccines|Vaccination]] is an effective means of control in areas where classical swine fever is endemic. In the past, the difficulty of distinguishing vaccinated and infected animals precluded the efficient use of a CSF vaccination. Now, however, gene deletion marker vaccines are available, and ELISA tests can be used to differentiate between infected and vaccinated swine.
 
−
 
 
−
Wild boar act as a reservoir of CSF infection, and so control must also be aimed at this population. As well as adequate surveillance, this involves utilising knowledge about factors influencing CSF epidemiology such as wild boar behaviour and population dynamics, and the influence of hunting strategies.  Wild boar vaccination schemes are currently being undertaken in parts of Europe using bait containing marker vaccines.
 
−
 
 
−
{{Learning
 
−
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22Classical+Swine+Fever%22%29+AND+%28title%3A%28transmission%29+OR+title%3A%28pathogenesis%29%29 Classical Swine fever transmission and/or pathogenesis publications]
 
−
 
 
−
[http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22classical+swine+fever%22&occuring1=title&rowId=2&options2=AND&q2=&occuring2=de&rowId=3&options3=AND&q3=&occuring3=freetext&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all&x=42&y=10 Classical Swine Fever publications since 2000]
 
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}}
 
−
 
 
−
==Links==
 
−
 
 
−
* [http://www.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/csf Defra - Classical Swine Fever]
 
−
 
 
−
==References==
 
−
 
 
−
#Moennig, V (2000) '''Introduction to classical swine fever: virus, disease and control policy''', ''Veterinary Microbiology'', 73, 93-102.
 
−
#Moennig, V et al (2003) '''Clinical Signs and Epidemiology of Classical Swine Fever: A Review of New Knowledge''', ''The Veterinary Journal'', 165, 11-20.
 
−
#Paton, DJ and Greiser-Wilke, I (2003) '''Classical swine fever – an update''', ''Research in Veterinary Science'', 75, 169-178.
 
  
 +
==Prognosis==
  
−
{{review}}
+
[[Category:Pestiviruses]][[Category:Pig]]
−
[[Category:Pestiviruses]][[Category:Haemorrhagic Diseases]][[Category:Enteritis,_Viral]][[Category:Enteritis,_Ulcerative]]
+
[[Category:Enteritis,_Viral]][[Category:Enteritis,_Ulcerative]]
−
[[Category:Pig Viruses]][[Category:Lymphoreticular and Haematopoietic Diseases - Pig]][[Category:Neurological Diseases - Pig]][[Category:Dermatological Diseases - Pig]][[Category:Intestinal Diseases - Pig]][[Category:Respiratory Diseases - Pig]][[Category:Musculoskeletal Diseases - Pig]]
+
[[Category:To_Do_-_Lizzie]]
−
[[Category:Brian Aldridge reviewing]]
 
−
[[Category:Cardiology Section]]
 

Revision as of 17:41, 6 August 2010


 This article is still under construction.


Description

Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a Togavirus. Presentation may be actue, sub-acute, chronic or persistent, and the disease is indistinguishable in the field from African Swine Fever. Acutely, classical swine fever is characterised by severe depression, high fever and superficial and internal haemorrhages, with many cases resulting in death. Depression, anorexia and pyrexia are seen in chronic classical swine fever. Transplacental infection is also possible and results in persistently infected piglets.

Aetiology

The causative agent of classical swine fever is a small, enveloped virus of around 40nm diameter. The genome is comprised of single stranded RNA, which is positive sense and contains about 12,300 bases. The sequence of the genome is known, and codes four structural and seven non-structural proteins. The classical swine fever virus is relatively stable in excretions and in fresh meat products including ham, salami and other similar sausages. It is, however, easily inactivated by detergents, common disinfectants and heat.

Classical swine fever virus is a Togavirus within the Pestivirus genus of the Flaviviridae. As such, it is closely related to the bovine viral diarrhoea (BVD) virus of cattle, and the border disease virus of sheep.

Signalment

Domestic pigs and other swine of any age may become infected with classical swine fever.

Transmission and Pathogenesis

In field cases of CSFV, transmission is mainly oronasal by direct or indirect contact with infected pigs. Infected feed or pork products may also cause spread of disease, and transmission in semen can occur. Once the virus gains entry to the host an incubation period of around 7 days ensues, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, classical swine fever virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to further tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also causes a thrombocytopenia which contributes to haemorrhage by impairing primary haemostasis. In acute CSF this angiopathy causes pig death in association with shock and the febrile response. Surviving swine go on to develop a chronic form of the disease where joint and enteric lesions are seen resulting from tissue infarction.

The outcome of transplacental infection of foetuses depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die from CSF.

Diagnosis

Clinical Signs

T et al., 2000). The incubation period in individual animals is about one week to 10 days. Under field conditions, symptoms may only become evident in a holding 2–4 weeks after virus introduction, or even later (Laevens et al., 1999). The severity of clinical signs mainly depends on the age of the animal and the virulence of the virus, and in older breeding pigs the course of the infection is often mild or subclinical. The virulence of a CSF virus isolate is difficult to determine on a rational basis (Mittelholzer et al., 2000), as the same CSF virus isolate can cause different forms of CSF depending on age, breed and immune status of the host animal (Floegel-Niesmann et al., unpublished observation). Acute, chronic and prenatal forms of CSF can be distinguished, and there is no array of classical symptoms that is invariably associated with the disease. Piglets up to 12 weeks of age most often display the acute form. A constant finding is pyrexia, usually higher than 40 �C, but in adults the temperature may not exceed 39.5 �C. Initial signs are anorexia, lethargy, conjunctivitis, enlarged and discoloured lymph nodes, respiratory signs and constipation followed by diarrhoea. Neurological signs are frequently seen, such as a staggering gait with weakness of hind legs, incoordination of movement, and convulsions (Fig. 1). The typical haemorrhages of the skin are usually observed on the ear, tail, abdomen and the inner side of the limbs during the second and third week after infection until death. The virus is shed from the infected animal by saliva, urine and faeces (Depner et al., 1994; Laevens et al., 1999). Pathological changes visible on post mortem examination are observed most often in lymph nodes, spleen and kidneys. The lymph nodes become swollen, oedematous and haemorrhagic (Fig. 2). Haemorrhages of the kidney may vary in size from petechiae to ecchymotic haemorrhages. Petechiae can also be observed in the urinary bladder, larynx, epiglottis and heart, and may be widespread over the serosae of the abdomen and chest. A non-purulent encephalitis is often present (Gruber et al., 1995). CSF virus causes severe leukopenia and immunosuppression, which often leads to secondary Fig. 1. Neurological signs of CSF. The back is hunched up and the hind legs are pushed under the abdomen. Wasting and haemorrhages on ears and hind legs are visible. Fig. 2. Swollen lymph nodes of the small intestine and necrosis of the ileocaecal valve (centre). 12 THE VETERINARY JOURNAL, 165, 1 enteric or respiratory infections. The signs of these secondary infections can mask or overlap the most typical signs of CSF and may mislead the veterinarian (Depner et al., 1999). In general, the acute form of African swine fever leads to a very similar clinical and pathological picture. CSF must also be considered in the differential diagnosis of erysipelas, porcine reproductive and respiratory syndrome (PRRS), cumarin poisoning, purpura haemorragica, post-weaning multisystemic wasting syndrome (PWMS), porcine dermatitis and nephropathy syndrome (PDNS), Salmonella or Pasteurella infections or any enteric or respiratory syndrome with fever not responding to antibiotic treatment. With increasing age of the infected pigs (fattening and breeding animals) the clinical signs are less specific and recovery with production of antibodies can occur. Antibodies against CSF virus become detectable 2–3 weeks postexposure to CSF virus (Laevens et al., 1998). CHRONIC COURSE OF CLASSICAL SWINE FEVER VIRUS INFECTION The chronic form of CSF is always fatal. It develops when pigs are not able to mount an effective immune response against the infection. Initial signs are similar to die acute infection. Later, predominantly non-specific signs are observed, e.g. intermittent fever, chronic enteritis and wasting. Animals may survive for 2–3 months before they die. CSF virus is shed from the onset of clinical signs constantly until death. Antibodies may be temporarily detected in serum samples, as the immune system starts to produce antibodies although they are not able to eliminate the virus from the host. Consequently the antibodies are neutralised by the virus and cease to be detectable (Depner et al., 1996). Pathological changes are less typical, especially the lack of haemorrhages on organs and serosae. In animals displaying chronic diarrhoea, necrotic and ulcerative lesions on the ileum, the ileocaecal valve and the rectum are common. Since clinical signs of chronic CSF are rather non-specific, a broad range of other diseases must be considered as part of any differential diagnosis. PRENATAL COURSE OF INFECTION AND LATE ONSET OF DISEASE Although the course of infection in the sow is often subclinical, CSF virus is able to cross the placenta of pregnant animals, thereby infecting fetuses during all stages of pregnancy. The outcome of transplacental infection of fetuses mainly depends on the time of gestation and viral virulence, respectively. Infection during early pregnancy may result in abortions and stillbirths, mummification and malformations. All of this will lead to a reduction in the fertility index in the holding. Infection of sows from about 50–70 days of pregnancy can lead to the birth of persistently viraemic piglets, which may be clinically normal at birth and survive for several months. After birth, theymay show poor growth, wasting or occasionally congenital tremor. This course of infection is referred to as �late onset CSF�. These piglets constantly shed large amounts of virus and are a dangerous virus reservoir, spreading the disease and maintaining the infection within the pig population (Van Oirschot and Terpstra, 1977). This situation is comparable to cattle persistendy infected with BVD virus. CSF must be considered in the differential diagnosis of reduced fertility due to parvovirus infection, PRRS, leptospirosis and Aujeszky�s disease.

Laboratory Tests

Pathology

Treatment

Control

  • NOTIFIABLE disease
  • Vaccination (live attenuated) in endemic countries:
    • Parts of EU are using vaccinated bait to control spread in wild boar population
    • Vaccination does not curtail spread: marker vaccine needed to distinguish virus exposure from vaccine-induced antibody

Prognosis

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