Difference between revisions of "Classical Swine Fever"

From WikiVet English
Jump to navigation Jump to search
 
(65 intermediate revisions by 4 users not shown)
Line 1: Line 1:
{{unfinished}}
+
Also known as: '''''CSF — Hog Cholera — Pig Plague — CSFV
  
==Description==
+
==Introduction==
 
+
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.
  
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 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.
 
 
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.
+
Domestic pigs and other swine of any age may become infected with classical swine fever virus.
 
 
==Pathogenesis==
 
  
After transmission by direct spread or by aerosol, classical swine fever virus gains entry to the host via mucous membranes or skin abrasions. 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.
+
==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.
  
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.
+
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.
  
 
==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===
The main route of infection in field cases is oronasal
+
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.
by direct or indirect contact with infected pigs or by
+
 
feed which is contaminated with virus, e.g., swill. In
+
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.  
areas with a high density of pigs, virus spread easily
+
 
occurs between neighbouring pig holdings (Fritzemeierj
+
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.
et al., 2000). Disease transmission via the
+
 
semen of infected boars may also occur (Floegel
+
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]].
et al., 2000). The incubation period in individual
+
 
animals is about one week to 10 days. Under field
+
===Pathology===
conditions, symptoms may only become evident in a
+
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.
holding 2–4 weeks after virus introduction, or even
+
 
later (Laevens et al., 1999). The severity of clinical
+
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.
signs mainly depends on the age of the animal and
+
 
the virulence of the virus, and in older breeding pigs
+
The most common finding in cases of congenital classical swine fever is CNS pathology, particularly cerebellar hypoplasia.
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===
 
===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==
+
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]
 +
}}
 +
 
 +
==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.
 +
 
  
[[Category:Pestiviruses]][[Category:Pig]]
+
{{review}}
[[Category:Enteritis,_Viral]][[Category:Enteritis,_Ulcerative]]
+
[[Category:Pestiviruses]][[Category:Haemorrhagic Diseases]][[Category:Enteritis,_Viral]][[Category:Enteritis,_Ulcerative]]
[[Category:To_Do_-_Lizzie]]
+
[[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:Brian Aldridge reviewing]]
 +
[[Category:Cardiology Section]]

Latest revision as of 14:57, 15 October 2013

Also known as: CSF — Hog Cholera — Pig Plague — CSFV

Introduction

Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a 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.

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 (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 virus.

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 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.

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.

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

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.

In the acute form, animals are almost always pyrexic. In piglets the fever may exceed 400C, but in adults temperatures may be no higher than 39.50C. 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, PRRS, purpura haemorragica, PMWS, PDNS, Salmonellosis and Pasteurellosis. Classical swine fever should also be considered in any pyrexic enteric or respiratory disease case that is not responsive to antibiotics.

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.

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 parvovirus, PRRS, leptospirosis and Aujeszky's disease.

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.

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.

The most common finding in cases of congenital classical swine fever is CNS pathology, particularly cerebellar hypoplasia.

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 Moennig1, 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. 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 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.

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.


Classical Swine Fever Learning Resources
CABICABI logo.jpg
Literature Search
Search for recent publications via CAB Abstract
(CABI log in required)
Classical Swine fever transmission and/or pathogenesis publications

Classical Swine Fever publications since 2000


Links

References

  1. Moennig, V (2000) Introduction to classical swine fever: virus, disease and control policy, Veterinary Microbiology, 73, 93-102.
  2. Moennig, V et al (2003) Clinical Signs and Epidemiology of Classical Swine Fever: A Review of New Knowledge, The Veterinary Journal, 165, 11-20.
  3. Paton, DJ and Greiser-Wilke, I (2003) Classical swine fever – an update, Research in Veterinary Science, 75, 169-178.