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→Clinical Signs
==Diagnosis==
==Diagnosis==
===Clinical Signs===
===Clinical Signs===
The main route of infection in field cases is oronasal
by direct or indirect contact with infected pigs or by
feed which is contaminated with virus, e.g., swill. In
areas with a high density of pigs, virus spread easily
occurs between neighbouring pig holdings (Fritzemeierj
et al., 2000). Disease transmission via the
semen of infected boars may also occur (Floegel
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et al., unpublished observation).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===
===Laboratory Tests===
===Pathology===
===Pathology===