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Ostali nazivi: svinjska kuga, pestis suis, swine plague, hog cholera,
classical swine fever
Prema odluci Ministarstva poljoprivrede i šumarstva vakcinacija svinja
protiv klasične svinjske kuge spada u javne potrebe u zdravstvenoj zaštiti
Prema istoj odluci sve svinje u dobi od 60 do 90 dana, krmače prije pripusta
a nerastovi dva puta godišnje, moraju biti vakcinirani protiv klasične
svinjske kuge vakcinom pripremljenom od atenuiranog virusa (K-soj), tako da
su stalno imune.
Na farmama s cjelovitim proizvodnim ciklusom prasad se može vakcinirati
najranije u dobi od 45 dana, nazimice i krmače prije pripusta a nerastovi
dva puta godišnje.
Svinje koje se izgoni na zajednicku odnosno sumsku ispasu, kao i divlje
svinje u ograđenim uzgajalištima, moraju prethodno biti vakcinirane i
održavane u stalnom imunitetnom stanju.
U promet se mogu staviti samo imune svinje, odnosno svinje koje su
vakcinirane najmanje sedam dana prije stavljanja u promet.
Promet svinja dopusten je samo na stocnim sajmovima, dogonima i drugim
otkupnim mjestima koja su pod veterinarsko-zdravstvenom kontrolom.
Zbog razlictih okolnosti ta metoda kontrole te zarazne bolesti nije posve
ucinkovita pa se klasicčna svinjska kuga pojavljuje rjeđe ili cesće u
pojedinim područjima Hrvatske. Zbog cijepljenja svinja protiv klasične
svinjske kuge Hrvatska ne može izvoziti svinje i proizvode podrijetlom od
svinjeceg mesa u zemlje Europske unije, pa niti u većinu drugih europskih
zemalja koje ne provode cijepljenje. Cijepljenjem se svake godine obuhvati
manji broj svinja od potrebitog sto taj postupak kontrole te zarazne bolesti
čini izuzetno skupim i nedjelotvornim.
Oblici klasične svinjske kuge
1)tipičan-perakutan,akutan,subakutan i kroničan
2)atipičan-nastaje radi razlike u virulenciji virusa i rezistencije
Inkubacija traje 3 do 6, a najviše 35 dana.
-perakutno:iznenadno ugibanje bez znakova bolesti.
-akutno:bolno i otežano hodanje,zavlače se u stelju,kasnije pareza stražnjeg
djela tijela, tremor, cijanoza rila, ušaka, udova i perineuma, boginjavi
osip po tijelu, nekroza kože.
-sljepljeni kapci,spojnice zažarene ili ikterične, kasnije slepoča,
nerijetko jaka krvarenja iz nosa.
-povračanje, začep se izmjenjuje sa proljevom, nerijetko kašalj, pobačaj
bređih krmača, smrt u komi ili grčevima.
U širenju bolesti veliku ulogu ima promet svinjama. Upravo iz tog razloga
obavezno je cijepljenje svinja prije stavljanja u promet. Svinje ugibaju
iznenada bez osobitih znakova, uz mogućnost pojave slijedećih simptoma:
svinja prestaje jesti, teško hoda, javlja se promuklim glasom, kapci su
slijepljeni, na nosnim otvorima sasušeni sekret. Svinje ugibaju u komi i
Subakutni i kronični tok ovise o sekundarnoj infekciji, i obično je
lokaliziran na dišnom i probavnom sustavu. Letalitet iznosi oko 80-100% u
područjima slobodnim od svinjske kuge. Dijagnoza se temelji na kliničkim
simptomima, epizotiološkim podacima, patoanatomskom nalazu, i laboratorijski
(imunofluorescencija, GDP-test, identifikacija uzročnika, homologni biološki
pokus. Liječenja nema, vrlo je bitna profilaksa sa cjepivom protiv svinjske
Hog cholera (HC) is a highly contagious viral disease of swine that
occurs in an acute, a subacute, a chronic, or a persistent form. In the
acute form, the disease is characterized by high fever, severe depression,
multiple superficial and internal hemorrhages, and high morbidity and
mortality. In the chronic form, the signs of depression, anorexia, and fever
are less severe than in the acute form, and recovery is occasionally seen in
mature animals. Transplacental infection with viral strains of low virulence
often results in persistently infected piglets, which constitute a major
cause of virus dissemination to noninfected farms.
Although minor antigenic variants of hog cholera virus (HCV) have been
reported, there is only one serotype. Hog cholera virus is a lipid-enveloped
pathogen belonging to the family Flaviviridae, genus Pestivirus. The
organism has a close antigenic relationship with the bovine viral diarrhea
virus (BVDV) and the border disease virus (BDV), as demonstrated in the
immunodiffusion and immunofluorescence tests. The serum neutralization test
can, however, differentiate between HCV and BVDV. In a protein-rich
environment, HCV is very stable and can survive for months in refrigerated
meat and for years in frozen meat. The virus is sensitive to drying
(desiccation) and is rapidly inactivated by a pH of less than 3 and greater
The hosts of HCV are the pig and wild boar.
According to the FAO—WHO—OIE Animal Health Yearbook 1989, HC is recognized
in 36 countries and is suspected of being present in another 2. The disease
has been eradicated in Australia, Canada, and the United States. Constant
progress toward eradication has been made in the countries of the European
Economic Community since the guidelines for HC control in individual member
states were accepted in 1980.
The pig is the only natural reservoir of HCV. Blood, tissues, secretions and
excretions from an infected animal contain HCV. Transmission occurs mostly
by the oral route, though infection can occur through the conjunctiva,
mucous membrane, skin abrasion, insemination, and percutaneous blood
transfer (e.g., common needle, contaminated instruments). Airborne
transmission is not thought to be important in the epizootiology of HC, but
such transmission could occur between mechanically ventilated units within
close proximity to each other.
Introduction of infected pigs is the principal source of infection in
HC-free herds. Farming activities such as auction sales, livestock shows,
visits by feed dealers, and rendering trucks are also potential sources of
contagion. Feeding of raw or insufficiently cooked garbage is a potent
source of HCV. During the warm season, HCV may be carried mechanically by
insect vectors that are common to the farm environment. There is no
evidence, however, that HCV replicates in invertebrate vectors. Husbandry
methods also play an important role in HC transmission. Large breeding units
(100 sows) have a higher risk of recycling infection than small herds. In
large breeding units where continuous farrowing is practiced, strains of low
virulence may be perpetuated indefinitely until the cycle is interrupted by
stamping-out procedures and a thorough cleaning and disinfection are carried
The incubation period is usually 3 to 4 days but can range from 2 to 14
The clinical signs of HC are determined by the virulence of the strain and
the susceptibility of the host pigs. Virulent strains cause the acute form
of the disease, whereas strains of low virulence induce a relatively high
proportion of chronic infections that may be inapparent or atypical. These
strains are also responsible for the "carrier-sow" syndrome from which
persistently infected piglets are produced.
Acute Hog Cholera
In acute HC, the pigs look and act sick. Their disease progresses to death
within 10 to 15 days, and remissions are rare. In an affected herd, some
pigs will become drowsy and inactive and will stand with arched backs. Other
pigs will stand with drooping heads and straight tails. Some pigs may vomit
a yellow fluid containing bile. The sick pigs will huddle and pile up on
each other in the warmest corner of the enclosure and will rise only if
prompted vigorously. Anorexia and constipation will accompany a high fever
that may reach 108° F (42.2° C) with an average of 106° F (41.1° C). Pigs
may continue to drink and may have diarrhea toward the end of the disease
process. Conjunctivitis (Fig. 65) is frequent and is manifested by
encrustation of the eyelids and the presence of dirty streaks below the eyes
caused by the accumulation of dust and feed particles. Sick pigs become
gaunt and have a weak, staggering gait related to posterior weakness. In
terminal stages, pigs will become recumbent, and convulsions may occur
shortly before death. In the terminal stage, a purplish discoloration of the
skin may be seen; if present, the lesions are most numerous on the abdomen
and the inner aspects of the thighs.
Chronic Hog Cholera
Chronic HC is characterized by prolonged and intermittent disease periods
with anorexia, fever, alternating diarrhea and constipation, and alopecia. A
chronically infected pig may have a disproportionately large head relative
to the small trunk. These runt pigs may stand with arched backs and their
hind legs placed under the body. Eventually, all chronically infected pigs
Congenital Hog Cholera
Congenital HCV infection by virulent strains will likely result in abortions
or in the birth of diseased pigs that will die shortly after birth.
Transplacental transmission with low-virulence strains may result in
mummification, stillbirth, or the birth of weak and "shaker" pigs.
Malformation of the visceral organs and of the central nervous system occurs
frequently. Some pigs may be born virtually healthy but persistently
infected with HCV. Such infection usually follows exposure of fetuses to HCV
of low virulence in the first trimester of fetal life. Pigs thus infected do
not produce neutralizing antibodies to HVC and have a lifelong viremia. The
pigs may be virtually free of disease for several months before developing
mild anorexia, depression, conjunctivitis, dermatitis, diarrhea, runting,
and locomotive disturbance leading to paresis and death. In breeding herds
affected with lowvirulence strains of HCV, poor reproductive performance may
be the only sign of disease.
Acute Hog Cholera
The most common lesion observed in pigs dying of acute HC is hemorrhage.
Externally, a purplish discoloration of the skin is the first observation.
There may be necrotic foci in the tonsils. Internally, the submandibular and
pharyngeal lymph nodes are the first to be affected and become swollen owing
to edema and hemorrhage. Because of the structure of the pig lymph node,
hemorrhages are located at the periphery of the node. As the disease
progresses, the hemorrhage and edema will spread to other lymph nodes. The
surface of the spleen, and particularly the edge of the organ, may have
raised, dark wedge-shaped areas. These are called splenic infarcts. Infarcts
are frequently observed in pigs infected experimentally with older strains
of HCV but are less commonly seen with the contemporary strains.
Pinpoint to ecchymotic hemorrhages on the surface of the kidney are very
common in HC. Such lesions are easier to see in the decapsulated kidney.
Hemorrhages are also found on the surface of the small and large intestine,
the larynx, the heart, the epiglottis, and the fascia lata of the back
muscles. All serous and mucosal surfaces may have petechial or ecchymotic
Accumulation of straw-colored fluids in the peritoneal and thoracic cavities
and in the pericardial sac may be present.
The lungs are congested and hemorrhagic and have zones of bronchopneumonia.
Chronic Hog Cholera
In chronic HC, the lesions are less severe and are often complicated by
secondary bacterial infections. In the large intestine, button ulcers are an
expression of such a secondary bacterial infection. In growing pigs
surviving for more than 30 days, lesions may be seen at the costochondral
junction of the ribs and at the growth plates of long bones.
Congenital Hog Cholera
In pigs infected transplacentally with HCV strains of low virulence, the
most commonly seen lesions are hypoplasia of the cerebellum, thymus atrophy,
ascites, and deformities of the head and of the limbs. Edema and petechial
hemorrhages of the skin and of the internal organs are seen at the terminal
stage of the disease.
Morbidity and Mortality
In acute HC, the morbidity and mortality are high.
Septicemic conditions in which pigs have high fever should be investigated
carefully. A thorough history from the herd owner should be obtained to
determine if raw garbage was fed, if unusual biological products were used,
or if recent additions were made to the herd. Careful observation of the
clinical signs and of the necropsy lesions should be recorded. In acute HC,
it is helpful to necropsy four or five pigs to increase the probability of
observing the representative lesions.
A marked leukopenia is detectable at the time of initial rise in body
temperature and persists throughout the course of the acute and chronic
disease. This feature was once widely used in the field diagnosis of HC.
Nowadays, with the development of more specific laboratory diagnostic
methods, which are aimed at demonstrating the virus or its structural
antigens in tissues or at detecting specific antibodies in the serum, the
white blood count is not as widely used. In endemic areas it could be
Specimens for Laboratory
For virus isolation and antigen detection, the tonsils are considered
essential. In addition, submandibular and mesenteric lymph nodes, spleen,
kidneys, and the distal part of the ileum should be collected. In live pigs,
tonsil biopsies and whole blood collected with anticoagulants are useful to
diagnose HC. Sample collection should be targeted to pigs having fever or
showing other signs of the disease. Each sample of tissue should be placed
in a separate plastic bag and identified. The samples should not be frozen
(interference with fluorescent antibody tissue section test) but kept at
refrigeration temperature. The material should be transported and stored in
leak-proof containers in accordance with national regulations for
transportation of diagnostic biologic samples.
Serum samples for antibody detection should be collected from animals that
have recovered from suspected infection or from sows known to have been in
contact with infected or suspected cases. A sufficient number of samples
should be collected to ensure a high probability of detecting infection.
A complete set of tissues, including the whole brain, should be submitted in
10 percent buffered formalin.
Any clinical diagnosis of HC must be confirmed by the submission of
specimens to a specialized diagnostic laboratory that should also have the
capability to distinguish between HC and African swine fever.
The laboratory diagnostic procedures for HC have evolved in parallel with
the emergence of new technologies. Until the 1960's, laboratory diagnosis
was restricted to recognition of gross lesions and confirmation by
histopathology. Inoculation of susceptible pigs was often used as final
confirmatory test and to determine the virulence of the viruses. Numerous
laboratory techniques have been described to diagnose HC, but only a few
have gained international acceptance and have been integrated into national
HC control programs. Only these will be discussed in this presentation.
In the fluorescent antibody tissue section test (FATST), direct fluorescent
antibody technique is applied to detect HC viral antigens in frozen tissues
of organs from dead pigs, in biopsy material, or in impression smears.
Theoretically, a diagnosis can be confirmed within hours from the reception
of the specimen. In countries where the disease has been eradicated, the
diagnosis of the "index case" by the FATST alone may be difficult, and
confirmation in cell culture may be needed. The FATST may not differentiate
HC from BVDV infection; an accurate distinction between the two viruses has
to be made before releasing a final diagnosis. Differentiation between HCV
and BVDV can readily be made with the immunoperoxidase test using monoclonal
antibodies or the serum neutralization test.
The isolation of HCV in cell culture and the identification using
fluorescein-labeled hog cholera antibody (fluorescent antibody cell culture
test) can provide confirmation in cases where the results of investigation
of frozen tissue sections are inconclusive.
As control measures for HC are implemented in a country, virulent strains of
HCV will be reduced, and there will be a relative increase of low-virulence
strains. As the proportion of subclinical cases in a national herd
increases, it will become increasingly difficult to recognize the disease.
The antigen detection systems previously described become less effective;
thus, serological tests are essential for a successful control and eventual
Approximately 75 percent of pigs infected with acute HC have microscopic
lesions of an encephalitis characterized by perivascular cuffing,
endothelial proliferation, and microgliosis. This feature is easily
recognized in a nonspecialized diagnostic laboratory and may constitute the
most important single factor that will cause the pathologist to suspect HC.
Differential diagnosis of HC should include African swine fever, erysipelas,
salmonellosis, eperythrozoonosis, and salt poisoning.
Over the years, numerous regimens of vaccination have been advocated with a
variable degree of success. In the past two decades, modified live vaccines
(MLV) with no residual virulence for pigs have become available. The
lapinized Chinese (C) strain, the Japanese guinea pig cell culture-adapted
strain, and the French Thiverval strain have been widely used. All three
strains are considered innocuous for pregnant sows and piglets over 2 weeks
Control and Eradication
In countries where HC is enzootic, a systematic vaccination program is
effective in preventing losses. Experience in the United States and in some
countries of the European Union has proven that a strict regimen of
vaccination will reduce the number of outbreaks to a level at which complete
eradication by sanitary measure alone will be feasible. At that point,
vaccination must be stopped. A successful eradication program requires a
massive input of funds from a central government and cooperation from the
government, the swine industry, and the veterinary profession. Eradication
measures will be assisted by strictly enforcing the garbage cooking laws,
having an effective swine identification system, and using serological
surveys targeted primarily to breeding sows to detect subclinical
In countries where HC has been eradicated and in which the threat of
reintroduction is significant, it is essential to initiate an effective
serological monitoring system. Sampling may be limited to strategic
locations such as the border of an infected neighbor country or be
intensified to target populations such as the garbage-fed herds. Such a
system has been in effect in the United States since successful eradication
in 1976; several thousand samples have been accessed annually.