Definition
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.
Etiology
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 than 11.
Host Range
The hosts of HCV are the pig and wild boar.
Geographic Distribution
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.
Transmission
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 out.
Incubation Period
The incubation period is usually 3 to 4 days but can range from 2
to 14 days.
Clinical Signs
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 will die.
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.
Gross Lesions
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 (Fig. 66). 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 (Fig. 67). 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 (Fig. 68).
Pinpoint to ecchymotic hemorrhages on the surface of the kidney
are very common in HC (Fig. 69). Such
lesions are easier to see in the decapsulated kidney. Hemorrhages are also found on the
surface of the small and large intestine (Fig. 70), the larynx, the heart, the epiglottis, and the fascia
lata of the back muscles. All serous and mucosal surfaces may have petechial or ecchymotic
hemorrhages.
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.
Diagnosis
Field Diagnosis
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 helpful.
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.
Laboratory Diagnosis
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 eradication program.
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
Differential diagnosis of HC should include African swine fever,
erysipelas, salmonellosis, eperythrozoonosis, and salt poisoning.
Vaccination
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 old.
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 infections.
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.
Public Health
Human beings are not susceptible to HCV infection.
GUIDE TO THE LITERATURE
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Gilles C. Dulac, D.V.M., M.Sc., Ph.D. Animal Diseases Research
Institute, Nepean, Ontario, Canada
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