How does hog cholera spread

In older breeding pigs the course of the infection is often mild or even subclinical. The symptoms are indistinguishable from those of African swine fever. EU information on Classical Swine Fever.

A list of data of potential antiviral agents interfering with membrane binding, genome replication or gene silencing siRNA specific inhibiting either CSFV or morbilliviruses was created. Reference material for PCR validation was produced. A list of validated, functional real-time RT-PCR assays useful for the sensitive, specific and robust detection of CSFV based on information of collected data has been compiled and summarized in a review article.

Genetic DIVA based on detection and differentiation of nucleic acid from some of the major live vaccines and wild-type CSFV have been implemented and partly validated.

Intervention Strategies A better knowledge of the functional states cytokines, chemokines, co-stimulatory molecules etc. Viruses used for the in vitroand in vivo infection experiments included classical swine fever virus CSFV , Experimental investigations continued to characterize the role of T cells and antigen presenting cells in different infection models including CSFV. The results of this reporting period contribute to a better understanding of the immune response to diseases caused by epizootic infections and to the characterization of immune correlates of protection against these diseases.

The complex use of DIVA vaccines in eradication of animal diseases from an endemic or epidemic situation has been evaluated based on demands and evaluation of CSF vaccines from a European perspective and has been discussed in a draft paper A list of data of potential antiviral agents interfering with membrane binding, genome replication or gene silencing siRNA specific inhibiting either CSFV or morbilliviruses was created.

Supplementary data from experimental infections on a wide variety of CSFV strains and data from clinical suspicions in the field are gathered to improve the system and turn it into an international hand held, computer aided system for easier and more uniform field clinical evaluation.

Risk Assessment Evaluation of a technical aid that helps to assess the risk that classical swine fever is present in a herd. In pig houses, excreta and bedding, virus can persist for days to weeks, depending upon temperatures. The virus survives some curing processes as well as in frozen pork for months to years, and in chilled meats for months. Classical swine fever is highly contagious and infection spreads rapidly by direct or indirect contact between infected and susceptible pigs.

Pigs with acute infection shed large amounts of virus before they are visibly ill, during illness, and after recovery. Live pigs infected as fetuses spread virus in their secretions and excretions. Uncooked waste food containing infectious pork scraps and subsequently fed to pigs has been well documented as initiating many outbreaks. Other methods of viral spread include farm equipment contaminated wagons, trucks, tractors, machinery , personnel careless farmers, salesmen, veterinarians , fomites, pets, birds and arthropods.

Airborne transmission probably is of little significance. After ingestion, the virus infects epithelial cells in the crypts of tonsils, spreads to adjacent lymph nodes and produces viremia within 24 hrs. Tonsils are the initial site of viral replication. Within three to four days, virus spreads to many epithelial-type cells and is present in excretions and secretions.

The virus causes lymphoid depletion which makes the swine more susceptible to other infections. Bone marrow damage leads to leukopenia and thrombocytopenia.

Thrombocytopenia, along with endothelial cell damage, results in petechial and ecchymotic hemorrhages at many sites. Swine with chronic CSF infection may develop glomerulonephritis from antigen-antibody complexes that damage glomeruli.

In pregnant sows and gilts, the virus may cross the placenta and infect some or all of the fetuses. The effect depends on the stage of pregnancy and can include abortion or production of mummified fetuses, stillborn piglets, or persistently infected live piglets. Fetal anomalies may result from in utero infection; a remarkable one is hypomyelinogenesis, a syndrome that results in shaking piglets myoclonia congenita.

In typical acute outbreaks, clinical signs are nonspecific. There may be diarrhea or constipation, and perhaps vomiting. Most affected pigs die within three weeks of onset. Outbreaks with less virulent virus or chronic cases seldom present with typical signs but often have conjunctivitis, diarrhea or constipation, and some degree of emaciation. Mildly virulent strains of the virus seem to be becoming more prevalent worldwide and present a significant opportunity for misdiagnosis by those veterinarians and producers unfamiliar with the disease.

Pigs infected as fetuses or neonates may present no signs. In typical acute CSF, lesions include petechial and ecchymotic hemorrhages at several common sites including the epiglottis, bladder mucosa, cortex and pelvis of the kidneys, gall bladder mucosa, on the lungs and heart, at the ileocecal junction and in the skin. Lesions sometimes considered of special value in diagnosis include single or multiple infarcts along the border of a spleen of normal size, subcapsular hemorrhage in many lymph nodes, and hemorrhages on the cortices of the kidneys and on the lungs.

There usually is some degree of congestion in the fundus of the stomach and small intestine. Small foci of necrosis may be present in the tonsils. Peracute cases may have no lesions. Grossly visible fetal lesions include ascites, hepatic nodularity, pulmonary hypoplasia, petechiation of the skin, microencephaly, hydrocephalus and cerebellar hypoplasia.

Microscopically, there is a panencephalitis more apparent in the medulla, pons, midbrain or thalamus. Glial cell nodules often cluster around destroyed capillaries. Vascular lesions are present at many sites, perhaps more pronounced in splenic follicular arteries.

Typical acute CSF should be suspected on the basis of history, clinical signs, temperatures and gross lesions. Numerous postmortem examinations will increase the accuracy of diagnosis.

Leucopenia in several suspected cases is suggestive of CSF. The lesions of typical, acute cholera closely resemble and must be carefully differentiated from those of African swine fever, acute salmonellosis and acute swine erysipelas. Infection with mildly virulent strains may be indistinguishable from many endemic systemic or respiratory pathogens.

Diagnostic testing is imperative whenever the combination of gross pathology, clinical signs, and response to therapy suggest that CSF is on the list of possible etiologies. Suspected outbreaks should be immediately reported to authorities to confirm diagnosis. Three laboratory procedures commonly used are: demonstration of CSF viral antigen in frozen tissue sections by immunoflorescence with preferred tissues being tonsil, pharyngeal lymph nodes, spleen, kidney and distal ileum; isolation of virus in cell culture and identification of viral antigen in the culture by the fluorescent antibody FA test; and identification of antibodies to CSF by virus neutralization tests.

A monoclonal antibody technique is available.