Classical Swine Fever / Hog Cholera

Classical Swine Fever (CSF), historically known as Hog Cholera, is a highly contagious viral disease of domestic pigs and wild boar caused by the Classical Swine Fever Virus (CSFV), a member of the genus Pestivirus within the family Flaviviridae. This disease represents one of the most economically important diseases of swine worldwide, characterized by fever, hemorrhages, high morbidity, and variable mortality depending on viral strain virulence. CSF is specific to pigs and wild boar and does not infect other species or humans, but its devastating economic impact on affected swine populations and the global pork trade makes it a disease of critical importance for animal health authorities and producers worldwide.

Classical Swine Fever affects all domestic pig breeds and wild boar of all ages, with no species or breed resistance to infection. The disease occurs in three main clinical forms—acute, chronic, and late-onset (congenital)—depending on viral strain virulence, age at infection, and individual animal factors. Young pigs are generally more susceptible to severe disease, while adult pigs may show milder clinical signs with some strains. Wild boar populations serve as important reservoirs for the virus in endemic areas, complicating eradication efforts and posing ongoing risks for reintroduction to domestic pig populations. The disease is present in parts of Central and South America, the Caribbean, Eastern Europe, and Asia, while many developed countries have achieved and maintain disease-free status.

The economic impact of Classical Swine Fever is substantial at both individual operation and national levels. Direct losses from clinical disease include mortality, reduced growth performance, reproductive losses, and costs of veterinary care and diagnostics. However, the indirect economic consequences often exceed direct losses, particularly the trade embargoes imposed on CSF-affected countries by disease-free trading partners. Countries experiencing CSF outbreaks face immediate restrictions on pork exports, potentially costing billions in lost trade revenue. The costs of eradication campaigns, including depopulation, compensation, surveillance, and movement restrictions, impose additional economic burdens. For these reasons, CSF is listed as a notifiable disease by the World Organisation for Animal Health (WOAH), and all member countries are obligated to report confirmed cases.

Treatment of Classical Swine Fever is not practiced, as no specific antiviral therapy exists and affected animals represent an ongoing source of viral shedding. Vaccines are available and effective but are prohibited in disease-free countries and restricted in others due to the interference with surveillance and trade implications of vaccinated animals. Prevention through rigorous biosecurity remains the primary defense for disease-free regions, while endemic countries rely on various combinations of vaccination, surveillance, and movement control. Early detection is absolutely essential, as rapid identification and response can limit outbreak size and facilitate faster return to disease-free status. Any suspicion of CSF must be reported immediately to veterinary authorities, triggering investigation and potential regulatory response.

Classical Swine Fever is caused by the Classical Swine Fever Virus (CSFV), an enveloped, single-stranded RNA virus belonging to the genus Pestivirus within the family Flaviviridae. Other members of this genus include Bovine Viral Diarrhea Virus (BVDV) and Border Disease Virus (BDV) of sheep, with which CSFV shares sufficient antigenic cross-reactivity to complicate some diagnostic tests. CSFV strains are classified into three genotypes (1, 2, and 3) with multiple subgenotypes, showing considerable variation in virulence from highly pathogenic strains causing acute disease with high mortality to low-virulence strains causing chronic or subclinical infections. The virus is moderately stable in the environment and can survive for extended periods in meat products, particularly when chilled or frozen.

Genetic predisposition to CSF resistance does not exist among domestic pig breeds, and all breeds are equally susceptible to infection. European and Asian breeds, commercial hybrid lines, and heritage breeds all experience similar clinical disease when exposed to CSFV of equivalent virulence. Wild boar populations are equally susceptible and play a critical role in disease maintenance and spread in endemic areas, particularly in Europe where wild boar density has increased substantially in recent decades. Some research has explored potential genetic factors influencing disease severity or immune response to vaccination, but no practical applications for breed selection have emerged.

Environmental and management factors significantly influence CSF transmission dynamics and outbreak patterns. The virus spreads primarily through direct contact between infected and susceptible pigs via oronasal secretions, though all bodily fluids and tissues of infected animals contain infectious virus. Indirect transmission occurs through contaminated fomites including vehicles, equipment, clothing, and feed. Feeding of insufficiently heated swill containing infected pork products has been responsible for numerous outbreaks and remains a critical risk factor. Airborne transmission can occur over short distances, particularly in conditions of high humidity and animal density. Contaminated semen can transmit infection, and transplacental transmission from infected sows to fetuses results in persistent infection or reproductive losses.

Risk factors for CSFV introduction and spread include proximity to endemic areas or infected wild boar populations, movement of live pigs and pork products from unknown or affected sources, inadequate biosecurity practices, and swill feeding. Small-scale and backyard pig operations often face heightened risk due to limited biosecurity infrastructure, informal animal trading, and traditional feeding practices. Large commercial operations may have better biosecurity but face greater consequences from disease introduction due to high animal numbers and densities. International travel and trade present ongoing risks through potentially contaminated meat products carried by travelers or illegal imports.

The pathophysiology of CSF involves initial viral replication in tonsillar tissue following oronasal exposure, with subsequent spread to regional lymph nodes and then systemic dissemination via viremia. CSFV has tropism for vascular endothelium, lymphoid tissue, and bone marrow, and infection results in profound immunosuppression due to lymphoid depletion. Vascular damage causes the characteristic hemorrhagic lesions in multiple organs. Thrombocytopenia from bone marrow suppression contributes to bleeding tendencies. In pregnant sows, transplacental infection can result in fetal death, mummification, abortion, or birth of persistently infected piglets that remain viremic for life while appearing clinically normal—these carrier pigs are particularly dangerous for disease spread.

Early warning signs of Classical Swine Fever are often nonspecific and may be overlooked, particularly with low-virulence strains or in the early stages of an outbreak. Initial signs typically include mild fever, transient inappetence, and subtle lethargy that could easily be attributed to many common conditions. Pigs may appear slightly dull or show reduced activity without obvious localizing signs. In breeding herds, early indicators might include scattered reproductive failures or increased returns to estrus. Recognition of these early, subtle signs requires careful observation and a high index of suspicion, particularly in regions where CSF is known to occur or in herds with recent animal introductions.

The classic presentation of acute CSF in domestic pigs involves high fever (40°C to 42°C or 104°F to 108°F), severe depression, huddling, anorexia, and progressive weakness. Affected pigs typically stand with an arched back and tucked abdomen, showing reluctance to move. Conjunctivitis with accumulation of ocular discharge is common. Constipation often occurs early, followed by diarrhea that may become bloody in advanced cases. Respiratory signs including coughing and labored breathing may develop as secondary bacterial pneumonia complicates viral infection. Neurological signs including posterior ataxia, weakness progressing to paralysis, and convulsions may occur, particularly in young pigs.

Behavioral changes associated with CSF are pronounced and can help differentiate this disease from other conditions. Affected pigs typically pile on each other seeking warmth despite high environmental temperatures. They become unresponsive to normal stimuli and show no interest in food or water. Social interactions cease, with sick animals separating from healthy groupmates or remaining stationary while others move about. Pigs that normally respond eagerly to feeding become completely indifferent. These behavioral changes occurring in multiple animals simultaneously, particularly with accompanying fever and hemorrhagic signs, should prompt immediate investigation for CSF.

Physical signs of Classical Swine Fever include characteristic skin lesions ranging from diffuse reddening to discrete hemorrhages. In white-skinned breeds, cyanosis (bluish discoloration) of the ears, tail, snout, and distal limbs is often visible. Petechial hemorrhages (pinpoint red spots) may be visible on the skin, particularly on the ventral abdomen and inner thighs. Hemorrhagic lesions may also occur on mucous membranes of the eyes and mouth. Lymph nodes, particularly those of the head and inguinal regions, may become visibly enlarged. In some cases, button ulcers—characteristic necrotic lesions—develop on the large intestine.

Symptom progression in acute CSF follows a relatively predictable course leading to death within 10 to 20 days in most cases with highly virulent strains. Following the initial febrile phase, hemorrhagic manifestations become more pronounced over several days. Pigs become progressively weaker and more depressed, eventually becoming recumbent and unable to rise. Mortality with highly virulent strains can exceed 90% in naive populations. Subacute forms caused by moderately virulent strains show prolonged illness over 3 to 4 weeks with lower mortality. Chronic CSF presents with persistent, fluctuating illness, intermittent fever, wasting, and poor performance over months. Congenital infections from in utero exposure can result in late-onset tremors, growth retardation, and persistent infection.

Emergency symptoms requiring immediate regulatory notification include sudden death in multiple pigs, high fever affecting numerous animals simultaneously, widespread hemorrhagic skin lesions, bloody diarrhea, and concurrent respiratory and neurological signs. Any combination of these findings should trigger immediate contact with veterinary authorities and regulatory agencies. Given that CSF is a notifiable disease with significant trade implications, producers and veterinarians have legal obligations to report suspect cases promptly. Delay in recognition and reporting can result in catastrophic spread and prolonged recovery periods.

Clinical examination for suspected Classical Swine Fever requires careful assessment of affected animals while maintaining strict biosecurity to prevent potential viral spread. Veterinarians evaluate body temperature, noting the characteristic high fever, and conduct thorough physical examination looking for hemorrhagic lesions, cyanosis, ocular discharge, and neurological abnormalities. Herd history including mortality patterns, recent animal movements, feed sources, and potential wildlife contact provides essential epidemiological context. While clinical signs can be highly suggestive of CSF, particularly in outbreaks with high mortality and hemorrhagic lesions, laboratory confirmation is absolutely essential due to the similarity with other hemorrhagic diseases and the regulatory implications of diagnosis.

Laboratory diagnosis of Classical Swine Fever employs various techniques for virus detection, viral RNA detection, and antibody detection. Reverse transcriptase polymerase chain reaction (RT-PCR) provides rapid and sensitive detection of viral RNA in blood, tissue samples, and oropharyngeal swabs. Virus isolation in cell culture remains a gold standard confirmatory test but requires specialized facilities and is more time-consuming. Antigen detection by immunofluorescence or immunoperoxidase staining can be performed on frozen or fixed tissue sections. Enzyme-linked immunosorbent assay (ELISA) detects both viral antigen and antibodies, with various formats available for screening and confirmation. Sequencing of viral isolates provides epidemiological information for outbreak investigation.

Differential diagnosis for CSF is extensive due to clinical similarities with other important swine diseases. African Swine Fever (ASF) is the primary differential and is clinically and pathologically indistinguishable from CSF, necessitating laboratory testing for both diseases whenever either is suspected. Other differential diagnoses include Porcine Reproductive and Respiratory Syndrome (PRRS), erysipelas, salmonellosis, Aujeszky's disease (pseudorabies), porcine dermatitis and nephropathy syndrome (PDNS), and acute septicemic conditions. The hemorrhagic and febrile nature of CSF also requires differentiation from warfarin poisoning and other causes of coagulopathy. Postmortem findings including splenic infarcts, button ulcers in the cecum and colon, and widespread petechial hemorrhages are suggestive but not pathognomonic.

Herd-level diagnostics and surveillance programs are essential components of CSF control, eradication, and proof of freedom. Active surveillance involves systematic sampling of pig populations at slaughter, in high-risk areas, and in wild boar populations. Passive surveillance relies on investigation of clinical cases and suspicious mortality events reported by producers and veterinarians. Seroprevalence surveys help assess disease distribution and inform control strategies. Following confirmed outbreaks, intensive surveillance in surrounding areas determines the extent of viral spread. In countries pursuing or maintaining disease-free status, ongoing surveillance programs provide evidence to support trade negotiations and disease-free declarations.

There is no specific treatment or cure for Classical Swine Fever, and treatment of infected animals is neither practiced nor permitted under disease control regulations in most jurisdictions. The absence of effective antiviral therapy, combined with the regulatory status of CSF as a notifiable disease, means that affected herds are managed through containment and depopulation rather than therapeutic intervention. Experimental antiviral approaches have been explored in research settings but have not yielded clinically applicable treatments. The priority upon CSF confirmation shifts immediately from individual animal care to preventing further viral spread and eliminating sources of infection.

Emergency response to suspected or confirmed CSF cases follows established regulatory protocols focused on containment, epidemiological investigation, and disease elimination. Upon reporting of suspect cases, veterinary authorities implement immediate movement standstill on the affected premises pending diagnostic testing. Confirmed cases trigger establishment of protection and surveillance zones around affected farms, with strict movement restrictions on pigs, pork products, and potentially contaminated materials. Epidemiological investigation traces animal movements, feed sources, and contacts to identify the source of infection and potential spread to other premises. International notification through WOAH alerts trading partners and neighboring countries.

Medical management of CSF is not undertaken because treatment would prolong viral shedding, increase transmission risk, and conflict with disease control objectives. Supportive care of affected animals is generally not provided except in limited circumstances where regulatory authorities approve delayed culling to gather additional diagnostic information or manage logistical constraints. Anti-inflammatory drugs may be administered for animal welfare purposes while awaiting culling, but this does not constitute treatment aimed at recovery. Euthanasia methods must be humane and conducted by trained personnel in accordance with regulatory requirements.

Depopulation (stamping out) of infected and contact herds is the standard approach for CSF eradication in disease-free or newly infected regions. All pigs on infected premises are killed using approved humane methods, typically carbon dioxide, captive bolt, or electrical stunning followed by exsanguination or adjunctive methods. Carcasses are disposed of through rendering, burial, or incineration according to regulatory guidelines and local capacity. Depopulation of pigs within defined protection zones may be required depending on outbreak circumstances. Cleaning and disinfection of premises follows established protocols to eliminate environmental contamination before potential restocking.

Vaccination plays a complex role in CSF management, with its use prohibited, restricted, or actively employed depending on disease status and control strategy. Disease-free countries typically prohibit CSF vaccination to maintain surveillance integrity and avoid trade complications from seropositive animals. In endemic areas, vaccination is used to reduce clinical disease and viral circulation, though it does not prevent infection or eliminate the virus from populations. Emergency vaccination may be employed in outbreak situations to reduce viral transmission and limit spread, particularly when depopulation alone is insufficient. Marker vaccines (DIVA vaccines) that allow differentiation of vaccinated from infected animals are available and facilitate eradication programs that combine vaccination with surveillance.

Treatment decisions in CSF situations fundamentally differ from typical veterinary medical decision-making because the response is regulatory rather than clinical. Producers facing CSF have no treatment options to consider; instead, they must comply with mandatory reporting, movement restrictions, and depopulation orders. The economic consequences are managed through compensation programs in most countries, with payments for culled animals partially offsetting losses. Insurance options for CSF-related losses vary by market. The focus for affected producers shifts to working with regulatory authorities, accessing available support programs, and planning for eventual business recovery following successful disease elimination.

Recovery from Classical Swine Fever at the individual animal level is possible with low-virulence strains, though survivors often suffer permanent effects and may remain chronically infected with ongoing viral shedding. Pigs that survive acute CSF may show stunted growth, poor feed efficiency, and increased susceptibility to secondary infections. Chronically infected animals experience prolonged illness with intermittent fever, progressive wasting, and poor performance over weeks to months. Persistently infected pigs born from in utero exposure appear healthy initially but remain viremic for life and shed virus continuously, representing a major threat for disease spread. For these reasons, recovery and retention of individual animals is not a management goal.

Recovery at the farm level following CSF depopulation requires thorough decontamination before restocking can be considered. The CSFV virus is susceptible to most common disinfectants including sodium hypochlorite, quaternary ammonium compounds, and various oxidizing agents, but thorough cleaning to remove organic matter must precede disinfection. All organic material must be removed from facilities, including feed, bedding, manure, and biological residues. Particular attention is required for porous surfaces, drainage systems, and areas where organic matter accumulates. Environmental persistence of the virus, while limited compared to some other pathogens, still requires appropriate downtime before restocking.

Prognosis for herd and regional recovery depends on outbreak magnitude, effectiveness of control measures, and success of decontamination efforts. Small, rapidly contained outbreaks in well-defined areas have better prospects for quick recovery than large, prolonged outbreaks affecting multiple premises. Involvement of wild boar populations significantly complicates recovery, as elimination of sylvatic infection is extremely difficult and may take years. Financial recovery depends on compensation levels, insurance coverage, and the producer's ability to sustain operations during the extended period without production. Return to export markets requires demonstration of disease freedom through surveillance and negotiation with trading partners.

Return to production following CSF eradication requires regulatory approval based on successful decontamination and appropriate sentinel testing. Following cleaning and disinfection, premises typically undergo an extended downtime period before restocking authorization. Introduction of sentinel animals with intensive monitoring confirms decontamination success. Ongoing surveillance requirements may apply to restocked premises and the surrounding area. For countries recovering from CSF outbreaks, restoration of disease-free status and normalization of trade relationships can take years of sustained surveillance and diplomatic effort.

Vaccination against Classical Swine Fever is highly effective at preventing clinical disease and reducing viral shedding but has complex policy implications that vary by country and disease status. Modified live virus (MLV) vaccines using attenuated CSFV strains provide robust, long-lasting immunity and have been used extensively for disease control. However, conventional vaccines produce antibodies indistinguishable from natural infection, complicating surveillance and affecting trade eligibility. Marker vaccines (DIVA vaccines) use viral constructs that allow serological differentiation between vaccinated and infected animals, enabling their use in eradication programs. Vaccination is prohibited in disease-free countries like the United States and much of the European Union to avoid surveillance interference, while endemic countries employ vaccination as a primary control measure.

Biosecurity measures form the cornerstone of CSF prevention for disease-free regions and herds. Strict control of animal introductions, with sourcing only from known CSF-free origins and appropriate quarantine and testing, prevents introduction through live animals. Prohibition of swill feeding and control of feed ingredient sources eliminate a major transmission route. Perimeter security prevents contact with wild boar populations that might harbor infection. Vehicle and equipment biosecurity, including cleaning and disinfection protocols and restriction of farm-specific equipment, prevents fomite transmission. Personnel biosecurity measures including farm-specific clothing, shower protocols, and restrictions on contact with other pig populations reduce human-mediated transmission risk.

Nutritional aspects of CSF prevention center on feed biosecurity rather than nutritional immunity. The absolute prohibition of feeding food waste containing pork products to pigs is critical, as swill feeding has been responsible for numerous CSF introductions over decades. Commercial feed should be sourced from suppliers with appropriate biosecurity measures and quality control. Feed storage must prevent contamination by wildlife, particularly in areas where wild boar may harbor infection. Some countries have implemented requirements for heat treatment or extended storage of feed ingredients as additional safeguards against viral survival.

Management practices for CSF prevention integrate biosecurity with operational procedures throughout the production system. All-in-all-out production reduces opportunities for transmission between groups and allows thorough cleaning and disinfection. Controlled animal sourcing and closed herd management minimize introduction risks. Personnel training ensures understanding and consistent implementation of biosecurity protocols. Visitor restrictions and documentation of farm access support both prevention and epidemiological investigation if needed. Dead animal disposal prevents scavenging that could spread infection, and manure management considers the potential for viral persistence and transmission.

Quarantine and testing protocols provide essential safeguards for animal movements and trade. Animals introduced to herds should undergo quarantine with health monitoring and appropriate testing before mixing with resident animals. Export and import requirements for live pigs include health certification and testing from accredited laboratories. Slaughter surveillance programs provide ongoing monitoring of disease status in pig populations. Wild boar surveillance through hunter-harvested samples and carcass monitoring is essential in regions where these populations may maintain infection. International cooperation and information sharing support global efforts to control CSF spread.

Daily management and monitoring for CSF prevention requires systematic health observation and prompt investigation of abnormalities. Daily checks should assess animals of all ages for fever, depression, respiratory signs, diarrhea, and skin lesions. Mortality recording and investigation, including diagnostic testing of unexplained deaths, enables early detection of disease incursion. Feed and water consumption monitoring at the group level can detect early signs of illness before clinical signs become obvious. Staff training in CSF recognition ensures that observations are interpreted appropriately and suspicious findings are reported immediately. Documentation of daily health observations supports both routine management and potential outbreak investigation.

Housing and environmental management contribute to CSF prevention by reducing exposure opportunities and supporting overall animal health. Facility design should incorporate biosecurity features including separation from public access, controlled entry points, and physical barriers between production areas. Perimeter fencing adequate to exclude wild boar is essential in regions where these populations may harbor infection. Proper ventilation, temperature control, and stocking densities support immune function and reduce stress. Cleaning and disinfection protocols between production groups eliminate potential pathogen accumulation. Environmental monitoring for wildlife intrusion or security breaches enables prompt corrective action.

Herd health programs in CSF-aware operations integrate disease prevention with overall health management. Regular veterinary involvement includes health assessments, review of production records, and guidance on biosecurity measures. Diagnostic testing protocols may include periodic surveillance testing in high-risk areas or following concerning clinical observations. Vaccination programs for other diseases support overall herd immunity and reduce clinical signs that could mask or be confused with CSF. Records of animal movements, health events, and production parameters support both routine management and outbreak investigation if needed.

Record keeping and monitoring systems provide essential documentation for CSF preparedness and response. Animal movement records enable rapid trace-back and trace-forward investigation if disease is detected. Health records documenting mortality, morbidity, and treatments support early detection of unusual disease patterns. Biosecurity logs recording personnel entry, visitors, vehicle movements, and incoming materials provide information for epidemiological investigation. Production records including growth rates, feed conversion, and reproductive performance can reveal subtle changes that might indicate subclinical disease. Digital record systems facilitate rapid analysis and reporting when needed.

Economic considerations for CSF prevention must balance biosecurity investments against disease risk and consequences. Initial capital costs for facility upgrades, fencing, and biosecurity infrastructure may be substantial but are justified by the catastrophic potential losses from CSF. Ongoing operational costs include staff time for biosecurity procedures, cleaning and disinfection supplies, and potentially higher costs for controlled animal and feed sourcing. Insurance options for CSF losses are limited in many markets, emphasizing the importance of prevention. Industry participation in regional biosecurity initiatives and surveillance programs provides collective benefits beyond individual farm protection.

All breeds of domestic pigs are fully susceptible to Classical Swine Fever without genetic variation in resistance. Commercial breeds including Large White, Landrace, Duroc, Pietrain, Hampshire, and their crosses experience similar clinical disease when infected with CSFV. Heritage breeds, indigenous breeds from various regions, and miniature pig varieties are equally susceptible. Wild boar throughout their global range are also fully susceptible and play important roles in disease maintenance in endemic areas. The universal susceptibility of pig genetics to CSF means that breed selection cannot serve as a prevention strategy, and control relies entirely on biosecurity, surveillance, and vaccination where permitted.

Production type influences CSF risk primarily through management factors and operational practices rather than inherent differences in susceptibility. Large commercial operations typically implement more comprehensive biosecurity measures but face severe consequences from disease introduction due to high animal numbers and densities that facilitate rapid within-herd spread. Small-scale and backyard pig production often operates with limited biosecurity infrastructure and may involve practices such as swill feeding that increase disease risk. Outdoor and free-range production systems face challenges in preventing contact with potentially infected wild boar. Breeding operations with frequent animal movements and multi-source introductions have higher exposure potential than closed commercial herds.

Genetic selection for CSF resistance is not currently feasible, and prevention relies on non-genetic approaches. Research has explored immune response variations following infection and vaccination, but no markers for resistance or enhanced protection have been identified for practical breeding applications. Some studies have investigated genetic factors influencing antibody responses to vaccination, which could potentially inform selection for improved vaccine efficacy, but these remain research findings rather than implementable strategies. Breeding programs in pigs focus on production traits, meat quality, and disease resistance for endemic pathogens rather than CSF resistance, while CSF control continues to depend on management interventions, vaccination where used, and progress toward regional elimination.

African Swine Fever (ASF) is the primary differential diagnosis for Classical Swine Fever and is clinically indistinguishable from CSF in the field. Both diseases cause high fever, depression, hemorrhagic lesions, and high mortality in pig populations. Laboratory testing is absolutely essential to differentiate these two diseases, and samples should routinely be submitted for both diagnostic panels when hemorrhagic disease is suspected in pigs. Unlike CSF, ASF currently has no approved vaccine, and the viruses are unrelated—CSF is caused by a pestivirus while ASF is caused by an asfarvirus. The concurrent consideration of both diseases is critical for appropriate response and regulatory notification.

Other conditions with overlapping clinical presentations include Porcine Reproductive and Respiratory Syndrome (PRRS), erysipelas, salmonellosis, Aujeszky's disease (pseudorabies), and porcine dermatitis and nephropathy syndrome (PDNS). PRRS causes reproductive failure and respiratory disease but typically with less dramatic hemorrhagic manifestations. Acute erysipelas can cause fever, skin lesions, and sudden death but usually affects scattered individuals rather than causing herd-wide epidemics. Thrombocytopenic conditions from various causes can produce hemorrhagic signs requiring differentiation. Toxic causes of sudden death and bleeding, including warfarin poisoning, should be considered in appropriate circumstances.

Complications and sequelae of CSF in surviving animals include chronic wasting syndrome, secondary bacterial infections, and persistent viremia in congenitally infected pigs. Survivors of acute disease often show poor growth performance and increased susceptibility to other pathogens due to CSF-induced immunosuppression. Reproductive sequelae in breeding herds include prolonged infertility and ongoing reproductive losses. Persistently infected pigs born from in utero exposure represent a particularly dangerous complication, as they appear healthy but shed virus continuously, potentially sustaining transmission in herds that believe they have recovered. Regional complications include establishment of endemic infection in wild boar populations, which can perpetuate viral circulation for years and continually threaten reinfection of domestic pigs.