Aujeszky's Disease / Pseudorabies

Aujeszky's Disease, commonly known as Pseudorabies, is a highly contagious viral disease of pigs caused by Suid Herpesvirus 1 (SuHV-1), a member of the family Herpesviridae. Despite its name, pseudorabies is not related to the rabies virus but was named for the similar intense pruritus (itching) and neurological signs it causes in non-porcine species. In pigs, the disease manifests primarily as a respiratory infection in older animals and devastating neurological disease in piglets, with reproductive failure occurring in breeding herds. Pigs are the only natural reservoir host and can survive infection to become lifelong latent carriers, while other species including cattle, sheep, dogs, cats, and various wildlife invariably die from infection.

Aujeszky's Disease affects domestic pigs of all breeds and ages, though clinical manifestations and mortality rates vary dramatically based on age at infection. Neonatal piglets under two weeks of age experience mortality rates approaching 100%, while weaned pigs and growing-finishing pigs typically show respiratory disease with much lower mortality. Adult breeding animals may show minimal clinical signs but can experience reproductive losses including abortion, stillbirth, and mummified fetuses. Wild boar populations serve as a reservoir for the virus in many regions, complicating eradication efforts and posing ongoing risk to domestic pig populations. The disease has been successfully eradicated from domestic pig populations in many developed countries through vaccination and test-and-removal programs.

The economic impact of Aujeszky's Disease in affected swine populations is substantial and multifaceted. Direct production losses include piglet mortality, reduced growth performance in growing pigs, reproductive losses in breeding herds, and increased medication costs for secondary infections. Perhaps more significantly, Aujeszky's Disease status affects international trade in pigs and pork products, with disease-free countries maintaining import restrictions against affected regions. Countries that have achieved eradication, including the United States, Canada, and most of the European Union, have invested heavily in surveillance to maintain disease-free status. For affected countries, the economic burden includes both production losses and exclusion from premium export markets.

Aujeszky's Disease is treatable only in the sense that supportive care may help older pigs survive respiratory infection, but no specific antiviral therapy exists. Prevention through vaccination is highly effective at reducing clinical disease and viral shedding, and marker vaccines allow serological differentiation between vaccinated and infected animals, enabling continued eradication efforts in vaccinated populations. Early detection remains critically important for control efforts, as latently infected carrier pigs can reactivate viral shedding during stress and introduce infection to naive populations. In countries where the disease remains present, comprehensive vaccination programs combined with biosecurity measures are essential for controlling losses. The disease is notifiable in many jurisdictions, requiring reporting to veterinary authorities upon diagnosis.

Aujeszky's Disease is caused by Suid Herpesvirus 1 (SuHV-1), also known as Pseudorabies Virus (PRV), a double-stranded DNA virus belonging to the subfamily Alphaherpesvirinae within the family Herpesviridae. This subfamily also includes other significant animal pathogens such as bovine herpesvirus 1 (infectious bovine rhinotracheitis), equine herpesvirus 1, and the human pathogens herpes simplex virus and varicella-zoster virus. Like all alphaherpesviruses, SuHV-1 establishes latent infection in sensory nerve ganglia following primary infection, allowing the virus to persist in recovered animals for life with periodic reactivation and shedding. Multiple strains of varying virulence exist globally, with genetic variations affecting pathogenicity and tissue tropism.

There is no recognized genetic resistance to Aujeszky's Disease among domestic pig breeds, and all breeds are considered equally susceptible to infection. However, genetic factors may influence the severity of clinical disease and the likelihood of survival following infection. Research has investigated potential genetic markers associated with resistance or tolerance to PRV infection, but no practical applications for breed selection have emerged. Wild boar populations are equally susceptible to infection and play an important role in viral maintenance in endemic areas, particularly in Europe and Asia where wild boar populations overlap with outdoor or free-range pig production systems.

Environmental and management factors significantly influence the transmission dynamics and clinical impact of Aujeszky's Disease in pig populations. The virus spreads primarily through direct nose-to-nose contact between infected and susceptible pigs, with infectious virus present in nasal secretions, saliva, and respiratory aerosols. Venereal transmission can occur through infected semen, and vertical transmission from infected sows to piglets occurs both in utero and during nursing. The virus can survive in the environment for variable periods depending on temperature and humidity, with longer survival in cool, moist conditions. Contaminated equipment, vehicles, and clothing can serve as fomites for mechanical transmission.

Risk factors for PRV infection and clinical disease include age at exposure, immune status, concurrent diseases, and stocking density. Neonatal piglets lacking maternal antibody protection are at highest risk for severe disease and death. Immunosuppression from other infections or stressors can increase susceptibility and clinical severity in older pigs. High-density housing and continuous-flow production systems facilitate viral transmission and expose large numbers of susceptible animals. Introduction of new animals, particularly from unknown disease status sources, represents a significant risk for herd introduction. Contact with wild boar through inadequate fencing or outdoor production increases exposure risk in endemic areas.

The pathophysiology of Aujeszky's Disease involves initial viral replication in the upper respiratory tract epithelium following oronasal exposure. From this primary site, the virus spreads via sensory nerves to the trigeminal ganglia and subsequently to the central nervous system, causing the characteristic neurological disease. Viremia occurs in severely affected animals, allowing dissemination to multiple organs including the lungs, liver, spleen, and reproductive tract. In pregnant sows, transplacental infection results in fetal death, mummification, or the birth of weak, viremic piglets. Following recovery from acute infection, the virus establishes latency in trigeminal ganglia neurons, where it persists indefinitely with potential for reactivation during stress, immunosuppression, or administration of corticosteroids.

Early warning signs of Aujeszky's Disease vary considerably depending on the age and immune status of affected pigs, with initial signs often subtle and easily attributed to other common conditions. In breeding herds experiencing first-time infection, early indicators may include scattered reproductive failures, increased returns to estrus, or subtle respiratory illness in finishing pigs. Sows in early gestation may resorb embryos without obvious clinical signs. Grower-finisher pigs may show mild sneezing, nasal discharge, or transient inappetence that could be mistaken for endemic respiratory diseases. Observation of any unexplained illness in herds with unknown or negative PRV status warrants diagnostic investigation.

The classic clinical presentation of Aujeszky's Disease in neonatal piglets involves acute onset of severe neurological signs followed rapidly by death. Affected piglets may show tremors, paddling, opisthotonus (backward arching of the head and spine), and convulsions. They typically display hyperthermia, become progressively unresponsive, and die within 24 to 48 hours of initial signs. Mortality in piglets under two weeks of age approaches 100% in naive populations. Piglets that survive may show permanent neurological deficits. Litters from naive sows experiencing primary infection during late gestation may be born weak, fail to nurse, and die rapidly.

Respiratory disease predominates in weaned and growing pigs, with severity inversely related to age at infection. Clinical signs include sneezing, coughing, nasal discharge, labored breathing, and fever ranging from 40°C to 42°C (104°F to 108°F). Anorexia and depression are common, with affected pigs huddling or isolating from groupmates. Secondary bacterial infections frequently complicate viral pneumonia, resulting in persistent respiratory disease and poor growth performance. Mortality in pigs over three weeks of age typically ranges from 1% to 5%, though morbidity may affect a high percentage of the herd. Some pigs develop neurological signs including ataxia, posterior paresis, and seizures concurrent with respiratory disease.

Reproductive manifestations of Aujeszky's Disease in breeding herds depend on the stage of gestation at which infection occurs. Infection during early gestation results in embryonic death and increased returns to estrus or irregular cycling patterns. Mid-gestation infection causes fetal death with resorption, mummification, or abortion depending on fetal age at the time of infection. Late gestation infection may result in stillbirths, weak-born pigs, or apparently normal piglets that are viremic and shed virus. Sows themselves may show mild respiratory signs or fever but often remain clinically normal despite active infection. Boars may develop orchitis and epididymitis with temporary or permanent infertility.

Progression of clinical disease follows predictable patterns based on age at infection. In piglets, disease progresses rapidly from initial signs to death within 24 to 72 hours, with limited opportunity for intervention. In older pigs, respiratory disease typically peaks 5 to 10 days post-infection, followed by gradual recovery in survivors over 2 to 3 weeks. Neurological signs may develop at any point during illness and generally indicate poor prognosis. Recovered pigs remain latently infected and may experience reactivation of viral shedding during stress periods. Chronic effects in survivors may include poor growth performance, increased susceptibility to secondary infections, and permanent neurological deficits in pigs that experienced central nervous system disease.

Emergency symptoms requiring immediate veterinary attention include sudden onset of neurological signs in multiple piglets, high fever with tremors or seizures, and abortion storms in breeding herds. Any suspicion of Aujeszky's Disease in herds with negative or unknown status warrants immediate investigation and potential regulatory notification. In non-porcine species on or near pig farms, acute onset of intense pruritus with self-mutilation, hypersalivation, and rapid neurological deterioration is virtually pathognomonic for Aujeszky's Disease and indicates active viral circulation that poses extreme risk to these dead-end hosts. Death in dogs or cats from suspected PRV infection should always trigger investigation of the pig population as the source.

Clinical examination for suspected Aujeszky's Disease begins with careful history taking and assessment of clinical signs across different age groups in the affected herd. Veterinarians evaluate animals for fever, respiratory signs, neurological abnormalities, and reproductive issues. Physical examination findings vary by disease manifestation but may include elevated body temperature, nasal discharge, abnormal lung sounds on auscultation, and various neurological deficits ranging from mild ataxia to complete paralysis and seizures. The pattern of clinical disease across age groups—high mortality in young piglets with respiratory disease in older pigs and reproductive losses in sows—is suggestive of Aujeszky's Disease and warrants laboratory investigation.

Laboratory diagnosis of Aujeszky's Disease employs various methods to detect the virus, viral DNA, or antibodies depending on the clinical situation. Polymerase chain reaction (PCR) testing provides rapid and sensitive detection of viral DNA in clinical samples including nasal swabs, tonsil tissue, lung, and brain. Virus isolation in cell culture remains a definitive diagnostic method but requires viable virus and specialized laboratory facilities. Immunofluorescence testing on frozen tissue sections can demonstrate viral antigen in affected tissues. For surveillance and herd monitoring, enzyme-linked immunosorbent assay (ELISA) testing for antibodies is widely used, with differential ELISAs capable of distinguishing vaccinated animals (using marker vaccines) from naturally infected animals.

Differential diagnosis for Aujeszky's Disease includes other causes of neurological disease, respiratory illness, and reproductive failure in pigs. Neurological differentials include bacterial meningitis, salt poisoning (water deprivation), classical swine fever, African swine fever, and various encephalitides. Respiratory disease must be differentiated from swine influenza, porcine reproductive and respiratory syndrome (PRRS), Mycoplasma hyopneumoniae infection, and various bacterial pneumonias. Reproductive losses have an extensive differential including PRRS, porcine parvovirus, leptospirosis, and various other infectious and non-infectious causes. The combination of neurological, respiratory, and reproductive manifestations affecting different age groups simultaneously is relatively specific for Aujeszky's Disease.

Herd-level diagnostics and surveillance are essential for monitoring disease status, managing eradication programs, and verifying freedom from infection. Serosurveillance programs use ELISA testing of representative samples to estimate herd prevalence and detect new infections. In eradication programs using marker vaccines, differential serological testing identifies naturally infected animals while allowing continued vaccination. Whole-herd testing may be required for animals moving from affected to free areas. Slaughter surveillance using blood or tissue samples provides ongoing monitoring of population-level disease status. Wild boar surveillance is important in areas where these populations may serve as a reservoir for reintroduction of infection to domestic herds.

There is no specific antiviral treatment for Aujeszky's Disease, and management of affected animals relies on supportive care and control of secondary infections. The herpesvirus family, while susceptible to certain antiviral drugs in human medicine, has not been successfully targeted with approved veterinary antivirals for Aujeszky's Disease. Acyclovir and related compounds have shown some in vitro activity against PRV but are not used clinically in pigs due to cost, impracticality of administration, and lack of demonstrated efficacy. Treatment efforts focus instead on supporting affected animals through the acute disease phase and preventing complications from secondary bacterial infections.

Emergency management of acute Aujeszky's Disease outbreaks in naive herds involves rapid implementation of biosecurity measures to limit within-herd spread while providing supportive care to affected animals. Sick animals should be isolated to reduce transmission to unexposed groups. Environmental cleaning and disinfection reduce viral load in housing areas. Movement restrictions prevent spread to other premises. Notification of veterinary authorities is required in many jurisdictions, and regulatory guidance on management options should be sought immediately. In some cases, emergency vaccination of unaffected animals may be implemented to reduce severity of disease as infection spreads through the herd.

Medical management of Aujeszky's Disease focuses on supportive care and treatment of secondary complications. Anti-inflammatory drugs including non-steroidal anti-inflammatory drugs (NSAIDs) such as meloxicam or flunixin meglumine can reduce fever and improve comfort. Antimicrobial therapy is indicated for secondary bacterial pneumonia or other infections, with drug selection based on common pathogens and local resistance patterns. Parenteral administration may be necessary for anorexic animals. Fluid and electrolyte support may benefit severely affected pigs with high fever and reduced water intake. Nutritional support through provision of palatable feed and ensuring water access helps maintain body condition during recovery.

Supportive care for pigs with neurological manifestations presents particular challenges and generally carries poor prognosis. Affected animals should be housed on soft bedding to prevent injury during seizures or involuntary movements. Quiet, darkened environments may reduce stimulation that could trigger seizure activity. Anticonvulsant medications such as diazepam may be considered for controlling severe seizures, though availability and regulatory status vary by jurisdiction. Humane euthanasia should be considered for animals with severe, progressive neurological disease that fails to respond to supportive care, as recovery is unlikely and suffering is significant.

Herd-level treatment strategies depend on the population's vaccination and disease status and regulatory requirements. In naive herds experiencing first-time outbreaks, mass vaccination with modified live or killed vaccines can reduce severity of ongoing disease and protect unexposed animals. In endemic situations, strategic vaccination of breeding animals and young pigs controls clinical disease while eradication programs work to identify and remove infected animals. Depopulation may be considered or required for valuable breeding stock or in the context of area eradication programs. Movement restrictions and enhanced biosecurity prevent spread to other herds during the outbreak period.

Treatment decisions for Aujeszky's Disease must consider regulatory requirements, economic factors, and long-term herd health goals. In countries with active eradication programs, treatment and retention of infected animals may not be permitted, and test-and-removal or whole-herd depopulation may be required. Economic analysis should consider treatment costs, production losses, long-term carrier status of survivors, and potential trade implications. For valuable breeding animals, the decision to treat versus cull must weigh individual animal value against the risk of maintaining latently infected carriers in the herd. Veterinary guidance and regulatory compliance are essential in navigating these decisions.

Recovery from acute Aujeszky's Disease depends heavily on age at infection and severity of clinical disease. Neonatal piglets rarely survive acute infection, and those that do often have permanent neurological deficits including blindness, ataxia, and behavioral abnormalities. Weaned and growing pigs with primarily respiratory disease have good survival rates with appropriate supportive care, typically recovering clinical normalcy within 2 to 3 weeks of infection onset. However, all surviving pigs become lifelong latent carriers of the virus, with the potential for reactivation and viral shedding during periods of stress, immunosuppression, or following corticosteroid administration.

Post-treatment care and monitoring of recovered pigs involves ongoing observation for complications and delayed effects of infection. Respiratory function should be monitored, as some animals develop chronic pneumonia or bronchiectasis following acute infection. Growth performance may be reduced in recovered pigs, warranting nutritional support and management adjustments. Neurological status should be assessed regularly in animals that experienced central nervous system involvement. From a herd health perspective, recovered animals represent a potential source of future virus shedding and should be managed accordingly based on the herd's disease control strategy.

Prognosis for individual animal recovery is generally good for older pigs with mild to moderate disease, guarded for animals with significant neurological involvement, and poor for neonatal piglets and non-porcine species. Factors influencing prognosis include age at infection, viral strain virulence, immune status (including maternal antibody and vaccination), and quality of supportive care provided. Prompt recognition and supportive treatment improve outcomes in clinically affected pigs. However, even animals with complete clinical recovery remain latently infected and pose biosecurity concerns for disease-free herds and compliance with eradication programs.

Return to production for recovered pigs must be considered in the context of overall herd health goals and regulatory requirements. From a productivity standpoint, pigs that recover from respiratory disease can return to normal growth and reach market weight, though feed efficiency may be reduced. Recovered breeding animals can resume normal reproductive function, though the risk of virus shedding during stress makes them problematic in disease control programs. In herds pursuing eradication, recovered animals are typically identified through serological testing and removed. In endemic situations where eradication is not the goal, recovered animals may remain in production with the understanding that they represent a reservoir for ongoing transmission.

Vaccination against Aujeszky's Disease is highly effective at preventing clinical disease and reducing viral shedding in infected animals. Both modified live virus (MLV) and killed (inactivated) vaccines are available, with MLV vaccines generally providing more rapid and robust immunity but carrying theoretical risks in pregnant animals. Marker vaccines, also known as DIVA (Differentiating Infected from Vaccinated Animals) vaccines, are deleted for specific viral glycoproteins (typically gE) and allow serological differentiation between vaccinated animals (gE-negative) and naturally infected animals (gE-positive). This technology enables continued vaccination during eradication programs while identifying and removing infected carriers. Vaccination protocols typically involve primary immunization of young pigs followed by booster vaccination of breeding stock.

Biosecurity measures form the foundation of Aujeszky's Disease prevention, particularly for herds in disease-free regions or those participating in eradication programs. Herd closure or strictly controlled sourcing of replacement animals from verified negative sources prevents introduction of infected pigs. Perimeter fencing and wildlife exclusion measures prevent contact with potentially infected wild boar populations. Quarantine of incoming animals with serological testing before introduction to the main herd provides additional security. Personnel biosecurity including shower protocols, farm-specific clothing, and restrictions on contact with other pig populations reduces risk of mechanical transmission.

Nutritional factors do not directly prevent Aujeszky's Disease infection but contribute to overall immune competence and ability to resist or recover from infection. Adequate colostrum intake by neonatal piglets provides maternal antibody protection during the critical early weeks of life. Balanced nutrition supporting optimal growth and immune function helps pigs mount effective responses to vaccination and resist severe clinical disease if exposed. Stress reduction through appropriate environmental conditions and management practices supports immune function and reduces the likelihood of viral reactivation in latently infected animals.

Management practices for Aujeszky's Disease prevention integrate biosecurity with strategic vaccination and surveillance. All-in-all-out production systems reduce opportunities for transmission between age groups and allow thorough cleaning and disinfection between groups. Segregated production by age and source minimizes contact between animals of different immune status. Semen biosecurity, including sourcing from PRV-negative boars and testing of fresh semen, prevents venereal transmission. Careful management of breeding herd immunity through strategic vaccination protects fetuses and neonatal piglets during the highest-risk periods.

Quarantine and testing protocols are essential components of Aujeszky's Disease control programs at both herd and regional levels. New animal introductions should be sourced from herds of known negative status and should undergo isolation and serological testing before mixing with resident animals. Multiple tests over time may be required to ensure detection of recently infected animals that have not yet seroconverted. Herd certification programs establish and verify disease-free status for trading purposes. At regional and national levels, surveillance programs monitor disease prevalence and detect new introductions, supporting efforts to achieve and maintain disease-free status.

Daily management and monitoring of pig herds for Aujeszky's Disease involves systematic observation of animal health status and prompt investigation of abnormalities. Daily health checks should include observation of all age groups for clinical signs including fever, respiratory distress, neurological abnormalities, and general demeanor. Mortality should be recorded and investigated, with submission of appropriate samples for diagnostic testing when unexplained deaths occur. Feed and water consumption monitoring at the group level can detect early signs of disease that precede obvious clinical manifestations. Any unexplained illness in animals of any age should prompt consideration of PRV as a potential cause, particularly in herds with unknown or uncertain disease status.

Housing and environmental management contribute to Aujeszky's Disease control by reducing transmission opportunities and supporting animal health. Proper ventilation reduces airborne viral transmission within and between rooms or buildings. All-in-all-out production with thorough cleaning and disinfection between groups eliminates residual environmental contamination. Temperature management reduces stress that could trigger viral reactivation in latently infected animals. Physical separation between age groups and production stages limits contact transmission. Outdoor housing requires secure fencing to prevent contact with wild boar, and feed storage must be protected from wildlife access.

Herd health programs for Aujeszky's Disease integrate vaccination, surveillance, and biosecurity into a comprehensive management approach. Vaccination protocols should be developed with veterinary guidance based on local disease pressure, herd immune status, and regulatory requirements. Regular serological monitoring verifies vaccine-induced immunity and screens for evidence of natural infection. In herds using marker vaccines, surveillance testing identifies infected animals for removal. Breeding herd management ensures adequate immunity in sows to provide colostral protection to piglets. Integration of PRV control with management of other diseases optimizes overall herd health outcomes.

Record keeping and monitoring systems support Aujeszky's Disease management through documentation of vaccination protocols, test results, health events, and animal movements. Vaccination records should include dates, products used, and animals treated, enabling verification of protocol compliance and scheduling of boosters. Serological test results document herd status over time and identify individual animals requiring action. Health event records including mortality, morbidity, and clinical observations support early detection of disease changes. Movement records are essential for traceability and compliance with regulatory requirements for disease control programs.

Economic considerations in Aujeszky's Disease management include vaccination costs, production impacts, and market access implications. Vaccination programs represent an ongoing cost but are generally cost-effective when compared to the production losses from clinical disease. The value of disease-free status for market access can be substantial, particularly for breeding stock sales and export markets. Economic analysis should consider direct costs of disease (mortality, reduced performance, reproductive losses) against the costs of prevention and control measures. For herds in endemic areas, the economic optimization point balances vaccination intensity against acceptable disease levels, while herds pursuing eradication must accept higher short-term costs for long-term benefits of disease-free status.

All domestic pig breeds are susceptible to Aujeszky's Disease without significant genetic variation in resistance. Commercial breeds including Large White, Landrace, Duroc, Pietrain, Hampshire, and Berkshire all experience similar clinical disease when infected with PRV. Heritage breeds, miniature pigs, and potbellied pigs are equally susceptible. The universal susceptibility across pig genetics means that breed selection cannot serve as a prevention strategy for Aujeszky's Disease. Research into genetic factors influencing disease severity or resistance has not yielded practical applications for breeding programs. Genetic selection in swine focuses on production traits, meat quality, and resistance to other diseases rather than PRV resistance.

Production type affects Aujeszky's Disease risk primarily through management factors rather than inherent differences in susceptibility. Large commercial operations typically have more robust biosecurity infrastructure but face greater consequences from disease introduction due to high animal density and rapid potential for within-herd spread. Small-scale and backyard operations may have limited biosecurity and informal animal sourcing that increases introduction risk. Outdoor and free-range production systems face particular challenges in preventing contact with wild boar populations that may harbor the virus. Breeding operations with multi-source animal introductions have higher exposure risk than closed herds. Show pigs and animals attending exhibitions face exposure risks from commingling with animals of unknown disease status.

Genetic selection strategies for Aujeszky's Disease resistance are not currently available, and prevention relies on vaccination and biosecurity rather than host genetics. Research has explored the genetic basis of differential responses to PRV infection, including variations in immune response genes and cellular receptors, but no practical markers for selection have been identified. Genomic studies continue to investigate host factors that might influence disease susceptibility or severity. For the foreseeable future, genetic improvement programs in pigs will focus on economically important production traits while disease control for Aujeszky's Disease continues to depend on management interventions, vaccination, and progress toward regional or national eradication where achievable.

Porcine Reproductive and Respiratory Syndrome (PRRS) is a common differential diagnosis for Aujeszky's Disease due to overlapping clinical presentations including respiratory disease and reproductive failure. Both diseases cause pneumonia in growing pigs and can result in abortion, stillbirth, and weak-born piglets in breeding herds. However, PRRS typically causes less dramatic neurological disease, and the pattern of clinical signs across age groups differs somewhat between the two diseases. Co-infection with both viruses can occur and may result in more severe clinical outcomes. Diagnostic testing for both diseases is often performed concurrently when respiratory or reproductive problems are investigated.

Other conditions presenting with similar clinical signs include swine influenza (respiratory disease), classical swine fever and African swine fever (neurological signs and high mortality), bacterial meningitis (neurological disease in young pigs), and various causes of reproductive failure including porcine parvovirus, leptospirosis, and Japanese encephalitis. Salt poisoning (water deprivation followed by rapid water intake) causes neurological signs that can mimic PRV infection. Fumonisin toxicosis can cause pulmonary edema with respiratory distress. The combination of respiratory, neurological, and reproductive manifestations across age groups is relatively distinctive for Aujeszky's Disease, but laboratory confirmation is essential for definitive diagnosis.

Complications and sequelae of Aujeszky's Disease include secondary bacterial infections, chronic respiratory disease, and permanent neurological deficits in survivors. Bacterial pneumonia commonly complicates viral respiratory disease, with pathogens including Pasteurella multocida, Actinobacillus pleuropneumoniae, and Streptococcus suis frequently involved. Chronic pneumonia and reduced lung capacity may persist in recovered animals, affecting long-term growth performance. Neurological sequelae in animals that survive central nervous system infection can include blindness, behavioral abnormalities, and motor deficits. The lifelong latent carrier state represents the most significant long-term consequence, as recovered animals can reactivate viral shedding and serve as sources of infection for naive animals indefinitely.