Swine fever virus

Classical Swine Fever (CSF) is an acute or chronic, febrile, highly contagious infectious disease in pigs caused by the Classical Swine Fever virus. It leads to widespread pinpoint hemorrhages throughout the body and splenic infarction, making it one of the most severe viral diseases threatening the pig industry. CSF has a global distribution, and due to its devastating impact, it causes significant economic losses to pig farming worldwide. As a result, the World Health Organization classifies this disease as a Class A notifiable infectious disease, while in China, it is designated as a Category I animal epidemic. According to our company's testing data from 2020 to 2023, the overall positive rate for CSF virus was 124.5%, with an RNA positivity rate of 1.6% and an antibody positivity rate of 48%. These figures clearly indicate that vaccination coverage and protective efficacy in China remain insufficient, underscoring the continued presence of CSF virus infections. Notably, CSFV exhibits strong host specificity in natural infections—pigs are the only known natural hosts, and all breeds, ages, and sexes are susceptible. Moreover, experimental studies have demonstrated that CSF virus can even infect cattle under certain conditions.

CSFV belongs to the genus Pestivirus within the family Flaviviridae. It is an approximately spherical, single-stranded positive-sense RNA virus with an average particle diameter of 44 nm. Inside, it features a 20-faced, highly symmetrical nucleocapsid measuring 24–30 nm in diameter, while externally, the virus is enveloped by a lipid-protein membrane studded with glycoprotein spikes that range from 6 to 8 nm in length. CSFV exhibits high genomic sequence homology and close antigenic relationships with bovine viral diarrhea virus, another member of the same genus. As a result, these two viruses not only show serological cross-reactions but also confer cross-protective immunity against each other.

There are significant antigenic differences among different CSFV strains, and virulence varies widely among field isolates, ranging from highly virulent, moderately virulent, low-virulent, to non-virulent strains, as well as strains capable of persistent infection. Highly virulent strains typically cause acute classical swine fever with high mortality rates, while moderately virulent strains usually lead to subacute or chronic infections. Low-virulent strains can infect fetuses, resulting in mild clinical signs or even subclinical infections. In contrast, the outcomes of infection by moderately virulent strains depend largely on host factors such as age, immune status, and nutritional condition—though these factors play a minimal role in determining the effects of highly or low-virulent strains. Notably, non-virulent strains can induce a state of persistent infection characterized by high levels of viremia, yet they fail to elicit any overt clinical symptoms.

Under natural conditions, the classical swine fever virus (CSFV) enters pigs through the nasal route, and in some cases, it can also penetrate via the conjunctiva of the eyes, mucous membranes of the reproductive tract, or skin lesions. Additionally, infection may occur through oral and non-intestinal routes. Infected pigs excrete large amounts of the virus in their feces, body fluids, and other secretions. Moreover, the virus is also highly concentrated in materials directly contacted by sick pigs, such as bedding, feed, and drinking water. As a result, urine and secretions from infected pigs remain highly infectious to healthy animals. Since pigs of all breeds and age groups are susceptible to CSFV, young piglets are particularly vulnerable. Once the virus enters the oral cavity or pharyngeal tissues of a healthy pig, it begins to replicate within the body. Initially, the virus multiplies primarily in tissues like the tonsils and lymph nodes, eventually leading to viremia—where the virus spreads throughout the bloodstream. The virus then infiltrates white blood cells and is carried via circulation to infect various organs across the body. Typically, the virus can first be detected in the blood as early as day 3 post-infection, with viral levels peaking between days 6 and 8. In areas where the disease is endemic, pig populations often develop partial immunity, resulting in lower incidence and mortality rates. However, in newly affected regions, the disease tends to strike hard, with morbidity and mortality rates exceeding 90%. Swine fever can occur year-round, though outbreaks are usually more severe during spring and autumn. Thanks to widespread preventive measures, including routine vaccination programs, most intensively managed pig herds now possess a degree of immunity. Consequently, the epidemiological patterns of classical swine fever have shifted in recent years, giving rise to atypical and mild forms of the disease that often manifest as sporadic outbreaks. These milder cases typically present with subtle or inconspicuous clinical symptoms, low mortality rates, and non-specific pathological changes, making laboratory diagnosis essential for accurate confirmation.

The natural incubation period for classical swine fever typically ranges from 5 to 7 days, with shorter cases as brief as 2 days and longer ones reaching up to 21 days. Based on the severity of symptoms and the disease progression, clinical presentations of classical swine fever have recently been classified into four main types: hyperacute, acute, chronic, and delayed-onset. 1. The hyperacute type, clinically… Bedding is relatively uncommon. In addition to elevated body temperature, sick pigs often show no obvious symptoms, frequently leading to sudden death within 1–2 days due to circulatory failure and shock. 2. The acute form of classical swine fever, the most common type, is caused by highly virulent CSFV strains. The incubation period typically lasts 3–5 days, during which the pig’s body temperature can soar as high as 41°C. At the onset of the disease, pigs exhibit extreme depression, sluggishness, shivering, and a tendency to lie down in an arched posture or visibly trembling from cold. Appetite completely disappears, accompanied by inflammation of the eye conjunctiva, resulting in purulent discharge from both eyes—sometimes even causing the eyelids to stick together, and in severe cases, completely sealing the eyes shut. As the illness progresses, breathing becomes rapid, initial symptoms include constipation, followed later by diarrhea that may contain blood. In advanced stages, small or larger hemorrhagic spots may appear beneath the skin on areas such as the limbs, abdomen, ear tips, inner thighs, and vulva. A minority of affected pigs may also display neurological symptoms like convulsions. Most infected pigs survive for only 1–2 weeks before succumbing to the disease, with mortality rates remaining alarmingly high. 3. The chronic form of classical swine fever is frequently observed in endemic regions, characterized by mild or subtle clinical signs and irregular fluctuations in body temperature. Initially, pigs experience reduced appetite, but after a few weeks, they may show slight improvement. However, constipation and diarrhea tend to alternate, leading to severe weight loss and anemia. Affected pigs become weak, especially in their hind limbs, making it difficult for them to walk. Some pigs develop bluish-purple discoloration or necrosis at the ear tips and extremities. The duration of the disease can extend to 3 weeks or even longer than a month in some cases. Notably, the chronic form primarily targets piglets. 4. In pregnant sows, infection with the virus can easily result in stillbirths, mummified fetuses, or unexplained miscarriages. If the sow is infected with a moderately virulent strain, she may give birth to piglets that appear healthy at first glance. Unfortunately, these piglets will carry the virus for life and continue shedding it over time. Common symptoms in affected sows include emaciation, anemia, and general weakness, often accompanied by frequent lying down, mild loss of appetite, and impaired coordination. Ultimately, most infected sows perish, while surviving piglets typically suffer from prolonged growth retardation.

In the most acute form of classical swine fever, necropsy typically reveals only a few scattered hemorrhages in the internal organs and mucous membranes, with no obvious macroscopic lesions in other tissues. In contrast, acute cases often show diffuse pinpoint or patchy hemorrhages on the mucosa, peritoneum, and serous membranes. Pathological changes in immune organs include enlarged, hemorrhagic lymph nodes with a marbled appearance, as well as splenic infarcts exhibiting jagged, serrated margins. Additional findings may also include petechial hemorrhages in the kidneys, submucosal bleeding in the stomach, petechiae on the epiglottic cartilage, pulmonary hemorrhages, and a characteristic cecal-valve nodular swelling accompanied by varying degrees of tonsillar necrosis. In chronic cases, the primary necropsy findings involve widespread hemorrhages throughout the body, often accompanied by fibrinous pneumonia. A hallmark lesion is necrotizing enteritis at the cecal valve, which manifests as button-like ulcers that expand outward, protruding prominently from the mucosal surface.

The swine fever virus exhibits a unique affinity for mesodermal tissues such as the hematopoietic system and blood vessels. In acutely infected pigs, CSFV damages the hematopoietic system and the mononuclear-phagocytic system, leading to a reduction in white blood cells in the bloodstream, swelling and degeneration of mononuclear phagocytes, followed by their gradual disappearance. Meanwhile, widespread necrosis of lymphoid-like cells occurs, profoundly altering the immune response. As a result, the body's secondary antibody response to lysozyme is weakened, and the overall cellular phagocytic capacity is significantly diminished, ultimately impairing the host's immune function.

If cases of swine fever occur, immediate eradication measures must be implemented: all pigs in the infected herd should be destroyed, while the source of infection and any potential contact animals are traced. Contaminated premises must then be thoroughly disinfected. In countries and regions where swine fever is endemic, vaccination is often employed; therefore, an effective immunization program should be established. Newborn piglets experience suppressed immune responses after vaccination due to maternal antibodies. To ensure optimal immunity, these piglets need to be vaccinated again at 6 weeks of age. A booster dose administered at 5 months of age will further enhance the overall herd immunity. In pig populations or areas already affected by swine fever, emergency vaccination of pigs presumed to be uninfected can help protect the majority of the herd.

After vaccination, it is essential to strengthen immune monitoring of the pig population. A well-immunized herd should maintain an overall protection rate of at least 90%. If the protection rate falls below 50%, it indicates either ineffective immunity or that the area is experiencing unstable classical swine fever conditions, necessitating enhanced immunization efforts. Typically, immune testing is conducted 10 to 15 days after a booster dose. Breeding pigs should have their antibody levels checked every six months, and based on these results, decisions can be made regarding whether an additional booster is needed—especially when antibody titers drop below 1:16, prompt vaccination is advised. It’s worth noting that CSFV exhibits weak resistance to environmental factors; it is highly sensitive to lipid-solvent agents such as ether and chloroform. Additionally, extreme pH levels—whether too acidic or too alkaline—can inactivate the virus. In particular, viruses are rapidly destroyed in solutions like sodium hydroxide or bleach. Among disinfectants, a 2% sodium hydroxide solution is considered the most effective choice for controlling the virus.

References

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