Porcine Respiratory Disease Syndrome

Porcine Reproductive and Respiratory Syndrome Virus

Porcine Reproductive and Respiratory Syndrome is an infectious disease characterized by reproductive disorders in pregnant sows, such as abortion, stillbirths, and mummified fetuses, as well as respiratory illnesses affecting pigs of all ages—particularly piglets. The causative agent of PRRS is the Porcine Reproductive and Respiratory Syndrome Virus, which belongs to the newly established order Nidovirales, family Arteriviridae, and genus Arterivirus. This genus also includes Equine Arteritis Virus and Monkey Hemorrhagic Fever Virus. In 1991, Wensvoort et al. from the Netherlands first isolated the virus—designated as Lelystad virus—from porcine alveolar macrophages. PRRSV can be classified into two major genotypes: the European type, represented by the LV strain, and the American type, represented by the VR2332 strain. Currently, the predominant PRRSV strains circulating in China belong to the American genotype.

PRRSV is a single-stranded, positive-sense RNA virus with an envelope. Purified viral particles exhibit pleomorphism, but most prominently feature a lipid bilayer membrane with small, inconspicuous surface spikes. Reports also indicate that the nucleocapsid has a diameter of 40–50 nm, adorned with short protrusions approximately 5 nm long, while the overall viral particle measures about 45–72 nm in diameter. Surrounding the nucleocapsid is a lipid envelope, enclosing a 15.1-kb, single-stranded, linear genomic RNA that is non-segmented, polyadenylated, and enveloped—making it the largest among the four members of the Arterivirus genus.

PRRSV has a buoyant density of 1.13–1.17 g/mL in sucrose and exhibits a sedimentation coefficient ranging between 214S and 230S. PRRSV is sensitive to both pH levels and heat: it can remain stable for several years at -20°C and -70°C, but its infectivity rapidly declines when stored at 4°C or when exposed to pH levels above 7.5 or below 6. Treatment with lipid-solvent agents such as chloroform and ether effectively inactivates the virus. Like most arteriviruses, including PRRSV, this virus is highly unstable in low-concentration detergent solutions, leading to disruption of its viral envelope and subsequent release of non-infectious core particles. Another key biological feature of PRRSV is its strong tropism for macrophages; porcine alveolar macrophages (PAM) serve as the primary target cells. Moreover, PRRSV demonstrates a broad affinity for various types of macrophages, including porcine alveolar macrophages (PAM), peripheral blood monocytes, and pulmonary intravascular macrophages (PIM).

Pigs are the only hosts susceptible to PRRSV, and pigs of all ages, genders, and breeds can become infected. However, susceptibility varies somewhat depending on the pig's age. Young pigs typically exhibit mild symptoms upon infection, while sows and piglets often show more severe signs, with mortality rates in newborn piglets reaching as high as 80–100%. Infected pigs and carrier pigs serve as the primary sources of infection. This virus is highly contagious and can spread rapidly once introduced into a population. The main transmission routes include: 1) Long-distance spread via the transportation of infected pigs, as the virus can persist in pigs for extended periods, leading to persistent infections within herds and facilitating its dissemination as pig populations move; 2) Airborne transmission, though this is influenced by environmental factors such as wind direction, wind speed, temperature, seasonality, as well as the virus's physical state, viability, and viral load. Clinically, Porcine Reproductive and Respiratory Syndrome (PRRS) primarily affects pigs of all ages, causing symptoms like fever, lethargy, and loss of appetite. In breeding sows, fertility rates decline, and pregnant sows may experience abortion, stillbirths, mummified fetuses, or the birth of weak piglets. Boars infected with the virus often suffer impaired semen quality and reduced sperm motility. Meanwhile, piglets and growing-finishing pigs commonly display respiratory signs, including coughing, sneezing, rapid breathing, and difficulty breathing, accompanied by cyanosis in the ears and extremities. Notably, due to significant variations in virulence among different PRRSV strains, clinical manifestations and epidemiological patterns can differ markedly across regions and among pig populations. In recent years, there has been a noticeable increase in cases of subclinical and chronic infections, while persistent infections have become increasingly common within pig herds.

Experimentally infecting 4-week-old SPF piglets with different PRRSV isolates resulted in decreased numbers of peripheral blood red cells, reduced hemoglobin levels, and lower packed cell volume (hematocrit) between 3 and 21 days post-infection. A similar reduction in white blood cell counts was also observed when PRRSV-infected pregnant sows were in mid-gestation. By day 7 post-infection, B lymphocyte counts dropped to their lowest point, while peripheral blood lymphocytes and monocytes declined by 1S91 between days 3 and 11. Rossow et al. noted a further decrease in cell numbers, accompanied by a rise in band-shaped neutrophils, beginning on day 4 after infection. The specific pathological changes are as follows:
(1) Granulomatous inflammation is observed in the lymph nodes, liver, spleen, tonsils, thymus, and Peyer’s patches.
(2) Macrophages and multinucleated giant cells frequently exhibit numerous, diverse, basophilic or amphophilic globular inclusions in their cytoplasm.

(3) Renal tissue lesions. Numerous lesions appear between lymphocytes and histiocytes, accompanied by interstitial nephritis and pyelitis, with areas of fibrinous hyperplasia surrounding the inflammatory sites.
(4) Lesions in the affected tissues. Infiltration of mononuclear cells—primarily macrophages and lymphocytes, with occasional multinucleated giant cells—as well as Type I mast cells leads to thickening of the alveolar septa. Multiple lesions often appear in the bronchial and bronchiolar regions and may even extend into the open tracheal layers. Characteristic pathological features include fibrinous bronchitis and bronchiolitis pneumonia. Meanwhile, the number of lymphocytes and plasma cells within the alveolar septa decreases, while the influx of mononuclear cells and macrophages causes significant thickening of the alveolar walls. Many alveoli are filled with abundant necrotic debris and densely populated by Type I mast cells, contributing to alveolar adhesions. Overall, PRRSV infection triggers a wide range of pathological changes across multiple tissues and organs, with the most distinctive alterations primarily observed in the respiratory system and lymphoid tissues. However, exceptions to each described pathological change occasionally occur, potentially linked to varying degrees of secondary infectious complications.

Clinically, diagnosis can be made based on clinical symptoms and epidemiological features. However, because PRRS shares highly similar clinical signs with many other diseases that cause reproductive disorders in pigs—such as porcine parvovirus, pseudorabies, classical swine fever, and Japanese encephalitis B—and given the significant variability in clinical presentations among different pig farms, especially when secondary bacterial or viral infections occur—as well as the increasing number of subclinical and chronic cases reported in recent years—the diagnostic process has become even more challenging. Therefore, laboratory-based diagnostics are essential for definitive confirmation. Laboratory diagnostic methods commonly include histopathological analysis, virus isolation and identification, serological testing, and RT-PCR. Among these, virus isolation and identification is considered the most reliable method for diagnosing PRRS in the lab. However, cell culture is a labor-intensive, time-consuming, and technically demanding procedure. On the other hand, while serological methods for PRRS diagnosis are relatively straightforward to perform, they often involve complex procedures. Moreover, due to substantial antigenic differences among various PRRSV strains, no single serological test currently exists that can reliably detect PRRSV antibodies across all strains. As a result, there remains an urgent need to develop an effective and practical diagnostic approach for PRRS. RT-PCR has now become a widely used tool for both clinical diagnosis and strain identification of PRRSV, with ongoing improvements and refinements in its methodology. Typically, viral RNA can be detected by RT-PCR as early as 24 hours post-infection. Importantly, for persistently infected individuals, RT-PCR results provide a more accurate reflection of their actual viral load status. Additionally, RT-PCR can effectively distinguish between different genotypes of PRRSV strains. Compared with virus isolation and serological methods, RT-PCR has demonstrated superior sensitivity and reliability. For instance, while viral RNA can be detected by RT-PCR as early as 24 hours post-infection, serological tests fail to identify antibodies in serum samples during this same period. Furthermore, in both early and late stages of infection (e.g., at 28 days), RT-PCR can still detect low levels of circulating virus, whereas virus isolation may yield negative results for certain samples. These findings clearly highlight RT-PCR’s effectiveness, enabling precise differentiation of PRRSV strains into American and European genotypes—a critical advantage that makes it a highly accurate and sensitive diagnostic tool.

1. Assess the infection status of this batch. Conduct PCR tests while also considering production performance indicators, such as the rapidly increasing rates of stillbirths and mummified fetuses, mortality among nursing piglets, and mortality in nursery pigs. Begin by testing aborting sows, followed by analyzing exudates from weak piglets born in farrowing crates or those with docked tails, and finally test weaned but still weak piglets. If any of these tests come back positive, it confirms that the sows are carrying the virus. However, if all results are negative, the sows themselves are likely healthy; yet, if subsequent testing in the nursery reveals positive findings, it suggests issues occurring during the rearing and finishing phases. It is understood that the ideal scenario for weaned weak piglets is when they test negative for antigens but positive for antibodies, as this indicates they already possess some level of immunity. Additionally, regarding gilts, Zhang Guihong emphasizes that gilts testing negative for antigens but positive for antibodies represent the optimal choice—these animals exhibit robust immunity. Conversely, if a gilt tests negative for both antigen and antibody, it implies the animal lacks any protective immunity, making newly introduced gilts more susceptible to infection and potentially destabilizing the entire herd. On the other hand, if a gilt tests positive for antigen—regardless of whether antibodies are present or absent—it signals the introduction of a new virus strain, which could disrupt the stability of the existing sow population.

2. Understand the current strain situation. Only by clearly grasping the details of this strain can we implement more effective, comprehensive disease control measures. Key strategies include eliminating the source of infection, breaking the transmission routes (by reducing the viral load in the environment), and protecting susceptible populations (by enhancing the herd's immunity).

3. For stable farms that test positive for Porcine Reproductive and Respiratory Syndrome (PRRS), maintaining the original control methods along with enhanced biosecurity measures is sufficient. However, unstable PRRS-positive farms can be managed from an economic perspective. Zhang Guihong points out that pig farming has entered an era of thin profits, making it crucial to control major diseases through an economic lens. For unstable PRRS-positive farms, the most cost-effective approach involves administering two rounds of vaccine immunization—administered 14 to 21 days apart (or even sooner)—followed by partial culling of infected pigs.

4. Strict biosecurity measures. Ensure thorough biosecurity management, restrict cross-fostering in farrowing rooms, and prohibit arbitrary pen changes.

5. Control boar semen.

6. Back-up pigs entering the group must be strictly managed.

The methods for controlling and eradicating blue ear disease are well-established, but preventing re-infection with the blue ear virus remains challenging. In essence, the overarching principles for managing blue ear disease involve maximizing immunity, minimizing infection, and effectively guarding against reinfection—strategies that also align with economic considerations in controlling the virus.

References

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