Research on Differential Diagnostic Methods for Porcine Parvovirus

Porcine parvovirus is one of the most common pathogens causing reproductive disorders in pig herds worldwide. Since the disease was first reported in the United Kingdom in 1967, it has now become widespread throughout the world. China began researching this disease in the early 1980s, and the China Institute of Veterinary Drug Control was the first in the country to isolate the virus in 1.982. Relevant statistics show that porcine parvovirus disease is already widespread and epidemic in China.

The economic losses caused by porcine parvovirus infection are also enormous. According to reports, the annual reproductive losses caused by this disease in the United States amount to 4.5 million US dollars. In China, Zhao Zhanmin investigated 15 porcine parvovirus-positive farms in Beijing, involving 1288 first-parity sows, with a rate of 59.16% for mummified and weak fetuses, and a stillbirth rate of 49.17; in Guangxi, an investigation of 2024 first-parity sows showed that abnormal piglets accounted for 42.2% of the total piglets born.

Porcine parvovirus infection causes sows, especially first-parity sows, to produce stillborn fetuses, malformed fetuses, mummified fetuses, abortions and weak piglets. Susceptible sows will develop this disease if infected with the virus within the first 70 days of gestation. Sows returning to estrus, pseudopregnancy (failure to farrow), reduced litter size, and overall decreased reproductive performance of the herd.

However, research in recent years has found that this virus is a synergistic pathogen causing circovirus infection, and is one of the reasons for the prevalence of the latter. Circovirus, on the other hand, is the main pathogen causing decreased body condition, emaciation, diarrhea, and respiratory difficulty in pigs, leading to post-weaning multisystemic wasting syndrome.

1 Etiology

The pathogen of porcine parvovirus is porcine parvovirus, which belongs to the family Parvoviridae, genus Parvovirus. The virus particles are round or hexagonal, non-enveloped, with a diameter of 20 nm, and the genome is single-stranded. The virus can grow and reproduce in primary porcine cells such as porcine kidney and porcine testicular cells, as well as in passaged cells such as, and can cause cytopathic effects. Immunofluorescence techniques can detect viral antigens in the cytoplasm, and the virus can produce intranuclear inclusion bodies in cells. The virus can agglutinate the red blood cells of humans, monkeys, guinea pigs, mice and chickens.

Parvovirus strains vary in virulence. (1) is a virulent strain; after infection of seronegative pregnant sows, it will cause viremia and vertically infect the fetus through the placenta, causing fetal death; (2) is an attenuated strain after cell adaptation; after infection of pregnant sows, it cannot infect the fetus through the placenta, and is used as an attenuated vaccine strain. Interfering defective particles exist in cells infected with the strain, which can interfere with or reduce the replication of the virus. This interference effect provides sufficient time for the host body to establish a resistant immune response, thereby preventing the occurrence of viremia and secondary placental infection.

This virus has strong heat resistance and is extremely stable at 4°C, allowing long-term preservation. After heating at 56°C for 30 min, its infectivity and ability to agglutinate red blood cells are not lost; at 70°C for 2 h, it still does not lose its infectivity and hemagglutination activity; it is only inactivated at 85°C for 5 min.

The virus has strong resistance to various disinfectants. It is insensitive to lipid solvents such as ether and chloroform. Short-term trypsin treatment not only has no effect on the virus suspension, but can also increase its infectious titer. Formaldehyde vapor and ultraviolet light also require a long time to kill the virus. PPV can survive for at least 14 weeks under natural conditions in pens and excreta. PPV can be killed by 0.5% bleaching powder or sodium hydroxide in 5 min, while 2% glutaraldehyde requires 20 minutes, and 3% formaldehyde requires 2 hours.

2 Epidemiology

Pigs are the only known susceptible animals, and domestic pigs and wild boars of different ages and sexes can all be infected. According to reports, specific antibodies also exist in the sera of cattle, sheep, cats, guinea pigs, mice and rats, and the antibody-positive rate of rodents from diseased pig farms is higher than that of rodents from negative pig farms.

Virus-carrying pigs are the main source of infection. The virus can be transmitted to the fetus through the placenta, forming vertical transmission. At the same time, after fetuses in one uterine horn are infected with PPV, it can be transmitted to fetuses in the other uterine horn. In addition to placental infection, mating and artificial insemination infection, sows, finishing pigs and boars are mainly infected through the respiratory tract and digestive tract or reproductive tract via infected food and environment. The secretions and excretions of virus-carrying pigs can remain infectious for several months, and contaminated pens are the main reservoir of PPV. Therefore, after diseased pigs are removed from contaminated pig houses, even after the pens have been empty for four and a half months and cleaned by conventional methods, susceptible pigs placed in them may still become infected.

Piglets infected in utero can carry the virus for at least 9 weeks, and some with immune tolerance may carry and shed the virus for life. Stillborn fetuses, live fetuses, piglets and uterine secretions from sows infected with this virus all contain high-titer virus.

The virus can be isolated from the sperm cells, spermatic cord, epididymis and accessory sex glands of infected boars, and is easily transmitted to susceptible sows during mating.

Fluorescent antibody examination proves that the virus is mainly distributed in some rapidly proliferating tissues in pigs, such as lymphoid germinal centers, colonic lamina propria, renal interstitium, and nasal turbinate periosteum.

3 Clinical Manifestations

This disease is commonly seen in first-parity sows and generally occurs in endemic or sporadic form. After the occurrence of this disease, pig farms may continuously experience sow reproductive failure for several years. When sows are infected in early pregnancy, the mortality rate of their embryos and fetuses can reach 80%-100%.

After acute infection with PPV in pigs, viremia can occur 1-6 days later, virus can be shed through feces 1-2 weeks later, and hemagglutination antibodies can be detected in serum 7-9 days later.

Acute infection in piglets and sows usually presents as subclinical cases, but the virus can be found in many tissues and organs (especially lymphoid tissues) in their bodies. Infection of sows at different stages of gestation can cause different symptoms such as stillbirth, mummified fetuses, and abortion. Infection at 30-50 days of gestation mainly causes mummified fetuses. Infection at 50-60 days of gestation mostly causes stillbirth. Sows infected at 70 days of gestation often show abortion symptoms. Sows infected in the middle and late stages of gestation can also develop transplacental infection, but at this time the fetuses can often survive in the uterus without obvious clinical symptoms. After 70 days of gestation, most fetuses can produce a meaningful immune response to viral infection and survive, but these piglets often carry antibodies and virus. When early embryos are infected, intrauterine spread of the virus may be relatively uncommon, because after embryonic death they can be rapidly absorbed by the mother, effectively eliminating the source of infection in the uterus.