Porcine Parvovirus
Lalrinkima1, S. Hemalatha2
Assistant Professor, Khalsa College of Veterinary and Animal Science, Amritsar
Professor, Department of Veterinary Pathology, Madras Veterinary College, Chennai
Introduction
Porcine parvovirus was considered as a major cause of reproductive failure in swine indicated by repeat estrus, abortion and delivery of stillborn fetuses. The occurrence of the PPV in pigs was first described by Cartwright and Huck in Germany and U.S.A in 1976. In 2012, Truyen and Streck reported that the virus was found in many areas of pig herds around the world. Porcine parvovirus was later discovered as the primary cause of SMEDI (S: stillbirth, M: mummification, ED: embryonic death and I: infertility) syndrome in the pig industry. Reproductive losses were typically low in vaccinated herds but PPV could cause devastating abortion storms in unvaccinated herds or if the vaccine was administered incorrectly or in the emergence of new antigenic types.
In 2010, Sharma and Saikumar reported the PPV disease for the first time in India associated with neonatal mortality and reproductive failure in crossbred Indian pigs. 1n 2016, Aishwarya and his co-worker reported first occurrence of PPV from Kerala in domestic and wild pigs. The diseases was also reported in Punjab, North Eastern states and Southern part of India.
Etiology
Porcine parvovirus is a DNA virus of the genus Parvovirus of subfamily Parvovirinae of family Parvoviridae. The family Parvoviridae consists of two subfamilies Parvovirinae and Densovirinae. Viruses in the subfamily Parvovirinae mainly infect vertebrate hosts whereas viruses in the subfamily Densovirinae mainly infect arthropods. PPVs 1-7 and porcine bocaviruses belong to the subfamily Parvovirinae.
Transmission
Infected boar or sperm used for breeding purpose or a seronegative boar infected during mating from an infected sow’s vaginal secretions could transmit the virus into a vulnerable farm. PPV might live in the body for months and infected fomites were a persistent source of infection in the farm. The virus could spread across herds via fomites such as farmers clothing, boots, equipment’s and outerwear. The disease could spread within a herd via infected pig’s feces, nasal and oral secretions.
Clinical signs
An increase in the number of gilts or sows returning to estrus 3-8 weeks after breeding was a common clinical sign of PPV infection in a herd. Some sows may remain “endocrinologically pregnant,” that indicated it might not go into estrus until the expected farrowing date. The infection that occurred later in the pregnancy was evident by small litter size and mummification at farrowing. A mild and transient lymphopenia was noticed sub clinically regardless of sex or age between 5 and 10 days after initial infection. PPV1 and PPV-like structures in diarrheic feces and isolation of PPV1 from “vesicle-like” skin lesions had been described earlier.
Pathology
Grossly, lesions were evident in embryos or fetuses. A discoloration of skin due to bleeding occurred giving the fetus a dark tonality after death of the fetus followed by progressive dehydration of tissues that led to mummification. Macroscopically, lesions included a variable degree of congestion, oedema and hemorrhage with accumulation of serosanguinous fluid in body cavities. Lungs were non collapable, edematous and congested with focal hemorrhage. The pericardium appeared thickened and opaque with pale streaks in myocardium. Intense congestion or pale/yellow discoloration was observed in liver.
Microscopically, lungs revealed mild to moderate interstitial pneumonia and patchy areas of alveolar necrosis. Myocarditis characterized by diffuse areas of mononuclear cells infiltration, edema and degeneration of myocardiocytes and mild hemorrhage was common. Kidneys revealed mild to focal interstitial nephritis due to infiltration of mononuclear cells, degeneration of epithelial lining cells of proximal convoluted tubules and hemorrhage in interstitum.
Still born fetus – Serosanguineous fluid in the Still born fetus: Heart – Focally extensive
thoracic cavity epicardial haemorrhage (arrow)
Diagnosis
Based on the clinical signs and symptoms. Multiplex PCR, real-time PCR and nano-PCR were increasingly employed as a tool for the diagnosis of PPV infection. Hemagglutination inhibition (HI) and Enzyme linked immunosorbent assays (ELISA) had been used for detection of PPV antibodies. Detection of viral antigen by Immunohistochemistry.
References
Cartwright, S.F. and R.A. Huck. 1967. Viruses isolated in association with herd infertility, abortions and stillbirths in pigs. Vet. Rec. 81:196–197.
Miao, L.F., C.F. Zhang, C.M. Chen and S.J. Cui. 2009. Real-time PCR to detect and analyze virulent PPV loads in artificially challenged sows and their fetuses. Vet. Microbiol. 138(1-2): 145-149.
Sharma, R and G. Saikumar. 2010. Porcine parvovirus-and porcine circovirus 2associated reproductive failure and neonatal mortality in crossbred Indian pigs. Trop. Anim. Health Prod. 42(3): 515–522.
Truyen, U. and A.F. Streck. 2012. Porcine parvovirus. In: Diseases of swine, Zimmerman J, Karriker L, Ramirez A, Schwartz K and Stevenson G, 10th edn., John wiley and Sons Inc., USA. pp. 447-455.
https://pubmed.ncbi.nlm.nih.gov/31822635/
