Naturally-infected boars have been documented to shed Senecavirus A (SVA) RNA in semen for up to three months after exhibiting vesicular disease.
Experimentally-infected boars shed SVA RNA in semen for up to three weeks post-inoculation.
The majority of experimentally-infected boars did not exhibit clinical signs or develop apparent lesions.
“This update shows that SVA RNA is shed in semen from both naturally-infected and experimentally-inoculated boars. The prolonged shedding of viral RNA in semen and the presence of SVA RNA in the testes and tonsils of the naturally-infected boars for up to three months are concerning findings and raises the possibility of persistent infection in boars. While the duration of shedding in semen for the experimentally-infected boars was considerably shorter than for the naturally-infected boars, the fact that all contemporary-strain boars had PCR-positive semen on at least one collection indicate that shedding in semen is a repeatable phenomenon and shedding occurred in some boars which did not exhibit clinical signs or develop vesicular lesions. It is currently unknown whether semen from infected boars can serve as a source of infection if used to inseminate susceptible females.”
More than 230 Senecavirus outbreaks have been confirmed after July 2015 in the United States and this is why it is important:
“The clinical signs in pigs infected with vesicular disease caused by SVA are variable and can range from no outward signs, to nonspecific signs such as decreased appetite or fever, or pigs may develop vesicles, or blisters, on the skin or in the mouth.[..]
While SVA continues to plague U.S. and global pork producers, it is important to be reminded of and understand some basic characteristics and behavior of this virus. SVA causes vesicular lesions affecting the skin, mouth and feet of pigs of all ages and has been associated with increased neonatal mortality which may be accompanied by neonatal diarrhea. If vesicular disease is present, your state animal health official must be notified in order to rule out other foreign animal diseases, such as FMD. The virus can be detected in multiple sample types but there is variability in the amount of time for which each sample type can be used for detection. Finally, SVA is extremely stable and contaminated facilities, transport vehicles and fomites are concerns for possible virus transmission but several disinfectants have been shown to be effective at neutralizing the virus.”
How long do sows and piglets shed Senecavirus A after a clinical outbreak? How long is the viremia? Those are the questions answered in this case study of a Senecavirus A outbreak in one US farm.
Objective and Methods
Senecavirus A is a challenge for producers and veterinarians because of its clinical similarity to Food and Mouth Disease (FMD). In this study, 34 sows and 30 individual piglets from 15 different litters were sampled at day 1 post-outbreak and later at 1, 2, 3, 4, 6, and 9 weeks post-outbreak (PO). Serum, and tonsil, rectal, and vesicular swabs were collected for all of the pigs included in the study. The objective of the study was to explore the viremia and shedding patterns in those infected animals. All samples were submitted to the University of Minnesota, Veterinary Diagnostic Laboratory to be tested by PCR.
Vesicular lesions were seen in sows only for 2 weeks and had the highest amount of virus. In sows, the detection of Senecavirus A in tonsil and rectal swabs was greater than 90% at 0 week PO and remained as high as 50% through 5 weeks PO. Generally, viremia was detected up to 1 week PO in sows but it is important to note that viremia was not detected in 11 out of 34 (32%) of the sows at any point during the study. Viremia was detected in 18 out of 30 (60%) and 19 out of 30 (63%) in the suckling piglets from site 1. Similar to sows, viremia was not detected in 9 out of 30 (30%) of the site 1 piglets enrolled in the study.
The detection of Senecavirus A in sows tonsil swabs peaked 1 week PO (94% positive) whereas it peaked at day 1 PO for piglets (83% positive). The detection of virus shedding decreased over time in sows and piglets, and a single sow and piglet tested positive at 9 weeks PO.
The peak of Senecavirus A detection from rectal swabs in sows (91%) occurred at day 1 PO and continued to steadily decrease and was not detected at 9 weeks PO. In site 1 piglets, the detection of SVA peaked at 1 week PO (90% positive). 64% of the rectal swabs were positive at 4 weeks PO in site 1 piglets. At 6 weeks PO, the detection of Senecavirus A was same for both site 1 and 2 piglets (11%); however, a single piglet from site 1 was still shedding SVA at 9 weeks PO.
The study assessed the shedding pattern of SVA in sows and piglets during an outbreak on a farm in the US and investigated the spread of SVA between pigs during the post weaning period. Vesicular lesions were seen in sows only for 2 weeks and had the highest amount of virus. In sows, the detection of SVA in tonsil and rectal swabs was greater than 90% at 0 week PO and remained as high as 50% through 5 weeks PO, these sample types should be collected and submitted, in addition to vesicular lesion swabs and fluid (if present), as part of FAD investigations for the detection of SVA.
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Background: The study highlights the shedding pattern of Senecavirus A (SVA) during an outbreak of vesicular disease in a sow farm from the South-central Minnesota, USA. In this study, 34 individual, mixed parity sows with clinical signs of vesicular lesions and 30 individual piglets from 15 individual litters from sows with vesicular lesions were conveniently selected for individual, longitudinal sampling. Serum, tonsil, rectal, and vesicular swabs were collected on day 1 post outbreak, and then again at 1, 2, 3, 4, 6, and 9 weeks post outbreak. Samples were tested at the University of Minnesota Veterinary Diagnostic Laboratory for SVA via Real Time Polymerase Chain Reaction (RT-PCR)
Results: In sows, vesicular lesions had the highest concentration of SVA, but had the shortest duration of detection lasting only 2 weeks. Viremia was detected for 1 week post outbreak, and quickly declined thereafter. SVA was detected at approximately the same frequency for both tonsil and rectal swabs with the highest percentage of SVA positive samples detected in the first 6 weeks post outbreak. In suckling piglets, viremia quickly declined 1 week post outbreak and was prevalent in low levels during the first week after weaning (4 weeks post outbreak) and was also detected in piglets that were co-mingled from a SVA negative sow farm. Similar to sows, SVA detection on rectal and tonsil swabs in piglets lasted approximately 6 weeks post outbreak.
Conclusion: The study illustrates the variation of SVA shedding patterns in different sample types over a 9 week period in sows and piglets, and suggests the potential for viral spread between piglets at weaning.
In Canada and the USA alike, Senecavirus A is a challenge for producers and veterinarians because of its clinical similarity to Food and Mouth Disease (FMD). Indeed, Senecavirus A, is a causative agent of swine vesicular disease with lesions developing on the snout, around the mouth and on the coronary band of the feet. Therefore, being able to differentiate Senecavirus A infections from FMD rapidly is of utmost importance to be able to take the appropriate measures.
In the past months, several diagnostic tests have been developed at the University of Minnesota to detect antibodies against Senecavirus A. The difference between those tests and the in situ hybridization (ISH) described here is that ISH targets the genetic material included in the viral particle and marks it as a red spot as can be seen on the figure below. This advantage of this method is to be able to locate the virus and gives additional information to researcher wanting to study the behavior of Senecavirus A in the body of the pig.
Seneca Valley virus (SVV) is the causative agent of an emerging vesicular disease in swine, which is clinically indistinguishable from other vesicular diseases such as foot-and-mouth disease. In addition, SVV has been associated with neonatal mortality in piglets. While a commercial SVV qRT-PCR is available, commercial antibodies are lacking to diagnose SVV infections by immunohistochemistry (IHC). Thus, a novel in situ hybridization technique—RNAscope (ISH) was developed to detect SVVRNA in infected tissues. From a total of 78 samples evaluated, 30 were positive by qRT-PCR and ISH-RNA, including vesicular lesions of affected sows, ulcerative lesions in the tongue of piglets and various other tissues with no evidence of histological lesions. Nineteen samples were negative for SVV by qRT-PCR and ISH-RNA. The Ct values of the qRT-PCR from ISH-RNA positive tissues varied from 12.0 to 32.6 (5.12 x 106 to 5.31 RNA copies/g, respectively). The ISH-RNA technique is an important tool in diagnosing and investigating the pathogenesis of SVV and other emerging pathogens.
Dr. Matt Sturos, diagnostic pathologist at the University of Minnesota, Veterinary Diagnostic Laboratory will be presenting the latest information on Senecavirus A in swine, tomorrow at 4pm in a learning session organized by the Minnesota Veterinary Medical Association (MVMA). Participants can join in person at the MVMA conference room or online via WebEX.