Each year approximately 3% of the sow farms have a PRRS outbreak during the summer.
The incidence of summer PRRS breaks has been constant over the last 9 years.
There are geographical areas with higher or lower risk of summer breaks.
A summer outbreak was defined as a PRRS case that happened between June 21st and September 21st of the year. The mean incidence of PRRS summer outbreaks was 3.2% between 2009 and 2017, ranging between 1.6% and 4.4%. The trend was stable among the years. (Figure 1) Not all areas are equal against summer outbreaks. Indeed, the region of Southern Minnesota – Northern Iowa is more at risk of outbreaks than others like Southern Iowa or Eastern North Carolina. (Figure 2)
Biosecurity measures against PRRSV should therefore be a concern all year round for swine producers!
After being introduced in 1999, PRRS was eradicated from the country in 2012.
In 2013 PRRS was again detected, sequence analysis suggested this was a new introduction to the country.
The Chilean swine industry and the Chilean Veterinary Services (SAG) expect to again eliminate the disease in the near future.
PRRS is a notifiable disease in Chile. It was first detected in 1999, and in 2000 both the swine industry and government joined efforts to eradicate the disease by a series of coordinated events including a mixture of herd closure and depopulation of infected premises. Vaccination was not allowed in the country to control PRRSV infection. The eradication program was completed in 2007 and as a result, Chile was declared PRRSV free in 2012. Nevertheless, on October 2013 clinical signs compatible with PRRSV were reported in a commercial sow farm. Since then, all commercial herds performed surveillance activities according to a risk score based on location and biosecurity measures. From October 2013 to October 2017, approximately 153,000 blood samples have been analyzed.
Viral sequences obtained during the 2013 outbreak were compared to sequences from the early 2000s outbreak in Chile. Results showed a large genetic difference between isolates from both outbreaks. Further analyses demonstrated that the Chilean virus was closely related to a virus circulating in the state of Indiana in the US at the time of introduction. These results suggested that the latest PRRSV outbreak in Chile was most likely due to a new introduction into the country rather than a reemergence of a strain previously detected in Chile.
By October 2017, the disease was restricted to approximately 45,000 animals in six commercial farms owned by two companies that currently have eradication programs in place. These six infected commercial sites are clustered in three areas. (See figure above)
Piglet birth weight and colostrum intake are positively associated with pre-weaning survival and weaning weight.
Compared to piglets of similar birth weight, piglets with greater weight gain within the first day of life showed improved average daily feed intake and average daily gain in finishing and required fewer days on feed to reach market weight.
The study followed 808 piglets from birth to weaning and measured birth weight, colostrum intake, weight at 24 hours of life and weight at weaning. Results showed that a 1 lb increase in birth weight resulted in a 2.8 lb increase in weaning weight and increased piglet survival chances. Similarly, a 1 g increase in colostrum intake was associated with an 8.8 g increase in weaning weight.
To study consequences of early-life parameters on later stages of production, feed intake was recorded for 448 piglets from 74 days of age until the average pen weight reached 265 lb. Results showed that in both the low and high birth weight, a high colostrum intake increased the average daily gain and decreased the age at market.
Systematic monitoring of key production performance indicators allowed for early detection of PRRS outbreaks.
Number of abortions was the most efficient parameter, detecting outbreaks up to 4 weeks before being reported to MSHMP.
Early detection of signals associated with disease outbreaks may help in preventing further spread of the virus to other herds, and allowing implementation of rapid response intervention(s).
Two-years worth of reproductive performance data from a production system with 14 breeding herds (1,512 herd weeks) was gathered. Weekly data on number of abortions, pre-weaning mortality (PWM) and difference between total born and born alive (neonatal losses), were merged with weekly MSHMP PRRSV status. A statistical process control method was used to scan production data for significant deviations from baseline.
The time-to-detect outbreak, percentage of early detection of PRRSv-associated productivity deviations, and relative sensitivity and specificity of the production data monitoring system were determined relative to the MSHMP.
Abortion signals were detected 1 to 4 weeks before outbreaks were reported to the MSHMP. Most pre-weaning mortality signals coincided with the outbreak date reported to the MSHMP, and prenatal losses signals were detected from 1 to 3 weeks after the MSHMP reported outbreak date. Overall, the models had high relative sensitivity (range 85.7 to 100%) and specificity (range 98.5% to 99.6%) when comparing to the changes in
PRRS status reported in the MSHMP database.
“Over the years, there’s been considerable progress in the development of strategies aimed at eliminating porcine respiratory and reproductive syndrome virus (PRRSV). I define successful PRRSV elimination as the absence of clinical disease in the breeding herd and, more importantly, the absence of the vertical transmission of virus to weaned pigs. Unfortunately, successful PRRS elimination isn’t always achieved in some herds, and I have several experiences that may help answer why.”
Dr. Stricker then compiles six reasons that, in her experience, led to a failure in PRRS elimination:
No break in disease cycle or insufficient herd closure
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.”
The diversity of influenza A viruses in growing pigs is dynamic
Influenza A viruses can replicate as a swarm of viruses that are identical, closely related to each other (>99%), or clearly distinct (H1 vs. H3 subtypes)
Influenza A viruses of the same genotype can re-infect pigs within a short period of time.
132 3-week old piglets selected at weaning and placed in a wean-to-finish farm were sampled weekly for 15 weeks (n=2080 samples). Samples were tested by RT-PCR and the complete genome of influenza was obtained from 93 samples using next generation sequencing.
Two epidemic waves of IAV infection were detected with 3 distinct viral groups (VG swarms) found (VG1, VG2 and VG3). An H1 gamma (VG1) dominated the first outbreak, an H3 (VG3) dominated the second outbreak and an H1 beta (VG2) was only recovered when none of the two other viruses dominated.