What the Vancouver conference told us about PRRS

Sunday, February 6, 2011

Some more highlights from the nearly 2,000 papers presented at the 21st International Pig Veterinary Society last July

by ERNEST SANFORD

In the last issue, I covered some of the highlights of the 21st IPVS (International Pig Veterinary Society) Congress held for the first time in Canada (in Vancouver), July 18-21, 2010.  I also gave brief summaries of a few of the nearly 2,000 papers presented, concentrating on the PCV2 (Circovirus) papers. In this issue, I shall switch to PRRS and papers on some other topics, but before doing so I'll review one more PCV2 paper.

Report on the impact of early exposure of PCV2 in a vaccinated flow – Tom Gillespie, p. 377
Background. A 1,100-sow, farrow-to-wean, PRRS-naïve, Mycoplasma-positive herd, in which PCVAD had been well controlled by vaccination, suddenly observed a shift in the dynamics of PCV2 virus circulation. This resulted in an increase from 2.5 per cent to 10.8 per cent in nursery mortality at three weeks post-weaning and an increase from 1.77 per cent to 4.25 per cent in finisher mortality.
Thirty gestating sows from different breeding weeks and different parities were PCV2-positive by qPCR. One aborted fetus from a P1 sow was PCV2-positive, as were hearts from six fetuses with myocarditis. In addition, lungs from 68-day-old pigs were strongly PCV2-positive and necropsies demonstrated PCV2 enterocolitis. Colostrum from one sow was PCV2-positive and 30 per cent of suckling pigs in the herd were PCV2-positive by 20 days of age.
Take Home. The sow herd was PCV2 positive and sows were transmitting PCV2 to suckling piglets. This resulted in early (pre-vaccination) PCV2 exposure, increased nursery mortality and poor growth in nursery and finisher pigs.
The problem was resolved by mass PCV2 vaccination of sow herd and by moving piglet vaccination to earlier age (three weeks).
N.B. We are also seeing a changing pattern in Canada of PCV2 infection in herds that have been vaccinating their pigs for three to four years. The pattern is changing in some herds to an earlier (nursery pigs rather than finishers) age of infection.

Now to the PRRS papers.

A comparison of individual versus pooled sample testing on pool-level and case-level PRRSV PCR detection sensitivity and specificity
– Polson D, et al., p 206
Background. Assessing "time-to-negative-pigs" (TTNP) using serum from piglets within one week or less of weaning is a measure of the effectiveness of PRRS intervention.
This study aimed to determine the effect of sample pooling 5:1 versus 10:1 on PCR PRRS detection sensitivity and specificity at the pool and case levels when estimating TTNP. 
Results. There were comparable sensitivities for pools 5:1 (84.5 per cent positive) versus 10:1 (82.6 per cent positive) with PCR. And both 5:1 and 10:1 pools had 100 per cent sensitivity and specificity at the case level.
Take home. Pooling 10:1 has comparable pool and case-level detection sensitivity to pooling 5:1. It can therefore reduce testing cost for estimating TTNP.

PRRSV vertical transmission in a sow herd
– Cano J.P, et al., p. 149
Background. This was a study to determine the prevalence of PRRSV infected pigs and litters at birth and at weaning in endemically infected herds given live virus inoculation (serum inoculation).
Results. At four weeks post infection (PI), 26 per cent of litters were PCR-positive for PRRSV; 55 per cent were positive at weaning. At 12 weeks PI, eight per cent were positive at birth; 31 per cent positive at weaning. Between 52 and 77 per cent of PCR-positive litters had only one or two pigs within a litter positive at birth or weaning.
Take home. Current herd monitoring protocols might not be sensitive enough to pick up low numbers of PRRSV-positive pigs. The study supports sampling pigs at late lactation or at weaning.

PRRSV herd status factors in low density areas in Quebec
– Lambert M-E, et al., p 116
Take Home. Significant factors associated with herds being PRRSV-positive were having a neighbouring pig site closer than 1,500 metres and the absence of a specified entry protocol.

Long distance airborne PRRSV and Mycoplasma hyopneumoniae
– Dee S, et al., p. 153
Background. Distance of airborne travel of PRRSV was investigated using three PRRSV strains – 1-8-4, 1-18-2 and 1-26-2. Airborne Mycoplasma hyopneumoniae was co-investigated.
Take Home. PRRSV (1-18-4) was identified up to 9.1 kilometres from the source and Mycoplasma hyopneumoniae at up to 9.2 kilometres from the source.

MRSA in conventional and organic herds and wild boars
– Blaha T, et al., p 118
Background. The researchers tested nasal swabs or barn dust from conventional and organic herds and nasal swabs from wild boars for the MRSA (methicillin resistant Staphylococcus aureus) bacterium.
Results. There was a much higher incidence of MRSA in conventional versus organic herds (see table, right.) Possible reasons given were:
•    Higher pig density in conventional herds making transmission much easier;
•    Pig movement among conventional herds (seldom movement between conventional and organic herds);
•    Differences in antibiotic use between conventional and organic herds.
Take home. Conventional herds have considerably higher incidence of MRSA infection than organic herds, while wild boars might not have any MRSA at all. The MRSA infection in conventional herds is not directly related to antibiotic use.

MRSA in herds of fattening pigs in Germany: Typing results and factors associated with detection in herds
– Tenhagen BA, et al., p 119
Background. Pooled dust samples from 290 herds were cultured with a selective enrichment medium for MRSA, confirmed by triplex PCR.
Results. MRSA was identified in 152 herds (52.4 per cent). Larger herds using antimicrobials were more likely to be MRSA-positive. Tetracycline (28.3 per cent of herds), amoxicillin (19.7 per cent) and tylosin (17.6 per cent) were most frequently used in positive herds. No disease was associated with the MRSA in the positive herds.
Buying pigs from several different sources or from wean-to-grow operations was associated with MRSA. Fully slatted floors and AIAO pig flow were associated with isolation of MRSA from the dust samples. Multivariate analysis showed that larger herds used antimicrobials more often and bought pigs from more sources.
In the final model analysis, only farm size and farm type remained as significant risk factors. The risk factor most strongly associated with a positive test was herd size. This might be due to buying from different sources. Antimicrobial use was not a significant risk factor in this multivariate model.
Take Home. Having a large herd and buying pigs from many different sources were the biggest risk factors for a herd being MRSA-positive. Use of antimicrobials was not a significant risk factor for being MRSA-positive in this study.
N.B. In these two studies, MRSA was easily cultured from barn dust.

Epidemiology survey of Clostridium difficile in an integrated swine operation
– Harvey R, et al., p 785
Background. The most common Clostridium difficile (Cd) strain in pigs is NAP7, Toxinotype V. A new, highly pathogenic strain in humans that emerged since 2003 is NAP1, Toxinotype III. This strain is associated with hospitalized patients, but some concerns exist that it might be coming from pigs or pork. In this study, the prevalence of Cd in multi-age production groups was compared in a Texas integrated swine operation.
Results. A total of 252 Cd isolates were made from fecal samples across the herd. Of these, 175 came from farrowing room pigs, 37 from grow-finishing pigs, 14 from nursery pigs and 26 from breeding animals. Of the 252 Cd isolates, 239 were NAP7 or NAP7-like and 236 were Toxinotype V + V-like
Take Home. In this study, the Clostridium difficile isolated from pigs was not related to the common human C. difficile, indicating that the pig is not the source of C. difficile in humans. And, as pigs age, infection with C. difficile diminishes. BP

S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington. ernest.sanford@boehringer-ingelheim.com