Human Spread of PRRS Virus Appears Unlikely

The virus that causes porcine reproductive and respiratory syndrome (PRRS) doesn't appear to easily spread from people to pigs.

The study done at the Purdue University research farm did show that people could be contaminated with PRRS viral RNA after exposure. But actual transmission from people to sentinel pigs could not be documented, according to Sandy Amass, DVM, lead researcher in the National Pork Producers Council project.

There is scant scientific evidence to support the theory that humans can spread porcine pathogens, she says. The only scientifically proven case is that of foot-and-mouth disease.

Yet many farms maintain strict biosecurity measures to keep people from spreading pig diseases.

In the study at Purdue, researchers placed 70 pigs - 12 days old and PRRS-free - in three treatment groups of 20 pigs each and one control group of 10 pigs. Each group was housed in separate rooms in isolation facilities.

The first three groups of pigs were sentinel groups. The fourth contained the pigs that were artificially infected at the isolation facility.

Ten people known not to have had contact with hogs for at least seven days prior to the study were divided into two groups. All 10 had direct contact with infected pigs for one hour, seven days after disease challenge, when pigs were showing clinical signs of PRRS.

Group 1 participants were immediately exposed to Group 1 sentinel pigs for one hour after their contact with infected pigs. The five people in Group 2 showered, changed clothes and put on new boots before exposure to Group 2 sentinel pigs. Group 3 sentinel pigs were control pigs and were not in contact with exposed people.

Saliva, nasal and fingernail swab samples were taken from participants before exposure to infected pigs to prove all were negative for PRRS. Samples were also taken following exposure to infected pigs, right after showering, at four to 10 hours after exposure and every 24 hours for 96 hours. PRRS virus was detected on two of 10 people in saliva and fingernail rinse samples immediately after one-hour contact with infected pigs. The virus was found on a third person in a fingernail rinse sample at five hours after contact, and it was found in a fourth person in a nasal swab sample 48 hours following contact with infected pigs.

No uninfected, sentinel pigs became infected with PRRS from exposure to persons in direct contact with PRRS-infected pigs, regardless of whether biosecurity practices were followed.

But Amass cautions those findings don't rule out the possibility that people are vectors for PRRS transmission. "The probability of pathogen transmission is dependent on multiple factors including host susceptibility, likelihood of pathogen shedding by infected pigs, exposure dose, frequency of exposure and viability of pathogen outside the host," she says.

Researchers: Sandra F. Amass, DVM; Gregory Stevenson, DVM; Purdue University. Phone Amass at (765) 494-8052 or e-mail amasss@vet.purdue.edu.

Vaccine Interaction Concerns Unfounded

Concerns that giving a modified-live-virus porcine reproductive and respiratory syndrome (PRRS) vaccine before Mycoplasmal pneumonia vaccination would interfere with mycoplasma vaccine protection are unfounded, according to Iowa State University (ISU) researchers.

In earlier work, ISU scientists found that PRRS vaccination or disease challenge during or after mycoplasma infection decreased the ability of mycoplasma vaccine to reduce disease following that experimental infection.

Many pork producers commonly vaccinate for PRRS at weaning before giving the first dose of mycoplasma vaccine rather than giving the PRRS vaccine before or after the second dose of mycoplasma vaccine.

ISU researchers obtained funding from the National Pork Producers Council to take the next step to find out if PRRS vaccination prior to mycoplasma vaccination decreased the efficacy of mycoplasma vaccination, says ISU lead researcher Eileen Thacker, DVM.

In this case, ISU scientists concluded that PRRS vaccination one week before mycoplasma vaccination had no impact on the efficacy of mycoplasma vaccination.

PRRS antibody titers (measure of how much antibody is circulating in the pig's bloodstream) were lower in pigs receiving both PRRS vaccine and two doses of mycoplasma vaccine, compared to those pigs receiving PRRS vaccine alone.

In contrast, mycoplasma antibody titers were highest in pigs receiving both PRRS and mycoplasma vaccines followed by mycoplasma disease challenge, says Thacker.

Analysis of lung fluids revealed that mycoplasma-vaccinated pigs had high levels of mycoplasma-specific antibodies regardless of PRRS vaccination status.

More importantly, PRRS vaccination didn't reduce protection against Mycoplasmal pneumonia provided by mycoplasma vaccination.

Researchers: Eileen Thacker, DVM, Pat Halbur, DVM, Brad Thacker, DVM, and Tamara Boettcher, DVM, Iowa State University. Phone Eileen Thacker at (515) 294-5097 or e-mail ethacker@iastate.edu.

Rotating Similar Antibiotics Produces Most Resistance

Significant levels of antibiotic resistance were recorded in trials in which similar antibiotics were used in rotation to treat artificially infected pigs.

University of Tennessee-Knoxville researcher Alan Mathew conducted two trials for the National Pork Producers Council to determine the effect of drug combinations and regimens on antibiotic resistance.

One hundred forty-four 18-day-old weaned pigs were given doses of Salmonella typhimurium and K88 E. coli before being placed on feed- and water-based antibiotics. Drug treatments included maximum label use, rotation of similar and non-similar antibiotics, increasing gradient doses and pulse doses for two weeks after disease challenge. There was also a control group that didn't receive any antibiotics.

Antibiotic resistance was observed to a greater degree in the non-pathogenic E. coli, compared to salmonella typhimurium. Greater resistance also was seen when similar antibiotics (apramycin, gentamicin, neomycin) were used in rotation, compared to other treatments and during label use.

Rotational use of like and unlike antibiotics produced the greatest resistance to sulfamethazine.

The highest levels of antibiotic resistance also were observed during or just after rotation of similar antibiotics.

The six treatment regimens and the results are detailed in Tables 1-4. Treatments included: (1) control, no antibiotics; (2) apramycin at 150 g./ton of feed for 14 days (maximum label duration); (3) gradient application with apramycin at 50 g./ton of feed for five days, then 100 g./ton of feed for five days, then 150 g./ton of feed for four days; (4) pulse dosing with apramycin at 150g/ton of feed for three days, off three days and repeating that sequence for 14 days; (5) rotation with apramycin for four days, followed by sulfamethazine in drinking water (118 mg./kg. of body weight) for four days, carbadox at 50g./ton of feed for four days; and (6) rotation with apramycin in the feed, gentamicin in drinking water (25 mg./gal. of water), neomycin sulfate (22 mg/kg body weight) in the drinking water.

To test these various antibiotic regimens, fecal samples were collected before antibiotic treatment and three days after disease challenge, at three, seven, 10, 14 and 28 days after start of antibiotics, then twice a month until pigs reached market weight.

Mathew offers several caveats for the study results.

First, recovery of pathogenic K88 E. coli was very low. This may have been due to competition from the presence of salmonella. This left only non-pathogenic E. coli for resistance testing.

Second, antibiotic resistance for salmonella remained relatively low in the study, in contrast to earlier work. This may have been due to housing the pigs in a new facility.

Third, antibiotic resistance decreased after drug withdrawal to the point that of no differences in resistance patterns compared to controls at 31 days post challenge.

Use of different antibiotics, other housing and management conditions, or prolonged use of antibiotics in pigs produces more long-term antibiotic resistance to bacteria, says Mathew.

Researcher: Alan Mathew, University of Tennessee-Knoxville. Phone Mathew at (865) 974-7291 or e-mail amathew @utk.edu.