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Genetically Resistant Line Stops E. coli Cold

Article-Genetically Resistant Line Stops E. coli Cold

Minnesota veterinarian Darwin Reicks had heard tales of how F18 E. coli scours ravaged North Carolina herds for several years. Top-producing nurseries were suddenly and sporadically hit with double-digit death loss rates. Control efforts showed limited results. Then last year, Reicks came face to face with the emerging E. coli disease in a 1,200-sow, farrow-to-finish operation he consults for, just

Minnesota veterinarian Darwin Reicks had heard tales of how F18 E. coli scours ravaged North Carolina herds for several years.

Top-producing nurseries were suddenly and sporadically hit with double-digit death loss rates. Control efforts showed limited results.

Then last year, Reicks came face to face with the emerging E. coli disease in a 1,200-sow, farrow-to-finish operation he consults for, just a short drive from his St. Peter, MN, Swine Vet Center office.

Sudden Impact

The impact was devastating in the operation's off-site, on-site, 1,000-head nursery. For over half a decade, this high-producing commercial operation consistently raised 24-27 pigs/sow/year with a very respectable 1% death loss in the nursery.

“All of a sudden, the nursery broke with this F18 toxigenic E. coli,” recalls Reicks. “All three production turns that went through this hot outbreak averaged 8-12% death loss. It would break very consistently at four weeks after entry, when pigs were 6 weeks old.” Pigs are weaned at 14 days of age.

Typically, pigs would look good one day, become severely dehydrated with a very watery diarrhea and die by the next day. Sometimes, they would lay on their sides and paddle, convulse and then die.

The infection would become widespread throughout the nursery, but unlike most viral infections, there were definitely some pigs that remained unaffected, notes Reicks.

The repeated losses ranked with the worst Reicks had ever seen in his 7½ years as a swine veterinarian.

Treatment Options Exhausted

After exhausting treatment options, live pigs were submitted for diagnostic workup to the University of Minnesota. Tests brought surprising results: the first case of F18 E. coli scours that Reicks had encountered.

During the first round of problems in the nursery, all pigs were injected with the antibiotic ceftiofur. Death loss still ended up about 8%, he says.

Before the second turn of pigs through the building, all eight conventional nursery rooms were washed and disinfected with two different disinfectants, fumigated and let sit empty for a week. Water medication, feeding the pigs gestation sow feed (Greatly reducing the protein level of the diet is supposed to lessen “feeding the bugs.”) and addition of a plasma protein product were all attempted.

All those efforts only dropped nursery death loss a couple of percentage points during that second turn of pigs, according to Reicks. And for the third group through the nursery, mortality was back to the 10-12% range.

Reicks says some pigs did bounce back, but others remained stunted, causing serious pig flow problems in finishing.

Boar Lines the Answer

Because he provides veterinary care for the PIC affiliate boar stud (Pork Storks) at Sleepy Eye, MN, the stud agreed to purchase DR2 (Disease Resistant marker 2) PIC boars which carry genes resistant for F18 E. coli. Those boars are specifically collected for the herd Reicks is treating for this enteric disease.

To achieve 100% genetic resistance to the F18 E. coli bacteria, both boar and sow lines must carry both copies of a recessive gene, he explains. The DR2 boars have been bred and identified to be totally resistant through the application of genetic marker technology.

This new breeding program is called EdemaGard, explains Butch Baker, DVM, director of Health Services in the Technical Services group of PIC. For more information, contact PIC at 1-800-325-3398 or access their Web site,

“The projections from PIC were that in this herd, just by using these terminal boars, the very first turn of pigs would be approximately 31% resistant,” Reicks says. A maternal PIC boar line is also being used to make replacements that are resistant. All sows are artificially inseminated.

That level of resistance is achieved in offspring by the producer using 100%-resistant grandparent boars (Line 19) to increase the population of resistant Camborough 22 sows on that farm, explains Reicks.

“So by increasing the percentage of resistance in the mother line down the road, and continuing to use 100%-resistant terminal boars, the percentage of resistance in the pigs will gradually climb from 31% to up around 70%,” predicts Reicks.

The number of resistant pigs in a nursery population required to prevent the expression of the disease is unknown and likely varies with different facilities and management, says Baker.

“What we are doing on this farm in southern Minnesota is changing this population to carry more and more of this resistant gene,” says Reicks.

Once semen from the DR2 line was used to produce disease-resistant offspring in the infected herd, the changes were immediate, observes Reicks. The very next turn through the nursery, performance rebounded (see Tables 1, 2). Death loss dropped back to about 1%. Average daily gains even exceeded those before the breaks, surpassing 1 lb./day, he notes. Before the break it was 0.8-0.85 lb./day. Nursery closeout weights jumped from 52 lb. to 62 lb.

And labor needs in the nursery dropped off significantly as staff discontinued regular treating and checking pigs and pulling out deads, says Reicks.

Except for the infusion of new genetics, feed and management programs remain unchanged from before the outbreak, he says.

Table 1. Nursery Performance with Genetic Marker Program (first turn)*
Total number in 1,063 head
Total number out 1,054 head
Avg. weight in 11.00 lb.
Avg. weight out 65.80 lb.
Total weight in 11,693 lb.
Total weight out 69,359 lb.
Total gain 57,666 lb.
Avg. daily gain 1.16 lb.
Feed efficiency 1.45 lb.
Total deaths 9 (0.9%)
*Assumes wean dates of April 11, 2001 (534 head) and April 18, 2001 (529 head).

Table 2. Nursery Performance with Genetic Marker Program (third turn)*
Total number in 1,108 head
Total number out 1,097 head
Avg. weight in 11.00 lb.
Avg. weight out 60.07 lb.
Total weight in 12,188 lb.
Total weight out 65,900 lb.
Total gain 53,712 lb.
Avg. daily gain 1.03 lb.
Feed efficiency 1.45 lb.
Total deaths 11 (1.0%)
*Assumes wean dates of Aug. 1, 2001 (544 head) and Aug. 9, 2001 (562 head).

Semen Cost, Payback

There's been a big savings in medication costs. No routine antibiotics are used. The herd is healthy except for being PRRS (porcine reproductive and respiratory syndrome) positive.

“The producer is paying a dollar per dose of semen more for this gene resistance,” says Reicks. Based on weaning a 10-pig average, the cost is 10-12 cents a pig.

He bases the return on investment (ROI) on just reduced death loss. A 10% death rate during the outbreak in the 1,000-head nursery is 100 head, minus the current 1% death rate is a 90-head difference. Ninety pigs multiplied by an estimated $40 feeder pig value equals $3,600. That figure, divided by the 1,000-head nursery capacity, equals $3.60/head on a 10-cent cost for a 30:1 ROI.


Management is topnotch. Nursery is run all-in, all-out with a two-week fill time. Sanitation is excellent. The farm has not had a history of E. coli scours or other serious disease problems.

All that effort apparently didn't stop F18 E. coli scours, he says. The only way it got in was during an expansion at the farm in 1999 when there was heightened truck and people traffic, he speculates.

In addition, the operation runs as a closed herd multiplier. Maternal boars are bred to an F1 female to produce internal gilt replacements. Just 25 females are brought into the herd twice a year to produce the F1 female line.

“A lot of herds have gone to this approach so they won't be introducing so many females all the time,” relates Reicks. Cost of gilt replacements was the same before and after the new breeding program was instituted, thus, not impacting the ROI, he notes.

Bacterial Pathogen Proves Hard to Treat

It hits top-performing herds hard. Poor nutrition and poor sanitation make it worse. Sometimes antibiotics, oral vaccines and other steps seem to help. Other times, they don't appear to help at all.

Welcome to the world of F18 E. coli scours, a bacterial pathogen that only strikes weaned pigs, explains Brad Bosworth, veterinarian for National Pig Development, the breeding stock division of Smithfield Foods of Virginia.

Bosworth was an early investigator into the F18 swine enteric disease problem several years back when he worked at the National Animal Disease Center in Ames, IA.

E. coli carry receptors that attach to the intestinal cell wall of the pig and produce enterotoxins that cause severe diarrhea. Some F18 are also able to produce what's known as a Shiga-like toxin that travels through the blood and causes damage to the lining of blood vessels. This damage causes edema disease (swelling of eyelids, forehead, etc.) and neurological symptoms.

A telltale sign of the F18 type of E. coli is its uncanny knack of striking pigs 2-3 weeks after placement in the nursery, says Bosworth. “Some producers can almost mark, to the day, when they are going to get it,” he says.

Like most swine enteric problems, transmission is fecal-borne, he stresses. Because there are a lot of lagoon recirculation systems in North Carolina, the organism thrived there first, he says. Sanitation and biosecurity are vital to breaking the cycle.

See Table 3 for a breakdown of enteric disease problems in North Carolina in 2000.

Farmland, IN, veterinarian Dale Hendrickson, who consults for five large clients in the Southeast, says, in his experience, cleanup takes extra effort.

Table 3. Incidence of Swine Enteric Problems in North Carolina (2000)*
Agent Percentages Found
Baby Pig Enteritis
Clostridium difficile 25
C. difficle with C. perfringens Type A 21
C. perfringens Type A 10
No infectious agent found 9
E. coli 8
C. difficle with E. coli 7
Coccidia 5
C. perfringens with E. coli 4
C. difficile with rotavirus 4
Transmissible gastroenteritis 2
Enterococcus durans 1
C. difficile with TGE 1
C. difficile with E. durans 1
C. perfringens with rotavirus 1
TGE with Coccidia 1
Postweaning Enteritis (partial list)
Ileitis 7.5
F18 E. coli 60
K88 E. coli 46
*Results compiled by Karen Post, DVM, Rollins Animal Disease Diagnostic Laboratory, North Carolina Department of Agriculture.

“If we got this bug in a nursery and didn't clean and disinfect and leave it sit empty a solid week to 10 days, we would about have to fumigate to kill it. Conventional disinfectant methods with leaving some manure in the pit hasn't broken the cycle very well,” he adds.

The F18 E. coli strain also has shown an ability to become resistant to antibiotics very quickly.

The problem with this strain is there is no commercially available vaccine approved, and that leaves producers with antibiotics as the major route of treatment, says Bosworth.

Hendrickson reports a number of producers are treating F18 E. coli fairly successfully with oral autogenous vaccine and the antibiotic combination BMD plus 3-Nitro (bacitracin plus roxarsone) from Alpharma. The antibiotic combination was introduced in the fall of 1998 with BMD at 30 g/ton and 3-Nitro at 34.1 g/ton for growth and feed efficiency in nursery and finisher pigs.

Alpharma says there have been reports of producer success in dealing with F18 and K88 E. coli problems when the antibiotic was used at 250 g/ton of BMD plus 3-Nitro at 34.1 g/ton. Company literature suggests the success of this combination may be related to the apparent synergy of the two compounds, which provides superior effectiveness to the use of either drug separately. For more information, log on to

While F18 E. coli seems to be gaining in intensity in the Midwest, it has slacked off a bit in the Southeast, says Hendrickson. For unknown reasons, the disease is highly sporadic.