DIAGNOSTIC NOTES, .

Diagnosis of Clostridium perfringenstype A enteritis in pigletsJim E Collins, DVM, PhD;Tim J Loula, DVM; Paul E Yeske, DVM

HistoryA 120-sow,continuously farrowing swine unit from Minnesotaexperienced an epidemic of diarrhea in 1- to 3-day-old pigs.Clinical illness, which usually began shortly after birth, wascharacterized by high morbidity (nearly 100%)and negligiblemortality « 1%).Diarrheic pigs remained vigorous, continuedto nurse, and recovered spontaneously in 4-5 days. Diarrheawas clinically unresponsive to treatment with gentamicin ortrimethoprim-sulfadimethoxine but respondedwell to spectin-omycin therapy. The illness did not adversely affect prewean-ing mortality rates, which remained low « 10%)despite thepersistent diarrhea in this herd throughout a 4-month period.Routine vaccination of sows against transmissible gastroen-teritis (TGB), rota virus, Clostridium perfringens type C, andEscherichia coli pilus types K88, K99, 987P,and F41 did not pre-vent or reduce the morbidity.

Laboratory exam inationsThree live, unmedicated, acutely diarrheic, 1- to 2-day-old pigswere presented for necropsy.The pigswere alert, active, ro-bust, and well hydrated and were excreting copious amountsof foamy,fluid, yellow feces. Grossly,lacteals throughout thelength of the small intestine contained chyle, and colonic me-senteries were slightly edematous. Microscopically,villi in thesmall intestine were long, slender, and lined by epithelial cellsdistended by colostral protein. A few neutrophils were in thelamina propria. Many spore-bearing Gram-positivebacilli werein the lumen and occasionally in apposition with epithelialcells at the tips of villi. Immunofluorescencetesting for TGBvirus and rotavirus were negative. Viruses were not seen byelectron microscopic examination of negatively stained feces.Aerobic culture of small intestine from each pig yielded amixedgrowth of coliforms. Anaerobic culture of small intes-tine of each pig yielded a dense growth of C perfringens.

Discussion

Clostridium perfringens type A enterotoxicosis, a sporadiccause of diarrhea in piglets, should be suspected in herds expe-

jEC: Department of Veterinary Diagnostic Medicine, University ofMinnesota, St. Paul, Minnesota 55108; TjL, PEY:Swine VeterinaryCenter, PA,St. Peter, Minnesota.

riencing diarrhea in nursing piglets if the following conditionsare present:

. diarrhea usually begins from 0-3 days of age;

. morbidity is high (> 90%)and mortality is low « 1%);

. affected piglets are robust, active, well-fed, and have liquidto creamy colonic contents;

. small intestine is normal in thickness and lacteals contain

chyle;

. other known enteropathogens are absent; and

. the disease often responds to antimicrobial therapy.

To establish a diagnosisof Clostridiumperfringens type Aenterotoxemia, specimens should first be examined for themore common enteric pathogens. Specimens required for opti-mal success in achieving an enteric disease diagnosis are listedin Table I.

If etiologic agents are not identified using conventionaldiagnostic methods, additional testing can be done to detectevidence of enterotoxigenic C perfringens. A diagnosis canusually be made based on history, absence of other entero-pathogens, the presence of typical small intestinal lesions, andby culturing a dense growth of C.perfringens from the je-junum. Microscopically, small intestinal villi are of normallength. There may be increased numbers of neutrophils in thelamina propria and large, Gram-positive, spore-bearing bacilliin the small intestinal lumen. (The microscopic lesions are inmarked contrast to the severe, highly fatal necrosis caused byCperfringens type C.)Anaerobic culture is useful if specimensare obtained from live pigs. Swabs should be collected fromjejunumbecauseCperfringensis part of the normal flora ofthe large intestine but is absent or found in low numbers inthe jejunum.Obtaininga densegrowthof Cperfringensfromthe jejunumof live, untreated pigsprovidesfurther evidenceof type A enterotoxemia. Detecting type A enterotoxin mayprovide additional supportive evidence, but this is not rou-tinely done and is not widely available to veterinarians in theUnited States.

Thepathogenesisof CperfringenstypeAdiarrheain pigletsisunclear. In humans, C perfringens type A causes food poison-ing by elaborating a 34,000-MWprotein enterotoxin whichacts on the mucosa of the intestinal tract, causing fluid and

24 SwineHealthand Production- September and October, 1994

electrolyte secretion in the ileum. The enterotoxin also in-duces secretion in the ileum of piglets. There are conflictingreports on the importance of enterotoxin in field cases of typeA enterotoxemia. Although some authors suggest that C.perfringens causes wasting, it has been our experience thatpiglets seldom die from the effects of C.perfringens type Aand growth rate is only mildly affected unless complicated byother enteric pathogens. Nonetheless, the disease is problem-atic because the diarrhea creates an unsanitary environmentand because producers often request veterinary intervention,it increases treatment costs.

Treatment and controlSpecific therapy and control procedures for C.perfringenstype A have not been determined. Procedures commonly usedfor C.perfringens type C have been implemented for type A.

. Sanitation procedures such as all-in-all-out pig flow andwashing and disinfecting between each farrowing groupreduce exposure. Washing the sow prior to bringing herinto the farrowing house also helps reduce piglet contami-nation, as does routine scraping of farrowing house sowmanure prior to farrowing and during the first week oflife.

. Colostrum uptake (timing, quality, and quantity) is veryimportant to get maximum benefit from the sow's naturalimmunity.

. Heat-lamp management is critical to avoid stress and im-munosuppression caused by chilling.

. Feed-grade antibiotics such as BMDTMat 250 g per ton havehad some benefit when fed from 2 weeks prefarrowingthrough lactation.

. Individual piglet treatment (oral or injectable routes) hasbeen successful in most cases,although evaluation of suchtreatment is questionable because many piglets recover ifleft un treated. In jecta ble gentamicin, penicillin,spectinomycin, and neomycin have been used successfullyto reduce clinical signs of piglet diarrhea.

. Back feeding has been practiced with som~ success, utiliz-ing manure from sows in the farrowing house and pigletdiarrhea. The material is fed to gestating animals one tothree times during the period 2-5 weeks prefarrowing.

. Success of autogenous vaccines is difficult to evaluate be-cause autogenous vaccination is usually just one of manytreatment or control procedures employed simultaneously.

More research and clinical trials must be conducted to deter-

mine the effects of C.perfringens type A on preweaning mor-tality and weaning weights.

References

1. Bergeland ME,Henry Sc. Infectious diarrheas of young pigs. In:Veterinary Clinics of North America: Large Animal Practice. Volume4. Symp on Diagn and Treat of Swine Diseases. 1982:389-399.

2. Collins JE, Bergeland ME,Bouley D, Ducommun AL,Francis DH,Yeske P. Diarrhea associated with Clostridium perfringens type Aenterotoxin in neonatal pigs. J Vet Diagn Invest 1989; 1:351-353.

3. Estrada Correa AE,Taylor DJ. Porcine Clostridium perfringens typeA spores, enterotoxin and antibody to enterotoxin. Vet Rec.1989;124:606-610.

4. van Damme-Jongsten M,Haagsma J, Notermans S. Testing strains ofClostridium perfringens type A isolated fr()m diarrheic piglets for thepresence of the entertoxin gene. VetRec. 1990;126:191-192.

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