Swine dysentery is a mucohemorrhagic, exudative disease with lesions confined to the large intestine of pigs. Estimates from a 1976 survey by the Livestock Conservation Institute indicate an 88% increase in incidence of the disease in the United States since a similar 1972 estimate. This approximates a total annual loss of $64 million to the swine industry

Glock, R. D.

Schwartz, K. J.

English

Swine dysentery is a mucohemorrhagic, exudative disease with lesions confined to the large intestine of pigs. Estimates from a 1976 survey by the Livestock Conservation Institute indicate an 88% increase in incidence of the disease in the United States since a similar 1972 estimate. This approximates a total annual loss of $64 million to the swine industry.</p

Schwartz, K.

Glock, R.

Digital Repository @ Iowa State University (ISU)

Swine Dysentery --A Practitioner Update by K. J. Schwartz, B.S.* R. D. Glock, D.V.M., Ph.D.t Swine dysentery is a mucohemorrhagic, exudative disease with lesions confined to the large intestine of pigs. Estimates from a 1976 survey by the Livestock Conservation Institute indicate an 88% increase in in-cidence of the disease in the United States since a similar 1972 estimate. This ap-proximates a total annual loss of $64 million to the swine industry. Swine dysentery as a specific disease was originally described by Whiting, et ai., in 1921 (18). At that time a spiral-shaped organism was associated with the disease, but oral administration of mixed cultures of spiral-shaped organisms failed to produce the disease. In 1948, Doyle reported successful reproduction of swine dysentery in conventional pigs by oral inoculation with Vibrio coli (1). This report, however, could not consistently be substantiated by other workers. The etiology remained largely unknown and unpursued until the 1960's when a trend toward confinement swine units and an emerging ineffectiveness of chemotherapeutic agents resulted in an increase in incidence of swine dystentery. Renewed research efforts again indicated a primary involvement of a large spirochete. Before 1971, the evidence of spirochete pathogenicity was largely circumstantial due to a failure to propagate the organisms in vitro, and consequently the inability to fulfill Koch's postulates. In 1971, Taylor and Alexander propagated a large anaerobic spirochete in pure culture and successfully induced swine dysentery by oral inoculation of pigs • K. Schwartz is a third year Veterinary student. t Dr. Glock is an professor of pathology at Iowa State University. 104 (16). The pathogenicity of the large spirochete was confirmed by Harris, et al., and further characterized and named Treponema hyodysenteriae by the Iowa State workers (5). Treponema hyodysen-teriae is now accepted as the primary pathogenic agent in swine dysentery, but in germ-free pigs this organism alone will not cause disease. Meyer, et al., has recently shown that germ-free pigs develop lesions similar to swine dysentery when inoculated with pure cultures of T. hyodysenteriae in the presence of four anaerobic gram-negative organisms (12). It is uncertain whether T. hyodysenteriae alone possesses all determinants necessary for pathogenicity. It is possible that the other organisms contribute pathogenic deter-minants or provide environmental factors necessary for the expression of pathogenicity by T. hyodysenteriae. Of course, other parasitic organisms may potentiate pathogenic effects of T. hyodysenteriae. The isolation and propagation of T. hyodysenteriae, once tedious, has now become a rather routine technique for researchers, as well as a diagnostic aid for the practicing veterinarian. Treponema hyodysenteriae is a gram negative, oxygen-tolerant, anaerobic spirochete always found in high numbers in the colon and cecum of acutely affected pigs (10). Morphologically, T. hyodysenteriae is a loosely coiled, spiral-shaped organism with motility by ser-pentine motion. The organism is hemolytic, stimulated by hydrogen and best propagated at a temperature of 42°C. Swine dysentery is most commonly observed in 30 to 170 pound pigs but may also occur in suckling and adult animals. Iowa State University Veterinarian 'I I ) I SUSCEPTIBLE TO CANINE DISTEMPER? Maybe yes, maybe no. It really doesn't matter. Because 96% of all puppies now can be protected against canine distemper as early as 6 weeks of age regardless of maternal immunity level. The answer is 'Enduracel D-M ' , the combination distemper-measles vaccine for use in puppies 6-12weeks of age, End the guesswork. Talk with your Norden Field Representative. Caution: This vaccine should not be used on female pups over 12 weeks of age or older b,tches because maternal measles immunity may override the vaccine when used in pups of the next generation. US Pa' 3.616.203 Canadian Pat 1969 829.277 ENDURACELE'D-M N 105 Pigs are the only known reservoirs of T. hyodysenteriae and may shed virulent T. hyodysenteriae in the absence of clinical signs. Transmission of the disease appears to be by ingestion of fecal material from either clinically affected or clinically normal carriers of T. hyodysenteriae. Acutely affected animals tend to shed organisms in very high numbers which may lead to rapid transmission and more severe, explosive outbreaks. Obviously, strict sanitation is of great value in limiting swine contact with contaminated feces. The organisms appear quite resistant wheri in moist en-vironmental conditions; they remain viable for 1 week in feces at room temperature. Also, feces-contaminated fomites such as boots, vehicles, and equipment may transport viable organisms, all of which underscore the need for strict sanitation procedures. The incubation period of swine dysentery is extremely variable but usually occurs within 10-14 days. Dia,rrhea is the most consistent clinical sign of swine dysentery, with .. classical signs including blood and mucus in feces (15). The severe diarrhea ultimately leads to dehydration, acidosis and death of the animal. The gross lesions include hyperemia and edema of the gut wall with severe mucofibrinous to hemorrhagic enteritis diffusely found in the large intestine. Gross and microscopic lesions, as well as other pathological changes, have been well described by Glock, 1971 (2). Diagnosis of swine dysentery should be attempted only with consideration of other potential causes of diarrhea that involve the large intestine, namely, salmonellosis and trichuriasis. Factors to consider include herd history, clinical signs, gross lesions, microscopic lesions and diagnostic aids. A highly reliable method of diagnosis in-cludes a thorough necropsy of affected animals with the microscopic observation of large numbers of spiral-shaped T. hyodysenteriae in colonic scrapings using darkfield examinations' of wet mounts or brightfield examinations of smears stained with crystal violet followed by Gram's iodine. Salmonella isolation should be attempted from colonic contents, mesenteric lymph nodes and other viscera to exclude salmonellosis, bearing in mind 106 that both diseases may occur simultaneously. It has become increasingly apparent that nonpathogenic forms of T. hyodysenteriae do exist in both normal and affected pigs. Obviously, nonpathogenic T. hyodysen-teriae complicate the diagnosis of acutely infected animals as well as the detection of carrier animals. Presently, the most reliable method of detecting asymptomatic carrier animals and confirming acute cases of swine dysentery involves the culture of rectal swabs or colonic scrapings. Songer, et ai., have developed a selective medium of trypticase soy agar with 5 % bovine blood containing 400 mcg spectinomycin per milliliter which is incubated at 42°C. in an anaerobic environment (14). Kinyon's method of differentiating pathogenic and nonpathogenic T. hyodysenteriae is based on the observation that pathogens are strongly beta hemolytic while non-pathogens are only weakly so (11). It has also been noted that both pathogenic and nonpathogenic T. hyodysenteriae may be present concurrently in the same animal. Diagnosis of acutely infected animals, then, can be confirmed by microscopic observation of T. hyodysenteriae and/or culture attempts. Culture techniques will detect some asymptomatic carriers but require more expertise and experience. It is thought that the technique may be useful on a herd basis rather than for screening individual animals. Serological tests, such as Joens' microtiter agglutination (9) or Jenkins' passive hemagglutination test (8), have been shown sensitive and reproducible in detecting antibodies to T. hyodysenteriae in convalescent animals following clinical disease but are not useful in detecting asymptomatic carriers. More research is needed to develop a rapid, accurate, and reliable test for carriers. Successful swine dysentery control must include careful analysis of the management situation and a judicious utilization of chemotherapeutic agents_ Management efforts must decrease stress that may be in the form of overcrowding, filth, ex-tremes of temperature, transportation, nutrition, or other disease. It is of major importance to practice strict sanitation procedures. Swine dysentery severity can be directly correlated with the amount of Iowa State University Veterinarian contaminated feces which are ingested. Poor sanitation increases the probability of transmission of the disease within the herd as well as contributes to clinical severity of the disease within individual animals. Movement of swine, vehicles and equip-ment between herds and infected pens should be carefully controlled_ Chemotherapeutic agents for swine dysentery, unfortunately, have not yielded consistent results in the elimination of T. hyodysenteriae from infected herds. Most drugs licensed in the U.S., if efficacious, serve only to temporarily suppress clinical disease with recurrence of dysentery in 3-6 weeks. Presently, drugs of choice used as feed additives for prevention and follow-up treatment include carbadox. lincomycin, and virginiamycin. Acute infections are best treated with injectable or water medications (see table) (6). At the present time gentamicin. lincomycin, nitroimidazoles. tylosin or arsenic com-pounds appear to be most efficacious. Practitioners should be cognizant of all regulations and withdrawal times gover-ning drug usage. Unofficial field reports from veterinarians indicate that prolonged treatment of problem herds with nitroimidazole compounds and possibly lincomycin may eliminate T. hyodysen-teriae from the infected herds. Currently, there are no nitroimidazole compounds labeled for use as feed additives for swine; to use them as such· is illegal. Nitroimidazoles may be legally prescribed by the veterinarian as a drinking water medication. However, both practitioner and client are then responsible and liable for its usage and withdrawal from market animals. Regardless of the medication program utilized, it may be useless if undertaken without proper management considerations. Initial treatment must be for a long enough period of time. usually at least two weeks. This must be followed by an adequate preventative treatment program. Any medication program must be coupled with providing a cleaner, less stressful environment for animals. Any treatment regimen must be carefully thought out and adapted to the individual producer's situation. Persistence of swine dysentery within a herd may indicate the need for total depopulation. Economic impact will be the major consideration since production will be lost for an extended period. To increase chances of success, depopulation should be undertaken during the warmer, dryer months of the year. The premises must be TABLE 28.2-Dosage level, duration of administration, and withdrawal time for various drugs used for the treatment and/or prevention of swine dysentery Treatment "'ithc!r;mal Compound I.c·eel Dnratio'l Prevcntivc Lcvel Timc (ria) • (ria) Bacitracin 100 g/ton fecd 6 50-100 g/ton feed :"\otle Carbadox 50 g/ton feed Continuously 50 g/ton feed 70 Chlortetracycline 100-200 g/ton feed 3-5 50-100 g/ton fecd ;-':onc Dimetridazole- 0.025% in water 5 100 g(ton feed :\Dt Furazolidone 300 g/ton feed 14 100 g/ton feed 1'\'ol1e Gentamicin- 50 mg/gal 3-5 :'\]) ;-':0 Ipronidazole- 0.005% in water 7 100 g/ton feed ::"-10 Lincomycin 100 g/ton feed 21 40 g/ton feed ::"-10 Neomycin 140 g/ton feed 3-5 100 g/ton feed 20 Oxytetracycline 100 g/ton feed 3-5 50 gl ton feed :'\one Ronidazole· 0.006% in water 5 :'\0 Sodium arsanilate 4.5 grains/gal water 5-7 5 90 g/ton feed 5-7 90 g/ton feed 5 Tylosin 0.25 g(gal water 5-6 100 g/ton feed :'\one 200 mg/da (injectable) 3 4 Virginiamycin 100 g/ton feed 14 25 g/ton feed :'\0111' - These compounds were not approved for administration to swine in the United States at the time this table was compiled. tNot determined. Table was reprinted from Diseases of Swine, 4th ed. by permission of ISU Press. Issue No.3, 1976 107 thoroughly cleaned and disinfected. Survivability of T. hyodysenteriae is not precisely known, but the organism is viable in moist feces at least I week and may survive in pits and lagoons for an un-determined time (3). Therefore, efforts must be made to eliminate all fecal con-tamination from the farm. If depopulation is undertaken, one must attempt to obtain uninfected replacement stock. Presently, there are no good detection methods available to the practitioner so one must rely on a complete history of the source herd. Specific pathogen free herds may be given consideration as a source of replacement of breeding stock. Eradication of swine dysentery is not feasible at this time. The high incidence of the disease, the lack of sensitive, accurate diagnostic techniques, and inadequate understanding of epidemiology and of etiological relationships all suggest that attempts must be made to control the disease rather than eradicate it. The chronicity of swine dysentery within herds and individual animals was long thought to indicate no stimulation of im-mune mechanisms. Terpstra, et al., demonstrated circulating antibodies specific for T. hyodysenteriae in con-valescent pigs (17). Olsen has shown that convalescent pigs exhibit resistance to reinfection with T hyodysenteriae (13). Attempts by Hudson, et ai., and Joens to orally immunize pigs with attentuated cultures of T. hyodysenteriae have failed (7). However, Glock, et ai., have reported that intravenous hyperimmunization of animals with inactivated T. hyodysenteriae has provided protection against an oral challenge with a homologous isolate (4). Glock has theorized that circulating an-tibodies may confer protection by exudation at the site of lesions but does not discount potential for local immune mechanisms to be involved. Presently, there is no practical way to immunize pigs against swine dysentery, but the search continues for an effective vaccination method. REFERENCES 1. Doyle, L. P. 1944. A Vibrio associated with swine dysentery. Am J. Vet. Res. 5;3 ..... 1948. The etiology of swine dysentery. J. Am. Vet. Med. Assoc. 9:50. 2. Glock, R. D. 1971. Studies on the etiology, 108 hematology. and pathology of swine dysentery. Ph.D. diss. Iowa State Univ. Ames. 3. Glock, R. D.; Vanderloo, K. J.; and Kinyon, J. M. 1974b. Survival of certain pathogenic organisms in swine waste lagoon water. J. Am. Vet. Med. Assoc. 4. Glock. R. D.; Schwartz, K. J.; and H~rris. D. L.; Experimental Immunization of Pigs Against Treponema hyodysenteriae in Proceedings. In· ternational Pig Veterinary Society Congress, Ames, Iowa (1976). 5. Harris. D. L.; Glock. R. D.; Christensen, C. R.; and Kinyon. J. M.; 1972. Swine dysentery: Inoculation of pigs with Treponema hyodysen· teriae (new species) and reproduction of the disease. Vet. Med./Small Animal Clin. 67:61. 6. Harris, D. L. and Glock, R. D.; Swine Dysentery. in 4th ed. Diseases of Swine edited by Dunne, H. W. and Leman. A. D. Iowa State University Press, Ames, Iowa. (\975) 7. Hudson. M. J.; Alexander, T. J. L.; Lysons, R. J.; and Wellstead. P. D. 1974. Swine dysentery: Failure of an attenuated strain of spirochaete, given orally. to protect pigs against subsequent challenge. Crit. Vet. J. 130:37. 8. Jenkins. E. M.; Vance, R. T.; Pier. A. C.; Sinhi, P. P.; Humoral Antibody to Treponema hyodysenteriae in Swine. Abstract in Proceedings, Conference of Research Workers in Animal Disease, Chicago. II (1975) 9. Joens, L. A.; Harris, D. L.; Kinyon, J. M.; and Kaeberly. M. L.: Detection of Antibodies to Treponema hyodysenteriae. Using a Microtiter Agglutination Test. In Proceedings, International Pig Veterinary Society Congress. Ames, Iowa (1976). 10. Kinyon. J. M.: 1974. Characterization of Treponema hyodysenteriae isolated from out-breaks of swine dysentery. M.S. thesis. Iowa State Univ., Ames. II. Kinyon, J. M.: Harris, D. L.; Glock, R. D.: En· teropathogluicity of various isolated of Treponema hyodysenteriae. "Bacterial and Mycotic In· fections." Submitted. . 12. Olson, L. D.: Clinical and Pathological Ob· servations on the Experimental Passage of Swine Dysentery. Canad. J. Compo Med. 38:7·13 (1974). 13. - - -. 1974. Clinical and pathological ob· servations on the experimental passage of swine dysentery. Can. J. Compo Med. 38:7. 14. Songer, G. J.: Kinyon J. M.: and Harris, D. L.: (1976) Selective Medium' for .Isolation of Treponema hyodysenteriae. J. of Clin. Micro. V. 4:57. 15. Sorensen. D. K. 1970. Dysentery. In Diseases of Swine, 3rd ed. Iowa State Univ. Press. Ames. p. 486. 16. Taylor, D. ].; and Alexander. T. J. L.: 1971. The production of dysentery in swine by feeding cultures containing a spirochaete. Crit. Vet. J. 127: 108. 17. Terpstra, J. I.: Akkermans. J.P.W.M.: and Ouwerkerk, H.: 1968. Investigations into the etiology of vibrionic dysentery (Doyle) in pigs. Neth. J. Vet. Sci. 1:5. 18. Whiting, R. A.: Doyle, L. P.; and Spray. R. S.: 1921. Swine dysentery. Purdue Univ. Agr. Exp. Sta. Bull. 257:3. Iowa State University Veterinarian 

Swine Dysentery - A Practitioner Update

https://dr.lib.iastate.edu/handle/20.500.12876/46899

Swine Dysentery - A Practitioner Update

Abstract

Similar works

Full text

Available Versions

Digital Repository @ Iowa State University (ISU)