Volume 19 | Issue 2 Article 6

1957 Enterotoxemia of Sheep Donald Wise Iowa State College

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Recommended Citation Wise, Donald (1957) "Enterotoxemia of Sheep," Iowa State University Veterinarian: Vol. 19 : Iss. 2 , Article 6. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol19/iss2/6

This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. ENTEROTOXEMIA OF SHEEP

Donald Wise

NFECTIOUS enterotoxemia i san tive fermentation of carbohydrates and I acute, highly fatal toxemia of sheep, the production of type D exotoxin.9 which is produced by the anaerobic bacil­ PATHOGENESIS lus, Clostridium perfringens (Clostridium welchii) type D, and is characterized by Enterotoxemia occurs in lambs that are sudden prostration and congestion of the receiving a large supply of their mother's abomasum and small intestineY milk, feeder lambs on a high carbohy­ The exotoxin is absorbed into the body drate ration and under conditions where through the intestinal wall. A close rela­ sheep are allowed to have access to large tionship exists between the production of amounts of feed such as pasturing down exotoxin by Clostridium perfringens and wheat fields. the heavy feeding of lambs, which is in­ Mechanism of Invasion dicated by the fact that under average feeding conditions Clostridium perfring­ Since Clostridium perfringens is a pro­ ens lives in the intestinal tract as a non­ ducer of an exotoxin, it follows that an pathogen. Heavy feeding is apparently a invasion of tissues is not a prerequisite predisposing factor that is necessary in for the production of a diseased condition. order that Clostridium perfringens may An absorptive surface such as the mucosa produce a fatal exotoxin that is absorbed ofthe intestine plus the exotoxin is all by the body. that is required to produce a :toxic con­ dition in the animal. Invasion of the in­ SYNONYMS testinal mucosa does occur and its extent is usually limited by the muscularis mu­ Exterotoxemia is known by other cosa.ll names, such as "pulpy kidney disease," The organisms are non-motile, thus "milk colic," "overeating disease," "apo­ motility is not involved in 10comotion.1O plexy" and "braxy-like disease." Movement of the organisms is done en­ tirely by peristalsis and other intestinal ETIOLOGY movements and movement of villi. Enterotoxemia is a combination of in­ The organisms enter the lumen of the fectious and nutritional disease problems. intestine and fill the intestinal crypts. If The etiology of enterotoxemia is the pre­ anaerobic conditions are present the bac­ sence of Clostridium perfringens, the ac- teria may multiply. 1\ Large amounts of milk ingested at this time neutralizes the acidity and the bacteria multiply at a very Mr. Wise is a senior in veterinary medicine. This paper was originally prepared for Dr. F. rapid rate. Toxin which is produced is K. Ramsey's course in special pathology. absorbed in very large amounts.

Issue 2, 1957 107 Natural cases of enterotoxemia in feed­ of toxin in the anterior portion of the er lambs are due to the feeding of large small intestine and some means of localiz­ quantities of corn, milk, barley, peas, cane ing the toxin for a period of time. 1 and other feeds which tend to produce an alkaline medium. The large quantities of Localization of Clostridium feed may cause engorgement of the intes­ perfringens in the Intestine. tine. The feeds swell as water is absorbed Clostridium perfringens is unable to and the result is a decreased rate of pas~ multiply in wounds, tissues or the blood sage of ingesta through the gut or stasis stream, which is due to the fact that the which allows time for absorption of toxic bacteria are anaeJ:1obic.ll The blood stream quantities of the exotoxin. The stretching contains oxygen which is bound with he­ of the intestinal wall by the food produces moglobin; thus Clostridium perfringens atony of the musculature. Atony of the is unable to produce a bacteremia. musculature results in a decrease of per­ Clostridium perfringens becomes local­ istalsis and a stasis of intestinal contents. ized in the intestinal tract because the Judging from Cole's statement the les­ portal of entry is the mouth and the mu­ sened exercise along with fatness encour­ cosa of ,the intestine is the only place ages the lowering of the tonus of the in­ where the extensive absorption of toxin testinal musculature, thus favoring stasis can 'Occur. The spores of the bacteria are of the ingesta.7 Experiments have shown that oral ad­ the forms that are ingested. The bacteria ministratron of Clostridium perfringens are unable to multiply in the rumen and exotoxin to sheep will not produce symp­ duodenum, because the high acidity des­ toms of enterotoxemia. However, enter­ troys all vegetative forms 'Of the bacteria. After the spores enter the intestinal tract oxemia is produced if opium or belladon­ i~ na are administered with the exotoxin. multiplication of bacteria is very rapid the alkaline medium, if anaerobic condi­ These two drugs are capable of inducing stasis of the intestinal contents by de­ tions are present. creasing peristalsis. . The engorgement of the intestine with Iron is an esential mineral for the feed, especially carbohydrates, is another growth of Clostridium perfringens and the factor which is important in the multipli­ homo lactic fermentation of this organism. catiqn of bacteria. Engorgement of the in­ Apparently the iron 'Of foodstuffs supplies testine decreases peristalsis and other in­ the necessary requirements f'Or growth in testinal movements, thus stasis of the food the intestine. Investigators beleive that results. This condition allows impaction of the essentiality for iron is due to the need the ingesta, which aids in the production for the function of aldolase. Aldolase is of anaerobic condition. Stasis of the food the enzyme which converts hexose phos­ also allows the necesary time which is re­ quired for the absorption of exotoxin into phate to triose phosphate in the forma­ tion of energy rich phosphate bonds.! the blood vessels of the mucosa. Another reas'On that explains why Clos­ Magnesium is another mineral that is tridium perfringens exerts its action in essential for the cell dividing mechanism the intestine is that trypsin is required of Clostridium perfringens. An excess or to activate the exotoxin. A large portion deficiency of magnesium results in the of the exotoxin is in the form of a proto­ formation of filamentous forms of the 01'­ toxin which is non-toxic. ganism.16 It has been suspected that enterotox­ Incubation Period. imia may be set up by histamine of bac­ terial origin. The incubation period for Clostridium Australian experimenters have round perfringens is very short in most cases of that the main factors permitting absorp­ the disease. Since Clostridium perfring­ tion of epsilon toxin of Clostridium per­ ens is a normal inbaditant of the intestine fringens type D from the bowel were a all that is required to produce toxemia high ,concentration of toxin, the presence are ideal conditions for multiplication.

108 Iowa State College Veterinarian Engorgement of the intestine in sheep oc­ scattered foci of edema throughout the curs very rapidly, which is due to large nervous tissue. Diseased nerve cells were quantities of the ration and the atony of found in foci of edema, hemorrhagic foci the intestinal musculature. As soon as the and in small groups in apparently normal stasis of the food occurs, the ideal condi­ tissues in the cerebrum, cerebellum, spin­ tions are present for the growth and rapid al bulb and medulla. Cells of the spinal multiplication of bacteria and the absorp­ medulla and bulb showed "acute swel­ tion of toxin are present. The ideal condi­ ling." Scattered foci of the cerebral cor­ tions referred to above are fermentation tex showed "cellular liquefaction." There of carbohydrates and the anaerobic con­ were a few shrunken, deeply colored cells ditions that are produced by impaction. with agglutinated Nissl's granules and sinuous dendrites, "wrinkled cells" and Symptoms. some lightly stained "shadow cells." Pro­ liferation of neuronphages and peripheral Most of the symptoms of this disease glial cells were present around the di­ are the result of lesions of the central ner­ seased foci. The nerve fibers showed vous system. Orthotonus, a form of te­ marked changes of the myelin sheathes, tanic spasms in which the neck and limbs which were sometimes unevenly stained, are held in a fixed straight line, is present. sometimes fragmented and sometimes dis­ Other symptoms are incoordination of torted into a baUoon shape. The neuroglial movement, walking in a circle, head proliferations and the myelin sheath thrown back on the side, pushing and changes were more extensive under the straining against fences, blindness, re­ conditions of chl'onic intoxication.13 cumbent coma during the later stages of the disease, rise in temeprature of two or Other Microscopic Lesions. three degrees and glucosuria of two to six The pulpy kidney is brownish yellow to percent sugar.9 The animal may jump in­ a distinct yellow in color. The yellow dis­ to the air, fall upon the ground and go in­ coloration is due to the fatty degeneration to convulsions. Injury of the renal cor­ of the kidney. The kidney is also soft, en­ puscle and renal tubule cells by the exo­ larged and friable, which is the reason for toxin produces a condition whereby the the name "pulpy kidney." The liver un­ kidneys are unable to prevent the escape dergoes fatty degeneration changes, and of glucose into the urine. Degenerate the release of glucose occurs. The liver changes of the liver permit glycogenoly­ is yellow in color. Gas bubbles may ]orm sis, which is also a contributory factor to under the capsule. The capsule may be glucosuria. Less acute attacks show re­ friable, and tawny areas appear on the gurgitation, diarrhea, inappetence and surface of the engorged liver. Degenera­ loss of condition. tive changes of the liver and kidney are Nervous Lesions. considered to be pathognomomic for the disease. These changes appear three or Lesions IQf this disease are produced as four hours after death and may be both a result of injury of the endothelial lining ante-mortem and post-mortem in na­ of the blood vessels and the characteristic ture.H,7 inflammatory reactions which accompany Gross Lesions. the hemorrhages. The nervous lesions were studied by ad­ Gross hemorrhagic lesions may be lack­ ministering the exotoxin t'O a dog. The le­ ing in acute cases of the disease, Petechial sions were hyperemia with small perivas­ and echymotic hemorrhages may be pre­ cular hemorrhages and larger extravasa­ sent under the epicardium. Subendocar­ tions accompanied by lesions in the nerv­ dial and subepicarial hemorrhages may be ous tissue. Perivascular infiltrations of present. Petechial hemorrhages are pre­ mononuclear cells were present in both sent under the serosa of the small intest­ the white and gray matter. All the ani­ tine. Contents of the ileum resemble may­ mals showed uniformly distributed and onaise in color and consistency. The

Issue 2, 1957 109 abomasum may become distended with 10. Merchant, I. A. Veterinary Bacteriology and Virology. gas and rupture. It is impossible to strip 11. Mercuse, K. and Eggart, E. Demonstration of the mesentery from the entire intestinal Clostridium welchii in tissues. Veterinary wall without tearing the intestine every Bulletin. 21:12, Art. No. 3497, 1950. 12. Newsom, 1. E. Sheep Diseases. few inches." Intramuscular hemorrhages 13. Pachio, G., Gardoso, R. A. DeA., and Costa, are present in the diaphragm and abdom­ G. A. Lesions in the central nervous sys­ inal muscles. The pericardial sac contains tem of dogs caused by Clostridium welchii toxin. Veterinary Bulletin. 19:6, Art. No. a straw colored fluid which may be coagu­ 1200, June, 1949. lated. The lymph nodes are edematous 14. Runnels, R. A. Animal Pathology. and hyperemic. The small intestine and 15. Sisson, S., and Grossman, J. D. Anatomy of Domesticated Animals. abomasum are hyperemic. Rare cases may 16. Webb, M, The growth of Clostridium welchii show mild enteritis and gastritis.:!' 7 in complex media deficient in magnesium. Hemorrhagic septicemia and paraty­ Veterinary Bulletin. 20:6, Art. No. 1586, June, phoid dysentery may be confused with 1950. this disease. Lack of pneumonia rules out hemorrhagic septicemia. Paratyphoid di­ sease may result in diarrhea which is sel­ * Tibial Injuries dom seen in enterotoxemia. Ecchymoses (continlLed from page 103) on the intestine and diaphragm and coagu­ be reduced by manipulation of the patel­ lated fluid in the pericardial sac will rule la. Force is applied by :the hand to the s out listeriosis. medial side of the patella as the affected leg is further extended. This will usually Cause of Death. allow the patella to move back to its nor­ Death of the animal may be due to par­ mal position. However, the luxation often .alysis of the respiratory center which recurs immediately. In some instances leads to cardiac failure. The symptoms of blistering the stifle fonowing manual re­ heart insufficiency and respiratory diffi­ placement have proven successful. Usu­ culties are observed. ally, sectioning the medial patellar liga­ ment will be found to be the most suc­ References cessful treatment. Following desmotomy, 1. Australia (1946) Twentieth Annual Report several months of stall rest along with a of the Council for Scientific and Industrial fortified ration is indicated. Research. Veterinary Bulletin. Art. No. 1726. 2. Baldwin, E. M., Frederick, L. D., and Ray. J. D. The control of ovine enterotoxemia by the use of Clostridium perfringens type D Estrogenic substances, Clasey related bacterin. American Journal of Vet. Research. to the stilbestrol used as a beef growth 9:32, July 1948. 3. Baldwin, E. M. Enterotoxemia of sheep and stimulant, has been found in high levels its control. Veterinary Medicine. 45:12, Dec. in the following forage plants: subter­ 1950. ranean clover, red clover, ladino clover, 4. Bard, R. C., Gunsalus, I. C. Glucose metab­ olism of Clostridium perfringens: existence alfalfa, birdsfoot trefoil, wheat, rye, oats, of a metallo-aldolase. Veterinary Bulletin. and beets. 20:8, Art. No. 2220, Aug. 1950. 5. Boughton, 1. B. Some sheep disease. North American Veterinarian. 32:230-231, 1951. 6. Bullen, J. J., Scarisbrick, R., and Maddock, Air-conditioning and heating to guaran­ A. Enterotoxemia of sheep: the fate of wash­ tee temperatures between 50 and 70 de­ ed suspensions of Clostridium welchii type grees the year round would put hogs on D introduced into the rumen of normal sheep. Veterinary Bulletin. 23:11, Art. No. the market 100 days 'after weaning on 32022, 1953. 600 pounds of feed or less, experts say. 7. Coles, E . H. Problems encountEred in an ovine practice.' Iowa State College Veterin~ arian. 14 (2) :81-82, 1952. 8. Forsyth, R. A. Diseases of sheep. Proceed­ A recent study revealed that mow­ ings Book, American Journal of Veterinary cured hay retained 64 per cent more of Medicine. 1953. the carotene of the green crop than sun­ 9. Merchant, 1. A. An Outline of Infectious Di­ seases of Domestic Animals. pp. 51-54. cured hay.

110 Iowa State College Veterinarian