LI 8R AR-Y , CAM?US. “ TEXAS AGRICULTURAL EXPERIMENT STATIIIN AGRICULTURAL AND MECHANICAL COLLEGE OF TEXAS W. B. BIZZELL, President EIULILETIREINO. 319" I I? w FEBEUARY 1924 “TEINTFAIIAVIIIENEESIEY FIELD AND LABORATORY NOTES RN A FATAL DISEASE 0E CATTLE NCCIIRRING 0N TIIE CRASTAL PLAINS 0E TEXAS (LOIN DISEASE) ---- ,- H I "\ I»"~"»" " IAIIIIIIIAI\\N'IINI;IIIII ---------- " B. YOUNGBLOEOD, DIRECTOR COLLEGE STATION, BRAZOS COUNTY, TEXAS TEXAS AGRICULTURAL EXPERIMENT STATION SYSTEMl AGRICULTURAL AND MECHANICAL COLLEGE OF TEXAS ' COLLEGE STATION, TEXAS STAFF: (As of February 15, 1924) ADMINISTRATION: AGRONOMY: B. YOUNGBLOOD, M. S., Ph. D., Director E. B. REYNOLDS, M. S., Chief A. B. CONNER, M. S., Vice Director G. N. STROMAN, Ph. D., Cotton Breeder A. H. LEIDIGH, M. S., Assistant Director C. H. MAHONEY, B. S., Ass’t. in Cotton i. Chief Cleric Breeding . . R , ecretary M_ P_ HOLLEMAN, B" I _ - PLANT PATHOLOGY AND PHYSIOLOGY: J. M. SCHAEDEL, hwecfiiii): Agglsetiin€lerk J- J- TAUBENHAUS’ Ph- D-- Ch"! C. J. GORZYCKI, Technical Assistant FARM AND RANCH ECQNQM]CS; . L. P. GABBARD, M. S., Chief Chief V. L. CORY, M. S., Grazing Research Botanist 1 H. SCHMIDT, 1). v. M., Vt 'n m . v. J. BRAUNER, D. v. Mqel/edlfileraifr-Lldlrian H- E- REA» B- S-- -4*8“‘“"‘ ‘ . son. SURVEY: CHEMISTRY‘ **w. T. CARTER, B. s., Chief S: E: Eétiféizptr.%r."2ii£i.§f.‘2‘éfl1.i?;i“‘ H~ W- HAWKER- M Surveyor W_ H_ WALKER, Assistant Chemist EDWARD TEMPLIN, B. S., Soil Surveyor A. G. PETERSON, B. S., Assistant Chemist BQTANY; J. E. TEAGUE, B. S., Assistant Chemist H_ NESS, M_ S" Chief J. K. BLUM, B. S., Assistant Chemist PUBLICATIONS: HORTICULTURE: ' A' T' POTTS’ M' s" Chief srilriz). zlliiccliisffunfffalzslszAacl-l "’§"“1‘v1"'§6§%§s'£“i‘ one H Lawfifistémg’; A . Ch - - » - -' _ . . , . ., icu turist ‘n argc J. L. LUSH, Ph. D., Animal Husbandman, A_ H_ ALE); B_ S" Qqfeeln 3,864; Breeding G. R. WARREN, B. S., Swine Husbandman MAIN STATION FARMi _ R. M. SHERWOOD, B. S., Poultry Hue- D. T- KILLOUGH. B- 8-. Superintendent bandman FEED CONTROL SERVICE: J‘ J‘ HUNT’ W”! Grad" B. YOUNGBLOOD, M. s., Ph. 1)., Director ENTOMOLOGY: F. D. FULLER, M. S., Chief M. C. TANQUARY, Ph. D., Chief; State S. D. PEARCE. Sefiflfw-Tll Entomologist ' J. H. ROGERS, Inspector H. J. REINHARD, B. S., Entomologist W. H. 'WOOD, Inspector C. S. RUDE, B. S., Entomologist. J. J. KELLY, Inspector W. O. VICTOR, JR., Apiary Inspector J. D. PREWIT, B. S., Inspector W. R. JORDAN, B. S., Apiary Inspector T. C. DAVIS, B. S., Inspector SUBSTATIONS: No. 1, Beeville, Bee County: No. 9, Balmorhea, Reeves County: R. A. HALL, B. S., Superintendent J. J. BAYLES, B. S., Superintendent No. 2, Troup, Smith County: No. 10, College Station, Brazos County: W. S. HOTCHKISS, Superintendent (Feeding and Breeding substation) No. 3, Angleton, Brazoria County: L. J. McCALL, Superintendent V. E. HAFNER, B. S., Superintendent No. 11, Nacogdoches, Nacogdoches County: No. 4, Beaumont, Jefferson County: G. T. McNESS, Superintendent R. H. WYCHE, B. S., Superintendent **No. 12, Chillicothe, Hardeman County: No. 5, Temple, Bell County: D. L. JONES, Superintendent A. B. CRON, B. S., Superintendent No. 14, Sonora, Sutton-Edwards Counties: No. 6, Denton, Denton County: E. M. PETERS, B. S., Superintendent P. B. DUNKLE, B. S., Superintendent D. H. BENNETT, V. M. D., Veterinarian No. 7, Spur, Dickens County: O. L. CARPENTER, Shepherd R. E. DICKSON, B. S., Superintendent No. 15, Llano Grande, Hidalgo County: No. 8, Lubbock, Lubbock County: W. H. FRIEND, B. S., Superintendent R. E. KARPER, B. S., Superintendent ~ Teachers in the School of Agriculture carrying cooperative projects on the Station: +8. W. BILSING, Professor of Entomology W. E. GARNETT, Professor of Rural W. L. STANGEL, Professor of Animal Hus- Sociology bandry, Hogs G. P. GROUT, Professor of Dairy Husbandry F. A. BUECHEL, Professor of Agricultural R. C. WHITE, Associate Professor of Rural Economics Sociology G. W. ADRIANCE, Associate Professor of Horticulture ‘In cooperation with School of Veterinary Medicine, A. and M. College of Texas. "In cooperation with United States Department of Agriculture. i-On leave i-On leave. A- disease of cattle manifesting itself by a sudden and complete breakdown of the organs of locomotion and lo- cally called loin disease or down-in-the-back is herein de- scribed. This disease is prevalent from May to September in the low flat area bordering on the Gulf of Mexico and af- fects cattle over 18 months of age in case such cattle have been subsisting entirely on the native vegetation for a period of at least one year. It is not observed in dairy cattle fed a dairy ration. The outbreaks of the disease simulate an infectious disease, but in repeated experiments pathogenic organ- isms could not be demonstrated. The cause of the disease is tentatively ascribed to toxins produced by bacterial’ action in carcass material on the prairie and the consumption of such putrid material by cattle. It is tentatively recommended to feed sweet bone meal to cattle in order to stop them from eating danger- ous carcass material; also to thoroughly clean all pas- tures of animal carcasses. Investigation of this disease is not yet complete and ~ experiments are under way to definitely prove whether putrid carcass material is the sole source of the toxin and to establish the best methods of preventing the disease. '7 "'“i:’j(+_ _"_—__ ti?” iEfiorts to Establish Etiology of Loin Disease . . . . . . . . . . . . . . CONTENTS History and Distribution of the Disease . .‘ . . . . . . . . . . . . . . . .. 5 Epizootology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . y Pathological Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Loin Disease Probably not Due to Bacterial Infection . . . . . . . . Loin Disease not Identical with Botulism . . . . . . . . . . . . . . . . . . . Loin‘ Disease not Due to Trypanosomes . . . . . . . . . . . . . . . . . . . Loin Disease Due to Toxic Carcass Material . . . . . . . . . . . . . . .. i Feeding Experiments with Putrid Bones . . . . . . . . . . . . . . . . . ..2 Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3 Bulletin No. 319 February, 1924 FIELD AND LABORATORY NOTES ON A FATAL DISEASE OF CATTLE OCCURRING ON THE COASTAL PLAINS OF TEXAS (Loin Disease) A PRELIMINARY REPORT H. Schmidt [HISTORY AND DISTRIBUTION OF THE DISEASE A rapidly fatal disease of cattle, known locally as “loin disease” or “down-in-tne-back,” occurring on the prairie re- gion along the Gulf of Mexico in the State of Texas has been known to cattlemen in that territory for a long time. Oc- casionally reports of this hitherto undescribedl malady of cat- tle reached the Division of Veterinary Science of the Texas Agricultural Experiment Station as early as 1910. These re- ports gradually became more numerous and calls for help more insistent, but it was not until 1918 that a small fund Was provided to investigate this malady. The funds available Were entirely inadequate to do much effective work and for that reason the activities of the Division of Veterinary Science were limited to making occasional calls whenever a report came in with the view of collecting material for microscopical and bacteriological study. ' This method of procedure proved entirely unsatisfactory for two reasons. In the first place, many times the animal could not be reached in time to satisfactorily collect material. In the second place, range cattle were so cheap that cattle- men would seldom take the trouble to call on the Division for help. For these reasons ‘it was impossible to make any satis- factory progress and it, therefore, became necessary to change the method of attack in spite of the handicap of limited funds available. It was, therefore, decided to place a man in the field during the seasonal prevalence of the disease in order to collect data on its occurrence and specimens for laboratory study. This plan was inaugurated in May, 1921, and as many cases studied as possible with our limited force. As the investigation progressed it was learned that the disease centered in Harris County, but reports of its occur- rence, apparently to a lesser degree, also reached the Division from Galveston, Colorado, Brazoria, Austin, Waller, Fort 1Dr. A. T. Kinsley, who was in the field with the writer during the 1921 outbreak published his observations on this disease in Veterinary Medicine, Chicago, Vol. XVI No. 7, p. 24. 6 Bulletin N0. 319 Bend, Matagorda, Wharton, Lavaca, and Hardin Counties. It ; is not yet definitely known whether the occurrence of the dis- ease is limited to these counties; however, it appears that the .. disease is limited to the low, flat area bordering on the Gulf of Mexico and extending inland to the north to a distance of 1- about 100 miles and ranging in elevation from sea level to about 250feet above. This area is traversed by numerous a creeks, bayous, and drainage ditches, but on the whole the drainage is very poor and many small, shallow surface ponds ' are found. The land, however, does not become boggy, but few bogs occurring excepting along the creeks and bayous. In the low places, especially along the bayous, in and around the surface ponds and in the drainage ditches along the roads, the coffee bean, (Daubentonia longifolia), grows very abun- dantly. Over the entire area grasses and many different ' kinds of weeds grow very luxuriantly. The soil is usually non-calcareous. Cattlemen who have been in the cattle business in the affected area for a long time say that this disease has been prevalent in Harris County for the last twenty years, or even longer. One man stated that he observed the disease during the Spanish-American War, at which time he was buying steers for a Galveston firm and which were being shipped to the American forces in Cuba. At that time he frequently ob- served that steers would get down and die without any ap- parent cause after he had bought them and before he could deliver them to the Galveston firm. He is convinced that the disease occurred in Harris County three or four years previous to that time. Others say that the disease was first observed in the pastures_of Calvin Ehrhardt at Bammel, Texas, in the northeastern part of Harris County, and that it was introduced by him with cattle which he is reported to have acquired in Louisiana. From Mr. Ehrhardt’s pastures the disease is re- ported to have spread westward. Answers to inquiries indi- cate, however, that this disease is not and never has been prevalent in Louisiana. How this spread may have taken place cannot yet be stated, as the cause of the disease has not" yet been determined. Mr. Ehrhardt cannot positively say that he was the first man to have observed the disease and Mr. J. J. Reibenstein, Catspring, in Austin County, observed the dis- , ease in 1902. In this year, Mr. Reibenstein lost 18 head of cattle from this disease and in the following year he lost 16 head from it. It will be noticed that this was only four years after the Spanish-American War, and if the above statements are correct, the disease would have spread from the north- eastern part of Harris County westward across Waller County to Austin County, a distance of about 80 miles. The signif- A Fatal Disease of Cattle 7 icance 0f this fact cannot be estimated until the cause of the disease and the manner as well as the rapidity with which it is spread are known. However, in searching for the cause, one must ever bear in mind that the manner and especially the rapidity with which it is spread bear some relation to the cause of the disease. Knowing the rapidity of spread and the distribution of a disease,_ one is justified in drawing some conclusions as to its probable cause, especially in the case of insect-borne diseases. EPIZOOTOLOGY Although the disease has been prevalent in this territory for a long time it was not until about 1917 that it began to cause such serious losses as to endanger the cattle industry of that section. Some pastures soon became so “infected” that they were entirely abandoned, while adjoining pastures re- mained entirely free from the disease. Although not all pas- tures in this area were “infected,” the disease did not re- main localized, for some pastures are known to have become “infected” in recent years. The following case may serve as an example. In 1919 the Martin-Settegast Cattle Company ob- served the first case of this disease on their ranches. In 1920 the cases were more numerous, while in 1921 the losses were very heavy. Cattlemen agree, and the writer has found it to be the case, that animals are found down only in certain parts of a pasture, especially around and in close proximity to ponds. Ofn the other hand one must not forget that these ponds are very numerous and one need not go far in order to find such a pond. This observation probably bears no direct relation to the disease, but one must keep an open mind and consider the water supply of the animals when looking into the nature of a disease as obscure as loin disease. Neverthe- less, there are hundreds of acres in some pastures where not a single animal has ever been found down with the disease. The disease seems to be localized within certain pastures. Here again one must consider the frequency with which animals graze over such apparently unaffected areas. One must not forget that the cause of the disease may enter the animal today, but the disease itself need not become manifest until several days or even a fortnight later. In the meantime the animal may have traveled many miles away from the place at which the cause of the disease was picked up. Since no accurate data have been kept by cattlemen in the affected area showing the exact distribution of the disease, contradic- tory reports are often obtained, thus making it indeed diffi- cult to point out suspicious or dangerous pastures with any degree of certainty. 8 Bulletin N0. 319 Cattlemen have also observed that when cattle are dying . in one pasture and are then moved to another pasture they i will stop dying either immediately or within 7 to 10 days . thereafter, although they may later again begin to die in the . pasture to which they have been moved. An interesting case ~ of this kind was reported from Austin County by Dallas Hill- bolt. He and his father each had 1000 acres of land sep- Z arated only by a railroad with a fence on either side of the 1A right-of-way. In 1917 the son had 300 head of cattle in his pasture and the father about 150 head in his. About the lat- ter part of April the son’s cattle began to die from loin dis- t ease and by July 10, 75 head had been lost. On this date both father and son decided to move their cattle to Brazoria County in order to escape further losses. Up to this time the i a father had not lost any cattle. The cattle were rounded up on said date and shipped to Brazoria County, where all cattle _ were released in a 48,000-acre pasture. Here the son’s cattle stopped dying immediately while the father lost 15 head with- in the next two Weeks, presumably from loin disease. It is said that losses cease entirely as soon as cattle are moved to timbered pastures and that no losses are known to have ever occurred in timbered areas. This is said to be the case in Harris County and is staunchly maintained by all cat- tlemen there. Also in Austin County cattlemen contend that _ this is the case. Information gathered in that county illus- trates this point very clearly. The southern part of this coun- j, ty is low and flat and almost entirely devoid of timber. Losses are quite heavy from this disease in the southern part of the I county, but cease quite suddenly as soon as the northern hilly 4 and timbered part is reached. It is quite true, however, that Y in the northern part of Austin County we have a more elevated I; country combined with timber, while in Harris County We have a low flat country combined with timber in certain parts. Cattlemen also contend that working the cattle, that is, rounding them up as is done in dipping or branding or shifting l. them from one pasture to another, has a tendency to check heavy losses. Losses are also said to be heaviest soon after *- a heavy rain and during showery Weather, While a long dry spell has a tendency to check losses considerably. In this con- nection it is interesting to note that as the disease begins to make its appearance in late April or early May, the rainfall of the affected area begins to increase noticeably as is shown by the observed average monthly precipitation during the last 25 years. This increased precipitation will continue till about the end of August, when it begins to decrease perceptibly. Comparing this with the incidence of the disease one finds that the disease makes its appearance in the latter part of A Fatal Disease of Cattle 9 April or the early part of May and continues unabatedly until the early part of August, after Which time only sporadic cases occur during the next three or four months, and then cease entirely. lt is apparent, therefore, that the prevalence of the disease coincides With the season of greatest rainfall and also With the season when the vegetation is at its best. However, one must also consider that the environment must be favor- able in order that some diseases may develop and flourish, and that dry, hot Weather lasting only for a fortnight or so may indeed noticeably check the occurrence of some diseases. The age of the animal plays an important role. Of all the animals observed the Writer has "never seen one affected . that Was less than 18 months old, With one exception Where the oWner said the animal Was a yearling. Likewise, the dis- ease has never been observed in dairy cattle. These two facts, coupled With the fact that cattle, moved into the affected area from the outside, do not contract the disease till they have been in the affected area for a year or longer, seem to have a very important bearing upon the cause of the disease. It will be a most important task to clear up the possible relation that these observations may bear to the cause of the disease. The most plausible explanation Would be that there is something lacking in the vegetation that the animal needs, but the fact that affected animals are usually in prime condi- tion seems to lend Weight to the contrary. An animal in con- tinued good health probably secures in the feed it consumes and may even have stored in tho body tissues all elements nec- essary to maintain this condition. Now, should this normal supply of necessary elements gradually or even suddenly cease, one Would expect the animal to manifest this condition by a gradual change in its health and physical condition. In loin disease, however, this is not the case. On the contrary, the animal is apparently in good health and condition and then goes doWn suddenly, almost Without Warning. The ani- mal may appear to be in perfect health at night and the next morning may be found doWn and unable to get up. The sex of the animal, on the other hand, is immaterial. One Will find bulls, steers, cows With calf at foot, pregnant cows, and heifers suffering from the disease. The majority of the animals are mature and range in age from 4 to 6 years. The territory in question is essentially a cow country and for that reason one Will find that the greater number of animals dying from loin disease are cows. The affected animals are, as a rule, in the pink of condition, robust and fat. Only sel- dom Will a thin animal be found suffering from the disease. Some cattlemen report losses as high as 15 per cent dur- 1O Bulletin N0. 319 ing some years while others estimate their losses at a much lower figure. The losses may vary considerably from year to year and from pasture to pasture. SYMPTOMS a When an animal is observed in the early stages of the disease and before it goes down, one will notice that the ani- mal only reluctantly follows the herd and frequently lies down to rest. The walk of such an animal is difficult to describe, varying but little from normal. A person not familiar with the habits and disposition of such an animal would not notice anything wrong at all. Again the observer may fancy that he can see a change in the animal’s habits and disposition, but upon taking a second look he is no longer so confident and may even conclude he was wrong. But soon the condition be- comes more pronounced; the animal does not walk quite as actively as when normal; it appears a little stiff; and the back may be slightly arched. An incoordination of movements seems to be developing. The cowman refers to this condition as “not trailing well behind.” The animal experiences ever- increasing difficulty in getting up after having lain down to - rest. Within a very short time, as early as 12 hours and sel- dom later than 24 hours after these symptoms have developed, the animal will be found down and unable to get up. When assisted up at first, that is, at a time when the animal is just at the stage of being unable to rise unassisted, it may still be Figrurc 1. Animal suffering from loin disease just found on the prairie. A Fatal Disease of Cattle 11 able to Walk a mile or so, but eventually the animal will go down again. One will notice that when the animal is dowgn it will not switch its tail although flies may be tormenting it at the time. The tail has become paretic. When an animal in this stage of the disease is approached on the range, it will make strenuous efforts to get up, but once down all efforts to rise again are useless. The animal otherwise makes the impression of being per- fectly healthy. The eyes are bright, the pulse, respiration and body temperature are normal, and the animal rests on its sternum. The feces are normal in color and consistency, but they are frequently covered with more or less clear mucus or may even be bloodstained. When the animal is examined as to the condition of the muscular functions, one will observe that the tail is paretic. When the tail is pricked with a pin the animal will not move it away or switch it, but one can ob- serve the animal making strenuous efforts to do so; however, it can only raise the end of the tail an inch or so off the ground. Cattlemen riding the prairie and seeing an animal lying down never approach it when they see it switch its tail, for they know that such an animal is not suffering from loin disease. When pricked along the rump, back, or sides the animal will instantly react with contractions of the muscles of this region and make an effort to rise. The animal at this stage will eat and drink. One may even observe such animals crawling round in a circle on their knees to graze, dragging their hind legs after them. l Figure 2. Animal making an effort to rise after it had been down with loin dis- ease for ten hours. 12 Bulletin N0. 319 The rapidity with which further symptoms develop de- pends somewhat upon weather conditions and the care given the animal. If the animal be turned over frequently it may remain bright and rest normally on its sternum for some days following. Soon, however, within 24 to 48 hours, one will ob- serve that thelmuscles of the neck also become affected; the head will now be found resting against the side of the animal presenting a typical “milk fever position.” If the head be raised Figure 3. The “milk fever position” in three-year-old bull suffering from loin dis- ease. Animal down for about 42 hours. by an assistant into its normal straight position and then re- leased, it will immediately drop back against the side of tno animal again. If the head be turned too far by the assistant before being released, and become overbalanced, the animal will not be able, despite all efforts, to balance it again, but it will now fall "flat on its side with outstretched head and legs to remain there. Frequently one will observe, when the animal is resting in a milk fever position, if the horns of the animal ' be grasped and its head raised into its normal resting position, that the neck of such an animal shows a sharp crook about at the point of the third and fourth cervical vertebrae. This can sometimes also be observed when an animal is found which is still barely able to handle its head. One may notice in such a case that the animal, if it raises its head at all, will do so slowly and in the normal manner until it reaches a point where it apparently can go no farther and the neck shows this sharp crook. The animal will now be seen to slowly raise the point of the nose until it is almost on a level with the poll, and now, with a sudden snap, the crook disappears and the A Fatal Disease of Cattle .13 Figure 4'. The same animal as above photographed a few minutes later after the animal had been pushed over on its side. neck becomes straightened out. This movement is apparently always accomplished with difficulty. As time goes on, howl- ever, the animal will no longer be able to raise its head and will, therefore, when it begins to struggle, come to lie on its side to remain there. Although the animal goes flat there is no paralysis of the legs. In a few cases hyperesthesia of the skin was observed. Once the animal is flat, the progress of the disease will depend to some extent upon the attention given the animal. Food, as a rule, will no longer be taken voluntarily for at least a number of days, but water will be taken when the animal is raised on to its sternum,—if not voluntarily, it will at least be swallowed when poured into the animal’s mouth as in drenching. Rumination ceases when the muscles of the neck become affected and the animal assumes the milk fever posi- tion, or has gone flat. Some animals may retain their normal resting position upon the sternum for as long a period as two weeks, taking food and water during that time, but eventually they will all go flat. If the animal be well bedded, frequently turned over and watered regularly it may begin to eat again in a week or ten days, and once such an animal begins to eat again its chances for recovery are good indeed. Should such an animal recover, which may happen after the animal has been down for several weeks, one will find that it suddenly gets up and walks away. Such cases of recovery are rare in- 14 Bulletin N0. 31.9 Figure 5. This cow had been down for three weeks with 10in disease. She sud- denly got up one morning and immediately charged the writer, who happened to be standing near. This photograph was taken a few minutes after the cow got up. deed. Animals recovering from this disease are not perma- nently immune, for they may have another attack as early as the following year and then usually die from it. On the other hand, if the animal be found down on the prairie and left there exposed to the hot sun without food or water, the progress of the disease will be very rapid. In this case the animal may be flat after being down for only 12 hours and be dead at the end of 36 hours after going down. No cases are on record where the animal dies suddenly without first going down. It will thus be seen from the above that the disease may run a slow course, which may be described as chronic, or the disease may terminate fatally more rapidly and one may then speak of it as taking an acute course. PATHOLOGICAL ANATOMY If one should sacrifice an animal suffering from loin dis- ease after it has become moribund and all hope for recovery has disappeared and examine the body carefully for lesions produced by the toxin, one would find a variable picture pre- senting itself. The autopsy lesions here reported have all been taken from such animals. It may be well to mention here that no pathognomonic lesion will be found, that is, a lesion to which one can point and confidently say that if that lesion is present one is dealing with loin disease. A Fatal Disease 0f Cattle 15 Upon removing the skin from the carcass one -will prob- ably find bruised places on different parts of the body caused by the animal’s lying and struggling on the ground. Fre- quently one will find no lesions at all; all organs and the meat in such cases have the appearance of a perfectly healthy and well nourished animal like one regularly slaughtered for the consumption of its meat. At other times lesions will be found in some of the organs, but these lesions vary greatly in char- acter and extent. Let them be described in some systematic manner: The lungs and trachea are nearly always normal; only sel- dom will petechial hemorrhages be found. In the heart, lesions are encountered more frequently. In about 25 per cent of all cases hemorrhages will be found on the endocar- dium of the left ventricle. Very rarely are such hemorrhages present on the endocardium of the auricles or the right ven- tricle. These hemorrhages vary in size from a pin point to very extensive patches, thus sometimes covering three-fourths of the surface of the left ventricle. In color they vary from a pale red to a deep red. When such hemorrhages are small and few in number, they may be present on the papillary muscles only. The myocardium, epicardium, and pericardium have been found normal in all cases examined. The liver is usually normal in color and consistency. Only occasionally will this organ show a yellowish tinge or be even pronouncedly yellow. In only four per cent of all cases ex- amined so far were hemorrhages about the size of a pin head found under Glisson’s capsule, Now and then one will find liver fiukes in the bile ducts. The gallbladder, as a rule, is well filled with bile and is frequently slightly, or even much enlarged. The bile itself is clear and of a greenish color. The mucous membrane of the gallbladder is sometimes found con- gested and in about 15 per cent of the cases hemorrhages will appear thereon. These hemorrhages vary in size from a pin point to that of a pea, are irregular in outline and usually very numerous. The spleen was always found normal in size, color, and consistency with the veins of the capsule well filled and stand- ing out prominently. The kidneys show lesions more frequently than any other organ, but even here the lesions are not consistently found and vary in character and extent. In about 30 per cent of the cases a congestion of the kidneys is present which is especially well marked in the medullary portion. Upon close scrutiny one will find in about 4O per cent of the cases, small pin point Bulletin N0. 31.9 red dots, inthe cortex. These are the congested glomeruli of I! This congestion of the glomeruli does not always l occur simultaneously with the congestion of the medullaryl the kidneys. portion. Only rarely will one find hemorrhages. i The urinary bladder may be empty or contain some urine. i’ Lesions on the mucous membrane of the urinary bladder have ' never been observed by the writer. The writer has never found lesions on the first three com- < In about 40 per cent of the cases ¢ The fourth M stomach has sometimes been found to contain small pieces of . The mucosa of the abomason may be diffusely red-7 Occasionally one will find ulcer-like In about 1O per cent of the partments of the stomach. a parasite, Paramphistomum cerml, was found. bone. dened and congested. areas or old scars on the mucosa. cases one will find distributed over the mucous membrane a few circumscribed areas closely studded with sharply defined deep red petechia varying in size from a pin point to that of a pin head. Bile will be found in the small intestines in about 50 per cent of the cases. The amount of bile varies; more frequently one Will find it in considerable quantities mixed with excessive amounts of mucus and some food material. The mucous membrane is often congested. The congested areas may be small and circumscribed or diffuse and extensive. The color of these areas varies from a deep red to a pale red. On the mucous membrane of the large intestines one may find more or less circumscribed or diffuse reddened areas and streaks, either on the ileo-caecal valve, the caecum, or the colon. The ingesta are sometimes mixed with mucus. No lesions are found on the mucous membrane of the rectum. The rectal contents are more or less covered with clear mucus. The lymph glands do not show any constant and char- acteristic lesions. The precrural, prescapular, portal and some groups of the mesenteric lymph glands may be found slightly congested around their periphery, but these four groups need not be simultaneously affected. Occasionally one or the other lymph gland of the body may be found more or less congested or even hemorrhagic, especially a small lymph gland located in the small curvature of the abomason. ‘ In a few cases one can find relatively large hemorrhagic spots on the omentum or the peritoneum, varying in color from a pale red to a bright red. The meninges of the brain may be found congested, but other lesions of the brain have not been observed. The spinal cord has always been found normal macroscopically. In a few cases the spinal fluid was found either milky or tinged with blood. . .....' .._“..-¢.;>..¢.;....ev~..._~.» . A Fatal Disease of Cattle . 1'7 EFFORTS TO ESTABLISH THE ETIOLC-GY OF LOIN DISEASE The first symptoms of 10in disease appear with but very little Warning; it strikes suddenly. In this respect it resem- bles an intoxication. Such an intoxication would naturally have to come about by the toxic material entering the body from the outside and in such quantities as to produce an im- pairment of the health of the animal. And since the toxic material Would have to "be introduced from the outside, one will have to search for it either in the food, in the water, or in both. " XVith the first possibility in mind the range has been searched for possible poisonous plants, but with the excep- tion of the coffee bean, which is not eaten by cattle, none were found. Nor did the epizootology of the disease suggest such a plant. If it were a poisonous plant, why do cattle under 18 months of age not die from the disease? They have at this time passed at least one entire grazing season on the affected area xvithout having contracted the disease. Surely there was opportunity to take up such a poisonous plant during this time. There is no record, so far as the writer knows, of a plant which is poisonous to animals of a certain age only. Why do dairy cattle not contract it while running on the af- fected range? And why do cattle, brought into the affected area from the outside, not develop the disease until they have passed at least a year therein? Such facts would not suggest a poisonous plant. However, one must not limit his investigation to known poisonous plants, plants readily detectable by the naked eye, but one must go beyond that and look into the nature of the microscopic plant life encountered on the range. The writer has in mind here especially that microscopic plant life gener- ally classed as bacteria. Here several possibilities present themselves. In the first place one must consider the, probabil- ity of its being an infectious disease. Here again one must consider two possibilities. 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EHYMFQJH-wuuvflkm 33L“ vfimum ucuwuLa W82: 2o . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . éEouwEafiwLwa Lou >Z>GU£ 23 .2252 mm >534 uL/mmcufinw “E32 @833 $35 w wubm cw 0:2 oEom mmnuuuun vuumuw . . . . . . . . . . . . . . . . . . . .. umcfl . . . . . . . . . . . . .. u UCuCU> wuwm LLoEu .2 2 v . _ . .2 .2 Lao no 09.223080: .235» 1839.8 MmmuLw vfiwuu .9232 50o “M3 223050? £2 E QZCuuLm Gucouiuansw uwbfi 33.32 >ow2 LL00 SmEm Lou E 30am wuwfvlofiu: wm i: vou onmommmm . ufiwcuoxww ,2 _ _ mMLoEoM mowLwwLmwfioH moLIM-WWLLuWoH _ cuwainvwouw $52M macaw Lo_%%%2m i L914, Mssq tmufl .02 _ _ Auwifizau. J HQMABH 20 Bullet'in N0. 31_9 But there is still another possibility to be considered. I is possible that the microorganisms do not enter the anima body at all, but multiply outside of the animal body, produc and liberate their toxin there, and this in turn gains access" i. the animal body. We can here cite a parallel case, that it botulism, occurring widely distributed over the world. Th microorganism must then have to be looked for in the foo consumed by the animal or in the water taken up. Failin in every other direction, the Writer turned his attention espe cially to the latter possibility. ‘ LOIN DISEASE PROBABLY NOT DUE TO BACTERIAL INFECTION . In the early part of the investigation, when material wasll hard to obtain, the possibility that the disease was of an in-f fectious nature was especially considered, it being constantlyii kept in mind that whatever organism might be encountered, it must be possible to reproduce the disease with it in all its details. A diligent search was, therefore, made for microor- ganisms in the blood, heart, liver, spleen, lymph glands,f spinal cord and brain, both in smears made from these organs and in cultures. Laboratory animals and cattle were also in-Q oculated, especially with blood and serous fluid from the peri- j cardial sac. The results were always negative. In May, 1921, 3 the writer had an opportunity to autopsy an animal in the field _ that had been down for ten days. Blood was drawn from the L jugular vein of this animal and the animal then destroyed. f Smears were also made from the heart, liver, spleen, and kid- neys. Fifty cubic centimeters of the blood drawn from the, jugular vein of this animal were injected subcutaneously on‘ the following day into a cow with negative results. Unfor- tunately no specimens of the organs for culture purposes were * secured. When the smears were examined numerous clusters of bacteria were found in all of them. Since the animal from f which these smears were made had been down for 10 days, i‘ it was thought worth while to consider the possibility that the , organisms responsible for the disease did not develop in the ‘p, animal body in such numbers as to be readily detectable until the animal had been down for some time. Such animals, how- e1 ever, could not be secured. - During the severe outbreak of 1921 it was possible to make a thorough study of the disease. A large number of animals were available for autopsy and a thorough survey of the epizootology could be made. The latter point has already, been discussed in the previous pages of this report. Unfor- A Fatal Disease of Cattle 21 tunately, only two cows were available for inoculation during this outbreak. These were kept under observation for two months in asmall enclosure, during/which time they were, at different times, inoculated with blood, spinal fluid, saline ex- tracts from the spleen, kidney, liver, and spinal cord and also drenched with the contents of the small intestines of animals suffering from loin disease. The animals were finally re- turned to their respective owners, but nothing untoward hap- pened to them during the next several months that they were kept under observation. At the same time numerous smears were made from the organs of sick animals and diligently searched for microorganisms, but none could be demonstrated that could be held responsible for the disease. Numerous cul- tures, both aerobic and anaerobic, were made from the organs of animals autopsied within a day or two after they were found down, using such media as plain nutrient bouillon, plain nutrient agar, brain media (von Hibler), liver media, and a combination of the latter two. Plates and tubes were also» incubated in anaerobic jars and still the results were neg- ative with one possible exception. In this case, No. 32, a small organism was obtained on plates that was very pathogenic for mice, guinea pigs, and rabbits. Its pathogenicity was then tested for cattle. For this purpose a twenty-four-hour bouillon culture was prepared and with 50cc of this culture a four- year-old cow was injected intravenously at 1 :30 p. m., on No- vember 9,1921. Let us call this cow CSlA. The following facts were recorded at the time: At 8:00 a. m., 11-10-21, cow very weak and down. The cow made four attempts to get up before she succeeded in re- gaining her feet. Breathing labored and accompanied by a light roaring noise. Number of respirations per minute 18; body temperature 97.2 F.; watery diarrhea. At 1:00 p. m., same day, cow lying down and regained her feet upon the second attempt to rise. At 5 :00 p. m., cow lying down again; this time in a different place. November 11, 1921, 8:00 a. m.: The animal evidently had been up during the night, for on this morning she was down in a different part of the lot from where she was last seen the previous night. Cow unable to rise. Number of respirations per minute 18; body temperature 98.6 F. The head was held in its natural position, but a slight crook appeared in the neck. Animal bright and alert; switches its tail. Some well-formed feces of a normal color had been passed during the night. At 11:00 a. m., same day, animal still down resting its head against the side of the body as in milk fever. When the head is lifted into its normal position, the animal will hold it there 22 Bulletin N0. 319 for a short time and then allow it to drop back against th side of the body. The alertness of the early morninghas did appeared and the previously naturally nervous animal n longer takes notice of its surroundings. At 1 :00 p. m., on th same day, animal flat, but still able to sit up when assiste upon its sternum. At 5:00 p. m. the animal flat, and can sti sit up when assisted. When the head is lifted into its norma- resting position, the animal resting on the sternum, a decide crook appears in the neck and when the head is released mechanically drops back against the side of the body. ' November 12, 1921, 8:00 a. m.: Animal flat, when assis ; , ed on to the sternum it drops its head against the side of th body to remain there a few minutes, after which time the anii- mal goes flat again. Body temperature 97.6 F. The animal " died at 10:00 a. m. on the same day. ' Autopsy findings: The animal was autopsied at 1:00 m., 11-12-21. Bruises under the skin at the sternum and w the sides of the body. Prescapular and precrural lymph glands normal. Peritoneum, no lesions. r Spleen, not enlarged; veins of capsule, injected; some. circumscribed and also some quite extensive, pale, wash' ’ hemorrhages on capsule. On section, pulp firm; trabecula and Malpighian bodies plainly visible; color normal. “i, Liver, firm; normal in color; no hemorrhages or othel lesions. Gallbladder contained 640 cc bile of a greenish color Mucous membrane of gallbladder greenish in color; no hemor _- rhages. ' Kidneys, firm; greyish in color (cloudy swelling); hy ‘ peremia; no hemorrhages. Urinary bladder, empty. == mucosa showed hemorrhages the size of a pin point to tha of a pin head. a The mucous membrane of the abomason showed sharpl l i defined hemorrhages from the size of a pin head to four time that large. ' The contents of the small intestines, mixed with bile.‘ Mucous mebrane, more or less hyperemic about one-half the length of the small intestines. The aggregated follicles, enlarged. . Large intestines: lleo-caecal valve, hyperemic and swoll- en. In the caecum, hyperemic streaks and folds near ile0-- caecallvalve and apex. Lymph glands in abdominal cavity, i norma . Lungs: Extensive pneumonia present. Mucosa of trachea, slightly hyperemic. A Fatal Disease of Cattle 23 The pericardial sac contained a large amount of reddish fluid. Epicardium, covered with fibrin and some hemor- rhages. Myocardium, firm and pale (cloudy swelling). En- docardium, a few hemorrhages about the size of a dime. Microscopical examinations of smears made from the dif- ferent organs showed numerous microorganisms similar to the one injected into the animal. The same organism was recov- ered in pure culture from the animal. To further test this organism, a twenty-four-hour bouillon culture was prepared and 35 cc of this culture injected into the jugular vein of an eighteen-months-old heifer, CSlB. This heifer showed some depression during the next several days but eventually recovered without ever showing symptoms re- sembling those observed in loin disease. On 11-25-21 at 5:00 p. m., an aged cow, CS2, was in- oculated intravenously with 75 cc of a thirty-hour bouillon cul- ture of the organism recovered from the heart of CSlA. At 8:00 a. m., 11-26-21, this cow was down and could not be in- duced to get up. Body temperature 97.2 F.; number of respir- ations, 72 per minute. Feces, normal in consistency and streaked with blood. At 11:00 a. m., the cow was up and walking around in the lot. At 5:30 p. m., on the same day, the cow was lying down again and could not be induced to getup. On the following day, at 8:00 a. m., the cow was found dead. Autopsy findings: Bloody discharge from the nostrils. Numerous large hemorrhages under the skin in the subcutane- ous tissue. Prescapular and precrural lymph glands, normal. Numerous hemorrhages on peritoneum, on both the parietal and visceral layer, especially on all four stomachs. Lymph glands in peritoneal cavity, normal. On mucous membrane of fourth stomach, numerous hem- orrhages, the majority about the size of a bean and consisting of a circular ring-shaped hemorrhagic line about 2 mm wide with a non-hemorrhagic center. Mucous membrane of small intestines, hyperemic; no hemorrhages present. No bile 1n small intestines. Mucous membrane of the large intestines, especially that of the colon, hyperemic. Liver, greyish in color, friable (cloudy swelling). Gall- bladder, normal in size; no hemorrhages on mucosa. Spleen, apparently normal. 24 Bulletin N0. 319 Kidneys, greyish in color; friable (cloudy swelling). . hemorrhages present. A few small hemorrhages on muc of urinary bladder. Urine, straw colored. ' Parietal pleura, covered with numerous large hem rhages. Extensive pneumonia 1n lungs. ‘ Many hemorrhages on epicardium; myocardium, grei ish in color, friable (cloudy swelling). Endocardium of -’_ ventricle almost entirely covered with one large hemorrha area. No hemorrhages on endocardium of other heart ca ities. . No lesions were found in the muscles of the legs a along the back, but the loose connective tissue accompanyi- the sciatic nerves showed profuse hemorrhages. ' The organism injected into the animal was recovere from the heart, liver, spleen and lungs in pure culture. N cultures were made from the kidneys. ‘ c’ Although the clinical symptoms and lesions observed i‘ cow CSlA closely resembled those found in cattle sufferin from loin disease, the symptoms and lesions observed g cow CS2 were so different as to preclude the possibility tha the organism injected into these animals was the causative o ganism of loin disease, and for this reason no further experif ments were undertaken with it. i p-lu Thinking that the negative results thus far obtaine might be due to the media—-plain agar, glucose agar, live agar, blood agar—used for purifying the cultures made inth field or inoculated in the laboratory from specimens brough in from the field, not being suitable for the growth of th _ causative organism, a mass culture was made by inoculating liver bouillon from original brain media cultures made from the spleen and either the heart or kidney of six different ani-z mals. This mass culture was incubated for three days, th fluid portion then strained through a cloth and a two-and-one-“Y half year old cow and a two-year-old goat drenched with it The cow received 1000 cc and the goat 300 cc of this fluid No symptoms developed in either of these animals. Rabbits ;._ and guinea pigs were also inoculated. subcutaneously with cul- ture fluid obtained by straining the fluid from brain media, cultures inoculated with tissue from the organs of animals suffering with loin disease. No attempt was made to first purify these cultures for fear that the organism might get lost in the attempt. The rabbits and guinea pigs thus inoc- ulated never became sick during the next two weeks follow- ing the inoculation. A Fatal Disease of Cattle 25 Experiments were also undertaken in which the intes- tinal and rumen content of animals suffering with loin dis- ease were used in an attempt to find the cause. The content of the rumen of case N0. 34 were carried t0 the laboratory, the fluid portion strained off and with this a healthy cow was drenched. No symptoms developed in this cow. No animal yvaas available to which the remaining solid content could be e . In another experiment the small and large intestines were removed from case No. 28 and the content, with the ex- ception of that of the rectum, placed in a bucket. The intes- tines were then flushed with water and the flushings com- bined with the intestinal content. This material was then used to drench a healthy cow. No symptoms developed. LOIN DISEASE NOT IDENTICAL WITH BOTULISM The possibility that loin disease was related to botulism was also considered and, therefore, some animals down with the disease were injected with varying amounts of polyvalent botulinus anti-toxin. Thus one animal that was found down in the pasture was immediately given 80 cc polyvadent botu- linus anti-toxin, intravenously. No improvement was ob- served and 36 hours later the animal was given another in- jection of 100 cc botulinus anti-toxin. The animal died some six hours after the last injection. lAnother animal was given 80 cc polyvalent botulinus anti-toxin in the early stages of the disease and before it was down. The animal was cast for this operation and when re- leased could not get up again. On the following day this ani- mal was given another 80 cc polyvalent botulinus anti-toxin, intravenously; on the third day another 80 cc, and finally, on the fourth day, another intravenous injection of 100 cc poly- valent botulinus anti-toxin. The animal died on the fifth day. A third animal was found down in the pen in the morn- ing where it had been placed the previous night, apparently in good health. At 4:30 p. m., on the following day, the ani- mal was given an intravenous injection of 200 cc (500 units) polyvalent botulinus anti-toxin. No beneficial effect could be observed from the injection. The animal gradually grew worse and was finally destroyed for autopsy four days later. LOIN DISEASE NOT DUE TO TRYPANOSOMES Although the symptoms of loin disease do not resemble those usually observed as due to trypanosomes, it was _ trypanosomes. These parasites could never be demonstrate 26 Bulletin N0. 31.9 considered worth while to test this theory. Trypanosom" could never be demonstrated in smears from the organs i; animals suffering with loin disease, and cattle given injectio of large quantities of blood from such animals always fail to show any reactions following the injections. Neither r“ any of the numerous rabbits given injections of blood and 7 tracts of organs from animals suffering with loin disease sho any suspicious symptoms, or trypanosomes in their bloo, Guinea pigs were given intraabdominally, injections of 10 P? of blood freshly drawn from animals suffering with loin d'. . ease. The blood of these guinea pigs was later examined f and all‘guinea pigs lived and thrived. CONSUMPTION OF TOXIC CARCASS MATERIAL RESPONSIBLE FOR LOIN DISEASE Failing entirely to get any tangible results from all the- ories considered thus far, the writer turned his attention to the carcasses left on the prairie. It was observed that many ani- mals in the affected area had a habit of chewing bones. The‘; mere fact that one occasionally saw an animal chewing a bone, did not, at first, arouse suspicion that the trouble might =1 found there. Closer attention was, therefore, paid to bone-craving, habit of these animals and it was observed tha the animals did not only consume sweet bones, as was at fir a; thought they did, but that they would even consume putri bones. Thus it was found that the bones of animals autopsie on the prairie would soon be consumed by other cattle run, ning in the pasture. It was, therefore, decided to feed thes‘ bones to cattle experimentally and observe results. To ob- tain such putrid bones from the prairie, it was found necesi sary to place them in some kind of an enclosure in order to, keep the cattle away from them. ' Preliminary experiments were started in 1921. A small. quantity of bones was at first obtained and ground up. One- half pound of such bone was fed to a cow, but no symptoms f, developed. In October, 1921, bones were obtained from an animal that had died of loin disease on August 4, 1921. When these bones were collected a considerable amount of dried f‘ and foul smelling meat was still adhering to them. The bones j were ground and with several grams of them one liter of brain 1i media was inoculated and incubated for three days. The liq- uid portion of the culture was then strained off and a two- and-one-half year old steer drenched with it. No symptoms developed in this animal. A Fatal Disease of Cattle 27 FEEDING EXPERIMENTS WITH PUTRID BONES Feeding ground bone to cattle in larger quantities was then undertaken. For this purpose, more bones were col- lected from animals that had died from 10in disease, the car- casses of which had been left on the prairie to rot. When the experiment was begun a supply of 70 pounds of bone was on hand. Two three-year-old steers were used in the experi- ment which was begun on April 24, 1923. Thirty-five pounds of bone was allotted to each animal. The ground bone was fed mixed with wheat bran and corn chops, as otherwise the animals would not eat it. Small quantities were given at first. By May 1, each animal was receiving and consuming reg- ularly two pounds of ground bone daily. On May 13 the available supply of bone allotted to steer CS8 Was exhausted. He ate it well on that day, but when on the following day he was offered two pounds of ground bone allotted to steer CS9 (these bones were from a different carcass) he refused to eat it. Previous to this, on the morning of May 12, the attendant noticed that steer CS8 was not walking as usual, but when on the same day the writer looked at the animal the peculiar walk could not be defected. When the attendant was again questioned about the matter he said, “The steer did not act like he used to.” The steer was kept in the same lot for fur- ther observation and on May 16, at 1 :00 p. m., the attendant observed from a distance of about ~100 yards that the steer, lying ‘down and resting apparently normally, suddenly bel- lowed and struggled to get up. Once on his feet, he made a run of about 15 yards and then dropped to the ground again. Here he made frequent attempts to get up without succeeding. The writer saw the animal an hour later. It made the impres- sion of a perfectly healthy animal resting normally on its sternum, but it could not get up. At 6:00 p. m., the animal’s condition was as follows: body temperature, 102.0 F.; respira- tion and pulse, normal; the animal could not get up and was resting on its sternum. May 17, 1923, 7:00 a. m.: Animal, fiat. When assisted on to its sternum it remained there. Body temperature, 100.4 ‘F.; respiration and pulse, normal. At 11:00 a. m., the ani- mal was visited again and was again flat; at 1:00 p. m. the animal was still flat and was now assisted on to its sternum. .1 Water was offered to the animal, but it did not drink. The 1 animal was then offered some hay, of which it ate a little. > The animal’s bowels had acted and the feces were normal in 1': color and consistency. At 5:00 p. m., the animal was again ~ flat. When assisted on to its sternum a crook was noticed in .1 the neck. The animal was offered some water and it drank 28 Bulletin N0. 319 itvvi) gallons from a bucket. The animal could not switch l a1 . “ _ May 18, 1923, 8:00 a. m.: Animal, flat. Assisted on its sternum the crook in the neck appeared more pronounc than on the previous night, but it could still hold its head The animal was observed to ruminate. Body temperatu 101.2 F. Feces had been passed during the night and were covered With much mucus and a few streaks of blo Up to this time the animal, when assisted on to its sternu ‘j could, at all times, hold its head up in its natural position. I this morning, however, when the animal was to be turn Figure 6. Steer CS8 fed ground bone from prairie. This photograph was made a after the animal had been down twenty-four hours. ~ - over on its other side and a rope placed around its horns for this purpose, it began to struggle and while doing so sudden-f’ ly dropped its head against its side Where it remained in a typical milk fever position. It could be plainly observed that the animal was making strong efforts to raise its head again, ; but could not do so. When the head was now raised by an assistant and released when in its normal position, it Would either drop back against the side of the body again, or it _, would turn in the opposite direction and the animal Would go flat. When the latter occurred the head would strike the i ground with the nose first. The condition of the animal did not improve during the day. May 19, 1923, 8:00 a. m.: Animal flat and in same con- dition as on previous night. Water and food had not been A Fatal Disease of Cattle 29 Figure 7. Steer’ CS8 fed ground bone from the prairie. This photograph shows the milk fever position assumed by the animal after it had been down forty-eight hours. taken for twenty-four hours. Body temperature, 101.8 F.; ' respiration, 18 per minute. Feces had been passed during the night. These Were well-formed, like those of a horse, slightly bloodstained and covered with much clear mucus. Asiit was feared that the animal Would not live very much longer, it was destroyed for autopsy at 9:00 a. m., 5-19-23. - Figure 8. Steer CS8 fed ground bone from prairie. This photograph shows the animal fiat forty-eight hours after it went down. Compare text. 30 Bulletin N0. 319 Autopsy findings: N0 hemorrhages on peritoneum. cosa of pyloric end of abomason, slightly hyperemic. ‘ Small intestines contained much bile and much sticky.‘ mucus on the mucous membrane; otherwise, they were empty; Mucosa slightly hyperemic in a few limited areas. Large intestines, no lesions. Few mesenteric lymph glands, slight peripheral hypere-‘i mia. Abdominal cavity contained about 50 to 75 cc clear, yellowish fiuid, which coagulated soon after exposure to airfi Liver: Left lobe atrophied to one-ha_1f normal size. On? cut surface a distinct yellowish/tinge. No other lesions. ‘a Gallbladder contained 880 cc bile. Mucosa, normal. Spleen, normal on cut surface. Capsule studded withi hypertrophic areas. Blood vessels of capsule prominent. g Kidneys, hyperemic, especially in medullary portion. Cortex showed many pin point red dots; otherwise, kidneys ' apparently normal. Heart: Endocardium of both auricles well marked and . extensive hemorrhages; otherwise, normal in color and con- sistency. Pleura, lungs and trachea, no lesions. Comparing the symptoms and lesions found in steer CS8f with those observed in field cases of loin disease, one will see‘: that they are almost identical. It seems probable that this: ‘was a typical case of loin disease. Since, however, a single. case produced experimentally does not furnish sufficient proof g that loin disease is due to cattle’s eating putrid bone in the pas- i ture, more experiments will have to be carried out along the same line. Such experiments are already projected. The second steer, CS9, used in the above described exper- - iment, consumed the 35 pounds of bone allotted to him, but at no time did he show symptoms of any kind, much less come down with loin disease. a From this experiment no definite conclusion can be drawn as to the period of incubation of loin disease. From the data obtained it can- either be a minimum of 3 1-2 days or a max- imum of 23 1-2 days. While working on the bone theory an effort was made t0 determine at what time the toxin-producing bacteria enter the bone. Bones were, therefore, brought to the laboratory A Fatal Disease of Cattle 31 from fresh field cases of 10in disease, and cultures, both aero- b1c and anaerobic, were made from the bone marrow. In no case could microorganisms be demonstrated. This would indicate that there is no organism present in the bones of animals suffering from loin disease at the time of their death. The bacteria producing the toxin responsible for loin disease, provided that the case produced in steer CS8 was a true case of loin disease, must, in that case, gain access to the bones after the animal has died. Probably the bacteria grow even more rapidly and abundantly in the flesh during decomposition than in the bones. Another interesting problem is to determine whether the bacteria gain access to the bones and flesh from the soil after the animal has died, or whether the bacteria also inhabit the intestinal tract of the animal and invade the flesh and bones from that point after the animal dies, or whether both cases may happen. If the bacteria enter the flesh and bones from the soil only, then the possibility of spread of the disease would be very limited. On the other hand, if the bacteria may also inhabit the intestinal tract without producing their dead- ly toxin there during the life of the animal, but only after the animal has died from any cause whatever, then, in that case, the disease could be spread from place to place by the trans- portation of the animals harboring such bacteria in their in- testinal tract and an outbreak of the disease may occur wherever such an animal dies and other cattle are wont to consume its putrid flesh and bones. RECOMMENDATION If no other than the toxic cause of loin disease exists, the results obtained in the above experiment clearly indicate that the logical procedure to stop the losses from this disease would be to check the bone-craving habit of the animals on the range. Feeding the animals sweet bone meal in sufficient amounts to supply the deficiency necessary for the upkeep and normal development of the body should stop the disease in all cases. Scrupulously cleaning the range of all carcasses and carcass material, not only of cattle, but also of all other animals, should have a tendency to decidedly check, if not entirely prevent losses, depending upon the degree of thor- oughness with which the cleaning is carried out. ' more than the control animals which did not receive bone meal. Sir Arnold .j 32 Bulletin N0. 319 Note: Upon a recent visit of Sir Arnold Theiler, Director of Ve, erinary Education and Research, Union of South Africa, to the Tex_ Agricultural Experiment Station, Sir Arnold saw some of the above da“ and expressed the belief that loin disease" is identical with lamziekte, l disease very prevalent in South Africa. Not all data have been publishe (but see 3d and 4th Reports, Nov. 1915; 5th and 6th Reports, April 1918 and 7th and 8th Reports, April 1918, by the Director of Veterinary R, search, Union of South Africa) on lamziekte, but Sir Arnold stated tha the disease is contracted by the animals when eating putrid bone on th, veld, and that he had been able to produce lamziekte by feeding the ani] mals such bones, but in no other way. The bone-craving, in turn, is dud’ to a lack of phosphorus in the soil and vegetation. Since lamziekte contracted by eating bones, it only remained to stop the animals from doing this in order to prevent the disease. This was successfully ac-' complished by feeding the animals three ounces of sweet bone meal dailfi all the year round. In order to prove his contention, Sir Arnold adminise‘ tered this ‘quantity of bone meal to each individual animal daily with the; result that of a large number of animals thus fed, all stopped the habit. of chewing bones in the pasture and none contracted the disease, whilea. the control animals, which had not received the bone meal and were other- wise kept under like conditions, continued the habit of chewing bones and all developed the disease. ' Not only did he stop the disease by this method, but he was also able i. to show that the animals receiving the bone meal for some time before they had reached maturity, made a much better growth and in the end developed into much better animals, weighing several hundred pounds > suggested that bone meal be mixed with stock salt at the rate of two pounds of bone meal to one pound of stock salt and placed in troughs in the pasture near watering places so that all animals may have easy access to them at all times. A sufficient number of troughs should be provided; so as to prevent the stronger animals from hooking away the weaker ones. f While working on this trouble Sir Arnold also found that anotherdis- ease of South Africa, known there as styfziekte, a disease probably iden- i tical with “creeps,” could be prevented in the same way. f iConsidering, then, Sir Arnold’s description of lamziekte, one must observe that the symptoms of this disease and loin disease are very sim- 1 ilar, if not identical. It has, however, not yet been shown experimentally that the two diseases have a common cause. The organism responsible for the production of the loin disease toxin has not even been cultivated,flf up to the present. The Texas Agricultural Experiment Station, Division of Veterinary r Science, has projected a number of experiments which will likely throw '11 some more light on the subject and also indicate the best method of feed- ing bone meal to cattle. t