Oak Poimning in Livestock TEXAS A8zM UNIVERSITY Texas Agricultural Experiment Station R. E. Patterson, Director, College Station, Texas Summary Oak poisoning is a major problem in the production of livestock in areas where oak occurs. The blossoms, buds, young leaves and acorns are poisonous. Cattle, sheep, goats, swine, rabbits and guinea pigs are susceptible to oak poisoning. A gallotannin isolated from oak has been demonstrated to be poisonous. Calcium hydroxide is an antidote for tannic acid. Calcium hydroxide, supplied in a supplementary feed, is an aid in preventing oak poisoning in cattle. Contents Summary ........................................................................................................ --2 Introduction ................................................................................................... -5 History of the Problem of Oak Poisoning . . . . . _ _ . . . . . . . . . -5 Clinical Signs and Lesions ..................................... 4 Recent Studies on Oak Toxicity ................................................................. --4 Evaluations of Possible Antidotes 5 Methods of Chemical Control of Oak ........ -- 8 Conclusions ............................................. -- 8 Literature Cited .................................................. -- 8 Acknowledgements The assistance of R. H. Godbolt, Marfa, Texas, in solving some of the manufacturing problems in formulat- ing this antidotal feed and his furnishing the feed for most of the experimental trials is gratefully acknowledged. The assistance of the County Commissioners Court of Andrews County, Texas is sincerely appreciated. Mem- bers of the West Texas Cattlemen’s Association, Andrews, Texas, furnished calves for the feeding trials which is sincerely appreciated. w. Dollahite, o. Housholder and 1. Camp* ‘ i espectively, professor and technician, Department Veterinary Pathology, College of Veterinary edicine; and professor, Department of Bio- emistry and Nutrition. MORE THAN 4O SPEcIEs and numerous varieties of oak are found in Texas (5). Some occur in every section of the state. The buds and young leaves of many of the oaks are poisonous when they make up a major portion of the diet of livestock. The low-growing forms of oaks usually cause the most trouble, and the species Quercm laavardii is considered to be the most serious offender. Q. lam/ardii grows in sandy soil from Crane and Ward counties north through the Plains and Panhandle area of Texas. Several coun- ties have reported losing mo-re than 1,000 cattle in a single year. The total annual loss in Texas from sand shin oak ( lmoardii) has been estimated to be more than $10,000,000. Total annual loss from all other oaks combined probably wo-uld equal this figure. a Oak Poisoning in Livestock In 1936, Boughton and Hardy (3) reported severe losses among cattle and sheep eating durandii var brevilo-ka in the Edwards Plateau region of Texas. gambellii was reported by Marsh e! al. (16) to be toxic. Losses have been observed by the authors in cattle that have eaten varieties of incrma (sandjack oak)1 and rtellata (post oak) (10). The authors have observed numerous cases of poisoning in cattle that resembled oak intoxication and were attributed to the ingestion of acorns. Economic losses attributed to oak occur: When acute poisoning results in a high mortality rate; when chronically poisoned animals remain unthrifty for long periods; when other feed is substituted when animals are removed from oak infested areas; when use of the range is lost during this period; and when grass production is lowered because of the competition with o-ak for water and soil nutrients. History of the Problem of Oak Poisoning Probably the earliest recorded statement on the toxicity of oak as a forage was made by Mascal (17) in 1662, who wrote, “Again oak leaves, if sheep eat thereof green, it is evil for them; especially for young lambs, which will kill them; and like-wise of other cattel”. The next reference on oak toxicity did not appear until 1895, when Cor- nevin (6) reported a severe outbreak of oak leaf poisoning in France during the spring. The lesions found in this outbreak were primarily gastroenteritis and nephrocystitis. Hemoglobinuria was reported. Cor- nevin presented a theoretical discussion on tannin as the toxic prin- ciple of oak leaves, but his views were not supported by experimental evidence. The reported work on oak from 1893 to 1915 was limited to case histories and discussion of forage values. In 1901, Harting (13) ‘Field observations in 1960. reported that goats coul-d safely eat oak twigs, but deer and cattle were fatally poisoned. Mackie (15), in 1903, reported on the nutritional value of oak as a forage, but did not mention any poisonous properties of the plant material. The Breeder's Gazette, in 1909, reported a case history of oak poisoning. Glover and Robbins (12), in 1915 proposed that oak poisoning was due to the ingestion of larkspur growing in scrub oak thickets. The scrub oaks, gambelii and havardii, were reported to be toxic by Marsh, et a]. (16) in 1919. These investigators conducted feeding trials at the Salina, Utah Experiment Station during the summers from 1915 to 1918 and at Monahans, Texas, in the spring of 1917. Q. brevilolm was reported to be toxic to sheep and cattle in 1936 (3). Towers (22) described signs and lesions of acorn poisoning in cattle which resembled those seen in animals poisoned by oak leaves and buds. Clark and Cutchin (4) isolated a hydrolyzable tannin from penduculata acorns. This tannin was toxic to a rabbit, a calf and to mice when injected intraperitoneally. The lethal dose to mice was of the same magnitude as commercial tannic acid. For almost 500 years, the toxicity of oaks has been recognized, but the causative agent has been largely specu- lative. Oak tannins have been suspected since the time of Cornevin, but only limited experimental work has been reported to confirm or refute this hypothesis. Work done at the Texas Agricultural Experiment Station in the past 5 years has demonstrated the toxicity of oak tannin (19). Clinical Signs and Lesions The clinical signs of oak poisoning (16) in ruminants usually become apparent 8 to 14 days after the animals start eating the plant material. The first indication is listlessness and loss of appetite. The hair coat becomes rough, and the animals appear gaunt and have a tucked-up appearance. A pronounced constipation occurs frequently followed in 1 to 8 days by a profuse diarrhea. The feces contains mucus and blood. Affected animals have a tendency to stay close to watering ‘places and drink fre- quently, though only small quantities of water are consumed each time. The animals may become anemic and lose weight. The respiration remains normal during the course of the illness, but the pulse is weak and slower than in healthy animals. The pulse may become more rapid just before death. Edema may occur with subcutaneous swellings con- taining a clear gelatinous material and no evidence of hemorrhage. Large quanties of clear fluid also may be present in the peritoneal cavity and in the pericardial sac. 4 The abomasum, or true stomach, usually shows a s a hemorrhagic gastritis. The lesions in the first part of p small intestines usually are similar to those seen in stomach. The kidneys frequently are inflamed and r contain petechial hemorrhages. i Smith (21) reported the presence of a red stai; mass of solid material in someofl the proximal convol and ascen-ding tubules of sections stained by the a toxylin and eosin method. He stated that this mat replaces the epithelium and occupies the lumen of tubules. He believed these findings to be an im] aid in the diagnosis of oak poisoning. i i Recent Studies on Oak Toxicity A study to determine the cause and control of poisoning in cattle was initiated in Texas in 1959. i) investigation had specific fundamental objectives: _ determine the time of the year an-d the stage of growth which the plant could best be used for chemical and fee) studies; to develop suitable methods of collection and V age of plant material for these studies; to determine p. laboratory animal could be used for chemical assay to isolate and identify the toxic agent in the plant; develop an antidote or some method of neutralizing _ toxic agent; and to attempt to supply supplemental i, which would prevent animals from eating suffif amounts of oak to produce injurious effects. Practical experience had taught ranchers that an could more safely be turned into oak pastures when leaves had lost their tender green tint and had deei in color. The first spring growth of oak was demonst i) to be more toxic by feeding trials. Rabbits were fedf fresh blossoms, buds and leaves of shin oak collect the spring and mature leaves collected in November. _. 64 rabbits receiving the fresh spring growth, 32 ~f definite signs of oak poisoning an-d 21 of these Those rabbits fed the November growth showed y»; emaciation and 2 pregnant rabbits aborted. No y signs were observed, and all animals gained weight raj when placed on other rations. ' Buds, blossoms and stems of shin oak were coll; by hand as they became available. The plant material spread on wire racks for air drying or was sealed in p bags, then frozen within 2 hours from the time of I‘ lection. Drying the oak for 3-5 days did not alt)‘: toxicity for calves or rabbits. Oak collected in the -_' and stored frozen was palatable and toxic to rabbits, the length of storage time increased, the oak becam palatable. After 1O months storage in a deep freezer oak was not palatable to rabbits. ‘ Fresh oak was fed to sheep and goats that t nursing lambs and kids, but was withheld from the 4- iiThe toxic principle did not appear to be trans- ’, gh the milk. The lambs and kids 10st weight, “lieved that this was due to the decreased milk i pigs and rabbits also were found to be sus- .1 oak poisoning. The clinical signs and patho- ’s in rabbits were similar to those seen in cattle, less severe lesions occurred in the kidneys and e lesions were found in the liver. The ease of ing rabbits made this animal more suitable for l» chemical fractions derived from oak. lotannin was isolated from shin oak in 1962 If annin" is a generic name for a group of complex l widely distributed i.n the higher plants. The 'ns" yield gallic acid when subjected to acid Commercial “tannic acid" is an example of a i» and is obtained from nutgalls, an insect excres- the young twigs of Q. infectoria and other allied vqoral toxicity of the isolated shin oak tannin was i by determining the amount necessary to kill 5O (LDM) of the assay animals. The multiple dose i "the oak tannin was determined with adult rab- it four animals per group. Four different levels nin were administered to t'he rabbits daily for The data were analyzed (2) and the oral multiple i5‘, was calculated to be 6.9 gm./kg./day, for the lated from havardii (19). ' the isolation procedure became more refined, the iof the more purified tannin was increased. The 1 tannin produced death in all rabbits in 1-2 days f‘- inistered orally at doses of 2 gm./kg./day and 1'1 75 percent of the animals in 5 days when fed 1 gm./kg./day.2 isolated tannin, purified tannin, fresh shin oak d frozen shin oak leaves were fed to rabbits, and fcal signs and gross post mortem lesions were The signs and lesions were similar in all cases. rabbits, which had received 1 gm./kg./day of , tannin3, were sacrificed at 4-7 day intervals for rtem examination. The characteristic lesions of "oning were observed. 4i ified shin oak tannin and commercial tannic acid ed to rabbits in parallel studies. The serium tan- els (18) (expressed as “tannic acid” equivalent) ' termined periodically. The times of death of rab- ‘ eiving lethal doses of these materials corresponded lamounts of tannin consumed and the level of tannin ed in the blood serum. ite, ]. W. and B. ]. Camp, unpublished research notes, iyite, ]. W. and B. ]. Camp, unpublished research notes, Samples of shin oak were collected at several stages of growth fro-m a 1-acre plot near Andrews, Texas. Chemical analyses indicated the following variations in tannin con- tent on a dry weight basis (expressed as percent) : April, 15.1; May, 8.7; August, 7.7; and October, 4.2. From the similar clinical signs and post mortem lesions produced by oak tannin and laavardii leaves, the oral toxicity of the isolated tannin in rabbits, and the high tannin content of the plant concomitant with the most to::ic period of the plant, it was concluded that the tannin of laavardii was the toxic principle. During the fall and early winter, from 1959 to 1965, the authors observed numerous cases of poisoning in cattle which apparently resulted from the ingestion of acorns. These cases occurred in the eastern part of Texas and were more numerous in 1965. Typical clinical signs and post-mortem lesions of oak poisoning were observed. The blood-urea-nitrogen (BUN) was elevated, indicating exten- sive damage to the kidneys. Evaluations of Possible Antidotes Commercial tannic acid representing the same class of tannins as isolated from shin oak was used in the preliminary attempts to find an antidote, or neutralizing agent, for oak poisoning. Numerous chemical compounds were administered to rabbits along with tannic acid in an effort to find one with beneficial effects. Ferrous citrate, calcium chloride, calcium lactate, calcium carbonate and calcium acetate failed to provide any protection against tannic acid poisoning Bone meal, defluorinated phos- phate, calcium gluconate, an-d dicalciurn phosphate pro- vided a slightly beneficial effect when administered in equal quantities with tannic acid. Calcium hydroxide prevented tannic acid poisoning when administered in the ratio of 1 part calcium hydroxide to 6 parts tannic acid. This chemical reduced the losses when administered in the ratio of 1 to 8. This finding suggested that calcium hydroxide be evaluated as a possible antidote for shin oak tannin. Numerous feed formulas containing varying amounts of calcium hydroxide were tried to find a combination that was effective, palatable, economical and practical to manufacture. Two feeds, containing 9 percent and 15 percent calcium hydroxide were used in the first evalua- tion against shin oak poisoning in cattle (9). These feeds were prepared as follows: 9% Feed 15% Feed Control Feed Ground alfalfa 36% 30% 45 41 percent protein cotton seed meal 20 20 20 Rice oil 5 5 5 Calcium hydroxide 9 15 0 Molasses 30 30 30 a Oak Fed, As % Body Wt. m Perc ent Morbidity r-I O O p, 8O z . g 60 Percent Mortallty 0d i=1 Qt 4O r 2O I I Of 6 Calves Of 6 Calves Of 6 Calves Fed Oak Fed Oak and Fed Oak and Supplementary Antidote Feed Feed Figure l. Comparison of average oak consumption, percent morbidity and percent mortality of calves fed Quevcus hawardii (sand shin oak) and supplements. Antidotal feeds contained 9 percent and 15 percent by weight of calcium hydroxide. The 9 percent calcium hydroxide feed was made into 3/ 8- inch cubes and the 15 percent feed made into 5 / 4-inch cubes for purposes of identification. Eighteen calves were fed as much fresh shin oak ( laaz/ardii) as they would consume for 19 days. Six calves were fed fresh shin oak exclusively. Four of these animals developed severe signs of intoxication and one died (Figure 1). Six calves were fed shin oak and 5 pounds of control feed daily without calcium hydroxide. Three became ill. Six calves were fed shin oak and 3 pounds of supplemental feeds daily containing calcium hydroxide (hydrated lime). Three animals received the 9 percent lime formula and three were started on the 15 percent formula. Difficulty was encountered in getting the calves to continue eating the 15 percent lime feed as prepared in this formulation. Only one animal ate this feed for the entire feeding period. The other two calves were changed to the 9 percent formula after 1O days, but one calf refused this formula also. By the thirteenth day, signs of oak poisoning developed in this calf. The other calves remained free of oak intoxication. A similar feeding trial was performed in 1964 to evaluate a 10 percent calcium hydroxide supplementary g Oak Fed, As % Body Wt. Perc ent Morbidity 100 Percent Mortality H 8O 5 U 6O 0d E 40 r 2O Of 6 Calves Of 6 Calves Of 6 Calves Fed Oak Fed Oak and Fed Oak and Supplementary Antidote Feed Feeds Figure 2. Comparison of average oak COIISUIDPUUII, percent morbidity and percent mortality of calves fed Quercus stellata (post oak) and supplements. Antidotal feed contained l0 percent by weight calcium hydroxide. 6 feed (10). Post oak (Q. rtellata) was fed d trial. The antidotal and supplementary feeds as follows: Supplementary feed, An I. pounds =_ Cottonseed meal 1,040 Dehydrated alfalfa leaf meal 600 Vegetable oil '1 l60 Calcium hydroxide (hydrated lime) 0 Eighteen calves of mixed breeding from; months of age and weighing from 160 to 595 n fed as much post oak (Q. rtellata) as they woul for 12 days. Six calves were fed an average of ' cent of their body weight on post oak blossoms. leaves. All developed severe signs of poisoning died (Figure 2). Six other calves were f‘ quantities averaging 32.1 percent of their bod and 1.8 pounds daily of supplementary feed. i‘, these developed signs of oak poisoning, and ti The surviving calves in this group lost weight. group of six calves was fed a total amount of averaged 50.2 percent of their body weight and daily of the antidotal feed. Three developed poisoning and two died. The surviving calves -.-'_. stantial weight gains while they were eating returning to a normal diet. 1 The calves in this feeding trial were per M choice of post oak in all three conditions of feedTf allowed unusually large quantities of oak to be , with a fixed amount of the antidotal feed. The \ cases of oak poisoning in the group fed this feed/i animals that consumed the greatest quantity of ate oak in total amounts which averaged 53.6 percent of their body weight. At these high rat intake the protective ratio of calcium hydroxid tanning probably was exceeded. To better define it became necessary to compare the feed at two 1 oak consumption. The 1965 feeding trial evaluated a lime ing 15 percent by weight of calcium hydroxi attempt to get the animals to eat more of the i The content of vegetable oil was reduced 0n?“ percent, since the cubes manufactured in 1964 y.) during storage. This resulted in a much harder} reduced the total cost. The following formulati used in the experimental feedings: l» Supplementary feed, pounds - ' Cottonseed meal 980 ‘f Dehydrated alfalfa leaf meal 600 Vegetable oil 120 Hydrated lime (Ca(0H)2) 0 Six calves were used as controls. They were choice post oak buds, blossoms and leaves, and the» .1 consumed was determined. This same quantity fed to six other calves together with 2 pounds e formulation. This condition of feeding repre- e level of oak consumption. The second level take was established by allowing another group ves free choice of oak together with 2 pounds of al feed daily. A final group of six calves was with 1.7 pounds of supplementary feed daily. A in the tabulation, the supplementary feed was ‘(formulation as the antidotal feed, but it contained in hydroxide. The 1.7 pounds of supplementary _ained the same amount of nutrients as 2 pounds p, 'dotal feed. control calves ate an average of 37.9 percent of y weight of post oak (Figure 3). One calf was _"»'-- five developed severe signs of poisoning, and these died. The six calves fed supplementary feed fr sumed an average of 41.7 percent of their body 50f oak. Two remained free of signs of post oak g, two became ill but recovered and two died. The 'eceiving the antidotal feed and post oak free choice 1d the plant material in an amount which averaged rcent of their body weight. Five calves were 1 ed, but one refused to eat the feed after 1 week, w- signs of poisoning and died. The group of receiving antidotal feed together with post oak tities approximating that eaten. by the control o remained free of signs of oak poisoning. ;t both levels of oak intake, the feed containing ‘ed lime was adequate in preventing illness and death " g as the calves continued to eat. One calf ate feed i. in an amount which averaged 60.4 percent of weight, but no signs of poisoning developed. This p} t of oak had been fatal in the 1964 evaluation of a ‘containing 1O percent by weight of calcium hydroxide. CWith the exception of the calf which refused to eat fmedicated feed, all animals fed the antidote and post _were safely maintained on a diet containing approxi- ily 1 part calcium hydroxide to 1 part oak tannin. This i. was calculated from the chemical assay of plant rial for tannin content and the known amounts of f ated lime and plant material fed. gThe results of these controlled feeding trials indicate i a good supplementary feed will reduce livestock losses F: oak poisoning but will not always prevent intoxica- ‘. The beneficial effects of a supplementary feed 9e reflected in a lowered incidence of intoxication and i ered death rate. A good supplementary feed containing idrated lime had more beneficial effects, as reflected by ‘l lower morbidity and mortality rates (Figures 1, 2 and The determination of blood-urea-nitrogen proved use- ‘l in following the renal impairment subsequent t0 oak PERCENT Cloak Fed, As "/0 Body wt. 100 Percent Morbidity ' "-* Percent Mortality 75 50 Z5 Of 6 Calves Of 6 Calves Of 6 Calves Of 6 Calves Fed Oak Fed Oak and Fed Oak and Fed Limited (Cmfilvls) Supplementary Antidotal Feed Oak and Anti- Feed dotal Feed Group l Group 2 Group 3 Group 4 Figure 3. Comparison of average oak consumption, percent morbidity and percent mortality of calves fed Quercus stellata (post oak) and supplements. Antidotal feed contained l5 percent by weight of calcium hydroxide. ingestion. The extent of change in this serum constituent as determined for calves on the different oak and supple- mental diets may be seen in Figure 4. Field trials were made in Andrews County, Texas in 1963, 1964 and 1965 to evaluate 10 percent calcium hydroxide antidotal feeds under range conditions. The formulation used in 1965 contained vegetable oil at a concentration of 6 percent. Approximately 100 tons of the feed were used during these evaluations. On mo-st of the ranches, the feed was supplied to one or more pastures while other types of supplementary feed, such as 41 percent cottonseed cake, 2O percent range cubes and protein blocks were fed in the remaining pastures. In all cases, ranchers reported that cows fed antidotal feed were in better condi- tion at the end of the feeding trial than cows on any other supplementary feed. The cows ate the cubs satisfactorily, but young calves would not always eat their share. Losses in cows eating the feed were practically nil at a time when "there were losses due to oak poisoning in adjoining pas- tures. The losses in calves due to oak poisoning usually Post Oak (Group l) . , , _ , , ,, Post Oak and Supplementary Feed (Group Z) .____ Post Oak and Antidotal Feed (Group 3) 150 __*__.Antidote Feed and Oak ‘l Held at Control Level (Group 4) SERUM UREA-NITROGEN (MG. /100 ML.) DAYS Figure 4. Average daily urea-nitrogen (B.U.N.) values for four groups of calves fed Quercus svtellaota (post oak) and supple- m€nt5i 7 were less severe than those experienced in adjoining pas- tures on the same ranch. One rancher fed the formula as a loose feed in troughs. This feed was readily eaten in this form. The opinion of ranchers is that a minimum of 4 pounds of this feed must be fed daily to each cow to pre- vent oak poisoning. They have suggested that a method, such as creep feeding, be used to encourage the calves to consume more of this feed. Methods of Chemical Control of Oak The success of chemical control of o-ak depends on the consecutive annual re-application of the herbicides, as described below. The growth of grass after chemical spraying is excellent, if moisture conditions are favorable, but regrowth of oak is frequent and complete eradication 1S rare. Aerial spray applications of herbicides have been used as an aid in the control of sand shin oak. One-half pound of low-volatile esters of 2,4,5-T in 4 gallons of a diesel oil- water emulsion (1 gallon diesel oil and water sufficient to make 4 gallons) per acre has been an effective aerial spray. Maximum control is obtained when applications are made for 3 consecutive years. Shin oak on limestone soil does not respond readily to aerial applications of herbicides. Effective control is obtained after two consecutive treatments of 1 pound of 2,4,5-T in 4 gallons of a i-diesel oil-water emulsion. Shin oak in tree form, post oak and blackjack oak may be controlled by trunk base application of 16 pounds of 2,4,5-T of low-volatile ester in 100 gallons of diesel ofl (20). Post and blackjack oaks may also be controlled by the aerial spray application of 2 pounds of 2,4,5-T esters in 4 gallons of diesel oil-water emulsion per acre. Repeat- ing the application with 11/2 po-unds of 2,4,5-T the follow- ing year obtains maximum control (7). Conclusions The severe economic losses to the cattle industry from oak poisoning can be reduced only by annual preven- tive measures.’ If available, oak-free pastures should be deferred for use during the problem season. Excessive oak growth in pastures may be controlled by one of the previ- ously described chemical methods. The use of a good supplementary feed is needed during the problem season. The addition of a calcium hydroxide, or hydrated lime, to the supplementary feed is recommended to help prevent losses from oak poisoning. The feed recommended (per ton) is: Cottonseed meal 1,080 pounds Dehydrated alfalfa leaf meal 600 pounds Vegetable oil 120: pounds Calcium hydroxide 200 pounds This feed may be used in the form of cubes or in i form in troughs. A minimum of 4 pounds per cow s 5 be put out daily. Calves should be fed a minimum '5 pounds per day in a creep feeder. a Literature Cited 1. Anonymous: Breeder’s Gazette"; 56, (1909): 369. 2. Bliss, C. I.: The Determination of the Dose-Mortality g for Small Numbers. Quart J. Pharm. 8t Pharmacal, 11, (19, 192-196. 3. Bougihton, I. B., and Hardy, W. T.: Oak Poisoning in,‘ ‘ Cattle and Sheep. J.A.V.M.A., 89, (Aug., 1936): 157-162: 4. Clark, E. G. (L, and Cutchin, E.: A Note on the Toxici l the Acorn, Brit. Vet. J., 112, (Apr., 1956): 135-139. ' 5. Cory, V. L., and Parks, H. B.: Catalog of the Flora of‘ State of Texas. (1937): 37. 5' 6. Cornevin, C. E.: Der Planter Veneneurer et der Empoi p’ ment: Qz/eller Determinent. Paris, 1893; 130 (Quoted by 7. Darrow, R. A. and McCully, W. G.: Brus.h Control a Range Improvement. Texas Agr. Exp. Sta. Bull. 942 (1959).'* s. Dollahite, J. w, and Camp, B. 1.; Calcium Hydroxide An Antidote for Tannic Acid Poisoning in Rabbits. Am. J. p R€S., 22 (NOV., 1962)Z 1271-1272. - 9. Dollahite, J. W, Housholder, G. T., and Camp, B. J.: t‘ cium Hydroxide, A Possible Antidote for Shin Oak (Qu L] laazlardii) Poisoning in Cattle. Southwest. Vet., 16, (W7 1963); 115-117. -- 10. Dollahite, J. W., Housholder, G. T., and Camp, B. J.: p cium Hydroxide (Hydrated Lime) in a Supplemental Feed a; Antidote for Oak Poisoning in Cattle. Texas Agr. Exp. Sta. ‘ Rep. 2319 (July, 1964). - 11. Dollahite, J. W., Housholder, G. T., and Camp, B. J.: v Effect of an Antidote Feed Containing Calcium Hydroxide <= Supplementary Feed on the Toxicity of Quercur rtellata ( Oak) in Calves. In Preparation. ” 12. Glover, G. H., and Robbins, W. W.: Colo. Agr. Exp. _ Bull. 211 (1915)! 27. . 13. Harting, J. R.: American Gardening, 22, (1901): 132. 14. Long, H. C.: Plants Poisonous to Livestock. Camb ,7 University Press, 1917: 69. _ 15. Mackie, W. W.: The Value of Oak Leaves for F0 Calif. Agr. Exp. Sta. Bull. 150 (1903). l 16. Marsh, C. D., Clawson, A. B., and Marsh, H.: Oak- Poisoning of Domestic Animals. U.S.D.A. Bull. 767 (19 50-51. 7' 17. Mascal, Leonard: The Government of Cartel. London, 1: Cited by Mash, U.S.D.A. Bull. 796 (1919). 18. Mosesson, E., Norberg, B., Rosenquist, H., and Wohlgr t On the Toxic Effect of Tannic Acid with Reference to the T, ment of Burns. Acta Physiol. Scand., 14, (1947): 144-157. ‘_ 19. Pigeon, R. F., Camp, B. J., and Dollahite, J. W.: Toxicity and Polyhydroxyphenal Moiety of Tannin Isolated f Quercur lmvardii (Shin Oak). Am. J. Vet. Res., 22, (Nov. l, 1268-1270. » 20. Robison, E. D.: Chemical Brush Control in West T Texas Agri. Progress 9 (3), (1963): 3-5. » 21. Smith, H. A.: The Diagnosis of Oak Poisoning. Sou t, Vet., 13, (Fall, 1959)! 34-37. i 22. Towers, K. G.: Acorn Poisoning in Heifers. Vet. Rec‘ (1950); 74. :