Serum samples from white-tailed deer (Odocoileus virginianus) in Iowa were checked for various disease antibodies from 1959 through 1963. Leptospirosis antibodies were found in 9.5% of 369 sera checked. L. grippotyphosa (3.9%) L. pomona (3.6%) and L. autumnalis (2.8%) were found most frequently. L. ballum, L. hardjo, L. sejroe, and L. autralis were also noted. No evidence of brucellosis was found in 231 sera checked. Evidence for western or California strains of encephalitis was noted. Anaplasmosis was also present. Johne\u27s disease antibodies were not found in a sample of deer from western Iowa

Haugen, Arnold O.

English

Name not available

Incidence of Some Disease Antibodies in Iowa Deer

University of Northern Iowa

Proceedings of the Iowa Academy of ScienceVolume 74 | Annual Issue Article 161967Incidence of Some Disease Antibodies in IowaDeerArnold O. HaugenIowa State UniversityCopyright © Copyright 1967 by the Iowa Academy of Science, Inc.Follow this and additional works at: http://scholarworks.uni.edu/piasThis Research is brought to you for free and open access by UNI ScholarWorks. It has been accepted for inclusion in Proceedings of the Iowa Academyof Science by an authorized editor of UNI ScholarWorks. For more information, please contact scholarworks@uni.edu.Recommended CitationHaugen, Arnold O. (1967) "Incidence of Some Disease Antibodies in Iowa Deer," Proceedings of the Iowa Academy of Science: Vol. 74:No. 1 , Article 16.Available at: http://scholarworks.uni.edu/pias/vol74/iss1/16Incidence of Some Disease Antibodies in Iowa Deer1 ARNOLD 0. HAUGEN 2 Abstract. Serum samples from white-tailed deer ( Oclocoil-eus Dirginianus) in Iowa were checked for various disease antibodies from 1959 through 1963. Leptospirosis antibodies were found in 9.5% of 369 sera checked. L. grippotyphosa (3.9%) L. pomona (3.6%) and L. autumnalis (2.8%) were found ~ost frequently. L. ballum, L. hardfo, L. sefroe, and L. autralis· were also noted. No evidence of brucellosis was found in 231 sera checked. Evidence for western or California strains of encephalitis was noted. Anaplasmosis was also pres-ent. Johne's disease antibodies were not found in a sample of deer from western Iowa. All populations of game animals have annual increases and losses. Losses result from a wide variety of causes. Our discus-sions today, however, will deal only with information on disease, tests for disease antibodies and information from autopsies on deer in Iowa. A search of the literature has nort been made to learn if disease caused any loss.es of deer between the late 1800's, when white-tailed deer weve reinrtroduced in Iowa, and the early 1950's. This paper, therefore, reflects mainly what has been learned about disease ,antibodies in Iowa deer since 1950. There are no records to show that the Iowa State University Diagnostic Laboratory necropsied any deer between 1946 and 1950 (Table 1). The deer population in Iowa at that time was still rather small, and little chance for detecting mortality existed under those conditions. Five deer were checked in the period 1951-53. The Unit annual report for 1954-55 nortes that four deer had been brought in for autopsy. Cause of death of one was diag-nosed as enterotoxemia. One checked in August 1955 was found with encepholomalacia. Seven specimens submitted between Aug. 20 and Nov. 18, 1956, showed various symptoms, including some hemorrhagic enteritis and some hemorrhages in muscula-ture, pericardia! sac, and/ or on the heart. Three of these were suspected of having died of enterotoxemia, and one of algae poi-soning. Dr. Hendrickson stated in 1957 that "a disease, possi'bly an epizootic hemorrhagic disorder, reduced deer numbers in scat-tered areas during the summer of 1956." This was about the same year in which Frank Heidelbauer, State Conservation Commis-1 Journal Paper No. J-5698 _of the Iowa Agr~cultur'.'1 aod Home Economics Experi-m".nt .Station, Ames, I_owa. Proiect No. 1895. J<;nntly fmaoced by the Iowa COoperative ~ildlife Research Umt, the Bureau of Sport Fisheries and Wildlife (U.S. Dept. Inter-ior), Iowa State University of Science aod Technology, Iowa State Conservation Com-mission, and the Wildlife Management Instih1te. Part of the work was done in connec-tion with a National Science Foundation Undergraduate Research Participation grant. 2 Professor and Leader, Iowa Cooperative \'lildlife Research Unit, Ames. 78 1Haugen: Incidence of Some Disease Antibodies in Iowa DeerPublished by UNI ScholarWorks, 19671967] DEER DISEASES 79 sion pilot, observed a number of dead deer during his flights at low levels in western Iowa. No evidence is available to indicate any occurrence of disease outbreaks or unusual mortality in deer in Iowa in the period 1957 through 1963. However, there have been a number of .autopsies of deer at the Diagnostic Laboratory. Two of these were brought in because they were "queer" acting. BOll:h had brain abscesses. A third had a "softening" of the brain due to a previous skull fracture. Bacterial infection in the rib section w.as found in two specimens. Streptococcus infection of the foot was found in one, arthritis of the hock joint was found in one, and five had suf-fered traumatic injuries of some sort. Six fawns that had been held in captivity died from different causes, some had scours. One fawn had suffered mower cuts and had an infection about the navel. One game-farm yearling male, autopsied by Eldie Mus-tard of the State Conservation Commission, showed some sus-picious hemorrhages and some enteritis. A 6-month buck, killed with a hammer because it chased a farmer's dog, evidently was only acting like any normal buck ought to behave in late Novem-ber. The rut was in progress. No evidence of disease was found. Evidence of past experience of animals with disease may be detem1ined through testing for antibodies. Such evidence is mostly lacking and not well understood in wild animals. The presence of antibodies of certain diseases can be detected, how-ever, even though the seriousness of the animal's past experience with the disease is unknown. Obviously, such an approach only provides information on animals that have been infected and have survived. A good general discussion on leptospirosis in wildlife is pre-sented by Roth et al. ( 1961). Fay ( 1961) published a similarly good summary of brucellosis in deer. The availability of these publications makes it unnecessary to here repeat general infor-mation on these diseases. MATERIALS AND METHODS Blood samples for the study were secured from 1959 through 1963. The samples from 1959-61 were collected mainly by dip-ping a vial into any pool of blood found in the body cavity when hunters brought their deer to checking stations operated at desig-nated locations in the state. Samples at the DeSoto Bend Refuge in 1962 and 1963 were taken directly from the aorta with a hy-podermic syringe by biologists who gutted the deer as part of the operational procedure at the checking station. The samples were allowed to clot; then the serum was removed by centrifug-ing and stored frozen at about -20°F. until tested. Tests for brucellosis were performed by Drs. Frank C. Stiles, 2Proceedings of the Iowa Academy of Science, Vol. 74 [1967], No. 1, Art. 16http://scholarworks.uni.edu/pias/vol74/iss1/1680 IOWA ACADEMY OF SCIENCE [VoL 74 Jr., of the Bruoellosis Unit of the ADE Diagnostic Laboratory and George Lambert of the National Animal Disease Laboratory, Ames, using the 1:25 brucellosis plate test. Information on antibodies of Leptospira was secured by the microscopic agglutination test performed by personnel at the National Animal Disease Laboratory, Ames, including Drs. Ed-ward A. Carbrey, D. E. Hughes, and 0. H. V. Stalheim. Tests for encephalitis and vesicular stornatitis were performed by Dr. Daniel 0. Trainer of the Univ,ersity of Wisconsin by the Hela cell metabolic-inhibition test. Sera for those tests were packed in dry ice and airmailed from Ames, Iowa, to Madison, Wisconsin. The tests for Johne's disease antibodies were performed with an experimental antigen developed and used by Dr. Aubrey B. Larsen of the National Animal Disease Laboratory, Ames. Dr. Larsen also made dhect observation on sections of the gut of many deer, looking for lesions of the disease. RESULTS Leptospirosis. Dming 1959-63, 285 samples of deer sera col-lected during December hunting seasons were tested for Lep-tospira antibodies; 9.8% were positive (Table 2). L. porrwna had an incidence of 3.6%. Other serotypes involved were L. grippo-typhosa 3.9%, L. autumna~is 2.8%, L. ballum 1.1%, L. hardjo 1.1% and L. sejroe 0.7%. Of the 28 animals showing a positive test, there was a cross-reaction with a second serotype in 8 tests, with the cross-reaction most commonly involving pomona and autumnalis. Table 1. Deer examined at Iowa Veterinary Diagnostic Laboratory up through 1956." Year and Num-date ber Origin Diagnosis 1946-'50 None 1951 June 18 1 Coon Rapids Malnutrition 1952 April 17 2 Marshalltown Blackleg Sept. 26 Fort Dodge Rabies-negative 1953 Feb. 11 2 Marion Corynebacteriosis Nov. 16 Des Moines Toxemia 1954 Jan. 4 3 E. L. Kozicky, I.S.U. Enterotoxemia Nov. 12 11 Traumatism Nov. 28 Jewell Decomposed 1955 Aug. 15 1 E. L. Kozicky, I.S.U. Encephalomalacia 1956 Aug. 20 7 Boone Enterotoxemia Sept. 11 Muscatine Bacteriological exam.-negative Sept. 17 Des Moines Poisoning, algae Sept. 19 Fort Dodge Rabies-negative Oct. 8 I.S.U. Enterotoxemia Oct. 31 Boone Polyarthritis Nov. 18 Jefferson Enterotoxemia " Based on a search of old records by Dr. Paul Bennett in May, 1963. 3Haugen: Incidence of Some Disease Antibodies in Iowa DeerPublished by UNI ScholarWorks, 1967>-"'-'° O:> ~ Table 2. Serotypes and titer for serotypes of Leptospirosis as indicated from blood samples routinely secured from deer shot in December hunting seasons in Iowa and the adjacent Nebraska portion of the DeSoto Bend National Wildlife Refuge (microscopic agglutination tests). Number Serotype and titer sera Numher Number L. L. L. grippo- L. L. L. Year Location Age Sex samples negative positive pomona sejroe typhosa hardjo autumnalis ballum 1959 Allamakee and Cherokee Cos. 35 29 6 T T T T t:I Allamakee Co. Ph F 1/400 J:i:j II ] 1/2 M 1/400 J:i:j !:!:! II lVz ~[ 1/400 II 21/2 M 1/400 1/400 t:I ...... Cherokee Co. ? ? 1/400 r.n J:i:j II 2Vz F 1/400 > 1960 Allamakee Co. 30 22 8 T T T T T r.n J:i:j // F F 1/100 r.n II l1/2 M 1/1000 1/100 II lVz M 1/100 II lVz M 1/100 II 21h M 1/100 1/1000 1960 Allamakee Co. 3Vz M 1/1000 1/1000 II 3Vz F l/100 1/100 II 3Vz M 1/100 1/100 1961 II 19 18 1 T T T T T II 41h F 1/400 00 ...... 4Proceedings of the Iowa Academy of Science, Vol. 74 [1967], No. 1, Art. 16http://scholarworks.uni.edu/pias/vol74/iss1/16Table 2. (Continued.) Year Location Age Sex 1961 Lucas Co. F F F M F M F M F F F F 3~ M 3~ M 1962 DeSoto Bend Refuge F M F F 2~ F 1962 DeSoto Bend 71h F Refuge ? F 1963 " Total positive for single serotype Total positive for two serotypes Grand totals Percent positive 1960-63 1960 and 1961 1962 1963 Number sera Number Number samples negative positive 22 14 8 109 104 5 L. pomona T T 1/200 1/20 L. sejroe Serotype and titer L. giippo-typhosa T 1/100 1/100 1/100 1/400 1/400 1/100 T 1/20 1/20 L. hardjo T 1/100 1/100 T L. L. autumnalis ballum T T 1/100 T 1/100 T 1/20 1/20 70 70 0 T T T 4 2 8 2 3 1 5 3 1 5 2 285 257 28 9 2 11 3 8 3 9.8 3.6 0.7 3.9 1.1 2.8 1.1 also tested for icterohemorrhagiae, canicola .• australis, pyrogenes, bataviae and hyos. also tested for hebdomadis. also tested for mini. - only tested for the three shown with a "T". 00 to ...... 0 ~ > ~ trj ~ 0 'rj rn 0 t;:j z 0 ti:] ~ '"" ii>-5Haugen: Incidence of Some Disease Antibodies in Iowa DeerPublished by UNI ScholarWorks, 19671967] DEER DISEASES 83 Fifteen deer killed accidentally during 1960-61 in scattered lo-cations of Iowa, when tested, were found positive for L. australis -1, L. grippotyphosa-1, autumnalis-1, and 1 showed cross-re-action between L. pomona and L. autumnalis (Table 3). Table 3. Serotypes and titre for Leptospirosis as indicated by blood samples from deer accidentally killed in various months and lo-cations in Iowa. Nega Posi-Year Location tive tive L. L. grippo- L. L. au-pomona typhosa australis tumnalis 1/10/60 Johnson 1 2/15/60 Fayette 1 2/19/60 Polle 1 3/8/60 II 1 3/17 /60 II 1 3/24/60 Allamakee 1 417160 Greene 1 6/20/60 Story 1 7 /27 /60 Hamilton 1 9/7/60 Boone 1 10/21/60 II 1 1/100 11/12/60 Iowa 1 1/1000 1/1000 11/16/60 Johnson 1 11/21/60 II 1 11/28/60 Story 1 12/20/60 Iowa 1 1/100 3/26/61 Johnson 1 3/30/61 Boone 1 1/100 8/6/61 Bremer 1 Total deer 15 4 Conservation Officer Harlan Frankel ( 1960), with assistance from local veterinarians, made tests for L. pomona on 32 blood samples from Clayton County in 1958 and on 37 from Clayton (14), Winuesh.iek (6), Jackson (1+), Fayette (5), and Delaware ( 3) counties in 1959. All the 1958. samples were negative, but 3 ( 2 bucks and 1 doe) of the 1959 samples were positive for L. po-mona. An overall occurrence of leptospirosis antibodies of 9.5% is in-dicated when the 369 samples of Iowa deer from this study and those of Frankel are considered collectively. · Bennett ( 1964), who checked 2,298 samples of blood secured from deer hearts collected in the 1963 December hunting season in Iowa, found 91 reactors ( 3.9%) for L. pomona. He did not check for other serotypes of leptospirosis. In Carroll County, Illinois, Ferris and Verts ( 1964) checked 319 sera and found that 10% ( 32) of the dear reacted with one or more antigens of Leptospira serotypes. Wisconsin studies indi-cate approxinmtely 28% of the deer tested (Trainer and Hanson, 1960) were positive for L. pomona but the incidence varied con-siderably from area to area, with the higher prevalence in dense populations. 6Proceedings of the Iowa Academy of Science, Vol. 74 [1967], No. 1, Art. 16http://scholarworks.uni.edu/pias/vol74/iss1/1684 IOWA ACADEMY OF SCIENCE [Vol. 74 Tests for L. pomona on 190 deer mainly from the wildland area of the upper part of Michigan's Lower Peninsula showed 26.3% positive ( Y ouatt et al., 1959 ) . This part of Michigan supports its densest deer population. Suggestions were made by each of the authors from Wisconsin, Michigan and Illinois that Leptospiral infections due to L. pomo-na were related to the population density of deer. This may not be true for Iowa. As an example, only 2 L. pomona reactors were found in a sample of 109 tests from 188 deer harvested from a herd estimated at 600 animals on a 2500-acre "is]and area," the DeSoto Bend National Wildlife Refuge in 1962. A y~ar later, there were no reactors in a sample of 70 sera from 92 deer killed on the same area. The numbers of reactors are too few for conclusions, but there is evidence that both sexes and all age groups, including fawns, are susceptible. Brucellosis. From 1958 through 1962, 231 blood samples taken from Iowa deer during the December hunting seasons were checked for the presence of antibodies of BruceUa abortus. Al'l 231 were negative (Table 4). An additional 13 samples taken £i·cin\ ·deer killed accidentaly in various seasons of the year were also negative (Table 5) . Table 4. Results of plate tests for antibodies of Brucellosis in sera from Iowa deer. Numbe1 sera Test Results Date Location samples No. - No.+ 1958 Clayton Co. 32 32 0 1959 NE Iowa 37 37 0 1960 Various counties 12 12 0 1960 Lansing and Allamakee Cos. 25 25 0 1960 Cherokee 6 6 0 1961 Allamakee and Lucas Cos. 41 41 0 1961 Bremer Co. 1 1 0 1962 DeSoto Bend 77 77 0 231 231 0 Bennett ( 1964), who ran tests on blood samples from the hearts of 2,298 deer taken from throughout Iowa in the 1963 hunting season, also found all sera negative. Iowa tests are in agueement with findings of Fay ( 1961) who concluded that bru-cellosis is of no importance and almost non-existent in white-tailed deer. His conclusion was based on results from 12,706 white-tailed deer tests in 24 states, with only 20 ( 0.16%) deer blood samples reacting. Encephalitis. Eighty-seven serum samples from deer taken in the December 1962 and 1963 hunting seasons on the Nebraska 7Haugen: Incidence of Some Disease Antibodies in Iowa DeerPublished by UNI ScholarWorks, 19671967] DEER DISEASES 85 Table 5. Results of plate tests for antibodies "Of Bmi::ellosis in blood sam-ples secured from Iowa deer during various seasons oLthe . year. Date Location 417 /60 Greene 417 /60 Boone 4/14/60 Hamilton 6120160 Story 9/7 /60 Boone 10/21/60 Boone 11/15/60 Johnson 11/12/60 Iowa 11/21/60 Johnson 3/26/60 Johnson 3/30/60 Boone 12/20/60 Iowa 8/6/61 Bremer No. sera samples 1 1 1 1 1 1 1 1 1 1 1 1 1 13 Test Results No. - No.+ 1 0 1 O' .. 1 0 1 0 1 0 1 0 1 0 1 0 1 0 1 0 1 0 1 0 :: 1 0 13 portion of the DeSoto Bend National Wildlife Refuge, on the east side of the Missouri River, were checked for various strains of encephalitis. Two male fawns of 67 deer from 1962 showed antibodies for western viral encephalitis, but were negative for eastern, St. Louis, an.d California strains. In 1963, 6 ( 1 female and 5 males, all rn years and older) of 20 deer sampled were positive for the California strain, but negative for eastern, St. Louis, and western strains. Sera from 12 deer taken near Burlington in Des Moines County in southeastern Iowa were negative for encephalitis. Vesicular Stomatitis. All of 20 DeSoto Bend and 12 Burlington samples of blood serum tested for vesicular stomatits were nega-tive. Anaplasmosis. Bennett ( 1964), using the capillary agglutina-tion test on 2298 Iowa deer heart blood samples from the 1963 season, found 91 ( 3.9%) reactors for anaplasmosis. The positive animals came from scattered locations throughout the state. Johne's Disease. In a check of 50 intestinal specimens and 91 serum samples from the 1962 DeSoto Bend deer season, no evi-dence was found of Mycobacterium paratubercul,osis, the organ-ism that causes Johne' s disease ( Larsen, 1963 ) . Chlorinated Hydrocarbon Insecticides in Deer. Body fat from about half a dozen white-tailed deer shot on the DeSoto Bend National Wildlife Refuge in 1962 was sent to the Denver Wildlife Research Center. Analysis at that center indicated the presence of DDE in a concentration of less than 0.5 p.p.m. ACKNOWLEDGMENTS Data for this report could not have been secured without the assistance of a number of individuals. Special thanks are due a 8Proceedings of the Iowa Academy of Science, Vol. 74 [1967], No. 1, Art. 16http://scholarworks.uni.edu/pias/vol74/iss1/1686 IOWA ACADEMY OF SCIENCE [Vol. 74 number of Iowa State Conservation Commission employees, es-pecially Eldie Mustard, Paul Kline, Wendell Simonson and Keith Larson. Thariks are also due Karl Menzel and Bob Havel of the Nebraska Game, Forestation and Parks Commission and to Ker-mit Dybsetter, Refuge Manager at the DeSoto National Wildlife Refuge. The help of Drs. David Roslien, Dale Hein and Paul Vohs and other graduate students is greatly appreciated. The technical assistance of Drs. Edward A. Carbrey, D. E. Hughes, 0. H. V. Stalheim, Aubrey Larsen, Frank C. Stiles and Daniel 0. Trainer, Jr. was extremely helpful and is sincerely appreciated. Literature Cited Bennett, Paul C. 1964. Unpublished letter to cooperators. Iowa Vet. Diag-nostic Lab. Ames. 7p. Fay, Dale. 1961. The current status of brucellosis in white-tailed deer n; the United States. Proc. N .Am. Wildl. Conf. 26:203-211. Ferris, D. H., and B. J. Verts. 1964. Leptospiral reactor rates among white-tailed deer and livestock in Carroll County, Illinois. J. Wildl. Mgmt. 28( 1) :35-41. Frankel, Harlan. 1960. Personal comunication to E. T. Rose. Larsen, Aubrey B. 1963. Personal communication. Roth, Earl E., W. V. Adams, G. E. Sanford, Betty Greer, and Patricia Mayeux. 1961. Leptospirosis in wildlife and domestic animals in the United States. Proc. N. Am. Wildl. Conf. 26:211-219. Trainer, Daniel 0., Jr., and R. P. Hanson. 1960. Leptospirosis and brucel-losis serological reactors in Wisconsin deer, 1957-1958. J. Wildl. Mgmt. 24( 1) :44-52. Youatt, W. G., L. D. Fay, G. L. Whitehead, and J. P. Newman. 1959. Brucellosis and leptospirosis in white-tailed deer in Michigan. J. Wildl. Mgmt. 23( 3) :345-348. 9Haugen: Incidence of Some Disease Antibodies in Iowa DeerPublished by UNI ScholarWorks, 1967

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