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University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln

USGS Northern Prairie Wildlife Research Center US Geological Survey

1996

Survival of Radiomarked Ducklings in Northwestern Minnesota

Carl E. Korschgen Upper Mississippi Science Center

Kevin P. Kenow Upper Mississippi Science Center

William L. Green Upper Mississippi Science Center

Douglas H. Johnson USGS Northern Prairie Wildlife Research Center, [email protected]

Michael D. Samuel National Wildlife Health Center

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Korschgen, Carl E.; Kenow, Kevin P.; Green, William L.; Johnson, Douglas H.; Samuel, Michael D.; and Sileo, Louis, "Survival of Radiomarked Canvasback Ducklings in Northwestern Minnesota" (1996). USGS Northern Prairie Wildlife Research Center. 222. https://digitalcommons.unl.edu/usgsnpwrc/222

This Article is brought to you for free and open access by the US Geological Survey at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in USGS Northern Prairie Wildlife Research Center by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Authors Carl E. Korschgen, Kevin P. Kenow, William L. Green, Douglas H. Johnson, Michael D. Samuel, and Louis Sileo

This article is available at DigitalCommons@University of Nebraska - Lincoln: https://digitalcommons.unl.edu/ usgsnpwrc/222 The Journal of Wildlife Management, Vol. 60, No. 1 (Jan., 1996), pp. 120-132

SURVIVALOF RADIOMARKEDCANVASBACK DUCKLINGS IN NORTHWESTERNMINNESOTA

CARLE. KORSCHGEN,National Biological Service, UpperMississippi Science Center,P. 0. Box 818, La Crosse, WI54602- 0818, USA KEVINP. KENOW,National Biological Service, UpperMississippi Science Center,P. 0. Box 818, La Crosse, Wl 54602-0818, USA WILLIAML. GREEN,National Biological Service, Upper Mississippi Science Center,P. O. Box 818, La Crosse, WI54602-0818, USA DOUGLASH. JOHNSON,National Biological Service, Northern Prairie Science Center,8711 37 Street Southeast, Jamestown, ND 58401, USA MICHAELD. SAMUEL,National Biological Service, NationalWildlife Health Center, 6006 SchroederRd., Madison,WI 53711, USA LOUISSILEO, National Biological Service, NationalWildlife Health Center, 6006 SchroederRd., Madison,WI 53711, USA

Abstract: Duckling survival, an important factor affecting annual recruitment, has not been determined adequately for ( valisineria). We investigated the magnitude, timing, and causes of mortality of canvasback ducklings from hatch to fledging at the Agassiz National Wildlife Refuge (NWR) in northwestern Minnesota during 1987-90. During the 4 years, 217 day-old ducklings were radiomarked and released in 52 broods. Another 141 ducklings were radiomarked at >4weeks of age. Survival was estimated with the Kaplan-Meier nonparametric estimator and the Weibull parametric model. Most mortalities occurred within 10 days after hatch. Total brood loss occurred in 18 (35%) of 52 broods released. The primary sources of mortality were predation, principally by mink (Mustela vison), and exposure to precipitation and cold temperature. For combined years, females had lower survival than males (P = 0.03). If the disparate survival between sexes of canvasbacks observed in this study is representative of canvasbacks in their breeding range, this phenomenon contributes to reduced reproductive potential and the male-biased sex ratio of the species. J. WILDL.MANAGE. 60(1):120-132

Key words: Agassiz National Wildlife Refuge, Aythya valisineria, canvasback, duckling survival, mortality, radiotelemetry, survival analysis.

Between 1981 and 1994, the continental ducklings have been difficult to determine be- breeding population of canvasbacks (Can. Wildl. cause broods are secretive, loss of entire broods Serv. and U.S. and Wildl. Serv. 1994) had may go unaccounted for, and brood intermixing not attained the management goal of 580,000 occurs as brood bonds weaken with age (Stoudt that was established for the North American 1982, Leonard 1990). Failure to account for losses Waterfowl Management Plan (U.S. Fish and of entire broods, for example, may lead to over- Wildl. Serv. and Can. Wildl. Serv. 1986). Be- estimation of survival (Ball et al. 1975, Reed cause of concern over reduced population levels, 1975, Ringelman and Longcore 1982, Talent et the U.S. Fish and Wildlife Service listed the al. 1983). Our objectives were to determine the canvasback as a species of special emphasis. Re- magnitude, timing, and causes of canvasback strictive hunting regulations to limit canvasback duckling mortality using innovative radiotelem- harvest have been in effect periodically since etry techniques. 1972. However, effective management cannot The assistance of B. M. Ballard, L. A. Bennett, be implemented without a better understanding P. J. Boma, A. F. Boysen, J. P. Cowardin, J. M. of recruitment and causes of mortality in this Coffey, M. D. Havlik, D. C. Hurt, J. J. Jansen, species. T. G. Maeder, D. F. Miller, L. C. Mueller, B. Duckling survival can be an important factor R. Paulson, R. D. Pritchert, D. R. Spuhler, B. affecting annual recruitment (Cowardin and D. Woodsen, and G. D. Zenitsky was greatly Johnson 1979, Cowardin et al. 1985, Orthmeyer appreciated. The staff of the Agassiz National and Ball 1990) but is probably the least under- Wildlife Refuge, especially V. D. Erickson, J. stood component of waterfowl demographics Kotok, J. P. Mattsson, G. D. Tischer, and B. J. (Ball et al. 1975, Cowardin et al. 1985). Survival Wickstrom supported our study. We are grate- rates and causes of mortality of canvasback ful to T. L. Shaffer for statistical advice. We

120 J. Wildl. Manage. 60(1):1996 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. 121 thank C. J. Brand, F. J. Dein, D. R. Goldberg, erage number of canvasback breeding pairs dur- and J. Langenberg for veterinary, pathology, ing 1973-82 was 183 ? 133 (SD) pairs; an es- and diagnostic assistance. We also thank J. R. timated 920 canvasbacks were produced at the Cary for assistance with software development, refuge in 1982 (C. D. Swanberg, U.S. Fish and W. E. Dodge for making telemetry program Wildl. Serv., pers. commun.). XYLOG available, C. R. Luna for consultation on radiotransmitter attachment, and M. D. METHODS Schwartz for programming support. F. W. An- Nest Searching derka developed miniature radiotransmitters for With an airboat, we found canvasback nests We the critical day-old ducklings. appreciate in May and June by systematically searching review of this E. Aus- manuscript provided by J. suitable emergent vegetation. We thoroughly tin, G. M. Haramis, W. L. Hohman, W. E. New- searched locations where we saw canvasback ton, and P. J. Pietz. females. To reduce airboat disturbance and to increase search efficiency, we also located nests STUDY AREA by observing the movements of radiomarked The Agassiz NWR is in the ecotone of the canvasback females. We captured females with prairie and northern forest ecosystems in north- decoy (Anderson et al. 1980) or bait (Haramis western Minnesota. The refuge occupied 24,878 et al. 1987) traps, and implanted radiotrans- ha in a remnant depression of glacial Lake Ag- mitters in the ' abdominal cavities (Korsch- assiz. The topography was relatively flat, and gen et al. 1984, Olsen et al. 1992) or subcuta- drainage of the area was slow. Construction of neously on their backs (Korschgen et al. 1996). dikes and watercontrol structures since 1937 had We monitored the birds with standard telem- formed 18 separate impoundments, which etry techniques. ranged from 75 to 4,000 ha. The average max- imum water depth of impoundments ranged Collection and Incubation of Eggs from 0.7 to 1.3 m. The area on the During 1987, eggs were removed from can- refuge totaled 15,748 ha. vasback nests regardless of stage of incubation Impoundments were categorized as persistent and placed in an incubator for hatching. In later emergent and aquatic-bed (Cowardin years, however, we allowed the female to in- et al. 1979). Emergent vegetation was predom- cubate the eggs for >10 days to achieve greater inantly common cattail ( latifolia), nar- hatching success and synchronization of hatch- rowleaf cattail (T. angustifolia), softstem bul- ing (see Doty 1972). In their place we substi- rush (Scirpus validus), tule bulrush (S. acutus), tuted water-filled plastic eggs, painted to match common reed (Phragmites communis), sedges the color of canvasback eggs, or (Ay- (Carex spp.), and giant burreed (Sparganium thya americana) eggs in a less advanced stage eurycarpum). Submersed vegetation included of development. To synchronize hatching, we fennelleaf pondweed (Potamogeton pectina- incubated all eggs from each brood in physical tus), baby pondweed (P. pusillus), common proximity. hornwort (Ceratophyllum demersum), com- mon bladderwort (Utricularia vulgaris), and Radiomarking Ducklings spiked watermilfoil (Myriophyllum exalbes- We used a clutch (set of eggs from the same cens). nest) of >4 eggs that hatched within 12 hours Waterfowl production and quality to as an experimental brood. When a clutch support waterfowl use are the primary objec- hatched, we determined body mass and sex for tives of the Agassiz NWR. In recent years, man- each duckling and we randomly assigned - agement at the Agassiz NWR has emphasized lings to be radiomarked. We also chose at ran- increased production of overwater-nesting wa- dom the order of radiomarking. We attempted terfowl. It was the only refuge in the midwest- to radiomark about 75% of ducklings in each ern United States with consistent canvasback brood. We also collected cloacal and tracheal production during 1954-74 (W. E. Green, U.S. swab samples from ducklings during the 1990 Fish and Wildl. Serv., pers. commun.). During field season as part of disease monitoring by the this 21-year period, the average annual use-days National Wildlife Health Center (NWHC), of canvasbacks was 46,293, and an average of Madison, Wisconsin (see Goldberg et al. 1995). 477 young were produced each year. The av- We implanted miniature radiotransmitters 122 CANVASBACKDUCKLING SURVIVAL * Korschgen et al. J. Wildl. Manage. 60(1):1996 subcutaneouslybetween the scapularsof duck- Natl. Biol. Serv., unpubl. software), a modified lings within hours after hatch. Handling and version of XYLOG4(Dodge and Steiner 1986). care of ducklings and surgical techniques The programalso was used to immediately cal- (Korschgenet al. 1996) were approved by the culate and display transmittertemperature and Care and Use Committee of the North- thereby determine live or dead status. Because ern Prairie Science Center, and comply with transmittersin day-old ducklings had a limited the Animal Welfare Act (Public Law 99-198 life, we used nightlighting techniques (Cum- and 9 CFR Parts 1, 2, and 3). We performed mings and Hewitt 1964) to recapture radi- surgery under as aseptic conditions as possible omarked ducklings and replace expiring trans- with the general anesthetic,isoflurane. We used mitters with larger transmitters(28 x 13 x 6 crystal-controlled,2-stage pulse, internally im- mm, 4.0 g) that had greaterradiated power and plantableradiotransmitters (model BD-2TI, Ho- longer life. We removed expiring transmitters lohil Systems, Ltd., Woodlawn, Ont., Canada and subcutaneouslyimplanted new transmitters KOA3MO; use of manufacturer'sname does not in a single surgicalprocedure. Unmarked duck- imply government endorsement).Transmitters lings (>4 weeks of age) were also captured by were encapsulatedin Scotchcastelectrical resin nightlightingand were radiomarked.All duck- 215 (3M Co., St. Paul, Minn.). The transmitters lings were returnedto the site of capture. If the were rectangular,measured about 20 x 9 x 5.5 hatch date of the duckling was unknown, we mm, weighed about 1.8 g, and had a life ex- determined age by development pectancy of 35 days. The antenna was a 170- (Dzubin 1959, Weller 1957). mm twisted (multi-strand)stainless-steel wire coated with black nylon that exited the duc- Determination of Cause of Death kling'sskin through a formedopening. The pulse rate of the transmitterwas thermistor-regulated Dead birds were recoveredas quickly as pos- for remote monitoring of duckling body tem- sible. If radiomarkedbroodmates were in the perature.This device also served as a mortality same area as the dead duckling, we delayed cue. recoveryuntil telemetry locationsindicated that the brood had left the area. In most predator- Duckling Release related mortalities, little of the carcass re- mained. Predator identification was based on Before we 1-2 releasing ducklings, placed location of carcassor transmitter in nests to stimulate recovery (e.g., pipping eggs experimental in a mink underneatha and the hen with sound and movement of den, raptorperch), hatching. evidence on carcassor transmitter.When cause were released <12 hours after hatch Ducklings of death was undetermined in 1988 and to enhance on the foster fe- 1989, nesting carcasseswere frozen for later at the male. To restrain on the nest until the necropsy ducklings NWHC. fresh carcasses were female we the duck- During 1990, nesting returned, placed to NWHC for immediate All in a made of hand towels. shipped necropsy. lings paper envelope carcassesexamined at NWHC received a com- We the of the closed and stapled top envelope examination se- covered it with nest material. After a of plete pathological including period lected and studies to time the the diagnostic histopathology ducklingseasily ripped open paper evaluate and A sam- after the had been viruses,bacteria, parasites. envelope, especially envelope of carcasseswas tested for wetted moisture from the nest bowl or the ple organophosphorus by and carbamate based on brain female. With video cameras exposure acetyl- returning nesting cholinesterase Rocke and at 22% = of the nest we confirmed activity (Hill 1988, (n 53) sites, Samuel Determinationof and that females broods released 1991). proximate nesting accepted causes of was based on in this manner. contributing mortality diagnostic findings in combination with field evidence, i.e., weatherconditions, brood history, Radiotracking and movements. We attempted to locate and determine trans- We classified causes of mortality in 5 cate- mitter temperaturesof all radiomarkedduck- gories: predation, disease, weather-related,in- lings several times daily from vehicles, boats, or anition (starvation),and unknown/other. Pre- aircraft. We processedtelemetry azimuth data dation was considered a contributing cause of in the field with portable personal computers death when predation-liketrauma was present and the program XYLOGAGZ(Kenow et al., at necropsy and field evidence suggested pre- J. Wildl. Manage. 60(1):1996 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. 123 dation, but cause of trauma was not certain. obtain precise survival estimates, but only about Disease-related mortality included pneumonia, 39% of our ducklings survived past 10 days of parasitism, and other incidental health prob- age. (In fact, the Kaplan-Meier method is only lems. We assessed weather conditions (daily about 60% efficient when applied to data from temperature and rainfall) at the Agassiz NWR the Weibull distribution [Miller 1983]). We con- headquarters 48 hours before death for duck- sequently used the Weibull model to further lings with no apparent cause of mortality. We analyze survival data. We used the LIFEREG considered weather a direct cause of death (ex- module of SAS (SAS Inst. Inc. 1989) to compute posure) of ducklings whose carcasses indicated estimated parameters of the Weibull survival good or fair body condition (primarily body fat models. deposits) when the proximate time of death co- The Weibull survival model was flexible incided with rainfall or cold (<11 C) temper- enough to accommodate our data; the mortality ature. We diagnosed inanition (Langenberg and rate was high among young birds and declined Montali 1983) when the carcass was emaciated with age. In general, parametric models provide but otherwise normal. We listed the cause of more precise estimates of survival if the model death as unknown if the carcass revealed no fits well (Miller 1983, Klein and Moeschberger clear pathological information, was too auto- 1989), as did our data. For the Weibull distri- lyzed for complete diagnostic procedures, or had bution, the survival function, which describes signs of uncommon causes of death (e.g., drown- the probability of survival as a function of age ing). In many cases, multiple factors probably (t), is S(t) = exp(-atj). The hazard rate, which contributed to the proximate cause of death. describes the instantaneous death rate, decreases Differences between (t-tests) and among with age if y < 1. The LIFEREG procedure of (analysis of variance) mean duckling body mass SAS estimates a scale parameter a and intercept by sex, year, and cause of death were identified JL, where a = y-' and a = exp(-,t/a). Under with SAS statistical software (SAS Inst. Inc. 1989). this parameterization, the hazard function de- creases with age if a > 1. If a = 1, survival follows an exponential, constant hazard distri- Survival Analysis bution. We estimated survival rates of ducklings ra- When transmitters on day-old ducklings failed diomarked at <1 day old and -4 weeks old prematurely after having performed irregular- (Class II ducklings). Some birds were in both ly, and we had no indication that the duckling groups. Survival rates of the two groups were had died, we assumed the transmitter had failed. estimated separately. Such observations were treated as right-cen- In our analyses, we treated all ducklings as if sored in the analysis; that is, we assumed the they were statistically independent. In reality, duckling survived until the transmitter failed. ducklings of the same brood probably do not When signals from some transmitters ended experience statistically independent fates but are without indication of irregular performance exposed to similar predation, weather, and other (symptomless transmitter failures), we suspect- risks. Treating ducklings as independent does ed that a predator destroyed the duckling and not result in biased estimators of survival, but transmitter. Because we did not know this with variance estimators are biased low (e.g., Pollock certainty, we conducted one survival analysis et al. 1989). for which such observations were treated as Day-old ducklings.-We initially used the deaths and a second analysis for which they nonparametric Kaplan-Meier approach (Kaplan were treated as right-censored at last observa- and Meier 1958) to calculate survival rates of tion. For the Kaplan-Meier analysis we assumed ducklings that were radiomarked at hatch. This that deaths occurred 12 hours after the last ob- method does not restrict the shape of the sur- servation. For the Weibull model we assumed vival curves to a particular parametric model. that deaths occurred sometime within the next We used the LIFETEST module in SAS (SAS 24 hours after the last observation (thus treating Inst. Inc. 1989) for fitting Kaplan-Meier curves. datum as interval-censored). If the time of re- Plots of log{-log[S(t)]} against log(time) ob- lease or rediscovery was not recorded in the from the Kaplan-Meier procedure were data, we used 1430 hours, which was a typical generally linear, indicating that a Weibull sur- time of day for those activities. vival model would adequately fit the data. The We first analyzed the data by considering Kaplan-Meier method requires large samples to mortality in total, regardless of the assigned 124 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. J. Wildl.Manage. 60(1):1996

Table 1. Fate of canvasbackbroods radiomarkedat hatch at the Agassiz NationalWildlife Refuge, 1987-90.

1987 1988 1989 1990 Total Brood deployments 5 11 23 13 52 Radiomarkedducklingsa 22 43 96 56 217 Brood lossesb total 2 4 5 7 18 partial 3 5 17 6 31 none 0 2 1 0 3

a Deployed with radiotransmitters within 1 day of hatch. b Includes loss sustained during period of radiocontact with brood. cause. This treatment permitted the most de- of 37 days. Few of these ducklings died, and tailed examination of the data. We also per- because we had no indication of an age-related formed some cause-specificanalyses, for which hazard function, we analyzed data of Class-II we distinguished4 mortalityfactors: predation, ducklingswith the Mayfield(1961) method,with weather, disease, and inanition. We also iden- standarderrors that were determinedaccording tified a category of mortality,termed suspected to Johnson (1979). Several transmittersfailed predation,which includedthe lossesfrom known withoutpreviously malfunctioning, and we again predationand transmitterfailures that were not treated the data in 2 ways, firstconsidering such preceded by abnormal transmissions.For the observationsas right-censored,and second con- cause-specificanalyses, we estimated mortality sidering them to be deaths. rates for each of the 5 factors as if it were the only source of mortality. Mortalityfrom other RESULTS sourceswas treatedas right-censoredat the time Duringthe 4-yearstudy, 52 canvasbackbroods of death because it was not always possible to totaling 217 day-old, radiomarked ducklings distinguish clearly among multiple causes of were placed in nests and bonded with attendant death. If the cause-specificfactor contributedto hens within hoursof hatch. Only 3 of 52 broods mortality, we included that death in the anal- fledged without the death of 1 or more radio- ysis. For example, a duckling judged to have marked ducklings, and 18 broods sustained succumbed from predation and disease would total loss (Table 1). be treated as a death in the analysis involving Causes of predation,a death in the analysisinvolving dis- Mortality ease, but as a right-censoredobservation in the Day-old ducklings.-We recovered portions analyses involving weather or inanition. of 135 duckling carcasses during 1987-90. In Class-II ducklings.-We radiomarked 141 many cases multiple factors contributed to the Class-IIducklings at an average estimated age cause of mortality. Predationand weather-re-

Table2. Contributingcauses of death of canvasbackducklings radiomarked at hatchat the Agassiz NationalWildlife Refuge, 1987-90a.

Known Possible Year Sex (nl,n2)b predation predationc Disease Weather Inanition Unknownd 1987 Female (8,0) 7 7 0 0 0 1 Male (6,3) 4 7 0 0 0 2 1988 Female (13,2) 5 7 1 4 1 4 Male(12,4) 5 9 0 2 1 5 1989 Female (33,11) 16 27 1 11 2 6 Male (20,17) 11 28 0 7 3 1 1990 Female (26,3) 19 22 3 2 1 3 Male (17,4) 13 17 1 1 0 3 All Female (80,16) 47 63 5 17 4 14 Male (55,28) 33 61 1 10 4 11 a Row sums may exceed the total number of mortalities for any year-sex class because some deaths have causes of b multiple mortality. nl refers to number of recovered carcasses, n2 refers to number of symptomless transmitter failures. c Includes known predation and symptomless failure of transmitter. d Cause of death could not be determined. J. Wildl. Manage. 60(1):1996 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. 125

Table 3. Numberof canvasbackducklings killed by predatorsat the Agassiz NationalWildlife Refuge, 1987-90.

1987 1988 1989 1990 Total Ducklings from hatch to 4 weeks of age Mink 11 5 9 15 40 (Bubo virginianus) 2 1 3 6 Black-crownednight-heron (Nycticorax nycticorax) 1 1 American coot (Fulica americana) 1 1 Other avian 4 5 9 Snapping (Chelydra serpentina) 1 1 Fox (Vulpes vulpes) 1 1 Unknown predator 2 8 7 17 Total depredations 11 10 23 32 76 Ducklings >4 weeks of age Mink 1 1 3 5 Snapping turtle 1 1 Unknown predator 1 1 Total depredations 3 1 3 7

lated factors were the major causes of mortality and 9 in 1990). None exhibited clinical depres- (Table 2). Among known mortalities, predation sion of brain acetylcholinesterase activity and was the cause of 59% of female and 60% of male we concluded that pesticide exposure probably deaths. Mink were the single greatest cause of was not a cause of mortality in canvasback duck- mortality (39-100%) each year (Table 3). When lings at the Agassiz NWR. suspected predation was included in the anal- Causes of mortality could not be determined ysis, predation accounted for 66% of female and for 25 (19%) of the 135 recovered carcasses. A 73% of the male deaths. complete pathological evaluation was conduct- Weather (exposure) was a contributing cause ed on 68 (50%) of the recovered ducklings. From of mortality for 6 of the 22 assigned causes (27%) this sample we identified 2 (3%) ducklings for in 1988, and 18 of the 74 assigned causes (24%) which the transmitter was a contributing or in 1989. Mortality often coincided with cold principal cause of mortality. We also found 7 weather, especially when accompanied by pre- (10%) ducklings for which our pathological ex- cipitation, as in 1989 (Fig. 2). Cold weather with amination revealed minor effects related to the precipitation occurred on 6-8 June and on 12- transmitter implant site. 14 June, 1989, and consequently, among duck- Class-II ducklings.-Predation was the only lings <10 days old, daily mortality rates were known cause of death among the Class-II duck- higher than the average rate of 0.08 + 0.12. lings and all of these losses were among females. Exposure accounted for 53% of mortality during Mink were the single greatest cause of mortality those periods (exposure mortality made up 37% (Table 3), as was the case with younger duck- of mortality that occurred outside of the 2 pe- lings. riods). Ducklings also died during less extreme Survival conditions of cold temperature and precipita- Analyses tion (e.g., 21-22 Jun), but at lower rates. Day-old ducklings. -We first considered Disease contributed to 6 (4%) of the 135 deaths overall mortality, regardless of its cause. Param- for which causes were assigned and inanition eter estimates from the Weibull model (Table was involved in 8 (6%) deaths. Bacterial pneu- 4) were used to produce survival curves (Fig. monia was the most common disease. Body mass 1). The consistency of scale parameters exceed- at hatch was lower for individuals for which the ing 1 (Table 4), and the frequent significance principal cause of death was inanition (43.2 + of those departures, demonstrates the need for 1.7 g; n = 7) than of surviving ducklings (46.3 the Weibull model over the more parsimonious + 3.4 g; n = 80) (t = -4.16, P = 0.002) and of exponential model. There was a consistent pat- individuals that died from other causes (45.6 + tern of higher survival rates for males than fe- 3.6 g; n = 125) (t = -3.42, P = 0.007). males in each year whether we censored symp- Thirty-one ducklings were tested for pesticide tomless transmitter failures or treated them as exposure during 1988-90 (5 in 1988, 17 in 1989, deaths (Table 5). Survival of males was higher 126 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. J. Wildl. Manage. 60(1):1996

1.00- 1.00- 1987 1988

0.75- 0.75-

0.50- 0.50-

\,I~~0^ -cCENSOR t-=. ^. -CENSOR 0.25 0.25- I"~- X L-CENSOR - o- d- DEATH d-DEATH 9-DEATH 0.25 ". -DEATH OR CENSOR v.W nnn-V W I l l Il lI l I l I l 0 5 10 15 20 25 30 35 40 0 5 10 15 20 25 30 35 40 AGE OF DUCKUNG(DAYS) AGE OF DUCKLING(DAYS) I 1.00 1.00 1989 1990

0.75 0.75-

0.50 \",'S.dL- ~ CENSOR 0.50- U ~ ~ ~ -_ _ II co ~ ~ - C -- -CENSOR 0.25 d- DEATH 025- " - CENSOR "" 2-DEATH -: -= oc-DEATH ''"""z - z9-CENSOR n - "-DEATH 0.00 I I I I I I I 1J.-~-? 0 5 10 15 20 25 30 35 40 0 5 10 15 20 25 30 35 40 AGE OF DUCKLING(DAYS) AGE OF DUCKUNG(DAYS)

Fig. 1. Survivalcurves of radiomarkedcanvasback ducklings at the Agassiz NationalWildlife Refuge, 1987-90. Curveslabeled withCENSOR indicate survival values when symptomlesstransmitter failures were treatedas censored and curves labeledwith DEATHindicate survival values when symptomless transmitterfailures were treated as deaths. Sample sizes were as follows: 1987, 10 females, 12 males; 1988, 20 females, 23 males; 1989, 52 females, 44 males; 1990, 33 females, 23 males.

(pooled estimate of the sex effect) when symp- Class-II ducklings.-Only 7 deaths were ob- tomless transmitter failures were treated as served during 3366.5 cumulative exposure-days deaths (P= 0.03) and when symptomless trans- of observation of 73 female and 68 male duck- mitter failures were considered as censored (P lings (Table 6). When symptomless transmitter = 0.003). Male (45.6 + 3.6 [SD] g; n = 104) and failures were included as deaths, the disparity female (46.0 ? 3.5 g; n = 113) ducklings did between the sexes diminished, with 27 female not differ in body mass at hatch (t = 0.74, P = and 16 male mortalities. When symptomless 0.46). Duckling body mass differed among years transmitter failures were treated as censored, (43.9 ? 3.2 g in 1990 versus 46.9 ? 3.9 g in daily survival rates pooled across years were 1987; F = 9.03; 3, 215 df; P < 0.0001). 0.996 for females and 1.0 for males; when symp- We estimated survival curves for each sex and tomless transmitter failures were treated as year, assuming in turn that each of the 5 mor- deaths, daily survival rates pooled across years tality factors was the only cause of death. As were 0.985 for females and 0.990 for males. expected, cause-specific survival rates were high These values correspond to survival rates for a except for predation and, in 1988 and 1989, for 26-day period (from an average age of 37 days weather. For example, estimated survival to 20 when radiomarked to fledging at 63 days) of days of age, averaged across all sex and year 0.91 for females and 1.0 for males when symp- groups, was 0.522 for known predation, 0.395 tomless transmitter failures were treated as cen- for known or suspected predation, 0.871 for sored, and 0.71 for females and 0.79 for males weather, 0.956 for inanition, and 0.959 for dis- when symptomless transmitter failures were ease. treated as deaths. J. Wildl. Manage. 60(1):1996 CANVASBACKDUCKLING SURVIVAL * Korschgenet al. 127

. .. 30 ... :0.7...... ,,,,,, , ,,...., ,,, .. . 0 .6

. u, . ,,, ...... S25- ......

2 . ... : : A : ::: -0.5 6 :...... A _ 5 0- :..

. u ... :: ;:::. .. : -0.4 l 15-/^;: A / : ::; : I " ..' .. ..*.. ",, ,,, ... 03 0 I- 1. n^~*~\,~/ ... ,> I~... ~ :

* .. 0 ...... ,...... '" :. '" ... 0. 2 3 5-: \J : :::: ::: ::: ::- W. 5- ......

5 10 15 20 25 30 5 JUN JUL

Fig. 2. Relationof canvasbackduckling mortalities with weather patternsat the Agassiz NationalWildlife Refuge, 1989. The solid line depicts daily mean temperatures.Shading extends below cloud on days with precipitation.Daily mortality rates of canvasbackducklings are representedby solid bars. 128 CANVASBACKDUCKLING SURVIVAL * Korschgen et al. J. Wildl. Manage. 60(1):1996

Table4. Estimatesof Weibullparameters for canvasbackducklings by sex and year at the Agassiz NationalWildlife Refuge, 1987-90.

Symptomlesstransmitter failures treated Symptomlesstransmitter failures treated as deaths as censored Year Sex Intercept Scale Intercept Scale 1987 Female 2.12 (0.67)8 1.50 (0.53) 2.12 (0.67) 1.50 (0.53) Male 2.72 (0.49) 1.19 (0.41) 3.38 (0.87) 1.54 (0.67) 1988 Female 2.67 (0.38) 1.46 (0.32) 2.90 (0.46) 1.64 (0.39) Male 2.87 (0.33) 1.27 (0.28) 3.43 (0.54) 1.64 (0.44) 1989 Female 2.67 (0.21) 1.39 (0.17) 3.12 (0.31) 1.75 (0.26) Male 3.09 (0.21) 1.26 (0.17) 4.20 (0.48) 1.91 (0.37) 1990 Female 1.75 (0.28) 1.49 (0.20) 1.86 (0.29) 1.54 (0.22) Male 2.49 (0.35) 1.57 (0.27) 2.80 (0.44) 1.82 (0.36)

a Valuesin parenthesesare standarderrors.

DISCUSSION paringcontrol and transmitter-implantedduck- Effects of on lings in 2 experiments (ducklings treated at 1 Radiomarking of in 1 and at 4 weeks of Duckling Survival day age experiment age in the other) (Zenitsky 1993). Surgery and Radiomarking and duckling deployment of transmittershad short-termef- this implantation techniques developed during study provid- fects on growth,most obviousimmediately after ed estimatesof survivalfrom hatch to duckling surgery, but treatment effects were not always without the bias associated fledging typically statisticallysignificant. The effect of an appar- with brood attrition.Anal- visuallydetermining ent initial delay in growth of implanted duck- of interactionsbetween females ysis video-taped lings on survivalis unknown,because ducklings and indicated that radio ducklings packages compensatedwith increasedgrowth rate shortly no with the females' posed apparent problems thereafter. Activities of control ducklings did of radiomarked acceptance ducklings. not differ from those of ducklings treated at 1 Krementzand Pendleton used the same (1991) day old (Zenitsky1993). Ducklings treated at 4 to radiomark technique ( platy- weeks of age foraged less than controls for 2 and rub- rhynchos) (A. after surgery, spending more time preen- on the and days ripes) ducklings Chesapeake Bay the implant site and antenna. By day 2, were able to more determine the ing accurately resumed normal foraging rates and causes of in with radioim- ducklings mortality ducklings site/antenna continued at a than for marked with external implant plants ducklings low percent of the time sampled. transmitters. also observation They compared In a related study, an assessmentof the po- rates of radiomarkedand control and ducklings tential thermoregulatoryenergetic costs of sub- concluded that the transmittershad implanted cutaneous radioimplants to ducklings, under no effect on survival. various of thermal stress,indicated that The effect of our subcutaneous transmitter degrees the presence of a radiotransmitterhad no sig- on the and behavior implant procedure growth nificant effect on net heat production (Bakken of redhead was evaluated com- ducklings by et al. 1996). The resultssuggested that ducklings radiomarkedwith subcutaneousimplants were no more vulnerableto exposurethan were con- Table5. Coefficientsfor sex effect in Weibullmodel, by year, for canvasbackducklings at the Agassiz NationalWildlife Ref- trol birds. uge, 1987-90. We also conductedpathological examinations on 68 (50%of all ducklings,but 56%of ducklings Symptomlesstransmitter Symptomlesstransmitter failurestreated failurestreated during 1988-90) ducklingsthat died during the as deaths as censored study. Only 2 of these birdshad sufficientpatho- Year Coefficient P-value Coefficient P-value logical findings associated with the transmitter 1987 0.61 0.46 1.24 0.23 implant or surgical procedure to influence the 1988 0.21 0.67 0.53 0.44 birds' survival. Both of these birds died within 1989 0.40 0.18 1.00 0.05 2 of the transmitter In 1990 0.77 0.07 0.98 0.05 days implant. addition, 7 duckling carcasseshad minor necrosis or in- J. Wildl. Manage. 60(1):1996 CANVASBACK DUCKLING SURVIVAL * Korschgenet al. 129

Table6. Mortalityand estimated daily survival rates (S?) of Class-llcanvasback ducklings at the AgassizNational Wildlife Refuge,1987-90.

Symptomless transmitter failures Symptomless transmitter failures treated as deaths treated as censored Days of Year Sex n exposure Deaths S SE Deaths S SE 1987 Female 15 210.0 6 0.971 0.011 0 1.000 0.000 Male 8 152.0 3 0.980 0.011 0 1.000 0.000 1988 Female 16 430.0 4 0.991 0.005 3 0.993 0.004 Male 20 467.0 1 0.998 0.002 0 1.000 0.000 1989 Female 25 805.0 8 0.990 0.003 1 0.999 0.001 Male 28 719.0 6 0.992 0.003 0 1.000 0.000 1990 Female 17 307.5 9 0.971 0.010 3 0.990 0.006 Male 12 276.0 6 0.978 0.009 0 1.000 0.000 All Female 73 1,752.5 27 0.985 0.003 7 0.996 0.002 Male 68 1,614.0 16 0.990 0.002 0 1.000 0.000

Survival rate calculated with the Mayfield (1961) method, with standard errors determined according to Johnson (1979). flammation at the transmitter site. These inci- 1969), American black duck (Reed 1975, Rin- dental effects ranged from inflammation caused gelman and Longcore 1982), ring-necked duck by bacterial infection to skin and muscle necro- (Aythya collaris) (McAuley and Longcore 1988), sis at the transmitter site, but were not consid- and mallard (Orthmeyer and Ball 1990). ered to be a direct contributor to the 's mor- tality. Causes of DucklingMortality We suspect that most methods of marking Causes of canvasback duckling mortality were waterfowl with radiotransmitters influence sur- consistent with that reported for other species vival rates to some degree (Wheeler 1991, Ward and included predation (Sargeant and Raveling and Flint 1995). Assuming that we conducted 1992), adverse weather conditions, inanition, and pathological examinations on a representative disease (Table 2). Adverse weather events sample of ducklings that died, we believe that marked by cold temperatures, precipitation, and our estimated survival rates may be biased low wind, or prolonged periods of mild cold stress because the radioimplant technique probably may affect ducklings both directly (hypother- contributed to the death of a few birds. Our mia) or indirectly (Johnson et al. 1992). Such pathology data suggests that about 3% (95% CI conditions predispose ducklings to other causes = 0.4-10%) of the estimated mortality may be of mortality through increased rate of energy a result of the transmitter implant. However, loss, changes in activity, reduced growth rate, radiotelemetry is the only reliable method avail- or reduced food availability. On the other hand, able that provides information to determine ac- disturbance from predation may predispose curately the time of death, location of carcasses, ducklings to cold stress. The brood histories and causes of mortality, detailed field evidence of movements in this study revealed that some en- habitat used, and detailed movements of indi- counters with predators scattered broods, re- viduals relative to one another (e.g., brood be- sulting in exposure deaths of ducklings no longer havior) of highly secretive and cryptic tended by hens. Vulnerability to predators, in- such as ducklings. clement weather, and starvation are probably affected by the quality of wetland habitat in Timingof Mortality which the broods reside. Risk of mortality for canvasback ducklings at Ducklings that died with signs of inanition the Agassiz NWR decreased through the period had a mean body mass of 3.2 g less at hatch from hatch to fledging (Fig. 1). Mortality was than ducklings that survived. Inanition also oc- greatest during the first 10 days; 10-day survival curs in domestic neonates (3-7 days) rates varied from a low of 0.26 in females in that never begin to eat and therefore starve to 1990 to a high of 0.69 in males in 1989. This death after their yolks are depleted (Langen- pattern of mortality is consistent with that re- berg and Montali 1983). Inanition in wild duck- ported for canvasback (Leonard 1990) and other lings may be complicated by cold weather and species: (Aix sponsa) (McGilvrey lack of food. Untergasser and Hayward (1972) 130 CANVASBACKDUCKLING SURVIVAL * Korschgenet al. J. Wildl. Manage. 60(1):1996 reported that body weight in 3 species of duck- Studies of duckling survivalin the wild have lings increased little, or not at all, during a pe- not involved birds of known sex. However, riod of a few cold and rainy days. The avail- among artificially incubated canvasbacks, ability of invertebrates (e.g., chironomids hatch- Hochbaum (1944) reported a slightly higher ing) may also be depressed during periods of embryonic mortality rate for females. Kear adverse weather to further reduce food intake. (1965) also observed a higher mortality rate for This type of mortality may be reduced through female than male mallard ducklings; most mor- improvement in the quality and quantity of tality occurred at hatching. . In event, brood-rearing any ducklings MANAGEMENTIMPLICATIONS suffering from inanition-related problems are probably at higher risk of mortality both from Predation and weather played key roles in predators and exposure. Johnson et al. (1992) the mortality of canvasback ducklings. The loss referenced several studies that suggested star- of ducklings to mink, other predators, and ex- vation as a probable major cause of mortality posure may be influenced by the quality of among young waterfowl. aquatic habitat and weather conditions during Disease mortality may also be difficult to doc- the first few weeks after hatch. Management of ument in young birds because generally they large impoundments, such as those at the Ag- have an undeveloped immune system, may be assiz NWR, can mediate these effects by pro- highly susceptible to infectious agents (which viding optimal water levels for (1) establishment are difficult to detect), and are subject to greater of brood cover, (2) production of invertebrate risk from predation than healthy individuals. foods, (3) protection from predatory mammals, Bacterial pneumonia was the most common and (4) creation of a large volume of water as cause of disease mortality among canvasback a thermal mass to buffer temperature extremes. ducklings. However, this source of disease mor- The behavioral and physiological basis of lower tality was never as prevalent in canvasback survival of female canvasback ducklings found ducklings as in on the Chesapeake Bay in this study is not understood and needs further (Krementzand Pendleton 1991), where during examination. Future research should be direct- 1 year of the study, 43% of radiomarked duck- ed to identify factors that lead to differential lings died of pneumonia. survival rates at this early age, and to determine the influence of radiomarking techniques on DifferentialSurvival Between Male survival. and Female Ducklings Estimatedsurvival rates for prefledgedduck- LITERATURECITED lings at the AgassizNWR were lower for females ANDERSON, M. G., R. D. SAYLER,AND A. D. AFTON. than for males. The cause of this disparity is 1980. A decoy trap for diving . J. Wildl. unknown and we can only speculate on the im- Manage. 44:217-219. G. P. S. K. P. of this Differential survival BAKKEN, S., REYNOLDS, KENOW,C. E. plications finding. KORSCHGEN,AND A. F. BOYSEN. 1996. Ther- rates were not related to size at duckling hatch, moregulatory effects of radiotelemetry transmit- and duckling growth curves have been shown ters on mallard ducklings. J. Wildl. 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Classification of wetlands and Latham believed a differ- deepwater habitats of the United States. U.S. Fish (1947) physiological and Wildl. Serv. Biol. Serv. ence between sexes was for observed Program, Washing- responsible ton, D.C. 103 pp. differential tolerance to extremes of climate and , AND D. H. JOHNSON. 1979. Mathematics starvation in ring-necked pheasant (Phasianus and mallardmanagement. J. Wildl. Manage.43: 18-35. colchicus) chicks for which, except for trials in- , D. S. GILMER,AND C. W. SHAIFFER. 1985. chicks <3 old, females survived at volving days Mallard recruitment in the agricultural environ- higher rates than males. ment of North Dakota. Wildl. Monogr. 92. J. Wildl. Manage. 60(1):1996 CANVASBACK DUCKLING SURVIVAL * Korschgen et al. 131

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IMPLANTINGINTRA-ABDOMINAL RADIOTRANSMITTERS WITH EXTERNALWHIP ANTENNAS IN DUCKS

CARLE. KORSCHGEN,National Biological Service, UpperMississippi Science Center,P. 0. Box 818, La Crosse, WI54602, USA KEVINP. KENOW,National Biological Service, UpperMississippi Science Center,P. 0. Box 818, La Crosse, WI54602, USA ANNETTEGENDRON-FITZPATRICK, Research AnimalResources Center,University of Wisconsin,2115 ObservatoryDrive, Madison,WI 53792, USA WILLIAML. GREEN,National Biological Service, UpperMississippi Science Center,P. 0. Box 818, La Crosse, WI54602, USA F. JOSHUADEIN, National Biological Service, NationalWildlife Health Center, 6006 SchroederRd., Madison,WI 53711, USA

Abstract: We developed and evaluated a surgical procedure for implanting intra-abdominalradiotrans- mitters with externalwhip antennasin captive mallards(Anas platyrhynchos).Transmitters were implanted in the abdominal cavity and the antennas exited through the caudal abdominal wall and skin. Birds with implanted transmittersdeveloped mild to moderate localized air sac reactions. These reactions involved adhesionsof the right anteriorabdominal air sac to the liver with contractionsaround the transmittersand antenna catheters.The adhesionswere reinforcedby a proliferationof connective tissue and lined by multi- nucleated giant cells (foreign body reaction).Casual observationindicated that neither behavior nor activity of the birds was altered by the histologicalreaction to the transmitterimplant. No increasein systemic lesions (particularlyliver or kidney) could be correlated with the histological reactions. Our evaluations indicate that the procedureis a reliable method for radiomarkingducks and the technique has been successfullyused in 2 field studies. J. WILDL.MANAGE. 60(1):132-137

Key words: Anas platyrhynchos,Aythya valisineria, radiomarking,surgical techniques, telemetry, trans- mitters, waterfowl.

Waterfowl are a prominent and important configured for intra-abdominal implants (Pe- group of migratory birds in . tersen et al. 1995). Management of this resource requires accurate Abdominally-implanted transmitters have and reliable data regarding populations, distri- typically used an internal coiled antenna bution, and causes of population fluctuations. (Korschgen et al. 1984, Olsen et al. 1992). How- Radiotelemetry has been used in past research ever, transmission path loss associated with an to investigate the movements and the survival internal transmitter antenna precludes their use of waterfowl species. for studies that are geographically extensive. To Despite the widespread use of telemetry in compensate for transmission path loss associated waterfowl research, external attachments, such with abdominal transmitter implants, an intra- as the backpack harness (Dwyer 1972) or nasal abdominal transmitter with an external whip saddle mount (Perry 1981), have caused behav- antenna was developed (Korschgen et al. 1995). ioral changes in several duck species. Recently, In this paper, we describe the surgical proce- abdominally-implanted radiotransmitters have dures used to implant intra-abdominal trans- provided both an alternative and a preferred mitters with external whip antennas and the attachment technique (Korschgen et al. 1984, data of the pathological effects of such implants. Olsen et al. 1992). In addition, waterfowl mi- We acknowledge the assistance of J. E. Austin, grations can be monitored using new technology A. F. Boysen, C. O. Kochanny, P. Thorsen, and that employs miniaturized satellite transmitters Z. J. Twardowski. M. R. Petersen and J. H. Schulz