Attempts to identify the source of avian vacuolar myelinopathy for waterbirds

Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots (Fulica americana), mallard ducks and ducklings (Anas platyrhynchos), quail (Coturnix japonica), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels (Falco sparverius), and American crows (Corvus brachyrhynchos). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla, or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.     

Failure to transmit avian vacuolar myelinopathy to mallard ducks

Avian vacuolar myelinopathy (AVM) is a neurologic disease that has been diagnosed in free-ranging birds in the southeastern United States. Bald eagles (Haliaeetus leuocephalus), American coots (Fulica americana), and mallards (Anas platyrhynchos) have been affected. Previous investigations have not determined the etiology of this disease. In November and December 2002, we attempted to induce AVM in game-farmed mallards through four, 7-day exposure trials. Mallards were housed in six groups of eight, with two of these groups serving as controls. One group was housed with AVM-affected coots; one group was tube fed daily with water from the lake where affected coots were captured; one group was tube fed daily with aquatic vegetation (Hydrilla verticillata) from the same lake; and another group was tube fed daily with sediment from the lake. No ducks exhibited clinical neurologic abnormalities consistent with AVM and no evidence of AVM was present at histopathologic examination of brain tissue. Although limitations in sample size, quantity of individual doses, frequency of dose administration, duration of exposure, and timing of these trials restrict the interpretation of the findings, AVM was not readily transmitted by direct contact, water, hydrilla, or sediment in this investigation.     

Establishing a food-chain link between aquatic plant material and avian vacuolar myelinopathy in mallards (Anas platyrhynchos)

Avian vacuolar myelinopathy (AVM) is a neurologic disease primarily affecting bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana). The disease was first characterized in bald eagles in Arkansas in 1994 and then in American coots in 1996. To date, AVM has been confirmed in six additional avian species. Attempts to identify the etiology of AVM have been unsuccessful to date. The objective of this study was to evaluate dermal and oral routes of exposure of birds to hydrilla (Hydrilla verticillata) and associated materials to evaluate their ability to induce AVM. Mallards (Anas platyrhynchos) were used in all trials; bobwhite quail (Colinus virginianus) also were used in one fresh hydrilla material exposure trial. Five trials were conducted, including two fresh hydrilla material exposure trials, two cyanobacteria exposure trials, and a frozen hydrilla material exposure trial. The cyanobacteria exposure trials and frozen hydrilla material trial involved gavaging mallards with either Pseudanabaena catenata (live culture), Hapalosiphon fontinalis, or frozen hydrilla material with both cyanobacteria species present. With the exception of one fresh hydrilla exposure trial, results were negative or inconclusive. In the 2002 hydrilla material exposure trial, six of nine treated ducks had histologic lesions of AVM. This established the first cause-effect link between aquatic vegetation and AVM and provided evidence supporting an aquatic source for the causal agent.     

Experimental vacuolar myelinopathy in red-tailed hawks

Avian vacuolar myelinopathy (AVM) was recognized in 1994 as a cause of wild bird mortality when 29 bald eagles (Haliaeetus leucocephalus) succumbed to the disease at DeGray Lake, Arkansas (USA). The cause of AVM and its source remain undetermined despite extensive diagnostic and research investigations. Two years later, when AVM killed 26 eagles in the same area in Arkansas, it became apparent that American coots (Fulica americana) had identical neurologic signs and lesions, and it was hypothesized that eagles acquired AVM via ingestion of affected coots. In order to test this hypothesis, we fed coot tissues (brain, liver, kidney, muscle, fat, and intestinal tract) to rehabilitated, non-releasable red-tailed hawks (Buteo jamaicensis). Five hawks received tissues from coots with AVM lesions, and one hawk received tissues from coots without brain lesions that had been collected at a site where AVM never has been documented. All hawks received 12-70 g/day (mean = 38 g) of coot tissues for 28 days. All six hawks remained clinically normal during the study. The birds were euthanatized on day 29 and microscopic lesions of AVM were found in all hawks that received tissues from affected coots, but not in the hawk that received tissues from unaffected coots. This marks the first time that AVM has been produced in birds under laboratory conditions and proves that birds of prey can acquire AVM via ingestion of tissues from affected coots.     

Attempts to reproduce vacuolar myelinopathy in domestic swine and chickens

Avian vacuolar myelinopathy (AVM) was first recognized as a cause of bald eagle (Haliaeetus leucocephalus) mortality in 1994 in Arkansas (USA) and has since caused over 90 bald eagle and numerous American coot (Fulica americana) mortalities in five southeastern states. The cause of AVM remains undetermined but is suspected to be a biotoxin. Naturally occurring AVM has been limited to wild waterbirds, raptors, and one species of shorebird, and has been reproduced experimentally in red-tailed hawks (Buteo jamaicensis). In this study, chickens and swine were evaluated for susceptibility to vacuolar myelinopathy with the intent of developing animal models for research and to identify specific tissues in affected coots that contain the causative agent. Additionally, submerged, aquatic vegetation, primarily hydrilla (Hydrilla verticillata), and associated material collected from a reservoir during an AVM outbreak was fed to chickens in an effort to reproduce the disease. In two separate experiments, six 4-wk-old leghorn chickens and ten 5-wk-old leghorn chickens were fed coot tissues. In a third experiment, five 3-mo-old domestic swine and one red-tailed hawk, serving as a positive control, were fed coot tissues. In these experiments, treatment animals received tissues (brain, fat, intestinal tract, kidney, liver, and/or muscle) from coots with AVM lesions collected at a lake during an AVM outbreak. Negative control chickens and one pig received tissues from coots without AVM lesions that had been collected at a lake where AVM has never been documented. In a fourth experiment, eight 3-wk-old leghorn chickens were fed aquatic vegetation material. Four chickens received material from the same lake from which coots with AVM lesions were collected for the previous experiments, and four control chickens were fed material from the lake where AVM has never been documented. Blood was collected and physical and neurologic exams were conducted on animals before and once per week during the trials. All animals were sacrificed and necropsies were performed on Day 29 of feeding, with the exception of one treated chicken that was sacrificed and necropsied on Day 15 of feeding. Microscopic lesions of vacuolar myelinopathy were present in the red-tailed hawk and five chickens that received a mixture of all tissues and two chickens that received only gastrointestinal tissues of coots with AVM lesions. Three of four treated chickens in the aquatic vegetation trial developed vacuolar lesions. None of four treatment pigs or any of the negative control animals developed vacuolar lesions. Chickens are susceptible to AVM and may serve as a useful animal model for future studies. Swine may be refractory to AVM or not affected by AVM at the same dose as are chickens and red-tailed hawks. The causative agent of AVM in affected coots is associated with the gastrointestinal tissues. Furthermore, AVM can be reproduced in chickens via ingestion of aquatic vegetation and associated materials collected from a lake during an AVM outbreak. The cause of AVM is most likely present in the materials associated with submerged vegetation because the vegetation itself (hydrilla) was the same at our AVM-positive and AVM-negative sites.     

Avian vacuolar myelinopathy outbreaks at a southeastern reservoir

Avian vacuolar myelinopathy (AVM) is a neurologic disease of unknown etiology that affects bald eagles (Haliaeetus leucocephalus), American coots (Fulica americana), and several species of waterfowl. An unidentified neurotoxin is suspected as the cause of AVM, which has been documented at several reservoirs in the southeastern United States. We conducted diagnostic and epidemiologic studies annually during October-March from 1998-2004 at Clarks Hill/Strom Thurmond Lake on the Georgia/South Carolina border to better understand the disease. Avian vacuolar myelinopathy was confirmed or suspected as the cause of morbidity and mortality of 28 bald eagles, 16 Canada geese (Branta canadensis), six American coots, two great-horned owls (Bubo virginianus), and one killdeer (Charadrius vociferus). Active surveillance during the outbreaks yielded annual average prevalence of vacuolar lesions in 17-94% of coots, but not in 10 beavers (Castor canadensis), four raccoons (Procyon lotor), and one gray fox (Urocyon cinereoargenteus) collected for the study. Brain lesions were not apparent in 30 Canada geese collected and examined in June 2002. The outbreaks at this location from 1998-2004 represent the most significant AVM-related bald eagle mortality since the Arkansas epornitics of 1994-95 and 1996-97, as well as the first confirmation of the disease in members of Strigiformes and Charadriiformes.     

Epizootiological features of avian cholera on the north coast of California

An avian cholera (Pasteurella multocida) epizootic was observed among wildfowl at the Centerville Gun Club, Humboldt County, California (USA) in January 1978. Compared to their live populations and use of the area, coots (Fulica americana) died in proportionately greater numbers than any other species. Coots collected by gunshot were evaluated for sex and age composition, and morphometry from November 1977 through mid-January 1978 at this site. There was no substantial difference in the sex, age or morphometry between birds dying of avian cholera and from those dying from gunshot. Assuming coots dying of gunshot are representative of the general population, it appears there was little selection among coots by P. multocida. There was evidence for a sequential mortality similar to that reported previously at this site: coots were the first birds to die, followed by American wigeon (Anas americana) and northern pintails (A. acuta acuta); northern shovelers (A. clypeata) and mallards (A. platyrhynchos) died late in the epizootic.     

Investigation of the link between avian vacuolar myelinopathy and a novel species of cyanobacteria through laboratory feeding trials

Avian vacuolar myelinopathy (AVM) is a neurologic disease affecting Bald Eagles (Haliaeetus leucocephalus), American Coots (Fulica americana), and other birds in the southeastern United States. The cause of the disease has not yet been determined, although it is generally thought to be a natural toxin. Previous studies have linked AVM to aquatic vegetation, and the current working hypothesis is that a species of cyanobacteria growing epiphytically on that vegetation is producing a toxin that causes AVM. Surveys of epiphytic communities have identified a novel species of cyanobacteria in the order Stigonematales as the most likely suspect. The purpose of this study was to further examine the relationship between the suspect Stigonematales species and induction of AVM, by using animal feeding trials. Adult Mallards and domestic chickens were fed aquatic vegetation from two study sites containing the suspect cyanobacterial epiphyte, as well as a control site that did not contain the Stigonematales species. Two trials were conducted. The first trial used vegetation collected during mid-October 2003, and the second trial used vegetation collected during November and December 2003. Neither treatment nor control birds in the first trial developed AVM lesions. Ten of 12 treatment Mallards in the second trial were diagnosed with AVM, and control birds were not affected. This study provides further evidence that the novel Stigonematales species may be involved with AVM induction, or at the least it is a good predictor of AVM toxin presence in a system. The results also demonstrate the seasonal nature of AVM events.     

Strain- and genotype-specific differences in virulence of Paenibacillus larvae subsp. larvae, a bacterial pathogen causing American foulbrood disease in honeybees

Virulence variations of Paenibacillus larvae subsp. larvae, the causative agent of American foulbrood disease of honeybees, were investigated by analysis of 16 field isolates of this pathogen, belonging to three previously characterized genotypes, as well as the type strain (ATCC 9545) of P. larvae subsp. larvae, with exposure bioassays. We demonstrated that the strain-specific 50% lethal concentrations varied within an order of magnitude and that differences in amount of time for the pathogen to kill 100% of the infected hosts (LT100) correlated with genotype. One genotype killed rather quickly, with a mean LT100 of 7.8 +/- 1.7 days postinfection, while the other genotypes acted more slowly, with mean LT100s of 11.2 +/- 0.8 and 11.6 +/- 0.6 days postinfection.     

Avian botulism during late autumn and early spring in Saskatchewan

Two outbreaks of botulism in central Saskatchewan in which mortality of waterfowl continued into late autumn and then recurred in the same marshes the following spring are described. Small numbers of birds were involved in each instance. Dabbling ducks (predominantly mallards, Anas platyrhynchos and pintails, Anas acuta) and American coots, Fulica americana were affected most commonly in autumn, whereas only diving ducks (predominantly lesser scaup, Aythya affinis) were found to be involved in spring. Live maggots present in carcasses despite sub-freezing temperatures were the probable source of intoxication in the autumn; the source of toxin in the spring was not determined.     

Correlations of daily activity with avian cholera mortality among wildfowl.

We tested the hypothesis that wildfowl activities can influence the risk of avian cholera (Pasteurella multocida infection) for susceptible birds at Centerville, Humboldt County, California (USA). Avian cholera mortality characteristics from past epizootics were correlated with variations in flock size, habitat use and 11 feeding and nonfeeding behaviors among six empirically defined groups of wildfowl: American coots (Fulica americana), tundra swans (Cygnus columbianus), American wigeon (Anas americana), northern pintails (A. acuta), northern shovelers (A. clypeata)/mallards (A. platyrhynchos), and teal (A. discors, A. crecca, A. cyanoptera). The position of these wildfowl groups in past mortality sequences was directly correlated with mean flock size, time spent on land, and time spent grazing on land or in shallow water. We propose that variations in bird density, habitat use and frequency of grazing may serve as predisposing factors to avian cholera among wildfowl.     

Large-scale seasonal variation in the prevalence and severity of chytridiomycosis

The chytrid fungus Batrachochytrium dendrobatidis has been implicated as the causative agent of mass mortalities, population declines and the extinctions of amphibian species worldwide. Although several studies have shown that the prevalence of chytridiomycosis (the disease caused by the fungus) increases in cooler months, the magnitude and timing of these seasonal fluctuations have yet to be accurately quantified. We conducted disease sampling in a single population of stony creek frogs Litoria wilcoxii on 13 occasions over a 21-month period and used quantitative real-time polymerase chain reaction to detect and quantify the number of B. dendrobatidis zoospores present on samples. Disease prevalence varied significantly across sampling sessions, peaking at 58.3% (in early spring) and dropping to as low as 0% on two occasions (late summer and early autumn). There was a significant negative relationship between disease prevalence and mean air temperature in the 30 days prior to sampling. These large-scale seasonal fluctuations in chytridiomycosis levels will strongly influence conservation programs and amphibian disease research.     

Serum cortisol levels in goats exhibit seasonal but not daily rhythmicity

The aim of the study was to find out whether there is a daily rhythm in goat serum cortisol concentrations, whether the concentration profiles differ between normal light:dark and constant dark conditions, and whether any seasonal variations might be detected in daily cortisol secretion patterns. Seven Finnish landrace goats were kept at indoor temperature (18-23°C) under artficial lighting that approximately simulated the annual changes of daylength at 60°N. Blood samples were collected for cortisol measurements by radioimmunoassay at 2h intervals during six times of the year: winter (light:dark 6:18h), early spring (10:14h), late spring (14:10h), summer (18:6h), early fall (14:10h), and late fall (10:14h). Cortisol profiles were determined for two consecutive days, first in light:dark (LD) conditions and then in continuous darkness (DD). There was no significant daily rhythm in serum cortisol levels in any time of the year, nor did the profiles in LD and DD conditions show any differences. A significant seasonal variation was, however, detected among the overall cortisol levels. In winter, the concentrations were higher than in any other season, and from early spring to summer they were at their lowest. Under equal photoperiods, the cortisol levels were higher in fall than spring. The difference between winter and summer was confirmed in the following year in LD conditions. There was no correlation between the serum cortisol and progesterone levels. The results suggest that the possible circadian variation of cortisol secretion in goats is completely masked by external factors, and the lighting conditions do not have immediate effects on the daily secretion patterns. The seasonal variation in the overall cortisol levels is most probably related to the changes in photoperiod, because other conditions were relatively constant during the experiment.     

Effect of time of early weaning and time of lambing on accelerated lambing in Polypay sheep

Effects of early weaning, lactation, and day-of-year lambing on the ability of Polypay ewes to rebreed following winter and summer lambings were evaluated. Winter lambing ewes did not successfully rebreed while lactating. However, when winter-born lambs were weaned at 31 days postpartum, more ewes rebred and produced summer lambs (35.7%) than when lambs were weaned at 41 days postpartum (23.6%). Ewes that lambed during the early part of the winter lambing period had an advantage over later lambing ewes in the percentage which subsequently lambed the following summer. This was apparently the result of a difference in length of breeding exposure rather than a higher fertility rate during the early part of the breeding period. When summer lambing ewes were rebred during the early part of the summer breeding period (late summer to early fall), stress associated with lactation did not affect subsequent winter lambing performance. Summer lambing ewes belonging to a late weaning (80 days) treatment group did not differ (P>0.05) from those belonging to an early weaning (31 days) treatment group in winter fertility, prolificacy, day-of-year lambing or lambing interval.     

Circadian and circannual variations in growth and cold resistance of warm acclimated rats and their relationship with the geomagnetic activity

In winter, summer, spring and fall, groups of 200 g Sprague Dawley male rats were kept for 14 days at constant Ta 28°C±°C and LD 12:12(07:00–19:00 h). They were fed a laboratory chow (P) or a semi-purified diet (H). They were weighed at 0, 7 and 14 days. Cold resistance was determined by the fall in rectal temperature during 4 hours of restrained exposure to +1°C either in the morning (09:00 – 13:00 h) or in the afternoon (14:00 – 18:00 h). Rats fed the H diet could better tolerate cold exposure in the morning than in the afternoon, whereas the chow-fed rats were more vulnerable and became severely hypothermic both in morning and afternoon. The greater morning resistance provided by the H diet was evident in summer and winter but not in spring or fall. With both diets, cold resistance as well as growth decreased during spring and fall. Frozen storage of the diets and the water for use during other seasons showed that the nutrients per se were not a factor in the observed seasonal cycle. Although humidity in the 28°C room varied between a minimum of 26.5% in April to a maximum of 44.3% in August, it was not a statistically significant factor in the growth cycle. Arguments are presented to rule out relative humidity as a significant factor in the seasonal variation in the degree of cold resistance. A significant correlation was found for growth and cold resistance with geomagnetic activity.NRCC # 17310     

Pintail and Mallard Survival in California Relative to Habitat,Abundance, and Hunting

ABSTRACT The influence of habitat, waterfowl abundance, and hunting on winter survival of waterfowl is not well understood. We studied late August-March survival of 163 after-hatch-year (AHY) and 128 hatch-year (HY) female mallards (Anas platyrhynchos) radiotagged in Sacramento Valley (SACV) and 885 AHY female northern pintails (A. acuta) radiotagged throughout the Central Valley of California, USA, relative to flooded habitat (HAB), January abundance of each species (JMAL or JPIN), hunter-days (HDY), and a hunting pressure index (HPI) that combined these variables. From EARLY (1987–1994) to LATE (1998–2000), HAB increased 39%, JPIN increased 45%, JMAL increased 53%, HDY increased 21%, duck-hunting season increased from 59 days to 100 days, and the female daily bag limit doubled to 2 for mallards but remained 1 for pintails. Survival (± SE) was greater during LATE versus EARLY for pintails radiotagged in each region (SACV: 93.2 ± 2.1% vs. 87.6 ± 3.0%; Suisun Marsh: 86.6 ± 3.2% vs. 77.0 ± 3.7%; San Joaquin Valley: 86.6 ± 3.1% vs. 76.9 ± 4.1%) but not for SACV mallards (AHY: 70.6 ± 7.2% to 74.4 ± 7.7% vs. 80.1 ± 7.2% to 82.8 ± 5.6%; HY: 48.7 ± 9.1% [1999–2000 only] vs. 63.5 ± 8.8% to 67.6 ± 8.0%). Most pintail (72%) and mallard (91%) deaths were from hunting, and lower HPI and higher JPIN or JMAL were associated with reduced mortality. Increased HAB was associated with reduced winter mortality for pintails but not for SACV mallards. Pintail survival rates that we measured were within the range reported for other North American wintering areas, and during LATE were higher than most, even though our study duration was 68–110 days longer. Winter survival rates of SACV mallards were also within the reported range. However, with higher bag limits and longer seasons, mallard survival during LATE was lower than in most other wintering areas, especially during 1999–2000, when high winds on opening weekend resulted in high hunting mortality. Habitat conservation and favorable agriculture practices helped create a Central Valley wintering environment where natural mortality of mallards and pintails was low and survival varied with hunting mortality. We recommend regulations and habitat management that continue to minimize natural mortality while allowing sustainable harvest at a level that helps maintain strong incentive for management of Central Valley waterfowl habitats, including the large portion that is privately owned.     

Strong seasonality of Bonamia sp. infection and induced Crassostrea ariakensis mortality in Bogue and Masonboro Sounds, North Carolina, USA

Asian oyster Crassostrea ariakensis is being considered for introduction to Atlantic coastal waters of the USA. Successful aquaculture of this species will depend partly on mitigating impacts by Bonamia sp., a parasite that has caused high C. ariakensis mortality south of Virginia. To better understand the biology of this parasite and identify strategies for management, we evaluated its seasonal pattern of infection in C. ariakensis at two North Carolina, USA, locations in 2005. Small (<50 mm) triploid C. ariakensis were deployed to upwellers on Bogue Sound in late spring (May), summer (July), early fall (September), late fall (November), and early winter (December) 2005; and two field sites on Masonboro Sound in September 2005. Oyster growth and mortality were evaluated biweekly at Bogue Sound, and weekly at Masonboro, with Bonamia sp. prevalence evaluated using parasite-specific PCR. We used histology to confirm infections in PCR-positive oysters. Bonamia sp. appeared in the late spring Bogue Sound deployment when temperatures approached 25 degrees C, six weeks post-deployment. Summer- and early fall-deployed oysters displayed Bonamia sp. infections after 3-4 weeks. Bonamia sp. prevalences were 75% in Bogue Sound, and 60% in Masonboro. While oyster mortality reached 100% in late spring and summer deployments, early fall deployments showed reduced (17-82%) mortality. Late fall and early winter deployments, made at temperatures <20 degrees C, developed no Bonamia sp. infections at all. Seasonal Bonamia sp. cycling, therefore, is influenced greatly by temperature. Avoiding peak seasonal Bonamia sp. activity will be essential for culturing C. ariakensis in Bonamia sp.-enzootic waters.     

Body temperature null distributions in reptiles with nonzero heat capacity: seasonal thermoregulation in the American alligator (Alligator mississippiensis)

Regulation of body temperature may increase fitness of animals by ensuring that biochemical and physiological processes proceed at an optimal rate. The validity of current methods of testing whether or not thermoregulation in reptiles occurs is often limited to very small species that have near zero heat capacity. The aim of this study was to develop a method that allows estimation of body temperature null distributions of large reptiles and to investigate seasonal thermoregulation in the American alligator (Alligator mississippiensis). Continuous body temperature records of wild alligators were obtained from implanted dataloggers in winter (n=7, mass range: 1.6-53.6 kg) and summer (n=7, mass range: 1.9-54.5 kg). Body temperature null distributions were calculated by randomising behavioural postures, thereby randomly altering relative animal surface areas exposed to different avenues of heat transfer. Core body temperatures were predicted by calculations of transient heat transfer by conduction and blood flow. Alligator body temperatures follow regular oscillations during the day. Occasionally, body temperature steadied during the day to fall within a relatively narrow range. Rather than indicating shuttling thermoregulation, however, this pattern could be predicted from random movements. Average daily body temperature increases with body mass in winter but not in summer. Daily amplitudes of body temperature decrease with increasing body mass in summer but not in winter. These patterns result from differential exposure to heat transfer mechanisms at different seasons. In summer, alligators are significantly cooler than predictions for a randomly moving animal, and the reverse is the case in winter. Theoretical predictions show, however, that alligators can be warmer in winter if they maximised their sun exposure. We concluded that alligators may not rely exclusively on regulation of body temperature but that they may also acclimatise biochemically to seasonally changing environmental conditions.     

Correlation of seasonal acclimatization in metabolic enzyme activity with preferred body temperature in the Eastern red spotted newt (Notophthalmus viridescens viridescens)

Eastern red spotted newts, as aquatic adults, are active year round. They are small and easy to handle, and thus lent themselves to a laboratory study of seasonal changes in preferred body temperature and biochemical acclimatization. We collected newts in summer (n=20), late fall (n=10) and winter (n=5). Ten each of the summer and late fall newts were subjected to an aquatic thermal gradient. Summer newts maintained higher cloacal temperatures than late fall newts (26.8+/-0.5 degrees C and 17.2+/-0.4 degrees C, respectively). In addition, the activity of three muscle metabolic enzymes (cytochrome c oxidase (CCO), citrate synthase (CS) and lactate dehydrogenase (LDH)) was studied in all newts collected. Newts compensated for lower late fall and winter temperatures by increasing the activity of CCO during those seasons over that in summer newts at all assay temperatures (8, 16 and 26 degrees C). The activity of CS was greater in winter over summer newts at 8 and 16 degrees C. No seasonal differences in LDH activity were demonstrated. These data in newts indicate that this amphibian modifies some muscle metabolic enzymes in relation to seasonal changes and can modify its behavioral in a way that correlates with those biochemical changes.     

Accumulation of lactate by supercooled hatchlings of the painted turtle (Chrysemys picta): implications for overwinter survival

Hatchlings of the North American painted turtle (Chrysemys picta) typically spend their first winter of life inside the shallow, subterranean nest where they completed embryogenesis the preceding summer. Neonates at northern localities consequently may be exposed during winter to subzero temperatures and frozen soil. Hatchlings apparently survive exposure to such conditions by supercooling, but the physiological consequences of this adaptive strategy have not been examined. We measured lactate in hatchling painted turtles after exposure to each of three temperatures (0 °C, −4 °C, and −8 °C) for three time periods (5 days, 15 days, and 25 days) to determine the extent to which overwintering hatchlings might rely on anaerobic metabolism to regenerate ATP. Whole-body lactate increased with increasing duration of exposure and decreasing temperature, and the highest levels were associated with the group that experienced the highest mortality. These results indicate that animals may develop a considerable lactic acidosis during a winter in which temperatures fall below 0 °C for weeks or months and that accumulation of lactate may contribute to mortality of overwintering animals. Accepted: 20 October 1999