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Platte River Ecology Study


Disease Concerns


Introduction

Because migratory bird losses to disease represent a major concern associated with habitat degradation on the study area, this section of the report has been prepared to provide detailed background information on the disease problem.

Four diseases with epizootic potential have been reported in migratory birds within the Platte River Study Area or in migratory bird populations which utilize the area. Botulism, originally known as western duck sickness, was reported in waterfowl in Nebraska before 1932 (Kalmbach and Gunderson 1934), and Nebraska ranks seventh among the western states and Canadian provinces in waterfowl losses to this disease (Rosen 1971a). In early 1973, an outbreak of duck plague, or duck virus enteritis, occurred in mallards and Canada geese at the Lake Andes National Wildlife Refuge and on the nearby Missouri River 274 km (170 miles) north of Grand Island, just across the Nebraska border in South Dakota (Berlinger et al. 1973). An outbreak of aspergillosis killed an estimated 1000-1500 crows in south central Nebraska in the fall of 1974 (Zinkl et al. 1977a), and avian cholera was confirmed in migratory waterfowl and crows in the Rainwater Basin in the spring of 1975 (Zinkl et al. 1977b). Botulism, duck plague, and avian cholera are discussed separately. Aspergillosis, although reported in migratory bird populations on the study area, is less likely to become a significant threat to waterfowl and crane populations as a result of habitat degradation problems described in this report and is not addressed in the following discussion.


Botulism

Botulism is a food poisoning caused by the ingestion of the toxin produced by the bacterium Clostridium botulinum. Most species of waterfowl and shorebirds are susceptible to type C botulinal toxin, but the incidence of the disease may be influenced by the food habits of the individual species and their occurrence on the outbreak area (Rosen 1971a). Summer outbreaks typically involve dabbling ducks and shorebirds. Although Canada geese are susceptible to the toxin, they usually are not present where botulism occurs during the summer, and when they do arrive, their feeding habits reduce the likelihood of their encountering the toxin (Jensen and Williams 1964). However, an outbreak of botulism at the Horicon National Wildlife Refuge in Wisconsin in 1978 did involve Canada geese. Raptors are more resistant to type C botulinal toxin and the disease has not been reported in sandhill or whooping cranes.

The basic epizootiology of waterfowl and shorebird botulism is relatively simple although the complete chain of events leading to a botulism outbreak may be complex. The "microenvironment concept" is now generally accepted by waterfowl botulism investigators. The concept suggests that C. botulinum. type C produces toxin in small, discrete, particulate food items, such as invertebrate carcasses, which provide the anaerobic conditions and nutrient requirements for growth of the bacterium independent of the surrounding wetland environment, and protect the toxin from dilution or inactivation (Bell et al. 1955; Enright 1971). Temperature requirements are readily met during warm summer days. This theory is supported by laboratory evidence of toxin production in aquatic and terrestrial invertebrate carcasses. Protection of toxin in particulate food items such as invertebrate carcasses, and preservation over winter by freezing also appear to be the most plausible explanations for spring outbreaks which sometimes occur before water temperatures have reached a point favorable for the growth of C. botulinum (Pearson and Jensen 1972).

Water conditions including water level, salinity, dissolved oxygen, available nutrients, toxic substances and other factors influence the amount of decaying animal protein available for the growth of C. botulinum (Pearson and Jensen 1972). Declining water levels and increased water temperature or salinity may cause marginal conditions for the survival of previously thriving invertebrate populations, or invertebrates may become stranded on mud flats used by waterfowl and shorebirds. Conversely, rising water levels may drown terrestrial invertebrates creating conditions conducive to toxin production, or may flood vegetation, causing a release of nutrients and stimulating the growth of aquatic invertebrate populations to unstable levels. In either circumstance, the collapse of these populations makes available large quantities of decaying animal protein particles for toxin production. Influxes of agricultural nutrients also may disrupt the nutrient budget of wetlands, thereby stimulating the growth of certain invertebrate populations, or algal blooms which lead to oxygen depletion followed by aquatic invertebrate or vertebrate mortality. The introduction of insecticides may cause direct mortality of invertebrates, whereas the application of herbicides can disrupt aquatic food chains by the sudden depression of phytoplankton production.

Although information is inadequate to evaluate thoroughly the impacts of changing conditions on the study area in relation to occurrence of botulism outbreaks, sufficient information is available to warrant discussion of the issue. Impacts of botulism on migratory bird populations are most likely to involve local breeding populations, and possibly early fall migrants, although spring migrants may also be exposed to botulinal toxin. Toxin produced during summer outbreaks can be preserved over winter in frozen invertebrate carcasses which can become available the following spring when large numbers of migrant waterfowl are using the area. Ducks periodically are affected in such spring outbreaks in South Dakota (Pearson, pers. comm.) and geese could also be expected to become involved if spring botulism outbreaks were to occur on wetlands in the Rainwater Basin Area. The potential threat from botulism is less severe than from other diseases which will be discussed later because sandhill and whooping cranes and most of the ducks and geese utilize the study area during the spring and then migrate on to other areas.

Whether or not sandhill or whooping cranes would be subjected to an increased risk of botulism would depend largely upon the specific sources of toxin in the outbreak, the occurrence of cranes on the outbreak area, and the specific food habits of the cranes. Whooping cranes utilize the Rainwater Basin wetlands and to a lesser extent the Platte River during their spring migration, and feed on aquatic and terrestrial invertebrates (see Whooping Crane Feeding Ecology section). It is not known if they feed on dead invertebrates, or on live invertebrates such as blowfly larvae which can accumulate toxin. Ingestion of these foods would markedly increase their risk of exposure to botulinal toxin. It is known that whooping cranes feed on fish, and Jensen et al. (1968) have shown that live fish consuming type C botulinal toxin can convey lethal doses of toxin when eaten by birds. If deteriorating habitat conditions on the Platte River result in significant numbers of sandhill cranes relocating to wetlands in the Rainwater Basin Area, sandhill cranes also could become affected by botulism outbreaks.

Certain man-induced changes in the environment of the study area have increased the likelihood of botulism outbreaks. Surface water drainage and lowering of groundwater levels associated with agricultural development already have severely altered or eliminated most of the natural wetlands in the Rainwater Basin Area. Further disruption from agricultural chemicals, drastic fluctuations in water levels, and nutrient enrichment in the remaining wetlands can be expected to increase the probability of botulism outbreaks by increasing the availability of decaying animal protein media for toxin production. Under these conditions, the occurrence and the magnitude of outbreaks becomes a function of the presence of susceptible birds. Concurrently, as wetlands continue to be lost, birds will tend to relocate on those which remain. Consequently, larger increments of the bird population are placed at risk when botulism outbreaks occur, and the probability of outbreaks also increases. Wells and associated facilities on 12 waterfowl production areas allow water to be pumped from underground aquifers. These wells allow some control over botulism outbreaks by stabilizing water conditions on wetlands.


Duck Plague

Duck plague is an acute, highly contagious herpes virus disease of ducks, geese, and swans (Leibovitz 1971). The 1973 duck plague outbreak at the Lake Andes National Wildlife Refuge in south central South Dakota killed an estimated 40% of 100,000 mallards and 3% of 9000 Canada geese wintering on the refuge and nearby Missouri River (Berlinger et al. 1973). The outbreak was the first major epizootic of this disease reported in free-flying wild waterfowl in the world (Proctor et al. 1975), although it had occurred in domestic ducks in Europe as early as 1923 and had been diagnosed in commercial duck flocks on Long Island, New York, in 1968 (Leibovitz 1971).

Evidence indicates that survivors of the disease may become chronically infected carriers which may perpetuate the virus within waterfowl populations and serve as the source for new outbreaks (Burgess et al. 1978). Banding data show that more than 10% of the mallards banded during the winter at Lake Andes between 1963 and 1969 were recovered in eastern Nebraska (Kuck 1971). Although it is probable that most of the survivors of the 1973 Lake Andes outbreak have by now been lost by attrition, it is evident that a potential does exist for the introduction of duck plague into waterfowl populations using the study area, just as it existed at Lake Andes.

The lack of additional reported epizootics of duck plague in free-flying waterfowl since the 1973 Lake Andes outbreak has prevented identification of the specific factors responsible for the occurrence of such outbreaks, other than the presence of the virus and susceptible waterfowl. The density of birds presumably was a contributing factor in the transmission of the virus when duck plague reached epizootic levels in waterfowl utilizing the limited area of open water in Owens Bay on the Lake Andes National Wildlife Refuge in 1973. However, substantially higher numbers of waterfowl had occurred on the area in previous years with no evidence of the disease (Berlinger et al. 1973), suggesting that the virus was not introduced until 1973, or that other unrecognized factors were responsible for triggering the outbreak. Until more definitive information is available on the epizootiology of duck plague in free-flying wildfowl it should be assumed that high numbers of waterfowl on limited water area, such as existed at Lake Andes in 1973, increases the potential for duck plague outbreaks.

Alteration of wetlands and diminished flows in the Platte are causing densities of both waterfowl and cranes to rise. High densities of waterfowl already occur on the study area during the spring migration, and continuing wetland destruction in the rainwater basins is further increasing densities of waterfowl on the remaining wetland areas. Similarly, reductions of flows in the Platte River effectively increase the density of birds per acre foot of water, even if their numbers and distribution are not affected.

It is important that adequate flows be maintained in the Platte during spring migration to disperse cranes and waterfowl and to reduce the potential for disease outbreaks, particularly if large numbers of birds are forced to move to the River. When duck plague occurred at Lake Andes in the winter of 1973, it was considered essential to avoid dispersing the infected birds to areas where other populations would be exposed, but also to implement a control program which would terminate the outbreak before the arrival of additional migrants. The control program sought to move the birds from the limited open water area of the Lake Andes National Wildlife Refuge to the Missouri River 7 miles away where releases of up to 565 m3/sec from the Fort Randall Dam created an extensive open water area for dispersal of the waterfowl and a high rate of flow for dilution of the virus, both of which contributed to a marked reduction in the density of birds per unit volume of water (Berlinger et al., unpubl. report).

Under present conditions, if duck plague were to occur in waterfowl within the Rainwater Basin Area, the Platte River would provide a possible area for dispersal of the birds and flows for dilution of the virus. Duck plague virus affects only waterfowl, thus such a control program would present no danger to cranes, eagles, or other species of wildlife (although the possible exposure of domestic waterfowl must be considered). If flows in the Platte River were to diminish, however, this option for disease control might be precluded.


Avian Cholera

Avian cholera, an infectious disease caused by the bacterium Pasteurella multocida, has been reported in a wide variety of domestic and wild birds (Rosen 1971b; Heddleston 1972). Outbreaks in wild birds have most frequently been reported in waterfowl (Rosen 1971b), but avian cholera also has been reported in the bald eagle (Rosen 1972) and other raptors (Rosen and Morse 1959; Hunter 1967; Rosen 1971b). Ten sandhill cranes out of a wintering population of 5600 died in a 1970-71 avian cholera outbreak in California (Rosen 1972). Individual sandhill cranes have died of avian cholera in Nebraska at the National Audubon Society Lillian Annette Rowe Bird Sanctuary on the Platte River in the spring of 1975 (James Hurt, pers. comm.), and on a Rainwater Basin wetland in the spring of 1977 (Chris Brandt, pers. comm.). Avian cholera has not been diagnosed in whooping cranes, but the wide host range of P. multocida in birds indicates that whooping cranes must be presumed to be susceptible to the disease (Zinkl et al. 1977b).

In migratory birds, avian cholera typically is an extremely acute disease, with few signs other than dead birds being evident (Jensen and Williams 1964; Rosen 1971b). Few sick birds usually are seen and they frequently die shortly after signs appear (Rosen and Bischoff 1949; Jensen and Williams 1964; Rosen 1971b; Zinkl et al. 1977b). Occasionally, waterfowl displaying disturbances of equilibrium and other neurological signs may be seen as outbreaks progress (Rosen and Bischoff 1949; Jensen and Williams 1964; McDougle et al. 1965; Vaught et al. 1967; Rosen 1971b; Zinkl et al. 1977b). In crows, however, avian cholera may occur in a chronic form (Zinkl et al. 1977b). Healthy, chronically infected P. multocida carriers occur in domestic poultry and are believed to be important in maintaining the infection and serving as the source of new outbreaks (Heddleston 1972). Chronically infected carriers may also occur in survivors of avian cholera outbreaks in migratory birds (Jensen and Williams 1964; Vaught et al. 1967; Donahue and Olson 1969; Rosen 1971b), and Korschgen et al. (1978) found a low incidence of P. multocida carriers in common eiders.

Dissemination of P. multocida among birds occurs via nasal exudates which contaminates the environment, especially food and water (Rosen 1971b; Heddleston 1972); feces are a much less significant source of contamination (Heddleston 1972). The nasal exudate of diseased birds contains large numbers of P. multocida (Rosen 1971b; Heddleston 1972) and copious quantities of this material may drain from the bills of birds immediately upon death (Rosen 1971b). P. multocida may survive for 2 months in carcasses at refrigerator temperatures and over 100 days in moist soil at 3 degrees C (Heddleston 1972). A pond in California was found to remain infective for 3 weeks after the last carcasses of avian cholera victims had been removed (Rosen 1969).

The most common routes of infection for P. multocida in birds probably are by ingestion or inhalation, with the organism gaining access through the mucous membranes of the mouth, pharynx, and upper air passages (Heddleston 1972). Infection also may occur via the eye (Heddleston 1972). Contaminated water, therefore, is thought to be an important source of infection, especially for waterfowl (Rosen 1971b) but contaminated food also may be a source (Rosen 1971b; Heddleston 1972).

Control of avian cholera through the use of antibiotics, chemotherapy, and vaccination, although effective in domestic poultry (Heddleston 1972), has had little application in dealing with the disease in migratory birds (Jensen and Williams 1964). Consequently, the available control measures generally are limited to practices aimed at reducing the level of transmission of the infection within and among migratory bird flocks. These practices typically include collection and disposal of carcasses and discouraging bird use of heavily contaminated areas by draining ponds or chasing the birds to other areas (Rosen and Bischoff 1949; Jensen and Williams 1964; Vaught et al. 1967; Rosen 1971b; Zinkl et al. 1977b). Killing of infected flocks may be feasible under some circumstances where dispersal of the birds can be avoided (Rosen 1971b Pursglove et al. 1976). Dispersal of migratory birds as an avian cholera control measure must be carefully evaluated on a case-by-case basis and, unless the movements of the infected birds can be predicted with a high degree of certainty, carries the risk of spreading the disease to other populations (Jensen and Williams 1964; Rosen 1971b). Measures to avoid the mixing of birds from different flocks are an important aspect of avian cholera prevention (Heddleston 1972).

The first confirmation of avian cholera in migratory birds in Nebraska occurred in waterfowl and crows in the Rainwater Basin Area in 1975 (Zinkl et al. 1977b); however, waterfowl with field signs suggestive of avian cholera were observed on the Platte River near Overton, Nebraska, during the springs of 1950 and 1964 (McDougle et al. 1965). An estimated 20,000-25,000 waterfowl died in the 1975 outbreak in the Rainwater Basin Area (Zinkl et al. 1977b), 7500-8500 were estimated to have died in the spring of 1976, and 7500-10,000 in the spring of 1977.

Losses in the Rainwater Basin Area were low in the spring of 1978, but 3100 birds, primarily coots, died of avian cholera on Lake McConaughy and at the Swanson Reservoir in Hitchcock County (Hurt 1978). Losses were low again in 1979, but in the spring of 1980, avian cholera occurred on at least SO wetlands in the Rainwater Basin Area, with 30,677 dead birds collected (A. Trout, unpubl. data). Sites of heavy waterfowl mortality and their distribution in relation to sandhill crane staging areas 1 and 2 are shown in Fig. 21. The principal species of waterfowl lost during the avian cholera outbreak in 1980 and numbers found are as follows: mallards, 9351; pintails, 8045; white-fronted geese, 6574; Canada geese, 2787; American wigeon, 1121; and redhead, 1114.

Although waterfowl mortalities in the 1975 Nebraska outbreak seemed to occur in proportion to the abundance of each species present (Zinkl et al. 1977b), differences in species susceptibility have been reported in other outbreaks (Rosen 1971b). Coots generally are reported to be highly susceptible to avian cholera and frequently are the first birds observed to die in outbreaks (Rosen and Bischoff 1949, 1950; Rosen and Morse 1959; Rosen 1969; Pursglove et al. 1976). Gulls are susceptible but appear to survive longer and may contribute to the local spread of the disease (Rosen and Bischoff 1949, 1950; Rosen and Morse 1959; Rosen 1971b). Petrides and Bryant (1951) noted during a 1949-50 avian cholera outbreak in Texas that the relationship between the abundance of waterfowl species and their mortality was not direct, and that 16 times more green-winged teal, but only half as many geese, died as than was expected, based upon their total numbers. Northern shovelers, American wigeons, canvasbacks, teal, and pintails were observed to be the most susceptible waterfowl, and mallards the least susceptible in the 1948-49 California outbreak (Rosen and Bischoff 1949). Rosen (1969) analyzed avian cholera mortalities in California waterfowl and found that in diminishing order of susceptibility the species were wigeon, shoveler, mallard, and pintail. He also found that white-fronted geese were more susceptible than snow geese or Canada geese, and that all three species of geese were more susceptible than mallards (Rosen 1969). Although differential species susceptibility to avian cholera occurs in domestic poultry (Heddleston 1972), differential mortality rates in migratory birds may be a reflection of relative exposure based upon different feeding habits and the utilization of different subhabitats, rather than differential resistance to the disease (Rosen and Bischoff 1949; Rosen 1969, 1971b).

Despite the long history and frequent occurrence of avian cholera in migratory birds, no comprehensive epizootiologic studies have been reported of the disease in wild bird populations and little objective information is available on the conditions which contribute to outbreaks (Jensen and Williams 1964; Rosen 1971b). In domestic poultry, withdrawal of feed and water, abrupt changes of diet, and environmental stress are reported to increase the incidence of avian cholera (Heddleston 1972). No correlation, however, was found between temperature and the mortality rate in the 1949-50 Texas outbreak in migratory waterfowl, although an apparent correlation was noted with wind (Petrides and Bryant 1951), and Bennett and Bolen (1978) found a correlation between wind velocity, relative humidity, and a stress response in wintering green-winged teal in Texas. The 1970 outbreak on Chesapeake Bay was preceded by several weeks of extremely cold weather (Locke et al. 1970). The 1964 outbreak at the Squaw Creek National Wildlife Refuge was associated with cold temperatures, a corn diet, and lead poisoning in mallards (McDougle et al. 1965). The 1975 Nebraska outbreak was preceded by a brief snow storm (Zinkl et al. 1977). However, no cause and effect relationship has been demonstrated between any of the aforementioned factors and the occurrence of avian cholera.

Nutrition has been suggested as an important factor in avian cholera (Rosen and Bischoff 1950), and outbreaks in common eiders occur during the nesting season when female eiders may lose up to 50% of their body weight (Korschgen et al. 1978). Avian cholera apparently also occurs in snow geese on their Canadian nesting grounds when females undergo weight loss during laying and incubation. However, diet had no apparent influence in the 1949-50 outbreak in waterfowl in Texas (Petrides and Bryant 1951) and, in fact, waterfowl dying in avian cholera outbreaks frequently are in excellent condition with abundant fat deposits (Quortrup et al. 1946; McDougle et al. 1965; Vaught et al. 1967; Locke et al. 1970; Zinkl et al. 1977; Wobeser et al. 1979). Rosen (1971b) postulated that the improving physical condition of waterfowl in spring as they are preparing to migrate to northern nesting grounds might be an important factor in preventing winter avian cholera outbreaks in California. However, the persistence of avian cholera within waterfowl undergoing rapid fat deposition on the spring staging area in Nebraska would appear to discount this hypothesis.

No consistent correlation exists between the total numbers of birds present and the total mortality in avian cholera outbreaks in migratory birds (Rosen 1969~ 1971b). Apparently the severity of outbreaks is influenced by factors other than population size. However, high bird densities are presumed to facilitate the transmission of contagious diseases (Rosen and Bischoff 1950; Jensen and Williams 1964), and overcrowding and "concentration" frequently are cited as factors associated with avian cholera outbreaks in migratory waterfowl (Rosen and Bischoff 1950 Petrides and Bryant 1951 Klukas and Locke 1969). The 1970 outbreak on Chesapeake Bay occurred when sea ducks concentrated on shallow portions of the bay after cold weather (Locke et al. 1970). The maintenance of open water by pumping at the Squaw Creek National Wildlife Refuge concentrated an estimated 300,000 waterfowl on small water areas and was thought to be an important factor in the 1964 outbreak (McDougle et al. 1965; Vaught et al. 1967). Late fall flooding followed by winter drought, which resulted in a decrease in the number and size of water areas and the concentration of waterfowl, was associated with the loss of an estimated 37,000 waterfowl in California in 1970-71 (Rosen 1972). High bird densities were cited as a factor in avian cholera outbreaks among nesting common eiders (Korschgen et al. 1978). Low water conditions and spring storms which delayed migration were cited as factors which may have concentrated waterfowl in Nebraska during the spring of 1975, contributing to an outbreak of avian cholera (Zinkl et al. 1977). However, Rosen (1969) explains that, "... population density is considered important in the transmission of disease per se, but another factor is not the total population of the waterfowl or of any one species, but rather how locally concentrated they are." However, studies relating actual bird densities to either total mortality or mortality rate in migratory waterfowl have not been reported, so the relationship remains unconfirmed.

Estimated waterfowl numbers, densities, total mortalities, and crude mortality rates for the 1980 spring avian cholera outbreak in the Rainwater Basin Area show no consistent patterns between either total waterfowl numbers or densities and either total mortality or crude mortality rate (Table 11). However, these population estimates are based upon numbers present on a single day and, therefore, are not indicative of total waterfowl use on these wetlands during the outbreak, or even the highest numbers present, so crude mortality rates may substantially overestimate the actual mortality rates. The total mortality counts also were cumulative and, along with the mortality rates, would be more meaningful if related to waterfowl use days.

Another major deficiency in understanding the epizootiology of avian cholera in migratory birds is the absence of information relating the occurrence and magnitude of outbreaks to the immune status of the populations involved. The pattern of the recent avian cholera mortalities in migratory waterfowl in Nebraska (an initial severe outbreak in 1975 with 20,000-25,000 deaths, followed by 2 years of reduced losses, 2 more years of low losses, and then another large outbreak in 1980 with 30,677 dead birds collected) is typical of what would be expected with the introduction of a contagious pathogen into a susceptible population. High losses would be expected in the first outbreak, because few individuals would be immune. Losses in subsequent outbreaks would continue at moderate levels until a substantial portion of the population had been exposed, followed by a decline in mortality to a very low level. As the immunity level of the population waned, or as recruitment replaced the immune birds, a susceptible population would again be created, and carriers within the population might then initiate another large outbreak. The 5-year interval between the serious outbreaks in 1975 and 1980 is compatible with the fluctuating immune status which would be expected in a migratory waterfowl population. Fluctuating levels of immunity within migratory bird populations might explain the difficulty of demonstrating consistent relationships between environmental factors and outbreaks, the variations in mortalities from year to year independent of total bird numbers, and variations in mortality rates within species during different outbreaks.

Until the combined relationships of environmental stresses, bird density, subhabitat utilization, and immunity to avian cholera in migratory birds are better understood, an assessment of the impacts of changing habitat conditions on the occurrence and magnitude of outbreaks will necessarily remain conjectural. Nevertheless, certain conclusions regarding avian cholera in migratory birds on the Platte River Study Area are warranted.

It is evident that avian cholera is now established within the migratory waterfowl and crow populations which utilize the study area. Experience with avian cholera in migratory waterfowl in Texas and California (Jensen and Williams 1964; Rosen 1971b), off the coast of Maine (Korschgen et al. 1978), and in the Chesapeake Bay area (Locke et al. 1970; Pursglove et al. 1976) indicates that after a pattern of outbreaks has been established, the disease can be expected to recur. Avian cholera has now occurred in migratory waterfowl and coots in Nebraska in each of the last 6 years.

It can also be assumed that all species of birds within the study area are susceptible to avian cholera including sandhill and whooping cranes, bald eagles, and other raptors (Rosen 1971b; Zinkl et al. 1977b). Exposure will vary among species and be dependent upon their occurrence on outbreak areas, the specific subhabitats occupied, food habits, and level of association with and exposure to infected birds.

With avian cholera established in migratory bird populations utilizing the study area, it can be assumed that habitat changes which would increase the densities of birds or the level of association between flocks and species of birds, or both, will magnify losses or the occurrence of the disease, or both, in different species. Although high bird densities per se do not cause disease outbreaks, high densities may facilitate transmission of contagious pathogens when suitable environmental conditions exist. If shrinkage of the wetland habitat base in the Rainwater Basin Area continues, it will very likely increase the densities of waterfowl on remaining wetlands and increase the potential for transmission during avian cholera outbreaks. Wetland habitat destruction in the Rainwater Basin Area also can be expected to increase the level of association between waterfowl and other species of migratory birds, e.g. whooping cranes, increasing their exposure to avian cholera. If loss of Rainwater Basin wetlands results in major shifts of the waterfowl population to the Platte River, this shift would increase the level of association with the sandhill crane population and increase its exposure to avian cholera. With inadequate flows in the Platte, the potential for high losses would exist on the River.

Loss of approximately two-thirds of the river channel as roosting habitat for sandhill cranes has resulted in high densities of birds on the remaining suitable areas (Fig. 7). Dilution and dispersal of the bacterium varies directly with volume of water passing through the channel, consequently, reduced flows significantly affect exposure even when numbers and distribution of birds do not change. Should continued loss and deterioration of habitat on the Platte River result in the sandhill cranes shifting to the Rainwater Basin Area, their level of association with waterfowl would increase as would their vulnerability to avian cholera.

Whooping crane use of the Rainwater Basin Area has increased in recent years concomitant with a decline in usage of the Platte River as described in a previous section. An indication of the potential hazard was shown in 1975 when nine whooping cranes congregated on a wetland within the epizootic area during the first confirmed avian cholera outbreak on the study area (Zinkl et al. 1977b). In the latter situation, weather prevented the chasing of the cranes from the area to the Platte River until the next day (Zinkl et al. 1977b). If avian cholera were transmitted to sandhill cranes within the Rainwater Basin Area, the risk of exposure of the whooping cranes would increase substantially due to the frequent association of these species on staging areas.

If a reduction in the acreage of harvested corn and other grains occurs, it can be expected to cause increased bird densities and more frequent association of different species on upland feeding sites and wetlands where food is most plentiful. Although water appears to be a major vehicle for transmission of avian cholera in waterfowl (Rosen 1971b), transmission may also occur by contaminated food (Rosen 1971b; Heddleston 1972). Contaminated food could become an important source of infection, especially if large numbers of infected waterfowl were to feed in fields being utilized by sandhill or whooping cranes.

In summary, habitat deterioration along the Platte River, if allowed to proceed, is likely to cause the sandhill crane population to abandon the present staging areas. A shift to wetlands in the Rainwater Basin Area where avian cholera outbreaks have become common in waterfowl could follow. A similar shift appears already to have occurred among whooping cranes and knowledge that sandhill cranes readily occupy similar habitat elsewhere along their migration route, plus evidence that some sandhill crane usage of Basin wetlands has occurred in recent years (Appendix K), adds to the plausibility of this scenario being realized. A serious threat could exist for both cranes and waterfowl if habitat conditions along the Platte deteriorate and flows during spring are reduced until slackwater conditions develop. With the combination of high population densities and high levels of association between populations in a non-flowing channel environment, avian cholera outbreaks likely would involve virtually all species, i.e. waterfowl, cranes, and eagles, with little prospect for control and with mortalities being limited only by the natural course of the epizootic.

P. multocida transmission may be preventable if there is sufficient water in the Platte River to assure a high rate of flushing and dilution and a low density of birds per acre-foot. One alternative is to move the migrant waterfowl from the Rainwater Basin to the river in order to reduce the potential for occurrence of avian cholera losses. However, such management steps should be applied only after research has clearly identified movement patterns of waterfowl within the Basin Area under various habitat conditions to ensure that more serious problems are not created by inadvertently causing infected birds to disperse to disease-free sites. Maintaining adequate flows in the Platte to meet needs of cranes and waterfowl may represent the only viable prospect for controlling migratory bird losses to avian cholera within the study area.


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