DISEASE PREVENTION AND MONITORING IN CAPTIVE-REARED WATERFOWL FOR RELEASE INTO THE WILD
Presented to the
North Carolina Wildlife Commission
May 13, 2004
Prepared by
Gary L. Pearson, D.V.M.
1305 Business Loop East
Jamestown, North Dakota 58401
Introduction
The release of captive-reared waterfowl for sporting purposes has been practiced throughout the world for centuries and it has become increasingly popular in the United States since the 1960s as huntable populations of wild waterfowl have declined in many areas (Reiger, 2001). Although both Federal and State wildlife agencies have participated in the propagation and release of captive-reared waterfowl for research, restoration and/or sporting purposes, concerns have been expressed in recent years about the potential for the release of captive-reared waterfowl to introduce diseases into wild waterfowl populations, increase hybridization with wild waterfowl species whose populations are declining, and skew wild waterfowl population data (U. S. Fish and Wildlife Service, 1993). Because the potential for disease transmission to wild waterfowl has been the primary concern expressed with the release of captive-reared waterfowl (Division of Migratory Bird Management, 2002), the issue merits further examination.
History of the Controversy Over Health Certification of Captive-Reared Waterfowl
The origin of the controversy over health certification of captive-reared waterfowl to be released into the wild can be traced back three decades to the establishment of the U. S. Fish and Wildlife Service’s National Wildlife Health Laboratory in 1974, where, without evidence that captive-reared waterfowl pose a significant threat for introducing diseases into migratory waterfowl populations and without consulting with captive-reared waterfowl interests, the director-designee of the laboratory cited as one of the reasons for selecting the University of Wisconsin for the location of the laboratory:
“It is located close to large cooperative game breeders (Jack Frost and the Max McGraw Foundation) which provides the opportunity for initiating a waterfowl certification program (DVE-free).” ( Anonymous, Undated a)
Four years later, the Service released a “Draft Migratory Bird Disease Contingency Plan,” which called for health certification of all captive-reared waterfowl released into the wild (U. S. Fish and Wildlife Service, 1978). The draft plan, which had originated from the Service’s National Wildlife Health Laboratory (now National Wildlife Health Center [NWHC] and under the U. S. Geological Survey’s Biological Resources Division), generated so much controversy among captive waterfowl producers that the late Jack Frost, founder of the Frost Waterfowl Trust, sought a meeting with Service officials to discuss the plan. As a result of numerous serious deficiencies identified at the January 3, 1979, meeting in Madison, Wisconsin, by such renowned experts as Dr. Louis Leibovitz of the Department of Avian and Aquatic Animal Medicine at Cornell University’s New York State College of Veterinary Medicine, Dr. Delmar Cassidy , Director of USDA’s National Veterinary Services Laboratory, and Dr. Frank Hayes, Director of the Southeastern Cooperative Wildlife Disease Study (Pearson, 1979), the Service asked Dr. Leibovitz to prepare a formal evaluation of the plan.
In his February 20, 1979, review of the Service’s Draft Migratory Bird Disease Contingency Plan, Dr. Leibovitz noted that:
“Apparently, the authors of the plan, with good intentions, attempted to create concepts of prevention and control of migratory bird diseases as a basic premise for their plan.” (Emphasis added)
and:
“In an effort to justify the Plan, many general statements are made as authoritative without the citation of the needed references.”
Regarding the “Preventive Management” portion of the Plan, Dr. Leibovitz said:
“Since the conceptual basis of the Plan is not valid, the preventive management portion contains many misconceptions.” (Emphasis added)
Regarding the Plan’s requirement for the release of “disease-free” captive birds, Dr. Leibovitz pointed out:
“Again, this is a conceptual error of the plan. Totally susceptible birds released into an infected environment would not only be less resistant to disease, but would magnify the problem and the consequences of disease outbreaks. Captive birds that are released, should be made more resistant to disease where possible rather than simply disease free.” (Emphasis added)
Regarding the Plan’s requirement for health certification of captive-reared waterfowl, Dr. Leibovitz noted that:
“The Plan fails to define the needed documentation for such status, the qualifications of the individuals who will make such judgements, and the methodology to be employed to make such an evaluation. Unfortunately, for the diseases selected [duck plague or duck virus enteritis and avian cholera], the sensitivity for the tests employed are not accurate enough to make such judgements possible. Again, the authors of the Plan tried to justify the selection of freedom from specific diseases as a requirement for certification without knowledge of the specific test procedures and the sensitivity of the tests employed…” (Emphasis added)
In summary, Dr. Leibovitz told the Service:
“The Plan, in its present form, is unacceptable.” (Emphasis added)
Dismissing Dr. Leibovitz’s stinging critique of the plan, officials of the National Wildlife Health Center and the Service’s Office of Migratory Bird Management continued to lobby State wildlife agencies to require health certification of captive-reared waterfowl released into the wild, claiming—despite published reports of 19 duck plague outbreaks in the United States where wild waterfowl were identified as the probable source of infection (Pearson, 1994), including the 1973 epizootic at the Lake Andes National Wildlife Refuge in South Dakota where over 100,000 potentially exposed survivors dispersed throughout all four flyways (Friend and Pearson, 1973; Pearson and Cassidy, 1997)—that duck plague was “not an established disease in wild North American waterfowl” (Brand, 1987).
Because of these activities, the controversy continued to build, and in 1982 the Director of the Fish and Wildlife Service appointed a panel of experts to review and report on:
“… the status of DVE [duck virus enteritis or duck plague] in wild waterfowl, benefits or possible problems associated with the use of DVE vaccine in waterfowl released in the wild, and the implications involved in requiring captive-produced waterfowl to be DVE-free before being released into the wild.” (Jantzen, 1982)
In its 1984 report, the Duck Plague (Duck Virus Enteritis) Panel concluded that:
1. The Service should recognize that DVE can no longer be considered an exotic disease among North American waterfowl.
2. Use of vaccine should be allowed in captive-reared waterfowl as a DVE preventive measure.
3. It is virtually impossible to assure that waterfowl removed from an open aquatic rearing area are free of DVE.
4. The Service’s policy of requiring waterfowl released on National Wildlife Refuges to be pathogen-free was unrealistic and if continued it would eliminate the release of captive-reared waterfowl on refuges. (Beard, et al., 1984)
In a June 19, 1984, letter to the chairman of the Duck Plague (Duck Virus Enteritis) Panel, the Acting Director of the Service said:
“We believe the Report reflects a highly professional and objective appraisal of the complex issues associated with DVE.” (Kutkhun, 1984)
Disregarding the conclusions and recommendations of the Service’s Duck Plague (Duck Virus Enteritis) Panel, however, the NWHC continued to maintain that duck plague was not enzootic (established) in migratory waterfowl and that duck plague mortalities in migratory waterfowl were the result of contact with infected non-migratory and captive waterfowl (Brand and Docherty, 1984), and the director of the NWHC continued to lobby the Service’s Office of Migratory Bird Management to press the Flyway Technical Committees and the Flyway Councils to endorse health certification of captive-reared waterfowl intended for release into the wild (Friend, 1989). In November 1991, the director of the NWHC prepared two briefing papers for the Assistant Secretary of the Interior for Fish and Wildlife and Parks on “Potential disease problems related to programs for the release of captive-bred waterfowl” (Anonymous, 1991a) and a “Health Certification Program for Captive-reared Waterfowl Release Activities” (Anonymous, 1991b). That month, he also sent a letter to the Director of the Southeastern Cooperative Wildlife Disease Study requesting assistance in arranging a meeting of State veterinarians from Maryland, Virginia and Delaware to discuss disease surveillance and monitoring for captive-reared waterfowl being released for sporting purposes (Friend, 1991). The meeting summary for the resulting December 11, 1991, “Tri-State Agency Meeting to Discuss Captive-Raised Waterfowl Health Concerns” reported, regarding the “Discussion of the Feasibility of a Health Certification Program for Captive-raised Mallards,” that:
“Diseases that potentially could be addressed in the health certification program included the following: avian cholera, duck plague, avian tuberculosis, duck virus hepatitis, avian influenza, pullorum, and Newcastle disease. Various aspects of testing for these diseases were discussed, and a number of technical problems were recognized in regard to the availability, reliability, and interpretation of tests…” (Anonymous, 1991c)
and:
“In closing the meeting, it was recognized that the data needed to make decisions on numerous technical questions pertaining to duck diseases and a health certification program were lacking.” (Anonymous, 1991c)
Never-the-less, a year and a half later, the Service published a Notice of Intent in the June 1, 1993, Federal Register to review all aspects of regulations pertaining to the release and harvest of captive-reared mallards, and as a basis for the review, the Service noted that released mallards are not required to be “certified disease-free” and it cited duck plague and avian cholera as examples of diseases of particular concern for transmission to wild waterfowl (U. S. Fish and Wildlife Service, 1993). However, because the concerns outlined in the Notice were not substantiated, a 1994 congressional appropriations bill prohibited the Service from expending funds to revise the regulations or promulgate new regulations for captive-reared waterfowl until it had addressed the issues raised in public comments on the Notice and had completed a study of duck release programs and provided it to the Committees on Appropriations.
In 1994, claiming new information, the Service modified its position on the status of duck plague and no longer maintained that it was not enzootic in wild waterfowl, but rather:
“The Service’s current position is that it cannot conclude that duck plague is established as a recurring source of mortality in migratory waterfowl.” (Emphasis added) (Frampton, 1994.) (See also Friend, 1994)
Of course, once a disease becomes enzootic in a host population, it is primarily the virulence of the agent and the susceptibility of the host that determine whether or not it is a recurring source of mortality.
When the Assistant Secretary for Fish and Wildlife and Parks repeatedly failed to respond substantively to requests made under the Freedom of Information Act (5 U.S.C. S. 562, 552A, 1982) for the information upon which this new position regarding the status of duck plague in migratory waterfowl was based, an action was filed in the United States District Court for the Northern District of Texas, Fort Worth Division, on August 24, 1995, petitioning the Court to compel the Department to provide that information (Feare. v. U. S. Department of the Interior, Case No. 4-95CV-662E). However, before the case reached trial, the Department acknowledged in settlement negotiations with the plaintiff that it had no new information to support its position.
Nine years after its 1993 Notice of Intent to review regulations pertaining to the release of captive-reared mallards, on July 10, 2002, the Service’s Division of Migratory Bird Management released a draft “Review of Captive-Reared Mallard Regulations on Shooting Preserves.” The Review stated, in part, that:
“Based upon this review, we believe there is cause for concern and evidence of increased disease transmission… The threat of disease transmission remains the primary concern among nearly all State wildlife agencies, and there is circumstantial evidence of an association between the releases of captive-reared mallards and duck plague outbreaks. These outbreaks appear to occur most frequently in areas where the largest numbers of captive-reared mallards are being released. Also, there is evidence of duck plague vaccine virus from captive-reared mallards spreading to migratory waterfowl in Maryland…” (Division of Migratory Bird Management, 2002)
and it continued to maintain that duck plague has not been shown to be enzootic in free-ranging migratory waterfowl in North America (Division of Migratory Bird Management, 2002).
The Review concluded by proposing:
“That the Service revise regulations in 50 CFR 21.13 to prohibit the release of captive-reared mallards in free-flighted or free-ranging condition and require tower-type releases to maintain control and restrict movements of captive-reared mallards to on-site premises.” (Division of Migratory Bird Management, 2002).
Careful reading of the Division’s review of the threat posed by the release of captive-reared mallards for introducing diseases into migratory waterfowl populations reveals, however, that it is based on unsubstantiated assertions, incomplete and inaccurate information, misinterpretation of the scientific literature, superficial and erroneous interpretation of data, and disregard for prevailing professional opinion (Pearson, 2002). For example, the Review does not cite a single instance where duck plague has been transmitted from captive-reared mallards to migratory waterfowl, let alone any “evidence of increased disease transmission,” and it even acknowledges that:
“Although large numbers of captive-reared mallards have been released in free-ranging condition on shooting preserves on Maryland’s Eastern Shore (primarily in Dorchester County) for over 15 years, a major epizootic event involving wild birds has not been recorded.” (Division of Migratory Bird Management, 2002)
The Review neglects to mention that information from the National Wildlife Health Center’s Quarterly Wildlife Mortality Reports reveals that 23 of the 38 reports of duck plague in non-migratory waterfowl in the Atlantic Flyway in the 15 years from 1987 to 2001 involved only muscovy ducks where the mortalities ranged from one to 100 birds, averaged 23 per episode and constituted 62.5% of the total mortalities for the period. An additional eight episodes involved muscovy ducks and either mallards or pekin ducks where the mortalities averaged 18 birds per episode. Thus, 31 of the 38 reported incidents of duck plague and 79% of the mortalities reported in the Atlantic Flyway during the 15 years from 1987 to 2001 involved muscovy ducks, which are recognized to be more susceptible to lethal duck plague infection in natural epizootics involving mixed species (Hwang et al., 1975), frequently to be the first or only ducks to die in natural epizootics involving mixed species (Newcomb, 1968; Snyder et al., 1973), and to suffer higher mortality rates than other species (Hall and Simmons, 1972; Snyder et al., 1973; Hwang et al., 1975; Hanson and Willis, 1976).
The Review also does not discuss the fact that data from the NWHC’s Quarterly Wildlife Mortality Reports show a total of 14 duck plague events in Maryland since 1987, involving from one to 22 birds each. Thirteen of the outbreaks involved muscovy ducks and three of those also included mallards. One involved 22 mixed avicultural waterfowl. Only one duck plague event has been reported in Maryland in the last decade, and that involved only muscovy ducks.
The Review states that a 1998 NWHC study of waterfowl on the Eastern Shore of Maryland found evidence of duck plague virus shedding in 32 percent of mallards raised in captivity and released for hunting, compared with 8 percent of the free-flying mallards sampled from the surrounding area. However, it neglects to mention that the NWHC study also found that 100 percent of the free-flying waterfowl tested in late May, when virus shedding by duck plague carrier waterfowl is reported to be the highest (Burgess and Yuill, 1983), were found to be shedding duck plague virus (Anonymous, Undated b). Duck plague infected waterfowl have been shown to shed the virus intermittently for at least four years (Burgess et al., 1979), so with 100 percent of the free-flying waterfowl in the area infected and with the high rate of commingling and potential for disease exchange that occurs among captive, feral and migratory waterfowl (Wobeser, 1997), there can be no question that duck plague is enzootic in all waterfowl populations in the area. The Review also neglects to note that the absence of reports of clinical duck plague disease in the face of this high rate of infection demonstrates that the duck plague virus strains circulating in waterfowl populations in the area generally are of low virulence and likely are inducing immunity to duck plague in those waterfowl.
The Review cites no evidence that captive-reared mallards in the Chesapeake Bay area of Maryland were the source of either the low-virulence field strains of duck plague virus or the duck plague vaccine virus found in wild waterfowl in the area and it cites no evidence that it was not feral or wild waterfowl that transmitted the viruses to the captive-reared mallards. For example, the NWHC study did not examine migratory waterfowl but it found that 100 percent of the free-flying non-migratory waterfowl in the area were positive for duck plague in mid-May (Anonymous, Undated b), so free-flying non-migratory waterfowl would be prime candidates for transmitting low-virulence duck plague viruses to both captive-reared mallards and migratory waterfowl. Duck plague vaccine is not generally approved for use in captive-reared waterfowl but it is commonly used in commercial waterfowl (Sandhu and Liebovitz, 1997), so it appears likely that commercial waterfowl, not captive-reared waterfowl, were the original source of the duck plague vaccine virus found in both released captive-reared mallards and wild migratory waterfowl in the area. Both free-flying feral waterfowl and migratory waterfowl commonly commingle with commercial waterfowl flocks (Leibovitz, 1968; Walker et al., 1969)
Finally, the Review does not address how it would be possible to produce and release captive-reared mallards in the area without their being exposed to duck plague viruses from feral and migratory waterfowl, and it cites no evidence that the duck plague viruses found in captive-reared mallards cause disease in captive, feral or wild waterfowl.
After considering the public comments received on the Division’s review, the Fish and Wildlife Service subsequently determined that the concern that the release of captive-reared mallards on shooting preserves poses a significant threat for introducing diseases into migratory waterfowl populations is not supported by the available scientific evidence.
Deficiencies of Health Certification Proposals for Captive-Reared Waterfowl
A review of the various proposals for health certification of captive-reared waterfowl for release into the wild developed by the Service reveals that they all are based upon and perpetuate the same deficiencies that Dr. Leibovitz identified in the Service’s 1978 Draft Migratory Bird Disease Contingency Plan 25 years ago, plus several others (Pearson, 1993, 2002).
• They attempt to create concepts of prevention and control of migratory bird diseases without adequate scientific foundation.
• They make statements as authoritative without citation of substantiating scientific data.
• They are based on broad generalizations that frequently either are erroneous or fail to consider important exceptions and qualifications.
• They frequently misinterpret or disregard scientific evidence.
• They fail to consider the significance of the evidence that most waterfowl diseases are enzootic in commercial, captive domestic, avicultural, free-flying feral and wild migratory waterfowl populations.
• They fail to recognize that migratory waterfowl routinely commingle with commercial, captive domestic, avicultural and free-flying feral waterfowl throughout their semi-annual migrations.
• They fail to consider objectively the relative significance of the potential for captive-reared waterfowl to introduce diseases into migratory waterfowl populations, compared with the potential for disease introductions resulting form the commingling of migratory waterfowl with commercial, captive domestic, avicultural, free-flying feral and other migratory waterfowl during their semi-annual transcontinental migrations.
• They fail to consider objectively the impacts on migratory waterfowl populations of the diseases for which health certification of captive-reared waterfowl is proposed, compared with other causes of mortality, ranging from random wire-strikes to the estimated 25-30 percent hunter crippling loss (5,000,000-6,000,000 per year in a continental waterfowl population of 80,000,000).
• They fail to evaluate objectively the actual effectiveness of proposed health certification programs in reducing mortalities in migratory waterfowl populations.
• They fail to consider the technical limitations, the reliability, the availability and the costs of current laboratory tests for identifying waterfowl infected with pathogenic microorganisms.
• A major deficiency of the proposals for health certification of captive-reared waterfowl that have appeared over the last quarter of a century has been the failure to involve those who will be most affected by the regulations in a meaningful way to develop realistic, reasonable and effective disease prevention programs. This unilateral approach to health certification of captive-reared waterfowl has led to polarization of the issue and antagonism between wildlife agencies and captive waterfowl interests.
Diseases of Concern in Migratory Waterfowl
More than 70 different diseases or potential disease conditions are recognized in wild migratory waterfowl, but three—lead poisoning, botulism and avian cholera—account for the greatest reported mortalities (Wobeser, 1997). A fourth disease—duck plague (duck virus enteritis, or DVE)—is of concern to many waterfowl managers despite the rare occurrence of epizootic mortalities in migratory waterfowl (Wobeser, 1997). Two other disease agents—highly pathogenic avian influenza viruses and exotic Newcastle disease viruses—are of increasing concern to the domestic poultry industry.
Lead Poisoning
Lead poisoning in migratory waterfowl most commonly results from the ingestion of spent lead shot pellets found in the bottom of marshes and ponds in waterfowl hunting areas (Wobeser, 1997). Prior to the 1991 U. S. ban on the use of lead shot in waterfowl hunting, from two to three percent of the fall waterfowl population (1,600,000 to 2,400,000 waterfowl in a population of 80,000,000) was estimated to die annually from lead poisoning in the United States (Wobeser, 1997), and losses continue today (Friend, 1999a). However, because lead poisoning is not a contagious disease, there is no risk of captive-reared waterfowl introducing it into wild waterfowl populations.
Botulism
Botulism is reported to have killed millions of migratory waterfowl in California and Utah in the early 20th century, and eight major outbreaks with estimated mortalities ranging from 50,000 to 5,000,000 have been reported in the U. S. and Canada since 1950 (Rocke and Friend, 1999). Botulism results from the ingestion of a toxin produced by the bacterium, Clostridium botulinum (usually Type C), which may develop during warm summer weather in any decaying animal protein in wetlands, including dead aquatic invertebrates, and it may concentrate in maggots that have fed on decaying carcasses of birds or fish (Wobeser, 1997). C. botulinum is widely dispersed in the environment and botulism is not a contagious disease (Wobeser, 1997), so there is no risk of captive-reared waterfowl introducing botulism into wild waterfowl populations.
Avian Cholera
Avian cholera is a contagious disease of birds caused by pathogenic strains of the bacterium, Pasteurella multocida (Wobeser, 1997). Water contaminated with excretions of infected birds appears to be an important mode of transmission of avain cholera in waterfowl (Wobeser, 1997). Chronically infected carriers of pathogenic strains of P. multocida are believed to maintain the disease in bird populations and to be responsible for the initiation of epizootics when conditions are favorable (Botzler, 1991;Wobeser, 1997). Although avian cholera was not reported in migratory waterfowl in North America until 1944 when it was diagnosed in wild ducks in conjunction with an outbreak in domestic poultry in Texas (Quortup et al., 1946), the disease likely has been present in North American wild waterfowl populations since at least the early 20th century (Jensen and Price, 1987). Since 1944, avian cholera epizootics have occurred periodically in migratory waterfowl from coast to coast in the U. S. and Canada, with mortalities estimated as high as 88,000 birds (Montgomery, et al., 1979; Friend, 1999b). Consequently, avian cholera is widely accepted as being enzootic in migratory waterfowl (Botzler, 1991; Wobeser, 1997).
Although there is no evidence that captive-reared waterfowl are an important source of avian cholera in migratory waterfowl, it is instructive to consider the impacts of the disease on wild waterfowl populations. It is believed that the introduction of avian cholera into susceptible waterfowl frequently results in only a few deaths which are not detected, but under conditions favorable for transmission, large epizootics may occasionally occur (Botzler, 1991). Although avian cholera epizootics killing 60,000-80,000 wild waterfowl have been reported, mortalities exceeding 100,000 apparently are rare (Wobeser, 1997; Friend, 1999b). Major avian cholera epizootics do not occur every year in migratory waterfowl, but the loss of 100,000 waterfowl would be equivalent to 0.25 percent of the total annual mortality in a continental population of 80,000,000 waterfowl.
Duck Plague (Duck Virus Enteritis, DVE)
Duck plague is a contagious viral disease that affects only waterfowl (ducks, geese and swans (Wobeser, 1997). Water appears to be the natural means of transmission of duck plague virus from infected to susceptible waterfowl (Sandhu and Leibovitz, 1977). Chronically infected carriers have been shown to shed virus intermittently for at least four years (Burgess, et al., 1979; Burgess and Yuill, 1983).
Duck plague was first diagnosed on North America in commercial pekin ducks on Long Island, New York, in 1967 (Leibovitz and Hwang, 1968), but it soon was reported in captive avicultural, free-flying feral and free-flying wild waterfowl in the area (Liebovitz, 1968; Walker et al., 1969). However, Leibovitz later realized that he had seen classic lesions of duck plague in waterfowl from Pennsylvania in 1956 (Pearson, 2001).
In 1973, an epizootic of duck plague killed an estimated 42,500 migratory waterfowl, primarily mallards, out of a population of 163,500 waterfowl wintering on the Lake Andes National Wildlife Refuge and nearby Missouri River in South Dakota (Pearson and Cassidy, 1997). Sampling of waterfowl collected during the epizootic showed that between 13 and 31 percent of the survivors had antibody to duck plague virus, indicating that they had been exposed to the virus and likely became carriers (Pearson and Cassidy, 1997). Band returns from waterfowl banded at the refuge in previous years showed that mallards from Lake Andes disperse to 26 states and four Canadian provinces in all four flyways (Pearson and Cassidy, 1997).
In a May 5, 1978, letter to the Director of the U. S. Fish and Wildlife Service, the Administrator of USDA’s Animal and Plant Health Inspection Service pointed out that:
“Experts throughout the United States agree that duck plague is an established pathogen in free-flying waterfowl.” (Mulhern, 1978)
However, despite the massive infusion of duck plague carriers into wild waterfowl populations across the continent from Lake Andes in 1973, the only epizootic reported in migratory waterfowl since then occurred in 1994 on the Finger Lakes in New York, where an estimated 1,200 waterfowl died out of a population of about 50,000 (Wobeser, 1997).
Both the preponderance of the scientific evidence (Friend and Pearson, 1973; Pearson, 1994, 2002; Pearson and Cassidy, 1997; Anonymous, Undated b; Division of Migratory Bird Management, 2002) and prevailing professional opinion (Mulhern, 1978; Beard et al., 1984; Wobeser, 1997) support the conclusion that duck plague is enzootic in North American migratory waterfowl populations.
An average of four duck plague outbreaks with total mortalities averaging 39 birds per year were reported in non-migratory waterfowl from 1967 through 1995, and the total reported losses of migratory waterfowl from duck plague since 1967 have been approximately 45,000 birds (Converse and Kidd, 2001). To put this into perspective, the total reported losses of migratory waterfowl from duck plague over the past 37 years are equivalent to about 0.1 percent of the total annual mortality in a continental population of 80,000,000 ducks.
Avian Influenza
Avian influenza is a contagious viral disease of wild and domestic birds (Swayne and Halvorson, 2003). Transmission occurs through direct contact between infected and susceptible birds, inhalation of aerosol droplets from the respiratory tracts of infected birds, and exposure to contaminated environments (Swayne and Halvorson, 2003). Water is a major vehicle of AI virus transmission in waterfowl and other water birds (Wobeser, 1997). Infected ducks have been shown to excrete AI virus for up to 30 days, chickens for up to 36 days and turkeys for up to 72 days (Swayne and Halvorson, 2003). The disease appears to be maintained in bird populations by continual low level transmission (Wobser, 1997).
Avian influenza viruses have worldwide distribution in birds, but the most frequent source of AI viruses has been free-flying aquatic birds, particularly waterfowl and shorebirds, gulls, terns and auks, which are believed to be the genetic reservoir of all AI viruses (Swayne and Halvorson, 2003). Avian influenza viruses have been isolated from all 11 North American species of dabbling ducks, especially mallards where up to 60 percent of the juvenile birds may be infected in late summer prior to the fall migration (Swayne and Halvorson, 2003). Despite the high rates of infection in wild ducks and other waterbirds, AI viruses rarely produce clinical signs in wild waterfowl (Wobeser, 1997) or other wild birds (Swayne and Halvorson, 2003). Although AI viruses are of little significance in wild waterfowl, certain highly pathogenic strains can have substantial impacts on the domestic poultry industry, and these are of concern to animal health regulatory agencies (Swayne and Halvorson, 2003). In addition, there is public health concern over the potential for the transfer of AI virus genetic material or even whole AI viruses from birds directly to humans, or from birds to swine where new strains may develop with the ability to infect humans (Swayne and Halvorson, 2003).
All avian influenza viruses are Type A, while Types B and C occur in humans and rarely in seals and pigs but not in birds (Swayne and Halvorson, 2003). Influenza viruses are further subtyped according to their hemagglutinin (HA) and neuraminidase (NA) surface antigens (Swayne and Halvorson, 2003). Currently, 15 HA and 9 NA subtypes of AI viruses are recognized and they may occur in any combination (Swayne and Halvorson, 2003). Avian influenza viruses are further grouped according to their pathogenicity as highly pathogenic (HP) or non-highly/moderately pathogenic (MP) (Swayne and Halvorson, 2003).
The epizootiology of avian influenza viruses is further complicated by the range of pathogenicity that occurs with the different subtypes and in different species. All highly-pathogenic AI viruses are subtype H5 or H7, but not all subtype H5 or H7 AI viruses are highly pathogenic, and there is evidence that HP AI viruses can emerge from MP AI outbreaks (Swayne and Halrovsron, 2003). In addition, pathogenicity may vary with the species of host, and AI viruses that are highly pathogenic in chickens and turkeys generally produce few clinical signs in wild birds and domestic ducks (Swayne and Halvorson, 2003). No HP AI viruses have been isolated from wild ducks and all of the AI viruses isolated from wild ducks are MP (Swayne and Halvorson, 2003). The introduction of MP AI viruses from wild ducks may or may not cause clinical disease in turkeys (Swayne and Halvorson, 2003).
From the perspective of wild waterfowl, AI viruses already are widespread in migratory waterfowl populations but do not cause recognized clinical disease or morality (Wobeser, 1997). However, there is concern about wild waterfowl serving as a reservoir of AI viruses or genetic material which could emerge to infect other species (Wobeser, 1997). If captive-reared waterfowl are not infected with MP AI viruses from visiting feral or wild waterfowl before they are released, they almost certainly will be infected after they are released. The principal concern with captive-reared waterfowl, therefore, would be if they were to become infected while in captivity with HP H5 or H7 AI viruses from domestic chickens or turkeys, and then transmit those viruses to other domestic poultry in areas where they are released. This is the same concern, however, that exits with the movement of domestic chickens and turkeys. Of course, if captive-reared waterfowl were being exposed to HP AI viruses from domestic poultry, that would mean mortalities would be occurring in domestic chickens and turkeys and the area would be under Federal and State quarantine so movement of birds from the area would be prohibited.
Newcastle Disease
Newcastle disease (ND) is a contagious viral disease of wild and domestic birds (Alexander, 2003). Infection may occur from inhalation of ND virus in aerosolized materials or ingestion of ND virus in feed or water contaminated with feces from infected birds (Alexander, 2003). Experimentally infected mallards were found to shed ND virus for 10-16 weeks, but the duration of virus shedding by naturally infected waterfowl is not known (Wobeser, 1997).
Newcastle disease virus also has worldwide distribution in birds and natural or experimental infections have been reported in 241 species from 27 of the 50 orders of birds (Alexander, 2003). There are very few reports of spontaneous ND in wild birds (Wobeser, 1997), but chickens are highly susceptible and turkeys somewhat less so, and the impact of the disease on the poultry industry globally is enormous (Alexander, 2003).
Newcastle disease viruses vary widely in their pathogenicity both between virus strains and between host species, and they are classified based on their virulence in chickens and their predilection for host tissues (Alexander, 2003). Newcastle disease viruses that are highly virulent in chickens are termed “velogenic,” those that are moderately virulent are termed “mesogenic,” and those that are of low virulence are termed “lentogenic” (Alexander, 2003). Newcastle disease viruses that produce signs and lesions related predominantly to the digestive tract are termed “viscerotropic,” those that produce signs and lesions related predominantly to the nervous system are termed “neurotropic,” and those that produce signs and lesions related predominantly to the respiratory system are termed “pneumotropic” (Wobeser, 1997; Alexander, 2003). A highly pathogenic ND virus producing signs and lesions predominantly in the digestive tracts of chickens would be a velogenic, viscerotropic Newcastle disease virus, or VVND. However, ducks, although readily infected, generally are resistant even to ND viruses that are highly virulent in chickens (Alexander, 2003).
Although it is believed, based on serological studies, that a significant portion of migratory waterfowl in North America regularly becomes infected with ND virus, ND virus isolation rates from migratory waterfowl generally have been low (0.5-2.5 percent) and reports of spontaneous disease in wild waterfowl are rare (Wobeser, 1997). However, outbreaks of velogenic ND have been reported in cormorants and other waterbirds in the U. S. and Canada in 1990, 1992 and 1997 (Docherty and Friend, 1999)
The resistance of waterfowl to ND was demonstrated during the 1972-1973 VVND epizootic in chickens in Southern California. A total of 3,222 wild ducks were collected within the quarantine area during the outbreak, but VVND virus was not isolated from any of them and other ND viruses were isolated from only 14 of the ducks (Pearson and McCann, 1975). Perhaps of even greater significance, VVND virus was isolated from only nine of 1,679 free-ranging semi-domestic and captive domestic ducks sampled during the outbreak, despite the fact that many of the domestic ducks lived in poultry houses with VVND infected chickens and fed on fly larvae in the manure below the chicken cages (Pearson and McCann, 1975). Furthermore, despite non-VVND viruses being widespread in the chickens, other ND viruses were isolated from only 17 of the 1,679 free-ranging semidomestic and captive domestic ducks sampled (Pearson and McCann, 1975).
Because of the economic impacts of highly virulent ND viruses on the domestic poultry industry, animal health regulatory agencies have launched costly programs to eradicate them when they have appeared in this country (Alexander, 2003). Therefore, although lentogenic and mesogenic ND viruses still are widespread in the U. S., velogenic strains are regarded as “exotic” and regulatory efforts are focused on surveillance for and eradication of velogenic strains when they appear, rather than on eradication of all ND viruses. The concept of “exotic” ND viruses is based on the premise that highly pathogenic ND viruses are not normally present in birds in North America, and that outbreaks of virulent ND result from the introduction of velogenic strains of the virus through the importation of infected birds, especially psittacine species, that are somewhat resistant to those virulent ND viruses. However, recent evidence has shown that virulent ND viruses may emerge as a result of mutation from ND viruses of low virulence, so the concept of “exotic” Newcastle disease may change (Alexander, 2003).
There is no evidence that velogenic ND viruses are present in migratory waterfowl and there is no evidence that the lentogenic strains that are present cause clinical disease (Wobeser, 1997). Although mortalities in domestic ducks from ND have been reported, these have been rare events, and ducks are considered generally to be resistant to virulent ND virus strains (Alexander, 2003). But, because ducks may be infected with ND viruses, it is possible for them to become infected through contact with chickens infected with velogenic ND virus stains. However, because the velogenic ND viruses would result in severe mortality in those chickens, the area would be placed under Federal and State quarantine so movement of all birds from the area would be prohibited.
Laboratory Testing of Captive-Reared Waterfowl
A number of factors need to be considered in determining the value of testing for diseases in captive-reared waterfowl for release into the wild. The first is whether the disease in question is contagious; if the disease is not transmitted from bird to bird, there is no point in testing captive-reared waterfowl for the disease even if it is an important cause of mortality in migratory waterfowl. Second is the status of the disease in migratory waterfowl and other wild and domestic species, and the availability of other sources of the disease agent. If a disease already is present in free-flying feral or migratory waterfowl or if other sources of the disease are readily available, then testing of captive-reared waterfowl for the disease is of little value in preventing its occurrence in migratory waterfowl. Third is whether testing is required in other domestic or captive birds in which the disease occurs. If testing is not required in commercial, captive domestic or avicultural waterfowl with which migratory waterfowl commonly associate, there would be little point in testing captive-reared waterfowl for release. Fourth is the type of test procedure employed. Serologic tests detect antibodies developed by animals as a result of exposure to disease agents, either through natural infection or vaccination, but they do not indicate whether the animal currently is actively infected. Serologic test results frequently are expressed as titers, which are the dilution at which positive results occur and they reflect the levels of antibody in the serum. However, it is not uncommon for cross-reactions or non-specific factors to cause false positive or false negative reactions. Isolation of a disease agent from an animal confirms that the animal was infected, but it does not in itself indicate whether the agent isolated was causing clinical disease. For example, it is not uncommon for non-pathogenic strains of disease agents to be isolated from healthy animals or animals that are sick or have died from other causes. Conversely, failure to isolate the agent does not necessarily mean that it was not the cause of the disease.
Four parameters must be considered in evaluating the accuracy and reliability of laboratory tests. Diagnostic sensitivity is a measure of the frequency of positive test results in animals in which the disease is present. A test with high sensitivity will identify a high percentage of the animals that are infected and it will produce few false negative results. Diagnostic specificity is a measure of the frequency of negative test results in animals in which the disease is not present. A test with high specificity will produce few false positive results. The predictive value of a laboratory test refers to the percentages of positive and negative results that are true positives and negatives. Finally, the efficiency of a laboratory test indicates the percentages of all animals that are correctly classified by the test results as either having or not having the disease in question. All of these parameters need to be established and validated for a laboratory test before its reliability and accuracy can be evaluated objectively.
Finally, the tests procedures and interpretations should be standardized and approved by animal health agencies and organizations and the tests should be generally available from diagnostic laboratories and not limited to experimental or research applications.
Lead Poisoning
Because lead poisoning is not a contagious disease, laboratory testing of captive-reared waterfowl is not an issue.
Botulism
Because botulism is not a contagious disease, laboratory testing of captive-reared waterfowl is not an issue.
Avian Cholera
Status
Avian cholera is a contagious disease of birds caused by the bacterium Pasteurella multocida. P. multocida is generally recognized already to be enzootic in migratory waterfowl (Botzler, 1991; Wobeser, 1997). Natural P. multocida infections have been reported in over 100 species of birds (Botzler, 1991) as well as in a number of species of domestic and wild mammals (Glisson et al., 2003), so many potential sources of infection besides captive-reared waterfowl exist (Botzler, 1991).
Serology
Serologic tests are of no value in identifying carriers of pathogenic P. multocida (Glisson et al., 2003).
Bacterial isolation
Sensitivity – P. multocida is readily isolated by standard bacteriologic procedures from birds that die of acute avian cholera and the isolates may be typed by several methods, including serology, phage sensitivity, Multi-Locus Enzyme Electophoresis and polymerase chain reaction (Glisson et al., 2003). However, carriers of virulent strains of P. multocida can be extremely difficult to identify (Wobeser, 1997).
Specificity - The pathogenicity of different stains of P. multocida can be highly variable (Wobeser, 1997), so the isolation of P. multocida without evidence of pathogenicity is of questionable significance.
Availability: Procedures for primary isolation of P. multocida are widely
available in veterinary diagnostic laboratories across the country.
Comment: Avian cholera is a contagious disease that already is enzootic in migratory waterfowl populations with numerous potential sources of the causative agent in captive, feral and wild birds and mammals. In addition, laboratory testing for virulent stains of the causative agent is fraught with problems that render it of little value in identifying carriers of the disease in captive-reared waterfowl. Testing for P.multocida is not required for domestic poultry under the National Poultry Improvement Plan or by state animal health regulatory agencies.
Duck Plague (Duck Virus Enteritis, DVE)
Status
Duck plague is a contagious viral disease of ducks, geese and swans (Wobeser, 1997). The preponderance of the scientific evidence (Friend and Pearson, 1973; Pearson, 1994; 2002, Pearson and Cassidy, 1997; Anonymous, Undated b; Division of Migratory Bird Management, 2002) and prevailing scientific opinion (Mulhern, 1978; Beard et al., 1984; Wobeser, 1997) support the conclusion that duck plague is enzootic in all classes of waterfowl in North America, including commercial, captive domestic, avicultural, free-flying feral and wild migratory waterfowl.
Serology
Virus neutralization titers can be used to demonstrate the progress of duck plague within captive waterfowl flocks (Sandhu and Shawky, 2003), but because infected waterfowl may remain healthy, shed large quantities of virus and yet have no detectable serum neutralizing antibodies, serology is not reliable in identifying sub-clinical infections or carrier waterfowl (Wobeser, 1997) (Burgess and Yuill, 1983).
Virus Isolation
A presumptive diagnosis of duck plague can be made on the basis of gross and histopathologic lesions but confirmation of the diagnosis is based on isolation and identification of the virus. Primary isolation of duck plague virus from birds requires inoculation of specimens into 1-day-old muscovy or pekin ducklings, 9-14-day-old embryonated duck eggs, or duck embryo fibroblast, liver or kidney cell tissue cultures (Wobeser, 1997; Sandhu and Shawky, 2003).
Sensitivity: Although virus isolation procedures are useful in confirming active duck plague infections, they are less reliable in detecting healthy carriers and latent infections (Wobeser, 1997; Pearson and Cassidy, 1997). For example, in the 1998 study by the National Wildlife Health Center of non-migratory waterfowl in the Chesapeake Bay area of Maryland, duck plague virus was not isolated from any of 366 samples tested, despite the demonstration of high levels of infection by other methods (Anonymous, Undated b). As a test for captive-reared waterfowl, virus isolation has a moderately high level of sensitivity in diagnosing duck plague in birds showing clinical signs, but it has a low degree of sensitivity in detecting carriers and latent infections from oral or cloacal swabs (Wobeser, 1997).
Specificity: Because different strains of duck plague virus can vary in pathogenicity (Wobeser, 1997) and a naturally occurring non-pathogenic stain (Lin et al., 1984) and even the vaccine strain (Division of Migratory Bird Management, 2002) have been identified in free-flying waterfowl, it is necessary to verify the pathogenicity of duck plague viruses that are isolated in order to evaluate their significance.
Availability: Because primary isolation of duck plague virus must be done either
in young ducklings or embryonated duck eggs that have limited seasonal availability or
in duck cell tissue culture systems that are not routinely maintained by most diagnostic
laboratories, the test generally is available only in laboratories that routinely process
waterfowl specimens.
Molecular Techniques: A polymerase chain reaction (PCR) assay has been developed for the detection of duck plague virus DNA in tissues of infected ducks or cell cultures (Sandhu and Shawky, 2003).
Sensitivity: The PCR appears to be substantially more sensitive in detecting healthy carrier waterfowl that are actively shedding duck plague virus than either serological or standard virus isolation procedures (Anonymous, Undated b). For example, in the 1998 study by the National Wildlife Health Center of duck plague in non-migratory waterfowl in the Chesapeake Bay area of Maryland, 100 percent of the free-flying waterfowl tested in late May were found to be positive by the PCR test, compared with 67 percent found to be positive by serology and zero percent found to be positive by standard virus isolation procedures (Anonymous, Undated b). However, by mid-June, the rate of detection of duck plague virus in free-flying waterfowl by PRC had dropped to only 26 percent (Anonymous, Undated b). Duck plague carrier waterfowl may shed virus intermittently for at least four years (Burgess et al., 1979), but the highest levels of virus shedding occur in May and then subside by June (Burgess and Yuill, 1983). This suggests that the PCR has high sensitivity in detecting duck plague virus in cloacal swabs from carriers that are actively shedding virus, but that it has very low sensitivity in detecting duck plague virus in cloacal swabs from ducks with latent infections
Specificity: The PCR assay appears to be highly specific for duck plague virus, but it does not differentiate between pathogenic and non-pathogenic strains of the virus. However, it can be combined with restriction endonuclease analysis to differentiate duck plague virus strains (Sandhu and Shawky, 2003)
Availability: The PCR assay has only recently been adapted for detection of duck plague virus (Plummer et al., 1998; Hansen et al., 2000), and it is not readily available for routine testing of captive-reared waterfowl.
Comment: With (1) duck plague enzootic in all classes of waterfowl, including captive domestic and commercial waterfowl, avicultural waterfowl, free-flying feral waterfowl and migratory waterfowl (Beard et al., 1984, Wobeser, 1997), (2) evidence of non-pathogenic duck plague virus strains occurring in captive and free-flying waterfowl (Lin et al., 1984; Anonymous, Undated b; Division of Migratory Bird Management, 2002), (3) the infrequent occurrence and low levels of clinical disease reported in captive domestic, avicultural and free-flying feral waterfowl (Converse and Kidd, 2001), (4) the rarity of reports of losses in migratory waterfowl (Wobeser, 1997; Converse and Kidd, 2001), (5) the absence of evidence of significant impacts on migratory waterfowl populations (Pearson and Cassidy, 1997), (6) the unreliability of available laboratory tests for identifying latent infections, (7) the limited availability of testing capability, and (8) the absence of requirements for testing of other classes of waterfowl, routine testing of captive-reared waterfowl for release in the absence of evidence of clinical disease has limited value or justification.
Avian Influenza
Status
Avian influenza (AI) occurs worldwide in birds with the most frequent isolations reported from waterfowl and other waterbirds, which are considered to be the genetic reservoir of all AI viruses (Swayne and Halvorson, 2003). Despite the high levels of infection of migratory waterfowl with AI viruses, the AI viruses isolated from migratory waterfowl all have been moderately pathogenic strains that produce no signs of disease in migratory waterfowl and rarely produce disease in domestic poultry (Wobeser, 1997; Swayne and Halvorson, 2003). Furthermore, AI virus strains that are highly pathogenic for domestic chickens rarely produce clinical signs in waterfowl (Swayne and Halvorson, 2003).
Serology
Serologic diagnosis of avian influenza is complicated by the great diversity of virus surface antigens and this is further compounded by the variability of the antibody response in different species, with ducks frequently having no detectable antibodies even when they are actively excreting virus (Wobeser, 1997; Swayne and Halvorson, 2003). Therefore, the diagnosis of avian influenza is based on the isolation and identification of AI virus or the direct detection of AI viral proteins or nucleic acid (Swayne and Halvorson, 2003)
Virus Isolation
Avian influenza virus isolation is performed by inoculating 10-11-day-old chicken embryos and demonstrating chicken erythrocyte hemagglutinating activity in the allantoic fluid of embryos that die between 48 and 72 hours after inoculation (Swayne and Halvorson, 2003). Serological methods are then used to identify and type AI viruses (Swayne and Halvorson, 2003).
Sensitivity: Virus isolation is moderately sensitive and if virus is present in the sample, it generally will grow sufficiently to be detected in the first egg passage (Swayne and Halvorson, 2003).
Specificity: With virus identification and classification to subtype, potentially highly pathogenic H5 and H7 strains can reliably be differentiated from moderately pathogenic strains (Swayne and Halvorson, 2003).
Availability: Avian influenza virus isolation is widely available in veterinary diagnostic laboratories.
Molecular Techniques
The direct detection of avian influenza proteins or genetic material is not routinely used for diagnosis at this time (Swayne and Halvorson, 2003). However, a polymerase chain reaction test has been developed that may be significantly more sensitive than traditional virus isolation procedures (Swayne and Halvorson, 2003)
Comment: Because of the potential impacts of highly pathogenic AI viruses on the domestic poultry industry, consideration is being given to incorporating a voluntary national H5/H7 low pathogenicity avian influenza surveillance program for commercial poultry in the National Poultry Improvement Plan. Although avian influenza viruses are widespread but do not cause clinical disease in migratory waterfowl, although captive-reared waterfowl pose little risk for introducing highly pathogenic AI viruses into migratory waterfowl (Wobeser, 1997; Swayne and Halvorson, 2003), and although H5 and H7 AI viruses have not been reported in migratory waterfowl (Swayne and Halvorson, 2003), should AI testing be required for domestic waterfowl at some time in the future, those same testing requirements would be applied to captive-reared waterfowl. Currently, however, there is little rationale for requiring testing of captive-reared waterfowl for AI in the absence of evidence of the presence of highly pathogenic AI viruses in domestic poultry in the area.
Newcastle Disease
Status
Newcastle disease (ND) virus has worldwide distribution in domestic, avicultural and wild birds, but there is no evidence that highly virulent ND viruses are present in migratory waterfowl or that the low virulence strains that are present cause clinical disease (Wobeser, 1997). There are few reports of spontaneous Newcastle disease in wild birds, but domestic chickens are highly susceptible and the impacts of the disease on the domestic poultry industry are very substantial (Alexander, 2003). Although ducks are can be infected with Newcastle disease virus and mortalities have been reported in domestic ducks, ducks are generally considered to be resistant even to virulent ND virus strains (Alexander, 2003).
Serology
Because Newcastle disease viruses are widespread in wild and domestic birds, and the presence of antibodies to ND virus provides little information on the infecting strain of the virus, serologic testing is of limited diagnostic value (Alexander, 2003).
Virus Isolation
Virus isolation with characterization of the virus currently is the accepted method of diagnosing Newcastle disease (Alexander, 2003). Although virulent ND viruses can be isolated in cell culture systems, inoculation of 9-10-day-old embryonated chicken eggs is the standard method, followed by identification and pathogenicity testing of the isolates (Alexander, 2003)
Sensitivity: Virus isolation in embryonated chicken eggs from specific-pathogen-free or at least ND free flocks is considered to be an extremely sensitive technique for isolating ND viruses (Alexander, 2003).
Specificity: With identification of the virus isolates and characterization by pathogenicity testing, virus isolation has a high degree of specificity in identifying and classifying Newcastle disease viruses (Alexander, 2003).
Availability: Newcastle disease virus isolation is widely available in veterinary
diagnostic laboratories.
Molecular Techniques
The polymerase chain reaction and reverse transcription have been used in conjunction with nucleotide sequencing for epidemiological studies of Newcastle disease, but other technical limitations diminish the efficacy of molecular techniques as a general diagnostic procedure for Newcastle disease (Alexander, 20003).
Comment: Because Newcastle disease viruses are widespread in domestic and wild birds, occur in strains of varying pathogenicity, and rarely cause clinical disease in waterfowl (Wobeser, 1997; Alexander, 2003), and because routine Newcastle disease testing of domestic poultry, including ducks, is not required, testing of captive-reared waterfowl in the absence of evidence of clinical disease in domestic poultry in the area has limited value or justification.
Principles of Proactive Disease Prevention and Monitoring in Captive-Reared Waterfowl
With the inherent problems and technical limitations of laboratory testing, a more comprehensive approach involving disease prevention and monitoring would more reliably minimize any risk that the release of captive-reared waterfowl might pose for introducing diseases into migratory waterfowl populations.
Because the major disease agents of concern in migratory waterfowl already are enzootic in captive domestic, avicultural, free-flying feral and migratory waterfowl (Wobeser, 1997), the primary concern is preventing and monitoring the introduction of virulent strains of those disease agents into captive-reared waterfowl in order to protect both captive-reared waterfowl flocks and migratory waterfowl when those captive-reared waterfowl are released. However, compared with domestic animals, disease prevention and monitoring in captive-reared waterfowl is complicated by the greater potential for exchange of diseases among captive domestic, avicultrual, free-flying feral and migratory flocks as a result of their close phylogenic relationship, the high mobility of free-flying feral and wild waterfowl and the frequent commingling of the various classes of waterfowl on open bodies of water (Wobeser, 1997). Although the details of disease prevention and monitoring programs for captive-reared waterfowl necessarily must be tailored to specific situations, the following basic elements should be included.
Isolation
The first element of isolation involves preventing the introduction of virulent disease agents into captive-reared waterfowl flocks through human activities, such as the location of facilities on bodies of water shared with other domestic or captive waterfowl or contaminated with domestic poultry wastes, the addition of birds from infected flocks, and traffic of contaminated personnel and equipment from infected flocks. The second element of isolation involves raising young waterfowl in separate groups and separate from the breeder flock, with thorough cleaning and disinfection of the facilities between the groups. The third element of isolation involves preventing contact, especially on open bodies of water, between captive-reared waterfowl and free-flying feral and wild waterfowl during the rearing period in order to avoid the introduction of virulent pathogens prior to their release.
Records
A system should be established for maintaining accurate and detailed records of production and mortality in the captive-reared waterfowl flock. This will assist in identifying the occurrence of disease problems and determining when and where they started and how they are progressing. In addition, detailed records should be maintained on all additions to and dispersals from the flock to facilitate tracing of any disease problems that might develop.
Monitoring
Monitoring involves the periodic submission of “routine” mortalities and the immediate submission of any unusual mortalities in the captive-reared waterfowl flock for diagnostic examination. The periodic submission of what appear to be routine mortalities may disclose non-epizootic but chronic disease problems that can be minimized by changes in management and it may also provide early evidence of the presence of virulent disease agents before the problem becomes serious. Of course, the occurrence of unusual mortalities is a signal that a significant disease problem may already have developed in the flock.
In some cases, monitoring could also include the use of susceptible sentinel birds to enhance detection of the presence of virulent disease agents in flocks of more resistant species.
Immunization
Where available, vaccination of captive-reared waterfowl should be utilized to prevent infection with virulent disease agents while they are in captivity and to avoid the release of susceptible waterfowl that are vulnerable to exposure to virulent disease agents from free-flying feral and wild waterfowl after release (Leibovitz, 1979). It should be noted specifically in this context that the U. S. Fish and Wildlife Service’s Duck Plague (Duck Virus Enteritis) Panel recommended in its 1984 report that use of the attenuated duck plague vaccine “should be allowed in captive waterfowl as a DVE preventative measure” (Beard et al., 1984).
Development of a Formal Disease Prevention and Monitoring Program
Consideration should be given to the development of a formal disease prevention and monitoring program for captive-reared waterfowl by a panel composed of independent waterfowl disease experts and captive-reared waterfowl interests. Because of the level of polarization and distrust that has developed between captive-reared waterfowl interests and Federal and State wildlife agencies as a result of scientifically unsound health certification requirements for released captive-reared waterfowl proposed by the U. S. Fish and Wildlife Service over the past 25 years, implementation of such a program will necessitate the re-establishment of trust and cooperation between the groups. In order to overcome these serious obstacles, the program (1) should be voluntary, with participation prompted by the resulting benefits to captive-reared waterfowl interests, and (2) it should be administered by a non-governmental body with an advisory board composed of independent waterfowl disease experts and representatives of the various captive-reared waterfowl interests involved.
REFERENCES
Alexander, D. J. Newcastle disease. pp. 64-87 In Diseases of Poultry. 11th Ed. Y. M. Saif, ed.
Iowa State University Press, Ames, Iowa. 1231 pp.
Anonymous. Undated a. Statement on the establishment of a fish and wildlife health laboratory.
2 pp. Attachment to June 10, 1974, memorandum from Director, Bureau of Sport
Fisheries and Wildlife, through Assistant Secretary for Fish and Wildlife and Parks, to
Assistant Secretary – Management on Establishment of Fish and Wildlife Health
Laboratory. 2 pp.
Anonymous. Undated b. Final report: the occurrence of duck plague virus in non-migratory
waterfowl in the Chesapeake Bay area of Maryland. U. S. Geological Survey,
Biological Resources Division, National Wildlife health Center, Madison, Wisconsin.
14 pp.
Anonymous. 1991a. Potential disease problems related to programs for the release of captive-
reared waterfowl. Briefing statement prepared for Assistant Secretary Hayden. Program
contact: Milton Friend, Director, National Wildlife Health Research Center, Madison,
Wisconsin. November 19. 2 pp.
Anonymous. 1991b. Health certification program for captive-reared waterfowl release activities.
Briefing statement prepared for Assistant Secretary Hayden. Program contact: Milton
Friend, Director, National Wildlife Health Research Center, Madison, Wisconsin.
November 19. 2 pp.
Anonymous. 1991c. Meeting summary. Tri-state agency meeting to discuss captive-reared
waterfowl health concerns. Annapolis, Maryland. December 11. 8 pp.
Beard, C. W., G. V. Burger, J. R. Cain, F. E. Kellogg and L. Leibovitz. 1984. Duck Plague
(Duck Virus Enteritis) Panel Report. U. S. Fish and Wildlife Service, Patuxent
Wildlife Research Center, Laurel, Maryland. 15 pp.
Botzler, R. G. 1991. Epizootiology of avian cholera in waterfowl. Journal of Wildlife Diseases
27:367-395.
Brand, C. J. 1987. Duck plague. pp. 117-127 In Field Guide to Wildlife Diseases, General Field
Procedures and Diseases of Migratory Birds. M. Friend, ed. United States Department
of the Interior, Fish and Wildlife Service. Washington, D. C. Resource Publication 167.
225 pp.
Brand, C. J. and D. E. Docherty. 1984. A survey of North American migratory waterfowl for
duck plague (duck virus enteritis) virus. Journal of Wildlife Diseases 20: 261-266.
Burgess, E. C., J. Ossa and T. M. Yuill. 1979. Duck plague: a carrier state in waterfowl. Avian
Diseases 23: 940-949.
Burgess, E. C. and T. M. Yuill. 1983. The influence of seven environmental and physiological
factors on duck plague virus shedding by carrier mallards. Journal of Wildlife Diseases.
19: 77-81.
Converse, K. A. and G. A. Kidd. 2001. Perspectives, duck plague epizootics in the United States,
1995- Journal of Wildlife Diseases 37: 347-357.
Division of Migratory Bird Management. 2002. (Draft) Review of captive-reared mallard
regulations on shooting preserves. U. S. Fish and Wildlife Service, Department of the
Interior. Washington, D. C. 46 pp.
Docherty, D. E. and M. Friend. 1999. Newcastle disease. pp. 175-179 In Field Manual of
Wildlife Diseases, General Field Procedures and Diseases of Birds. M. Friend and
J. C. Franson, eds. U. S. Department of the Interior, U. S. Geological Survey,
Biological Resources Division, National Wildlife Health Center, Madison,
Wisconsin. Information and Technology Report 1999-001. 426 pp.
Friend, M. 1989. Captive-reared waterfowl. Memorandum from Director, National Wildlife
Health Research Center, Madison, Wisconsin, to Acting Chief, Office of Migratory
Bird Management, 2 pp., with attached Health Certification of Captive-Reared
Waterfowl Intended for Release into the Wild. July 5. 3 pp.
Friend, M. 1991. Letter from Director, National Wildlife Health Research Center, Madison,
Wisconsin, to Dr. Victor Nettles, Director, Southeastern Cooperative Wildlife Disease
Study, University of Georgia, Athens, Georgia. November 4. 2 pp.
Friend, M. 1994. Duck plague: A viewpoint on behalf of North American waterfowl (Draft).
Wildlife Disease Association, Waterfowl Disease Symposium. Pacific Grove,
California. 11 pp.
Friend, M. 1999a. Lead. pp. 317-334 In Field Manual of Wildlife Diseases, General Field
Procedures and Diseases of Birds. M. Friend and J. C. Franson, eds. U. S.
Department of the Interior, U. S. Geological Survey, Biological Resources Division,
National Wildlife Health Center, Madison, Wisconsin. Information and Technology
Report 1999-001. 426 pp.
Friend, M. 1999b. Avian cholera. pp. 75-92 In Field Manual of Wildlife Diseases, General
Field Procedures and Diseases of Birds. M. Friend and J. C. Franson, eds. U. S.
Department of the Interior, U. S. Geological Survey, Biological Resources Division,
National Wildlife Health Center, Madison, Wisconsin. Information and Technology
Report 1999-001. 426 pp.
Friend, M. and G. L. Pearson. 1973. Duck plague: the present situation. pp. 315-325 In
Proceedings of the 53rd Annual Conference of the Western Association of State Game
and Fish Commissioners. Salt Lake City, Utah.
Frampton, G. T., Jr. 1994. Letter from Assistant Secretary for Fish and Wildlife and Parks,
Office of the Secretary, U. S. Department of the Interior, Washington, D. C., to J. D.
Hughes, Chairman, Duck Committee, North American Gamebird Association, Inc.,
Hugo, Minnesota. June 22. 2 pp.
Glisson, J. R., C. L. Hofacre and J. P. Christensen. 2002. Fowl cholera. pp. 658-676 In Diseases
of Poultry. 11th Ed. Y. M. Saif, ed. Iowa State University Press, Ames, Iowa. 1231 pp.
Halls, S. A. and J. R. Simmons. 1972. Duck plague (duck virus enteritis) in Britain. The
Veterinary Record 90: 691.
Hansen, W. R., S. W. Nashold, D. E. Docherty, S. E. Brown and D. L. Knudson. 2000.
Diagnosis of duck plague in waterfowl by polymerase chain reaction. Avian Diseases
44: 266-274.
Hanson, H. A. and N. G. Willis. 1976. An outbreak of duck virus enteritis (duck plague) in
Alberta. Journal of Wildlife Diseases 12: 258-262.
Hwang, J., E. T. Mallinson and R. E. Yoxheimer. 1975. Case report – occurrence of duck virus
enteritis (duck plague) in Pennsylvania, 1968-74. Avian Diseases 19: 382-384.
Jantzen, R. A. 1982. Letter from Director, United States Department of the Interior, Fish
and Wildlife Service, Washington, D. C, to Dr. Roy Anderson, President,
Wildlife Disease Association, Ames, Iowa. March 1. 1 p.
Jensen, W. I. and J. I. Price. 1987. The global importance of type C botulism in birds. pp. 33-54
In Avian Botulism: An International Perspective. M. W. Eklund and V. R. Dowell, Jr.,
eds. Charles C. Thomas Publisher, Springfield, Illinois. 405 pp.
Kutkuhn, J. D. 1984. Letter from Acting Director, United States Department of the Interior,
Fish and Wildlife Service, Washington, D. C., top Dr. J. Richard Cain, Poultry Science
Department, Texas A&M University, College Station Texas. 1 p.
Leibovitz, L. 1968. Progress report: duck plague surveillance on American Anseriformes.
Bulletin of the Wildlife Disease Association 4: 87-91.
Leibovitz, L. 1979. Letter from Associate Profession, Department of Avian and Aquatic
Animal Medicine, New York State College of Veterinary Medicine, Cornell University,
Ithaca, New York, to Harvey Nelson, Associate Director, U. S. Department of the
Interior, U. S. Fish and Wildlife Service, Washington, D. C. February 20.
4 pp.
Leibovitz, L. and J. Hwang. 1968. Duck plague on the American Continent. Avian Diseases
12: 361-378.
Lin, W., K. M. Lan, and W. E. Clark. 1984. Isolation of an apathogenic immunogenic strain
of duck enteritis virus from waterfowl in California. Avian Diseases 28: 641-650.
Montgomery, R. D., G. Stein, Jr., V. D. Stotts and F. H. Settle. 1979. The 1978 epornitic of
avian cholera on the Chesapeake Bay. Avian Diseases 24:966-978.
Mulhern, F. J. 1978. Letter from Administrator, U. S. Department of Agriculture, Animal and
Plant Health Inspection Service, Washington, D. C., to Lynn A. Greenwalt, U. S.
Department of the Interior, Fish and Wildlife Service, Washington, D. C. May 5. 2 pp.
Newcomb, S. S. 1968. Duck virus enteritis (duck plague) epizootiology and related
investigations. Journal of the American Veterinary Medical Association 153: 1897-1902.
Pearson, G. L. 1979. U. S. Fish and Wildlife Services Migratory Bird Contingency Plan.
American Pheasant and Waterfowl Society Magazine 79-3: 19-23.
Pearson, G. L. 1993. Comments on the U. S. Fish and Wildlife Service Notice of Intent to
review regulations pertaining to captive-reared waterfowl. Submitted to Director, U. S.
Fish and Wildlife Service, Department of the Interior, Washington, D. C. 24 pp.
Pearson, G. L. 1994. Lake Andes revisited: duck plague in free-flying wild waterfowl. Wildlife
Disease Association, Waterfowl Disease Symposium. Pacific Grove, California. 12 pp.
Pearson, G. L. 2001. Book review: Field Manual of Wildlife Diseases: General Field Procedures
and Diseases of Birds. Journal of Wildlife Diseases 37: 208-211.
Pearson, G. L. 2002. A review of Potential areas of conflict – Disease transmission In (Draft)
Review of Captive-Reared Mallard Regulations on Shooting Preserves, U. S. Fish and
Wildlife Service, Division of Migratory Bird Management. Unpub. 35 pp.
Pearson, G. L. and D. R. Cassidy. 1997. Perspectives on the diagnosis, epizootiology, and
control of the 1973 duck plague epizootic in wild waterfowl at Lake Andes, South
Dakota. Journal of Wildlife Diseases 33: 681-705.
Pearson, G. L. and M. K. McCann. 1975. The role of indigenous wild, semidomestic, and exotic
birds in the epizootiology of velogenic, viscerotropic Newcastle disease in Southern
California, 1972-1973. Journal of the American Veterinary Medical Association 167:
610-614.
Plummer, P. J., T. Alefantis, S. Kaplan, P. O’Connell, S. Shawky and K. A. Schat. 1998.
Detection of duck enteritis virus by polymerase chain reaction. Avian Diseases
42: 554-564.
Quortrup, E. R., F. B. Quees and L. J. Merouka. 1946. An outbreak of pasteurellosis in wild
ducks. Journal of the American Veterinary Medical Association 108: 94-100.
Reiger, G. 2001. History of duck releases and their role in the future of waterfowling.
South Carolina Waterfowl Association Waterfowl & Wetlands. Issue 59: 26-28.
Rocke, T. E. and M. Friend. 1999. Avian botulism. pp. 271-281 In Field Manual of Wildlife
Diseases, General Field Procedures and Diseases of Birds. M. Friend and J. C. Franson,
eds. U. S. Department of the Interior, U. S. Geological Survey, Biological Resources
Division, National Wildlife Health Center, Madison, Wisconsin. Information and
Technology Report 1999-01. 426 pp.
Sandhu, T. S. and L. Leibovitz. 1997. Duck virus enteritis (duck plague). pp. 675-683 In
Diseases of Poultry. 10th Ed. B. W. Calnek, ed. Iowa State University Press, Ames,
Iowa. 1080 pp.
Sandhu, T. S. and S. A. Shawky. 2003. Duck virus enteritis (duck plague). pp. 354-363 In
Diseases of Poultry. 11th Ed. Y. M. Saif, ed. Iowa State University Press, Ames,
Iowa. 1231 pp.
Snyder, S. B., J. G. Fox, L. H. Campbell, K. F. Tam and O. A. Soave. 1973. An epornitic of
duck virus enteritis (duck plague) in California. Journal of the American Veterinary
Medical Association 163: 647-652.
Swayne, D. E. and D. A. Halvorson. 2003. Influenza. pp. 135-160 In Diseases of Poultry. 11th
Ed. Y. M. Saif, ed. Iowa State University Press, Ames, Iowa. 1231 pp.
U. S. Fish and Wildlife Service. 1978. Draft Migratory Bird Disease Contingency Plan.
Department of the Interior, Washington, D. C. 47 pp.
U. S. Fish and Wildlife Service. 1993. Release of captive-reared mallards. Federal Register
58(103): 31247-31249.
Walker, J. W., C. J. Pfow, S. S. Newcomb, W. D. Urban, H. E. Nadler and L. N. Locke. 1969.
Status of duck virus enteritis (duck plague) in the United States. pp. 254-278 In
Proceedings of the 73rd Meeting, United States Animal Health Association, Richmond,
Virginia.
Wobeser, G. A. 1997. Diseases of Wild Waterfowl. 2nd Ed. Plenum Press, New York,
New York. 324 pp.
|
|
|
NCWA
exists to conserve, enhance and perpetuate our waterfowl heritage.
