OVERVIEW
Fish and wildlife are susceptible to naturally occurring and introduced diseases caused by a variety of pathogens, including viruses, bacteria, fungi, prions, and protozoans. Animals exposed to pathogens may exhibit illness or they may show no signs of disease if the pathogen is cleared by the animal’s immune system. In some cases, animals may serve as carriers or reservoirs of the pathogen or may die as a result of the infection. In susceptible individuals and species, disease spreads quickly when large numbers of animals are concentrated. This can occur during migration, in species that live in groups or use colonial nesting or rest sites, during breeding, or when animals are forced into small areas of habitat due to habitat loss and fragmentation or attracted to specific sites when they are fed by people. Emerging and novel diseases can have devastating effects on wildlife, human health, and local economies. Climate change may increase the vulnerability of fish and wildlife to disease by altering ecosystem dynamics, increasing opportunities for disease spread, and raising animals’ stress, potentially making them more susceptible to disease and illness if they become exposed.
Anyone can help to prevent human-caused disease outbreaks by regularly cleaning and sanitizing bird feeders, vaccinating pets, removing invasive species, and providing and managing natural habitat. Licensed Oregon wildlife rehabilitators care for sick or injured wild animals with the goal of returning them to their natural habitat. Rehabilitators often also provide valuable educational information and outreach to the public. In addition, accredited Association of Zoos and Aquariums facilities in Oregon (e.g., Oregon Zoo, Wildlife Safari, Oregon Coast Aquarium) provide valuable public education, outreach, and conservation projects related to the health of Oregon’s fish and wildlife and their native habitats.
Endemic disease is an inherent part of every ecosystem. However, introduced and emerging diseases not only threaten population or ecosystem health but can be very difficult and costly to eradicate once established. The best action to avoid unwanted disease outbreaks is prevention. Oregon’s biologists, veterinarians, and wildlife administrators make every effort to protect the state’s fish and wildlife through surveillance, monitoring, training, response plans, active disease response and mitigation, policy, and regulation. Listed below are the diseases that are of the greatest management or conservation concern or that present significant or recurring health risks to Oregon’s fish and wildlife. This list includes diseases that occur naturally or are endemic in Oregon, as well as diseases that are introduced or emerging. The list is not inclusive of all diseases identified in Oregon fish and wildlife species.
WILDLIFE DISEASES OF MANAGEMENT CONCERN
Table 1. Examples of diseases that pose the greatest management concern or present significant or recurring health risk to Oregon’s wildlife.
| Disease or Disease-Causing Organism | Vulnerable Species | Conditions that Promote Disease Issues | Management Approaches |
|---|---|---|---|
| Ranavirus | All amphibians and reptiles | Conditions that weaken immune response (e.g., UV-B light, pesticides). Movement of infected animals. | Maintain high water quality. Investigate the natural distribution of ranavirus to determine if it is spreading to new areas. Avoid human-caused movement of amphibians and reptiles to new areas. Remove invasive amphibian and reptile species. Follow disinfection protocols for field equipment. |
| Chytrid skin fungus (Batrachochytrium dendrobatidis) | All amphibians, although some species may be more vulnerable | Conditions that weaken immune response (e.g., UV-B light, pesticides). Movement of infected animals. | Maintain high water quality. Investigate the natural distribution of chytrid fungus to determine if it is spreading to new areas. Avoid human-caused movement of amphibians to new areas. Remove invasive amphibian species. Follow disinfection protocols for field equipment. |
| Egg-destroying pathogen (Saprolegnia ferax, a watermold) | All amphibians, although some species may be more vulnerable | Conditions that weaken immune response (e.g., UV-B light, pesticides) | Maintain high water quality. Investigate the role of introduced fish in spread between water bodies. |
| Amphibian deformities (multiple legs and other deformities caused by a trematode, Ribeiroia sp.) | All amphibians, but seen most often in some frog species | High nutrient levels that increase densities of intermediate hosts (snails) | Maintain high water quality. Monitor incidence of amphibian deformities. Avoid human-caused movement of amphibians to new areas. If possible, control habitat nutrient levels (e.g., reduce agricultural runoff) to control intermediate host densities. |
| Emydomyces testavorans associated shell disease | Aquatic native turtles of the Pacific Northwest, primarily the Western Pond turtle | Movement of infected animals. Cause presently unknown but there is an association with the fungus Emydomyces testavorans. Occurrence also highest with captive-reared animals. | Avoid human-caused movement of turtles to new areas. Remove invasive turtles. Continue research to identify cause in PNW turtles and determine population impacts. |
| Avian cholera (caused by the bacterium Pasturella multocida) | Waterfowl most susceptible. In Oregon, snow geese are most often at risk, but the disease can also impact gulls, terns, coots, and crows. | Observed in northeastern and in southern wetlands of the state in winter from concentration of waterfowl during migration. Waterfowl concentrations increase when the amount of open water is reduced (e.g., during drought, freezing temperatures, or due to habitat loss). Freezing temperatures also increase vulnerability by weakening immune systems. | Maintain and restore wetland habitats important for migratory waterfowl. Manage major die-offs through carcass removal and appropriate disposal to reduce local point sources and minimize impacts to populations. |
| Bird feeder diseases (salmonellosis, mycoplasmal conjunctivitis, avian poxvirus, trichomoniasis) | Songbirds. Finch species can be highly impacted. | Concentration of birds at bird feeders. Contaminated feeder surfaces and fecal-contaminated bird food. Bacterial pathogens may be zoonotic. | Conduct outreach regarding prevention methods. Implement frequent sanitation measures at bird feeders or cessation of wild bird feeding. |
| Newcastle virus | Double-crested Cormorants. Many other bird species are at risk. | Occurs in breeding colonies along the Columbia River and Northwest coast. Appears to occur on an every-other-year cycle, typically in odd-numbered years (2013, 2015, etc.) and peaks in the spring-fall at breeding colonies. | Monitor and conduct surveillance of colonies. Work with wildlife rehabilitators to avoid and manage potential disease risk in facilities. |
| West Nile virus (Zoonotic disease passed by mosquito vectors) | Birds in the family Corvidae and sage-grouse, other bird species, some mammals (e.g., squirrels) | Conditions conducive to wet habitats and breeding areas, responding density of vectors, and over-winter survival of competent host mosquito species. | Reduce mosquito breeding areas in urban environments. Follow Centers for Disease Control and Prevention recommendations. Place warning guidance at wetland management areas. |
| Highly pathogenic avian influenza (HPAI) | Naive waterfowl, shorebirds, and raptors are most susceptible to succumbing to disease. Many wild bird species are hosts to low and high path AI strains. Waterfowl and shorebirds are the principal hosts to highly pathogenic (HPAI H5, H7) strains and most responsible for viral spread and distribution. Some strains and genotypes are zoonotic. | Waterfowl, shorebirds, and many wetland wild bird species serve as hosts to most of the 144 strains of the virus. Specific genotypes within highly pathogenic virus strains can have devastating impacts to the poultry industry, dairy cows, other livestock, and human health, in addition to causing death in many wild birds. Poor biosecurity in backyard ponds, falconry birds, rehabilitation facilities, and waterfowl hunt clubs can contribute to outbreaks and spread of avian influenza. Most affected birds are observed during spring and fall migration. | Monitor and conduct surveillance of captured or translocated birds, including waterfowl (duck banding), mountain quail, turkeys, grouse, and farmed game birds. Increase education to landowners, poultry owners, falconers, rehabilitators, and hunt clubs regarding biosecurity. |
| Botulism (caused by a nerve toxin produced by the bacterium Clostridium botulinum) | Waterfowl, shorebirds, and avian scavengers | Associated with shallow wetland habitats during warm weather. Botulism can be made worse by fluctuating water levels. It is often associated with carcasses (waterfowl, fish kills). Fly larvae can bioconcentrate this toxin. Most cases occur during late summer/ fall. | Manage water levels, flow, flushing, and changes at important migration areas to prevent botulism. Manage all known and major die-offs by carcass removal and proper disposal to minimize further impacts to local populations. |
| Mycoses (diseases caused by fungi, including toxins produced by mold), Aspergillosis (aflatoxins) | Many bird species. Aspergillosis is most common in waterfowl, gulls, corvids, and raptors. | Transmitted from moldy corn or acquired from soil or damp organic materials. Stressed or diseased animals may have increased susceptibility. | Aspergillosis: Monitoring and surveillance. Minimize access to source sites if known, such as moldy silage piles. Manage major die-offs by removing carcasses. |
| Cryptococcus gattii | C. gattii has been identified in harbor porpoises, Dall’s porpoises, Roosevelt elk, domestic animals, and humans along the coast and Willamette Valley. | Geographic and local environmental factors are important in development of fungal infection. | Additional research is needed to understand the location of environmental “hot spots”. |
| Harmful Algal Blooms (HAB, Cyanobacteria toxic bloom) | Waterfowl and other wildlife species as well as humans and domestic dogs. | Warmer, stagnant water bodies with high nutrient content can cause anoxic conditions for fish and toxic algal blooms for avian and terrestrial species. Most cases peak in late summer/ fall. | Maintain good water quality, flushing, and flow. Reduce high nitrogen/phosphate/nutrient runoff. Manage major die-offs by removing carcasses and disposing of them appropriately. |
| Rodent control poisons (anticoagulants, hypercalcemia products, zinc phosphide toxicosis) | Non-target species, particularly waterfowl (zinc phosphide in cackling geese) and raptors, wild canids, mustelids, and felids (anticoagulant rodenticides), and pasture-based migratory songbirds in the Willamette Valley (zinc phosphide). | Application during high rodent population seasons and cycles, and when applied off-label by inappropriate methods of delivery and during periods identified as high-risk for non-target species and secondary toxicities (anticoagulants). | Applicators must follow label restrictions for legal application and avoidance of primary and secondary toxicity to non-target species. Involve ODA Pesticides Staff and USFWS in die-offs including migratory species or off- label application of product. |
| Canine distemper | Raccoons, foxes, skunks, coyotes, wolves, and seals | Observed in raccoon and fox populations when population densities are high. Spillover from domestic dogs can occur. Infected wildlife also put unvaccinated dogs at risk. | Continue to promote prevention (e.g., by securing garbage, not leaving any pet food outdoors, etc.). Use caution when moving nuisance raccoons. Promote vaccination programs in domestic pets. |
| Rabies | Bats (primary reservoir in Oregon and the only variant to be detected in the state). Occasional pathogen spill-over into other terrestrial mammals (e.g. raccoons, skunks, foxes, and coyotes). All mammals are susceptible including unvaccinated domestic pets (primarily dogs, cats, and livestock). Human rabies cases are rare in the U.S. | Zoonotic disease. Handling of sick or dead bats, exposure of pets to sick bats or other wild mammals resulting in contact or a biting incident, and unvaccinated domestic pets can result in transmission. Bat strain rabies occurs naturally at very low prevalence levels (<1%) in bat populations in Oregon. Southwestern Oregon has had repeated bat strain rabies outbreaks in non-bat mammalian wildlife. | Continue to promote vaccination programs in domestic pets. Conduct outreach and education to teach people to avoid sick wild mammals or those with unusual behavior. Follow zoonotic disease guidance by the Centers for Disease Control and Prevention. |
| Canine parvovirus (includes several closely related viruses, such as feline panleucopenia) | Raccoons, foxes, coyotes, and wolves, principally. Canine parvovirus can infect unvaccinated domestic cats. | Wildlife exposure to unvaccinated dogs and domestic cats (e.g., outdoor cats, abandoned cats, and feral cat colonies) | Promote pet vaccination programs. Promote benefits to cats, wildlife, and people when cats are kept indoors. Discourage community feral cat colonies. |
| Leptospirosis | All mammalian wildlife are susceptible. Multiple pathogenic serovars affect rats, mice, squirrels, raccoons, skunks, opossums, foxes, deer, and marine mammals (seals, sea lions, porpoises) | A zoonotic multi-serotype bacterial disease transmitted from contaminated urine of infected animals | Conduct outreach regarding the importance of avoiding contact with seals and sea lions and carcasses along Oregon's coast. Leptospirosis is considered a zoonotic disease. |
| Tularemia | All mammals are susceptible (except coyotes) but especially rodent and lagomorph species. Several bird and amphibian are also susceptible. | Tularemia can be transmitted through inoculation from parasitic blood feeding arthropod vectors (mosquitos, fleas, tabanid flies, and ticks), ingestion of contaminated food or water, by direct contact with infected blood or tissues through dermal or ocular mucous membranes, or by inhalation of aerosolized pathogen. This bacterial disease can be more prevalent when mammalian hosts occur at higher population densities. | Tularemia is a zoonotic disease with a North American and European distribution but has not been identified in Central or South America, or Africa. Sick or deceased rodents or rabbits should not be handled without gloves, mask, and eye protection. |
| Plague | Rodent species (particularly mice) can serve as hosts and can suffer high rates of mortality (e.g., prairie dogs). Many mammals are susceptible; canids are refractory. | Fleas act as vectors. Conditions are most conducive to transmission during high rodent population cycles. Birds, lagomorphs, and carnivores may maintain or disseminate the disease by transporting fleas or ticks or infected prey. | Plague is widespread in wild rodent populations west of the 100th meridian (west of the central U.S.). Control can be achieved through an oral vaccination program or burrow dusting with insecticides. Plague is a zoonotic disease. |
| Notoedric mange | Western grey squirrels, northern and southern flying squirrels | Transmission is primarily through direct contact of affected and unaffected animals and transfer of the mite Notoedres centrifera. Increased squirrel densities associated with competition for sparse food resources can be conducive to spread. | Restrict artificial feeding and animal congregations and movement of host or carrier animals. |
| Exotic biting lice (Cervicola (Damalinia spp., Bovicola tibialis)- Deer hair loss syndrome | Black-tailed, white-tailed, and mule deer | Lice are passed through direct contact between deer and indirectly from common use of bedding sites. | Conduct public education to discourage feeding or baiting deer, which congregates animals and can increase spread of lice. Cervicola spp. is widespread in the black-tailed deer population from Washington to central California. Bovicola tibialis is found in scattered pockets of mule deer in Oregon, Nevada, Idaho, Washington, and California. |
| Adenovirus hemorrhagic disease (AHD)- caused by Odocoileus adenovirus (OdADV-1) | Black-tailed, white-tailed, and mule deer. Younger deer are more susceptible. | Transmission is through direct nose to nose contact between infected and uninfected deer. Exposed animals may become diseased in acute or chronic state or mount an antibody response. Outbreaks in deer fawns in rehabilitation facilities have resulted in high mortality. Most cases occur during late summer/ fall but can occur at any time of the year. | Avoid movement of adult deer and deer fawns to unaffected populations or areas. Conduct public education to discourage feeding or baiting, which congregates animals and increases disease spread. Restrict rehabilitating deer fawns at facilities with consistent adenoviral hemorrhagic disease outbreaks. |
| Epizootic hemorrhagic disease (EHD) | White-tailed deer are highly susceptible. Black-tailed and mule deer can also be impacted. | Culicoides spp. midges are the insect vectors of this virus. Drought and low water conditions concentrate susceptible animals at limited watering sites and provide conditions for midge-to-deer transmission conducive to amplification of the virus and disease outbreaks in riparian habitats. Spikes of disease typically occur in late summer/ fall. | Continue annual surveillance in previously affected areas. Conduct public education to discourage feeding or baiting, which congregates deer and can increase disease spread. |
| Treponeme-associated elk hoof disease (TAHD) | Roosevelt and Rocky Mountain elk | Found statewide in elk populations, with a higher incidence in Roosevelt elk. Present distribution includes Washington, Oregon, Idaho, and California. Causal bacterial agent belongs to the genus Treponema. Wet pastures and environmental conditions are thought to facilitate spread and infection. | Avoid movement and translocation of elk and soils from infected areas. Consider targeted removals of severely affected animals (via hunting or agency staff). Continue monitoring with the aid of citizen science and hunters. |
| Bluetongue virus (BTV) | Bighorn sheep and pronghorn appear to be most susceptible, with the occasional occurrence in deer. | Similar to EHD, this virus is spread via Culicoides spp. midges. Drought and low water conditions concentrate midges and susceptible animals. Proximity to affected livestock herds also influences disease transmission between livestock and wildlife. Spikes of disease typically occur in late summer/ fall | Continued disease surveillance and testing in suspect cases. Maintain communication with Oregon Department of Agriculture about livestock and wildlife cases. Conduct public education to discourage feeding or baiting, which congregates deer and can increase disease spread. |
| Bighorn sheep pneumonia | Rocky Mountain bighorn sheep, California bighorn sheep | Mycoplasma ovipneumoniae (M. ovi) is transmitted between domestic sheep and goats and wild sheep. Acting independently, or with other pathogens like lungworms, or Manheimia and Pasteurella spp. of bacteria, M. ovi. suppresses the respiratory system of wild sheep and results in potentially lethal pneumonia. Once contracted, M. ovi. spreads quickly throughout the herd and can result in an extreme all age die-off. Surviving individuals with chronic symptoms may serve as a source of disease for newborn lamb which causes low recruitment, and may infect other populations in the area. | Maintain separation between domestic sheep/goats and wild bighorns. Maintain frequent disease monitoring and testing programs throughout restored bighorn herds in Oregon. Support research designed to mitigate effects of respiratory disease on sheep populations. Implement adaptive management strategies in infected herds such as test and remove protocols for chronic carriers. Implement management actions to enhance habitat to improve population health and vigor when faced with risk of disease. |
| Salmon poisoning disease | The disease occurs in wild canids and ursids and is caused by a rickettsial organism (Neorickettsia helminthoeca) present in a trematode parasite (Nanophyetus salmincola). Domestic dogs are also susceptible. | This disease is primarily found in the Cascade and Coast Ranges and in associated tributaries. Salmonids and a small number of non-salmonid fish species acquire the rickettsial parasite, which infects a stream snail (Oxytrema silicula) commonly eaten by the fish. Canids and bears can then acquire the rickettsial infection upon ingesting infected fish leading to acute illness and death of some affected individuals. | Educate pet owners about the potential risks to themselves from handling parasitized salmon and for dogs ingesting parasitized salmon, clinical signs of the disease in pets, and when to seek veterinary care for required antibiotic treatment. No treatment in wild canids and ursids is conducted as the disease is not population limiting in wildlife. |
| White-nose syndrome (WNS) | Cave-dwelling, hibernating bat species (13 of 15 Oregon species) | Low temperatures and high humidity; bat hibernacula in caves. Potential effects on migratory tree bats are unknown. Primary cause of mortality is skin infection by Pseudogymnoascus destructans, particularly on the wing areas essential for flight, and impacts to other vital physiologic processes like heat exchange, circulation, and water balance. Hibernating bats affected by WNS wake up frequently during winter due to the associated infection, which results in bats using up fat reserves and often starving to death before spring arrives. | Conduct active surveillance of susceptible bats, guano and habitats. Follow recommendations in interagency management plan and decontamination protocols. |
FISH DISEASES OF MANAGEMENT CONCERN
Table 2. Examples of diseases that pose the greatest management concern or present significant or recurring health risk to Oregon’s fish.
| Disease or Disease-Causing Organism | Vulnerable Species | Conditions that Promote Disease Issues | Management Approaches |
|---|---|---|---|
| Sea-star wasting-densovirus (SSWD; Parvoviradae) | Many species of sea stars | SSWD is caused by the bacterium Vibrio pectenicida. SSWD causes rapid degeneration of the animal and is associated with high levels of mortality. Urchins carry disease but have not yet been detected expressing it. | Research the factors that drive disease outbreaks and promote resilience. Continue monitoring SSWD. Monitor effectiveness of treatments. |
| Infectious hematopoietic necrosis virus | Most salmonids | Stress situations, such as spawning or adverse environmental conditions | Reduce movements of infected fish and track different isolates of the virus. |
| Erythrocytic inclusion body syndrome | Several salmonids | Unknown, but condition depresses immune system and other diseases become patent | Nutrition may affect severity of infection. |
| Viral hemorrhagic septicemia virus | North American strain can cause high losses in marine species like herring, sardines, and mackerel. | Young immuno-incompetent fish and spawning adults. Fish spread the virus horizontally. Virus may be passed on to progeny. | Avoid by limiting exposure. Monitor for the presence of the European strain which is much more virulent. |
| Infectious pancreatic necrosis virus | Most salmonids and a few other marine species | Fish to fish transmission. Also vertically transmitted from parent to progeny. | Avoid by limiting exposure. Screen spawning adults for virus and cull eggs from positive parental groups. |
| White sturgeon iridovirus, white sturgeon herpesvirus | White sturgeon and possibly other related species | Likely vertically transmitted from parents to progeny. High stress environmental conditions may lead to outbreaks. | Limit transfer of known carriers. Examine fish and stock history. |
| Bacterial kidney disease caused by Renibacterium salmoninarum | Salmonids | Exposure to infected fish and transferred within the egg from infected females | In hatcheries, reduce the pathogen by culling eggs from infected females and using antibiotic injections and feedings. |
| Columnaris disease caused by the bacterium Flavobacterium columnare | Freshwater fish, relatively uncommon in cold water marine fish | Warm water conditions, exposure to other infected individuals | Maintain adequate temperature and water flow. Where possible, augment flows to increase water quantity and decrease temperature. |
| Furunculosis caused by the bacterium Aeromonas salmonicida | Salmonids, some other species | Exposure to infected fish | Use antibiotic treatments where possible. |
| External fungal infections (water molds) caused by multiple species of fungi | Most common in freshwater fish | Stress situations, such as spawning, low water, low temperature (particularly a rapid temperature drop for freshwater fish), and body injuries | Fungal spores are ubiquitous and no possible control of environmental conditions. Educate about condition. |
| Tapioca disease, caused by the myxosporean parasite Henneguya salminicola | Several species but most noted in Chinook and coho salmon | Unknown. Rarely detrimental to fish but a concern for anglers due to cysts in flesh. | Provide education on the parasite and the safety of consuming flesh. |
| Ceratomyxosis caused by the myxosporean parasite Ceratomyxa shasta | Salmonids | Exposure to infectious stage of parasite that originates in a worm. Warm, slow water and low flows can increase contact with agent. | Where possible, augment water flows to increase quantity and decrease temperature. |
| White spot caused by the protozoan Ichthyophthirius multifiliis | Freshwater fish | Exposure to infected individuals, warm water conditions | Where possible, augment water flows to increase quantity and decrease temperature. |
| Tapeworms caused by Proteocephalus sp., Diphyllobothrium sp., Bothriocephalus sp. | All fish | Ingestion of intermediate host carrying infectious stage of the parasite | Provide education on the source of the parasites and the proper handling of fish for consumption. Zoonotic potential. |
| Copepods, fish lice, and anchor worms caused by Salmincola sp., Argulus sp., Lernaea sp. | All fish | Exposure to infected individuals, low water conditions, or overpopulation | Where possible, augment water flows to increase quantity and decrease temperature. |
| NIX (Nuclear Inclusion X) | Razor clams | Unknown. Affects gill tissue (branchial epithelium). Associated with high levels of mortality in Washington. | Further research and monitoring are needed. |
| Trematode | Razor clams | Unknown. Found in the gonad. | Further research and monitoring are needed. |
| Domoic acid (DA) diatom (Pseudo-nitzschia sp.) | Primarily affects marine birds and mammals. Can also contaminate shellfish, especially razor clams, posing a risk to humans who consume them. | DA is a naturally occurring toxin produced by the diatom Pseudo-nitzschia sp., a microscopic marine alga. Algae “blooms” increase the amount of biotoxin-producing algae. The exact combination of conditions that cause blooms is not yet known. A shellfish biotoxin closure is issued immediately if Domoic Acid levels rise above the alert level of 20ppm. | Oregon Department of Agriculture (ODA) and ODFW jointly issue recreational shellfish closures when biotoxin test results exceed safe levels. Involve Oregon Health Authority, National Oceanic and Atmospheric Administration, Oregon State University, and ODFW in research and monitoring. |
| Paralytic shellfish toxin (PST) -dinoflagellate | Bivalve shellfish like clams, mussels, oysters, and scallops, as well as some gastropods and crustaceans. People who consume contaminated shellfish are at risk. May affect seabirds and marine mammals. | Unknown environmental conditions. A shellfish biotoxin closure is issued immediately if PST levels rise above the alert level of 80 micrograms per 100 grams of shellfish meat. Shellfish contaminated with PST can cause minor to severe illness, and even death. | ODA monitors PST levels and, with ODFW, jointly issues recreational shellfish closures when biotoxin test results exceed safe levels. Involve Oregon Health Authority, National Oceanic and Atmospheric Administration, Oregon State University, and ODFW in research and monitoring. |
| Shrimp barnacle (Sylon sp.) | Pink shrimp (Pandalus jordani), spot prawns (Pandalus platyceros) | Unknown. Widely distributed in shrimp and prawns in the Northern Hemisphere but only recently noted by Oregon shrimpers fishing in southern Washington. Parasite generally kills host. | Further research and monitoring are needed. |
| Needle disease-microsporidian (Nadelspora canceri) | Dungeness crab | Unknown. More prevalent in Dungeness crab living in bays and estuaries. Needle-shaped spores are found in the muscle. Can greatly increase crab mortality. | Further research and monitoring are needed. |
| Vibrio pathogen (Vibrio tubiashii) | Oysters and clams | Causes premature death in larvae. | Further research and monitoring are needed. |
| Parasitic isopod (Orthione griffenis) | Mud shrimp (Upogebia pugettensis) | Probable introduction from Asia. Gill parasite associated with population decline. | Further research and monitoring are needed. |
| Whirling disease | Salmonids (particularly trout and salmon). Young fish are most vulnerable. Some cyprinids serve as intermediate hosts for the parasite. | The parasite that causes whirling disease thrives in cold water. Poor water quality (low dissolved oxygen and high sediment) can facilitate transmission. | Monitoring and surveillance. Improve or maintain high water quality. Outreach and education on disease prevention and disinfection protocols. Restrict movement of fish from infected areas. Research parasite ecology to inform effective treatments. |
| Thiamine deficiency | Salmonids. Predatory fish can be indirectly affected from consuming prey fish. Young fish are most vulnerable. | Altered prey availability can result in inadequate intake of thiamine. Environmental contaminants can interfere with thiamine metabolism. | Maintain adequate populations of thiamine-rich prey species. Implement pollution control measures. |
| Sanguinicola blood fluke | Salmonids and perch species. Other freshwater fish may be at risk. Juvenile fish are especially vulnerable. | Warm water temperatures accelerate the life cycle of Sanguinicola. High populations of intermediate hosts (often snails) increase transmission rates. Low water quality can stress fish and make them more susceptible to infection. | Control of intermediate host populations. Improve or maintain high water quality. Control environmental factors that promote the life cycle of blood flukes. |
| Gram-positive septicemias (Lactococcus sp., Streptococcus sp.) | Various species of fish, as well as shellfish. Rainbow trout and other salmonids are particularly susceptible to Lactococcus sp. infections. | Poor water quality and elevated water temperatures can stress fish and promote bacterial growth. Infected fish can shed the bacteria into the water and spread disease. | Increase and maintain water quality. Reduce organic load to reduce bacterial proliferation. Manage environmental stressors. |
| Bacterial Cold Water Disease (BCWD) | Cold-water fish species, particularly salmonids. | Colder water temperatures (4-18°C), which are optimal for bacterium’s growth. Poor water quality. | Improve and maintain high water quality. Manage environmental stressors. Improve or maintain water flow. |
| Spring Viremia of Carp virus (SVCv) | Carp species and other cyprinids. | Outbreaks are more common during spring and early summer. Water temperatures 10-25°C. Poor water quality. | Monitor temperature and water quality. Improve and maintain high water quality. Control environmental stressors. Follow disinfection protocols for fishing and handling equipment. |
| Koi Herpesvirus (KHV) | Carp species and koi fish | Warm water temperatures promote the replication of the virus, especially during summer months. Poor water quality. | Optimize water conditions. Monitor water temperature and quality. Improve water flow. Restrict movement of fish from infected areas. |
| Asian Tapeworm | (Bothriocephalus acheilognathi) | Freshwater fish. Particularly cyprinids, such as carp, but may affect rainbow trout and other salmonids. | High-density fish populations. Poor water quality and warm water temperatures. Movement of infected individuals. Abundance of aquatic invertebrate intermediate hosts (e.g., copepods) facilitate the tapeworm’s life cycle. |
| Avoid human-caused movement of infected fish to new areas. Follow disinfection protocols for field and aquaculture equipment. Reduce populations of intermediate hosts. Monitor water temperature and quality. | Aphanomyces infection | Salmonids, particularly rainbow trout, and cyprinids. Some species of shrimp. Certain amphibians may be susceptible. | High-density fish populations. Poor water quality. Nutrient pollution and organic waste accumulation can favor fungal development. Some species of Aphanomyces are more virulent under certain temperature conditions. |
| Improve water quality. Control organic matter and reduce excess nutrients. Monitor water temperature. | Channel catfish virus (CCV) | Primarily affects catfish and other species in the Ictaluridae family. Juvenile or fingerling catfish are especially vulnerable. | CCV outbreaks are more common in warmer months, as the virus thrives at higher temperatures. Poor water quality can make fish more vulnerable to infections. |
| Improve or maintain water quality. Monitor water temperature. | Largemouth Bass Virus (LMBV) | Primarily affects largemouth bass and other species in the Centrarchidae family, which includes bass and sunfish. | Warm water temperatures (68-86°F) promote the replication and spread of the virus. Outbreaks are more common in summer months. Poor water quality can make fish more vulnerable to infections. |
EMERGING DISEASES OF MANAGEMENT CONCERN
Table 3. Examples of emerging fish and wildlife diseases with the potential to spread and establish in Oregon with significant impacts to fish and wildlife.
| Disease or Disease-Causing Organism | Vulnerable Species | Conditions that Promote Disease Issues | Surveillance and Management Recommendations |
|---|---|---|---|
| Chronic wasting disease of cervids (CWD) | Deer, elk, moose. Captive caribou and reindeer are also at risk. | A fatal neurological prion-associated disease transmitted via direct contact between infected and non-infected susceptible cervids through saliva, urine, and feces. Indirect contact infection is also possible from long-term environmental contamination. | Conduct surveillance of vehicle-struck and hunter-harvested animals and animals observed with clinical signs. Ban importation and movement of live cervids and hunter-harvested neural tissues imported from wild cervids taken in other states. |
| Meningeal worm or “brain worm” (Parelaphostrongylus tenuis) | White-tailed deer. Moose, elk, mule deer, black-tailed deer, and pronghorn are aberrant hosts. | Non-pathogenic to white-tailed deer but causes severe neurologic signs and death in aberrant hosts. | Prevent movement of wild cervids from meningeal worm endemic areas. Consider increasing surveillance using molecular tools. |
| Meningoencephalitis associated with Carnobacterium maltaromaticum-like bacteria | Juvenile salmon sharks | Unknown. Documented in juvenile salmon sharks breeding along the California coast during late summer and early fall. | Further research and monitoring are needed. |
| Morbillivirus (phocine and cetacean) in marine mammals | Seals, dolphins, whales | Morbilliviruses are highly contagious and cause serious disease with immunosuppression in their hosts. The virus is likely to infect most of the immunologically naive individuals in a population. Herd formation and migration increase the probability of transmission. | Further research and monitoring are needed. Monitor global mass mortality events such as those seen along the eastern U.S. and eastern Pacific in dolphins. |
| Pigeon paramyxovirus (PPMV-1) | Pigeons and doves | Congregation of birds at feeders or watering sites promotes spread of the disease since it is spread via direct contact and feces. | Consider surveillance and monitoring to detect PPMV-1. Maintain biosecurity around poultry operations. |
| Salamander chytrid fungus (Batrachochytrium salamandrivorans) | Salamanders, especially newts | Unknown. Globalization and lack of biosecurity, importation of infected species via the pet trade, and internet shipments of amphibians likely promote spread. | Maintain strict biosecurity and importation protocols. Evaluate novel biosecurity measures. Increase public awareness and education regarding risks to conservation, species impacts, and global health. Further research and monitoring are needed. |
| Snake fungal diseases (Ophidiomyces ophiodiicola and Parananizziopsis sp.) | Snakes | A disease in snakes caused by the fungus Ophidiomyces ophiodiicola. This fungus was first isolated from captive snakes in Europe and the United States in the mid-1980s, and now experts consider it to be an emergent pathogen across North America. | Restrict the interstate movement of wild caught snakes through collectors or the pet trade. Conduct surveillance, research and monitoring. |