One Health

Posted in Fact Sheets

With increasing awareness of the inter-relatedness of human and veterinary health as well as the ecosystem, a collaborative initiative is underway incorporating veterinarians, physicians, public and environmental health experts, and researchers to advance health care across all areas. Veterinary pathologists, with unique expertise in comparative and translational medicine, have an important role in One Health. 

Click here for more information and an overview of the role of veterinary pathologists in One Health, as described by medical pathologist Dr. Robert Cardiff along with ACVP Diplomates Dr. Jerrold Ward and Dr. Stephen Barthold.

Michael D. Lairmore, DVM, PhD, DACVP, DACVM, is the dean of the U.C. Davis School of Veterinary Medicine, and has been involved in the One Health initiative since its beginning. Learn more about his career-long work with One Health. 

Michael Lairmore, DVM, PhD Dr. Michael D. Lairmore


West Nile Virus Factsheet

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West Nile Virus (WNV) is one of several viruses that may be transmitted to people and animals via insect bites. WNV, a member of the genus flavivirus, is carried primarily by birds and is transmitted from bird to bird by mosquitoes. Birds in the "enzootic cycle" are relatively resistant to disease and serve to maintain the virus in the avian population. Susceptible avian species, other animals and people may also be infected when bitten by a mosquito carrying the virus. Horses and humans have proven to be the mammalian species most likely to become ill following WNV infection, although there have been occasional reports of illness and even death in many other species, including dogs, cats, rabbits, sheep, alpacas and llamas.

In the past five years, WNV associated illness has been diagnosed in over 14,000 people in the United States, with over 500 deaths. In the same time period, over 20,000 horses have been affected with a mortality rate of approximately 35 percent. Although mosquito bites are the most likely means of human infection, virus transmission through blood transfusion, breast milk and organ transplantation has also been reported.

WNV was first identified in a woman in Uganda in 1937. Since then, the virus has caused outbreaks of illness in people and animals in other parts of Africa, the Middle East, Western Asia and Eastern Europe. In the summer of 1999, WNV was identified as the cause of encephalitis (inflammation of the brain) in a cluster of human patients and in several native and exotic birds in the New York City area. This was the first time the virus had been identified in the Western Hemisphere. The virus has continued to spread across North America—first along the East Coast of the United States, then west, reaching the Pacific Coast for the first time in 2003, including Canada and Mexico. WNV is probably now permanently established in the Western Hemisphere.

Infection in Humans
Although the numbers of reported cases of human illness associated with WNV over the past five years may be alarming, it is believed that most people who are bitten by a WNV-carrying mosquito will show no symptoms at all. One in five will develop mild "flu-like" symptoms that last a few days. Signs of headache, fever and lethargy are all associated with the syndrome "West Nile Fever." A very small number, one in 150, of infected individuals will exhibit more serious signs of "West Nile Neuroinvasive Disease," with encephalitis or meningitis (inflammation of the covering of the brain or spinal cord). Symptoms in these cases may include severe headache, stiff neck, disorientation, tremors, extreme muscle weakness, paralysis, and/or seizures. Elderly patients have the highest risk of developing serious illness from WNV infection.

Sick Seas Factsheet

Infection in Horses
Horses have proven uniquely susceptible to WNV infection, comprising more than 99 percent of veterinary mammalian cases. Clinical signs in affected horses include weakness, incoordination, depression, fever and muscle twitching, especially of the face and muzzle. The course of illness varies from a few days to a few weeks and may be rapidly or slowly progressive. Horses that become recumbent have a poor prognosis for recovery. Most horses that reach this stage are euthanized or die. The majority of horses, however, completely recover from the infection.

Infection in Birds
Birds in the family Corvidae, which includes crows, blue jays and ravens, have proven to be the most highly susceptible to illness following WNV infection among avian species, thus becoming the focus of WNV surveillance efforts by regional and federal health agencies across the United States and Canada. Identification of infected corvids through testing of blood, tissue and swabs of oral cavities or droppings has been used to forecast virus activity in humans and horses.

WNV infection has been identified in over 200 avian species during the North American outbreak. Although this list includes over 150 native North American birds, crows and blue jays account for between 50 and 90 percent of reported avian cases. During the summer of 2002, significant numbers of raptor species (owls, hawks, etc.), especially in the Midwestern United States, were infected with the virus. Domestic poultry (chickens and turkeys) and pet birds (budgerigars, cockatoos, cockatiels) seem fairly resistant to WNV disease. Most infected corvids are simply found dead or show signs of incoordinated flying or walking, weakness, lethargy, tremors and abnormal head posture.

Limiting exposure and improving strategies to diminish or eliminate mosquito numbers are the best ways to protect humans and animals from WNV disease. Vaccines are commercially available for horses and are under development for humans and birds.

Sick Seas Factsheet

Posted in Fact Sheets

Domoic Acid
In 2003, domoic acid caused the second-largest marine mammal die-off in U.S. history. Domoic acid is a naturally occurring toxin produced by blooms of microscopic phytoplankton. The toxin is concentrated in filter-feeding animals such as anchovies, sardines and shellfish, which are in turn eaten by marine mammals like dolphins, sea lions and manatees. As the toxin is absorbed into the body of these mammals, it inhibits the brain's neurochemical processes. Common effects of domoic acid seen in animals washed ashore include head weaving and seizures, which may lead to permanent brain damage and death.

In 2003, domoic acid was the cause of death of 685 sea lions and 98 dolphins in Southern California. Some experts from the California Dept. of Fish and Game believe the rise in domoic acid is due to an increase in run-off pollution into the ocean. Pollution may also have weakened the immune system of the sea mammals, causing them to become more susceptible to domoic acid poisoning.

Protozoal encephalitis
A significant percentage of mortality in sea otters is due to the one-celled organism, Toxoplasma gondii. Sea otters exposed to T. gondii can develop protozoal encephalitis, a deadly brain infection. An otter with this condition develops tremors in its front legs and loses muscle function, making it hard to groom and dive for food. Grooming is essential to a sea otter's survival. Sea otters have no blubber, so for insulation against freezing ocean waters, sea otters rely on their dense fur. An otter with protozoal encephalitis loses its defense against the cold water and has a significantly increased chance of dying.

It is estimated that over 70,000 chemicals are currently in use as industrial compounds, pesticides, food additives and other purposes. This number is increasing by approximately 1,000 each year. Of particular concern to the health of marine mammal populations are the halogenated hydrocarbons (HHCs) such as the PCBs and DDT.

There are a number of possible effects these contaminants can have on marine mammals. These include infertility and reproductive failure, birth defects, cancer, behavioral change, immune and nervous system dysfunction, damage to kidneys, liver and other organs. High levels of pollutants such as DDT and PCBs have been found in the blubber of sea lions and whales.

SARS Factsheet

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Severe acute respiratory syndrome (SARS) is caused by the newly described SARS-associated coronavirus (SARS-CoV), an RNA virus. Certain coronaviruses are a common cause of mild to moderate upper-respiratory illness in humans and have been linked to pneumonia in vulnerable populations. In animals, coronaviruses are known to cause severe respiratory, neurological, gastrointestinal and liver disease.

SARS is the first newly emerging, severe and readily transmissible infectious disease of the 21st century.

Evidence suggests that SARS emerged in the Guangdong Province in southern China in November 2002. More than 33 percent of the cases reported before February 1, 2003 involved people who handled, killed or sold wildlife destined for human consumption, or prepared and served such food.

As of August 7, 2003, a total of 8,422 cumulative probable cases and 916 deaths were reported in 29 countries. Approximately 5,324 cases and 349 deaths were reported from Mainland China. In the face of an emerging epidemic and pandemic, Singapore was the first city to begin mass quarantines, isolating a total of 8,000 people and threatening them with jail fines if they left home. The World Health Organization (WHO) declared the outbreak over on July 5, 2003.

As of January 15, 2004, one confirmed case and two suspect cases of SARS have been reported in the Guangdong Province of southern China. The suspect cases are undergoing further testing.

Cause and Transmission
The disease's spread appears to be primarily through direct mucous membrane exposure (eye, nose, mouth) to infectious respiratory droplets and/or contact with contaminated objects such as clothing or dishes.

Transmission can be prevented to a large degree by basic infection and public health control measures, such as rapid identification and reporting of cases, case isolation, tracing of contacts, basic hand washing and the use of personal protective equipment.

Animal Link
Evidence links SARS with the handling and slaughter of wildlife for human consumption in southern China. A survey of wildlife taken from open markets in the region found coronaviruses in masked palm civets and raccoon dogs that were very similar to SARS-CoV. Another species, the Chinese ferret badger, showed antibodies against SARS-CoV. Other species that have tested positive include cynomologus macaques, fruit bats, snakes and wild pigs. Although these species may have acquired the virus from other, yet unidentified, species, the data suggest that some of these species may be functioning as intermediate hosts that enable the virus to cross species to humans through Chinese culinary practices. Of 508 animal handlers tested in the Guangdong markets, 66 were serologically positive, i.e., infected but did not develop disease. This indicates that SARS-CoV exists outside a human host.

Environmental contamination, with possible animal vectors, was implicated in the transmission of SARS-CoV in some multiple living unit complexes in Hong Kong. In these instances, several companion animals (dogs and cats) tested positive for SARS-CoV. Cockroaches carried the virus on their body surfaces and in their gut contents and may have acted as mechanical vectors.

Prevention and the Search for a Vaccine
The origin of SARS-CoV is unknown, meaning that early identification and containment of the next outbreak will rely upon infection control and isolation/quarantine measures. Research in the hunt for the natural reservoir has stalled. Several research teams are pursuing developing a safe and efficacious vaccine with an adenovirus-based vaccine candidate holding promise. However, some believe that SARS-CoV's potential for rapid and unpredictable change (host-species shifting), characteristic of coronaviruses, may prove challenging for those identifying and developing a vaccine and therapeutics.

Ranavirus FACT SHEET

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The Pathogen
Ranavirus is a genus within the family Iridoviridae (other Genera currently include: Iridovus, Chloriridovirus, Megalocytivirus, and Lymphocystivirus).  Ranaviruses are large (120-300 nm diameter) icosahedral with linear, dsDNA genomes.  They are enveloped viruses; however, they maintain their infectivity without the envelope.  Recent evidence suggests that the virus originated in fish and underwent multiple host-shifts.  Environmental persistence outside of the host remains unknown and likely varies with ambient conditions; however, experimental evidence suggests that ranaviruses may be able to remain viable for over 1 month.

The Hosts
Ranaviruses infect amphibians, reptiles, and fish; however, susceptibility varies by species and across phylogenetic lineages.  For amphibians, the orders Anura and Caudata are affected and, to date, natural infections have been documented in at least 72 species, representing 14 families with most cases reported from the family Ranidae.  Currently, ranaviruses have been reported in several species of boney fish and FV3-like ranaviruses have caused die-offs in pallid sturgeon (Scaphirhynchus albus) and threespine stickleback (Gasterostelus aculeatus).  Ranaviruses also have been associated with disease in snakes, lizards, and chelonians, and may best be known for die-offs in eastern box turtles (Terrapene carolina carolina).  All age groups may be susceptible but this may vary by species.  In general, hatchling and metamorphs are the most susceptible age groups in amphibians; however, adults are reported most often in die-offs of several European amphibian species.  The egg appears to protect embryos from infection.

Distribution:  Ranaviruses are globally distributed; currently reported from 5 continents.  Anthropogenic spread (e.g., infected animals used as live fishing bait, field and recreational equipment, boots, import/export of infected animals for food or pets) has resulted in exposure of naïve populations and subsequent mortality events.

Transmission and Pathogenesis:  Transmission is horizontal via direct contact, ingestion of virus or infected animals and water exposure.  Vertical transmission is suspected but remains unknown. Frequency-dependent transmission is possible. There is considerable evidence, in nature and from laboratory experiments, for interclass transmission among amphibians, reptiles and fish. The pathogenesis of ranaviral disease is under investigation but current research findings support viral entry through epithelial surfaces, with subsequent dissemination through the body.  Studies have shown that infection can begin within seconds of contact.  Disease (and deaths) may be established in as short as 3 days but also may take weeks, and likely is dependent on host susceptibility (species and age group) and pathogenicity and amount of the ranavirus.  Although it is not always clear to determine how ranaviruses kill their host, in most cases, death results from severe cellular/organ necrosis. Clinical signs may include lethargy, buoyancy problems, erratic swimming, and gasping for air (chelonians).  Gross lesions may include swelling (neck, appendages, body), hemorrhages (especially on ventrum and legs [amphibians]), tan friable organs, ulceration, and oral necrotic tan plaques (chelonians).  Microscopic lesions may include, hemorrhage, swelling (edema), cellular necrosis (e.g., hematopoietic tissue, hepatocytes, epithelial cells, endothelial cells), and inclusion bodies (intracytoplasmic; however, intranuclear have been reported but are rare). Subclinical infection has been detected in wild amphibians and in experimental challenges.   

Significance: Ranaviral diseases may be enzootic or epizootic with high mortality (100% in some species).  Ranaviruses are not distributed uniformly across the landscape; infection hotspots exist.  Therefore, these viruses may have negative impacts on conservation measures, especially in cases of repatriation of endangered species.  Rare species that are highly susceptible (e.g., Lithobates capito) are at greatest risk. In general, translocation of animals into environments from where they did not originate, should be discouraged.  Statistically valid sampling practices still need to be defined. 

Treatment:  Currently there is no reliable treatment.  Quarantine of infected animals is recommended.  Treatment of secondary invaders also may limit the severity of the disease.

Disinfection:  A minimum of 1 minute contact time with > 3% Bleach, > 1% Virkon or > 0.75% Nolvasan will inactivate the virus.

Prevention and Control:  Vaccination or chemotherapeutics are not currently available.  Newly acquired animals should be isolated and tested prior to introducing them to captive colonies. Water in captive facilities should be disinfected to inactivate the virus prior to discarding it from tanks/enclosures housing infected animals.  If possible, each tank/pond should have a separate water source.  All equipment and surfaces of captive facilities should be disinfected after use.  Similarly, equipment and boots used at a field site should be disinfected before proceeding to a new field site.  Translocation of hosts, including those used for fishing bait, should be discouraged.

Zoonotic potential: None

Wildlife Impact: Susceptible species may experience population declines. Current (and on-going) research suggests that community composition may play a role in emergence within an ecosystem. Die-offs may begin and end in less than 2 weeks.

Status:  Amphibian diseases caused by ranaviruses are listed as notifiable by the World Organization of Animal Health (OIE). Information regarding the OIE listing can be found within the Aquatic Animal health Code, with ranavirus specific information at 

The OIE approved diagnostic tests can be found within the Manual of Diagnostic Tests for Aquatic Animals, with ranavirus specific information found at: