Chapter 7 Viral zoonoses.
The order Mononegavirales contains viral species that have a nonsegmented, single-stranded negative sense RNA genome. The order includes four families: Bornaviridae, Rhabdoviridae, Filoviridae, and Paramyxoviridae. The family Rhabdoviridae includes two genera of plant viruses and three genera of animal viruses. The three animal virus genera are Lyssavirus, Vesiculovirus, and Ephemerovirus; only Lyssavirus and Vesiculovirus are zoonotic. Tables 7-17 and 7-18 list the various zoonotic viruses in the Rhabdoviridae family. The two main zoonotic rhabdoviral diseases are rabies and vesicular stomatitis. In general, rhabdoviruses have a worldwide distribution with some virus found in specific areas such as Africa, Europe, and Australia.
Rhabdoviruses are medium-sized, enveloped, single-stranded, negative sense RNA viruses. Although these viruses have an envelope, their capsid is helical, which makes the viruses appear bullet-shaped. Rhabdoviruses carry genes encoding for five proteins: nucleocapside protein (N), phosphoprotein (P), matrix protein (M), receptor binding protein (G), and polymerase (L). The N, P, and L are attached to the nucleocapsid within the virus particle. The M protein is located between the nucleocapside and the outer membrane. The G protein is the only glycoprotein, which combines the functions of receptor binding and fusion. The nucleocapsid consists of an RNA and N protein complex together with an NS (M1) protein and is surrounded by a lipid envelope containing M (M2) protein. The nucleocapsid contains transcriptase activity and is infectious. The shape of the virus that infects vertebrates is a bullet (rhabdo is Greek for rod) with one blunt and one pointed end.
Rabies is an ancient viral infection of the CNS and is considered the oldest communicable disease of humans. The word rabies originates from the term rabhas, which means to do violence. The first recorded reference to rabies was in the 23rd century B.C. when Babylonian law described the financial penalty for the owner of a rabid animal that bites a human. The writers Homer (approximately 700 B.C.), Democritus (420 B.C.), and Aristotle (approximately 300 B.C.) both used descriptions of rabies in their works.
The first outbreak of dog rabies extensively recorded occurred in Italy in 1708. Rabies did not appear in the Western Hemisphere until the mid-18th century, when dogs caught the virus in Virginia in 1753. During the 19th century, rabies ravaged Europe and fear of this condition escalated to hysteria. Calming the terror people felt about this disease soon became the job of Louis Pasteur. Rabies virus was first isolated by Pasteur in 1885 (although other scientists were testing it before this time). Pasteur and his group of scientists began injecting the "disease" into rabbits to determine the amount of time it took for the virus to affect the spinal cords of these rabbits. Pasteur then began injecting dogs with weakened versions of the virus and observed that these injections could prevent the disease before and after exposure. In time, Pasteur produced the first rabies vaccine by inactivating the virus using ultraviolet light (the first vaccine was given to 9-year-old Alsatian boy named Joseph Meister, who later survived a rabid bite). Rabies has been reduced in many countries through pet control and careful quarantines, but it is still enzootic in various wild animals in the Americas and in domestic and wild animals throughout Africa and Asia.
Rabies is a preventable neurologic disease caused by a rhabdovirus. The Rhabdoviridae family is in the order Mononegavirales and is a nonsegmented, single-stranded, negative sense RNA virus. Rabies virus is neurotropic (seeks out nervous cells) and is typically found in one species in a given area. There are different variants of this virus and each variant is responsible for rabies transmitted between members of the same species in a given area.
Rhabdo means rod-shaped; viruses the rhabdovirus family have a distinct bullet shape.
Epizootiology and Public Health Significance
Rabies has a worldwide distribution in both wild and domestic animals with the exceptions of Australia, the United Kingdom, Ireland, New Zealand, Japan, Antarctica, Scandinavia, and Hawaii; however, the reservoir varies geographically. In the United States and Canada, rabies in wildlife populations typically includes skunks, raccoons, and bats. Distinct variants are responsible for rabies in different species; there is a distinct variant for dogs and coyotes, a different variant for skunks, and a different variant for foxes. In general, each variant found in bats belongs to a predominant bat species. In the United States, most cases of rabies in humans in the past decade have been caused by bat rabies variants. Cats, cattle, and dogs are also frequently infected with rabies in the United States. Wildlife that are common sources of rabies virus are raccoons, skunks, foxes, and coyotes. The number of postexposure prophylaxis treatments given in the United States is not tabulated, but is estimated to be around 40,000 per year. The estimated annual cost of rabies vaccination in the United States is over $300,000 (the majority of the cost is for dog vaccinations). Worldwide, 40,000 to 50,000 human fatalities from rabies (especially from wild animal rabies) occur annually, mainly in rabies-endemic areas such as Asia and Africa.
All mammals can get rabies; however, small rodents (squirrels, rats, mice, hamsters, Guinea pigs, gerbils, and chipmunks) and lagomorphs (rabbits and hares) are rarely infected with rabies. Birds, fish, reptiles, and insects do not get rabies.
Rabies virus may be present in saliva and transmitted by an infected animal several days before the onset of clinical signs (dogs can shed virus 5 to 7 days before clinical signs and cats can shed virus 3 days before clinical signs). Rabies is almost always transmitted by introduction of virus-laden saliva into tissues. The virus-laden saliva usually is introduced into tissue by a rabid animal bite; however, the virus can also be introduced into fresh wounds (a scratch or abrasion that is exposed to infective saliva) or through intact mucous membranes (eyes, nose, and by ingestion of the virus through the mouth). Aerosol transmission in a laboratory setting and in caves where bats roost has also been shown to transmit the virus, but a high concentration of suspended viral particles is needed for these types of transmission. Viral spread via blood is extremely rare. Rabies-contaminated transplants are also a source of rabies infection. The only documented cases of rabies caused by human-to-human transmission are through corneal transplants and solid organ transplants.
Rabies is a fatal disease that usually causes death within 10 days after the onset of clinical signs. The incubation period from exposure to clinical signs is extremely variable. The incubation period for rabies virus is unusually long and the virus can remain at the inoculation site for a long time. In dogs most cases of rabies occur approximately 20 to 80 days after viral exposure, but the incubation period may be longer or shorter. Rabies virus replicates in muscle cells near the inoculation site and then travels to the spinal cord via the peripheral nerves. The animal does not appear abnormal at this time. From the spinal cord the virus travels to the gray matter of the brain (mainly in neurons of the limbic system, midbrain, and hypothalamus) and finally to the salivary glands via the peripheral nerves. After the virus has multiplied in the brain, most animals begin to show signs of rabies. Within 3 to 5 days, the virus has caused enough brain damage that the animal begins to show neurologic signs of rabies.
Clinical Signs in Animals
Rabid animals exhibit CNS signs that vary slightly among species. All species infected with rabies virus exhibit behavioral changes and paralysis. The first sign to appear in all animals is a change in behavior, such as anorexia, irritability, and nervousness. These changes may be difficult to distinguish from early infectious disease, injury, an oral foreign body causing excessive salivation, or gastrointestinal disorders. Change in body temperature is usually not significant. Animals infected with rabies virus usually stop eating and drinking. Some animals seek solitude. An irritated urogenitial system may result in frequent urination and increased sexual desire.
Rabies is often described as either being furious or dumb. Animals display either the furious or dumb phase of rabies 1 to 3 days after infection. Furious rabies, often described as the classical "mad-dog" rabies or vicious rabies, refers to animals that have a pronounced aggressive phase. During this phase the animal becomes irrational and with slight provocation becomes aggressive. The animal is alert, anxious, has mydriasis (dilated pupils), and will attack with auditory stimulation. Specific species examples include:
* Rabid dogs may show behavioral changes and may chew cages and other restraint devices, and attempt to bite (Figure 7-38). Some dogs may eat dirt, sticks, and other objects. Some dogs are dysphagic (have difficulty eating), which will cause profuse salivation. Seizures, paralysis (including facial and pharyngeal), and death may follow the hypersalivation phase.
* Rabid cats may show behavioral changes and will show an excitatory phase where they may attack suddenly by biting and scratching. The pronounced excitatory phase is usually followed by progressive paralysis.
* Rabid equines (such as horses and mules) often present with signs of spinal cord disease such as ataxia (incoordination). Some rabid equines will bite with the slightest provocation. Equines frequently show signs of distress and agitation, and may roll (may be interpreted by some as a sign of colic). Increased vocalization is seen in some rabid equines.
* Rabid cattle typically begin with hind limb ataxia and paresis (weakness). Cattle may butt any moving object, attacking and pursuing humans and other animals. In dairy cattle, lactation stops abruptly. Yawning and tail paralysis may be seen in some rabid cattle. Facial expressions change from a placid expression to one of alertness. Eye and ear movements follow sound. Abnormal bellowing may continue intermittently until just prior to death.
* Rabid pigs will show behavior changes, which typically include biting and becoming aggressive.
* Rabid goats and sheep will show increases in bleating, hind-leg weakness, difficulty in walking, aggression, excessive sexual activity, and paddling.
* Rabid wildlife act abnormally. Rabid foxes and coyotes will invade yards and may attack pets and people. Rabid raccoons and skunks typically do not fear people and are ataxic, aggressive, and active during the day (even though they are nocturnal animals in nature). Rabid bats can be seen flying during the day, resting on the ground, attacking people and animals, or fighting.
[FIGURE 7-38 OMITTED]
Dumb rabies, often described as the paralytic form of rabies, manifests itself as paralysis of the throat and chewing muscles. In dogs dropping of the mandible, profuse salivation, and inability to swallow may be seen. Owners should not attempt to examine the mouth of the animal or administer medication to these animals as they are exposing themselves to the rabies virus. Animals displaying the dumb form of rabies are not vicious and do not attempt to bite. Paralysis will progress rapidly to all parts of the animal's body with coma and death occurring in a few hours.
Furious rabies is most commonly seen in carnivores, equine, and wild animals; dumb rabies is most often seen in ruminants. Each form occurs about 50% of the time in swine.
Clinical Signs in Humans
People who contract rabies usually have a history of an animal bite, although some people are unaware of their bite wounds if the wound is inflicted by bats. The site of the wound initially feels painful followed by a period of burning and increased sensitivity to temperature changes. The first symptoms of rabies may be nonspecific flu-like signs such as fever or headache. In time drinking becomes extremely painful as a result of laryngeal spasm and the person refuses to drink (hydrophobia). Behavior changes such as restlessness or extreme excitability may occur. Muscle spasm and laryngospasm are followed by convulsions at which time large amounts of thick saliva are present.
Diagnosis in Animals
The pathology of rabies infection involves the development of encephalitis and myelitis. Lymphocytes, segmented neutrophils, and plasma cells infiltrate perivascular areas throughout the CNS. Rabies virus frequently produces round or oval cytoplasmic inclusion bodies in neurons. These inclusions are known as Negri bodies, named after Dr. Adelchi Negri who identified them in 1903. Negri bodies are the sites of active viral replication and range in size from 0.25 to 0.27 [micro]m (Figure 7-39). Negri bodies are found in neurons of the brain (especially the cerebellum), salivary glands, tongue, and other organs.
It is difficult to clinically diagnose rabies because in its early stages rabies can be confused with other diseases. When rabies is suspected in an animal, laboratory confirmation of fresh brain tissue is warranted. The laboratory test of choice for rabies identification in animals is a fluorescent antibody (FA) test that has been utilized for approximately forty years. A benefit of the rabies FA test is that it provides a highly specific diagnosis within a few hours. Fresh brain tissue including the hippocampus, cerebellum, and medulla oblongata must be obtained for testing. The brain tissue must be preserved by refrigeration with wet ice or cold packs; not frozen. The FA test for rabies identification is based on the fact that rabies-infected animals have rabies virus proteins (antigens) in their tissues. Fluorescent labeled antibody to this viral protein is incubated with suspect brain tissue. If rabies viral protein is present, the fluorescent labeled antibody will bind to it. Any unbound labeled antibody is washed away. The sample is then examined with a fluorescent microscope and fluorescent labeled antibody bound to the antigen will be seen as a fluorescent green area if present in the tissue.
[FIGURE 7-39 OMITTED]
The outcome of rabies exposure depends on the variant of the virus, the amount of virus inoculum, the route of exposure, the location of exposure, and host factors.
Diagnosis in Humans
Brain tissue and meninges that are infected with rabies virus have a variety of changes seen on histopathologic analysis. These changes include Negri bodies, Babes nodules of glial cells, lymphocyte foci, perivascular cuffing of lymphocytes or segmented neutrophils (Figure 7-40), and mononuclear infiltration. Stains such as Mann's, Giemsa, or Sellers stains can differentiate rabies inclusions from other intracellular inclusions.
[FIGURE 7-40 OMITTED]
Immunohistochemistry methods for rabies detection are used to detect rabies in formalin-fixed brain samples. These methods are more sensitive than histologic stain methods. These methods use specific antibodies and enzyme-labeling to detect rabies virus inclusions.
Electron microscopy can also be used to examine the ultrastructure of rabies virus and its inclusions. Rabies viruses are seen as bullet-shaped particles using electron microscopy. Amplification methods can be used to identify rabies virus in samples suspected of containing small amounts of virus. Rabies virus replicates in cell culture using mouse neuroblastoma cells or baby hamster kidney cells (BHK cells). Cell culture techniques increase the numbers of viral antigens to help identify positive cases that have low viral load. Another method for increasing the viral concentration is by using reverse transcriptase-polymerase chain reaction (RT-PCR). In this technique, rabies virus RNA from saliva or skin biopsy samples is enzymatically amplified as DNA copies. Rabies RNA is first copied into a DNA molecule using reverse transcriptase. The rabies DNA copy is then amplified using PCR techniques.
Fixed sample preparations can still be infectious and need to be handled appropriately. Histologic examination of brain tissue from clinically rabid animals shows Negri bodies in approximately 50% of the samples. In contrast, FA tests show binding of fluorescent-labeled antibody in nearly 100% of the samples.
Rapid and accurate laboratory diagnosis of rabies in humans is essential for timely administration of postexposure rabies prophylaxis. Antemortem (before death) testing for rabies in humans requires several tests that are performed on a variety of samples including salvia, serum, spinal fluid, and skin biopsies of hair follicles at the nape of the neck. Saliva is tested by viral cell culture or RT-PCR. Serum and spinal fluid are tested for antibodies to rabies virus, whereas skin biopsy samples are examined for rabies antigen.
Treatment in Animals
Treatment of rabid animals is not attempted as a result of the zoonotic and usually fatal nature of the disease. Rabid animals are euthanized and their brains are tested.
Treatment in Humans
Treatment of human rabies depends upon the point of disease recognition and symptoms present in the person. Any animal bite that may have come from a potentially rabid animal needs to be seen by medical personnel that should perform vigorous washing and first aid of the wound. State or local health departments, veterinarians, and animal control officers need to be made aware of a possible rabies exposure. Post-exposure rabies prophylaxis (PEP) is indicated for people who have been potentially exposed to a rabid animal (bite wound, mucous membrane contamination, transplantation of contaminated tissue, etc.) or a person with rabies (exposed to the person 14 days preceding the appearance of clinical signs until the person's recovery or death). Post-exposure prophylaxis is begun as soon as possible after exposure and when given promptly has been successful. Currently, postexposure prophylaxis is a regimen of one dose of immune globulin (antibody) that provides immediate but temporary protection, a dose of rabies vaccine, which starts the body producing its own antibodies, and four additional doses of rabies vaccine over a 28-day period. Additional doses of rabies vaccine are given on days 3, 7, 14, and 28 after the first vaccination. Human rabies immune globulin is also infiltrated around the wound. Current vaccines are relatively painless and given intramuscularly in the arm. Adverse reactions to the rabies vaccine and immune globulin are not common and may include pain, redness, swelling, or itching at the injection site. Low-grade fever may be seen following injection with rabies immune globulin.
Any animal showing neurologic signs should be considered a rabies suspect and veterinary staff should protect themselves against exposure (by wearing gloves and protective clothing).
There are only six documented cases of human survival from clinical rabies and five of these included a history of either pre- or postexposure vaccination. The first case of rabies survival without pre- or postexposure vaccination was documented in Wisconsin in 2004 in which a 15-year-old girl contracted rabies from a bat bite and developed symptoms of rabies. Blood, spinal fluid, saliva, and skin samples were confirmed rabies positive by the CDC and she was put into a drug-induced coma for 1 week. During that one week's time she produced massive amounts of antibodies against rabies virus and no longer showed signs of infection. After 10 weeks of hospitalization she was discharged from the hospital and is regaining neurologic function (she graduated from high school in June 2007).
Management and Control in Animals
Rabies in the United States has changed over the past 100 years and now more than 90% of all animal cases reported to the CDC occur in wildlife (before 1960 the majority of cases were in domestic animals). In the United States, human fatalities from rabies have declined from over 100 annually to approximately 1 to 2 annually (usually as a result of people unaware of their exposure). Raccoons are the most frequently reported rabid wildlife species (about 40%), followed by skunks (about 30%), bats (about 17%), foxes (about 6%), and other wild animals. Cases of rabies in raccoons are especially high along the eastern coast of the United States. The Compendium of Animal Rabies Control, updated annually by the National Association of State Public Health Veterinarians (NASPHV), monitors current USDA-licensed rabies vaccines and their recommended protocols. Both modified live virus and killed vaccines are available for use in dogs worldwide. Currently available vaccines in the United States are effective for either 1 or 3 years and several types are available for use in dogs, cats, ferrets, horses, cattle, and sheep. The increased incidence of rabies in cats has made cat vaccination extremely important. As of June 2007 a newly approved vaccine for cats labeled for use every four years has been approved. Oral vaccines distributed in baits have been effective in Europe and Canada for control of fox rabies.
Any animal bitten or scratched by a wild, carnivorous mammal or bat is considered to have been exposed to rabies. The NASPHV recommends that any unvaccinated dog or cat exposed to rabies be immediately destroyed and tested. If the owner does not consent to this, the animal is strictly quarantined for 6 months and vaccinated for rabies one month before release. If the exposed animal is currently vaccinated, it should be revaccinated and observed for 45 days. Vaccinated or unvaccinated animals that have bitten someone, yet are considered to have not been exposed to rabies and are healthy, are quarantined for 10 days. If the animal develops any signs of rabies during this time period, it is humanely euthanized and its brain submitted for rabies testing. If the animal is a stray or unwanted, it may be euthanized and its brain submitted for rabies testing.
Guidelines for control of rabies in dogs prepared by WHO include the following:
* Notification of suspected cases and destruction of dogs with clinical signs as well as dogs bitten by a rabies-suspect animal,
* Reduction of contact with susceptible dogs by introduction of leash laws and quarantine,
* Immunization of dogs,
* Stray dog control and destruction of unvaccinated dogs, and
* Dog registration.
In May 2007, an updated rabies vaccination certificate was released by the National Association of State Public Health Veterinarians which includes a space for microchip number and more space for animal and vaccine information (the form is known as Form 51).
Management and Control in Humans
Pre-exposure vaccination for rabies is recommended for high-risk people such as veterinarians, animal handlers, wildlife workers, and laboratory workers. International travelers likely to be exposed to enzootic dog rabies should consider pre-exposure prophylaxis. Pre-exposure prophylaxis consists of three doses of rabies vaccine given intramuscularly on days 0, 7, and either day 21 or 28. There are currently three types of rabies vaccines made from killed rabies virus: human diploid cell vaccine (HDCV), rabies vaccine adsorbed (RVA), and purified chick embryo cell culture (PCEC). Human rabies vaccines are effective when given properly. High-risk individuals who have received the pre-exposure prophylactic vaccine series should routinely have antibody titers drawn to make sure their antibody numbers are at a protective level. If antibody levels are low, a booster vaccine is given.
Some time is needed following the initial inoculation of rabies vaccine to when the body mounts a sufficient response to achieve protection. Studies have shown that this time period is 28 days following the initial vaccination. Clients need to be aware that their vaccinated pets are not protected during this time and risks of contracting rabies need to be avoided.
Rabies is a preventable viral disease of mammals. Rabies virus, a rhabdovirus, is an RNA virus that causes acute encephalitis and myelitis in all warm-blooded animals including people. The outcome is almost always fatal. All species of mammals are susceptible to rabies infection; however, only a few species are important as reservoirs for the disease (such as raccoons, skunks, foxes, coyotes). In addition to terrestrial reservoirs, several species of insect-eating bats are reservoirs for rabies.
Transmission of rabies virus is usually through virus-laden saliva following an animal bite. Other routes of transmission include contaminated scratches, contaminated mucous membranes, aerosol transmission, and transplants (Figure 7-41).
Rabid animals exhibit CNS signs that vary slightly among species. Rabies virus infects the CNS, causing encephalitis and death, usually within 10 days of developing clinical signs. Rabies is often described as either being furious or dumb. Animals display either the furious or dumb phase of rabies 1 to 3 days after infection. People who contract rabies usually have a history of an animal bite, although some people are unaware of their bite wounds if the wound is inflicted by bats. The site of the wound initially feels painful followed by a period of burning and increased sensitivity to temperature changes. The first symptoms of rabies may be nonspecific flu-like signs such as fever or headache. Behavior changes such as restlessness or extreme excitability may occur. Muscle spasm and laryngospasm are followed by convulsions at which time large amounts of thick saliva are present. The laboratory test of choice for rabies identification in animals is a fluorescent antibody (FA) test on unfrozen brain tissue. Immunohistochemistry methods for rabies detection are used to detect rabies in formalin-fixed human brain samples. Electron microscopy can also be used to examine the ultrastructure of rabies virus and its inclusions. Animals are not treated for rabies. Post-exposure rabies prophylaxis is begun in people as soon as possible after exposure and when given promptly has been successful. Currently, postexposure prophylaxis is a regimen of one dose of immune globulin (antibody) that provides immediate but temporary protection, a dose of rabies vaccine, which starts the body producing its own antibodies, and four additional doses of rabies vaccine over a 28-day period. Additional doses of rabies vaccine are given on days 3, 7, 14, and 28 after the first vaccination. Human rabies immune globulin is also infiltrated around the wound. Vaccines are available for animals and humans. Animal control and vaccination laws are used to manage rabies.
[FIGURE 7-41 OMITTED]
Vesicular stomatitis (VS), also called sore mouth of cattle, is a highly contagious, sporadic disease of livestock characterized by vesicular (blisters and ulcers) lesions on the tongue, mouth, teats, or coronary bands. In addition to vesicular lesions, classic signs in horses, cattle, and swine include excessive salivation and lameness. VS was first reported in 1897 by Theiler who described an outbreak in horses and mules in Transvall, South Africa, in 1884. Affected animals had a fever, were anorexic, and had excessive salivation. Vesicles appear on the gums, tongue, and lips; ruptured-producing reddish ulcerations; and healed within 6 to 7 days. Although the disease has not been a problem in Africa since 1900 (unconfirmed cases may have occurred in 1934, 1938, and 1943), it sporadically appears in North and South America. The first officially reported case of VS in the United States was described in the veterinary literature in 1916 in the Denver stockyards; however, cavalry horses in the Civil War were described as having a disease similar to VS as early as 1862. J. R. Mohler in 1904 described a disease occurring in summer and fall, which affected the mouths (causing drooling and inability to eat) and feet (producing painful fissures near the coronary band) of cattle in some eastern and central western states. In 1906 Heiny described cases of VS in western Colorado and in 1907 horses in the Chicago stockyards were also described as having a disease similar to VS. In 1926 a major outbreak of VS occurred in New Jersey in mid-October and lasted until mid-November affecting 752 cattle on 33 farms in a 300 square mile area and 12 horses. In 1937 VS appeared in Wisconsin, Minnesota, the Dakotas, and Manitoba in both cattle and horses. VS was reported for the first time in South America in 1939 in horses and cattle of the La Plata region of Argentina. Two years later a major outbreak occurred in Venezuela involving 715 cattle, 195 horses, and 48 pigs (the first account of swine infection). In 1942 another VS strain appeared in Colorado (Indiana type) affected cattle and horses and was the last time this strain was seen in the United States. The Indiana serotype has been responsible for outbreaks of VS in 1942, 1956, 1964, 1965, and 1997 to 1998. The other VS serotype, the New Jersey serotype, has occurred in the United States in 1944, 1949, 1957, 1959, 1963, 1982 to 1983, 1995, and 2005 (470 cases during this outbreak).
The major concerns with vesicular stomatitis are its similar appearance to foot-and-mouth disease, its highly contagious nature, and the trade restrictions associated with it.
Vesicular stomatitis virus (VSV) is a member of the Rhabdoviridae family in the genus Vesiculovirus. It is a large (70 to 175 nm) bullet-shaped, helical, single-stranded, negative sense RNA virus (Figure 7-42). Its envelope has 10 nm spikes and is comprised of two virus-specific proteins (an internally situated nucleocapsid membrane protein (M) and an externally located, type-specific glycoprotein (G)). There are more than twenty serotypes in this viral genus, but only four are important as human pathogens (2 strains of VSV, Chandipura virus, and Piry virus). The two strains of VSV are the Indiana (VSV-I, which has subtypes 1 (Alagoas), 2 (cocal or Argentina), and 3 the New Jersey strains (VSV-NJ). The Indiana-1 and New Jersey strains of VSV are endemic in the Americas (Central and South America and Mexico) and have been responsible for the U.S. outbreaks. Three strains are found in South America: Indiana-2, Indiana-3, and Piry.
[FIGURE 7-42 OMITTED]
Epizootiology and Public Health Significance
VS is found in the warmer regions of North, Central, and South America. Outbreaks have occasionally occurred in the more temperate regions of the Western hemisphere. In Central and South America, VS can occur anytime but is especially common at the end of the rainy season. In the southwestern United States, VS is more common during the warmer months. The Indiana and New Jersey serotypes occur in North and South America and are responsible for most outbreaks. VS occurs occasionally in the southern United States with small outbreaks in horses occurring in 1998 and 2004. Other subtypes of VSV have been identified in Brazil (Alagoas or subtype 1) and South America (cocal, Argentina, or subtype 2). Outbreaks have been reported in France, but those cases were seen in horses shipped from the United States to Europe.
The most important serotypes of VSV are the Indiana and New Jersey variants. VS Indiana virus was the first arbovirus identified in the United States.
VS in people is rare and typically a self-limiting disease. In the United States, VS can affect the economy through reduced milk production, increased animal culling, increased morbidity, and veterinary and labor costs. Morbidity in animals is approximately 90%; however, mortality is rare.
The transmission of VS remains unclear, but is believed to be transmitted by insect vectors because of its typical occurrence during the warm months along rivers and in valleys. The sand fly and blackfly are the most important vectors of VSV. VSV-New Jersey has been isolated from several possible vectors including biting insects (Culicoides [biting midges], Simuliidae [black flies] (Figure 6-75), Aedes [mosquitoes], Lutzomyia [sand flies]) and nonbiting insects (Chloropidae [eye gnats], Anthomyiidae, Musca [house flies]). Vectors for VSV-Indiana include Aedes mosquitoes (Figure 6-76), Simuliidae (black flies), and Lutzomyia (sand flies). Transovarial transmission occurs in these arthropods.
Once in a herd or group of animals, VSV is transmitted between animals by direct contact (oral wounds and abrasions), fomites contaminated with saliva (milking machines, trailers, feed, bedding, cleaning equipment, etc.), indirect transmission from the hands of contaminated workers, or from the fluid of ruptured vesicles. Humans become infected by contact with vesicular fluid or saliva from infected animals. In laboratories aerosol transmission is possible. Arthropod transmission is also possible in people.
VS has an incubation period of 2 to 8 days in animals with clinical signs typically appearing in 3 to 5 days. Once the virus is inside a host cell VSV will shut down a host cell's system for protein synthesis. VSV then takes over the cell and makes its own proteins so it can replicate and spread. Histologic changes include intercellular edema of the middle layers of the epidermis, necrosis of epithelial cells in the middle layers, and inflammatory cellular infiltration of monocytes into necrotic epithelial areas. Edema in the skin can escape through vertical cracks in some layers of the epidermis. Large vesicles lose their overlying epithelial layers giving the lesions their eroded appearance. Healing of these lesions occur by regrowth of the epithelium from the basement membrane.
Clinical Signs in Animals
VS can occur in a variety of animals including horses, cattle, pigs, donkeys, mules, South American camelids, and some experimentally infected animals such as deer, raccoons, bobcats, and monkeys. Sheep and goats appear to be resistant to VS. The first clinical sign in most animals is excessive salivation, followed by development of vesicles. Just prior to or at the time vesicles appear, the affected animal may develop a fever. The characteristic vesicular lesions are raised blisters that may be seen on the lips, nares, hooves, teats, or in the mouth. Vesicles may be small or large. In horses, vesicles are typically on the dorsal surface of the tongue, the gums, lips, nares, and corners of the mouth. In cattle, vesicles are typically found on the hard palate, lips, gums, nares, and muzzle (Figure 7-43). In horses and cattle, hooves may have secondary lesions. In pigs, vesicles typically appear first on the feet and the pig may be lame. The muzzle is also commonly affected in pigs.
Vesicular lesions with VS are typically found in only one area of the body.
The vesicles associated with VS will eventually swell, break open, become painful, and produce erosions. At this point, animals may become anorexic, refuse to drink as a result of vesicular pain, and develop lameness. Weight loss and a drop in milk production may be seen in dairy animals. Animal recover in approximately 2 weeks unless secondary bacterial infections develop. Heart and rumen lesions may be seen on necropsy.
Clinical Signs in Humans
The incidence of VS in people is low and is most frequently contracted in the laboratory rather than from animal sources. Most people with VS are asymptomatic or may have influenza-like symptoms. The incubation period is 1 to 6 days. If people develop clinical signs they may develop a high fever, headaches, muscle and joint pain, ocular pain, and nausea. The formation of vesicles in people is rare and if found occur on the oral mucosa, lips, and nose. The disease is self-limiting in people. Recovery in humans may be long.
VS is not as contagious as foot-and-mouth disease.
[FIGURE 7-43 OMITTED]
Diagnosis in Animals
VS cannot be distinguished visually from other vesicular diseases such as foot-and-mouth disease and swine vesicular disease; therefore, laboratory diagnosis is needed. Federal and state veterinarians need to be contacted of any suspected vesicular disease. Proper authorities should be contacted prior to sample collection and submission. Samples must be sent under secure conditions and sent to authorized laboratories. Acceptable clinical specimens should be collected early in the disease and include vesicular fluid, saliva, and affected mucous membranes. Rapid diagnosis of VS is needed to exclude the diagnosis of foot-and-mouth disease. Virus detection from vesicle material is diagnostic through propagation of the virus in cell culture. A presumptive diagnosis can be achieved quickly by the electron microscopic demonstration of rhabdovirus in distilled H2O lysates of lesion material. Viral antigen is detected by serologic tests such as ELISA, complement fixation, and virus neutralization; antibody levels are detected by paired serum serologic tests using ELISA, complement fixation, and virus neutralization. Virus isolation has been used (tissue culture, embryonated chicken eggs, or unweaned mice) but has been unsuccessful.
Precautions such as wearing gloves should be taken when examining animals for evidence of VS.
Diagnosis in Humans
Human disease typically occurs during animal outbreaks. Human VS infections can be diagnosed with virus isolation from throat swabs or from blood using RT-PCR techniques or serologic tests.
Paired serum test taken 1 to 2 weeks apart are used in the United States to determine if an outbreak is occurring nationwide; after an outbreak is verified, a single positive complement fixation test is adequate for VS diagnosis.
Treatment in Animals
There is no anti-viral treatment for VS. Therapy is aimed at elevating pain and making sure the animal eats during the period in which vesicles are present. Oral ulcers can be swabbed with a 1% to 2% solution of Lugol's iodine and foot ulcers can be treated with copper sulfate to help prevent secondary infections. Feeding soft feeds may reduce mouth discomfort, administering anti-inflammatory drugs to minimize swelling and pain, and treating secondary bacterial infection of ulcerated areas are all measures that can help animals feel more comfortable during VS outbreaks.
Treatment in Humans
There is no anti-viral treatment for VS in humans. Therapy is symptomatic to relieve pain and to prevent secondary infections.
Management and Control in Animals
VS can spread rapidly within a herd. The following precautions can be taken to limit the spread of VSV.
* Clean feed bunks and water sources daily.
* Use foot protection, different boots, or disinfectant footbaths when moving between clean and infected areas. Phenolic disinfectants work best.
* Use individual rather than communal feeders and equipment.
* Practice arthropod control.
* Limit grazing during peak insect feeding times.
* Avoid the use of rough, coarse feed during outbreaks to prevent pain. Any leftover feed should be properly disposed of daily (burning).
* Know whether new animals added to a herd had clinical signs of VS within the past 3 months.
* Isolate newly purchased animals for at least 21 days. Animals can become reinfected with VSV after only a few weeks.
* Spray carcasses around the mouth, teats, and feet with disinfectant and treat them with insecticide if they cannot be disposed of immediately.
* Avoid livestock contact with other animals, such as dogs, cats, rodents, birds, and insects that can serve as vectors of VSV.
* Keep service personnel, farriers, and other visitors entering the premises to a minimum. Showers and clothes changes are recommended for these people. If possible, prevent feed, delivery, supplies, and other trucks from directly entering the unit.
* Limit use of farm vehicles transporting cattle to slaughter or driving to places where other cattle-hauling trucks and producers congregate.
* Vaccinate cattle for vesicular stomatitis (available intermittently during outbreak years).
During an outbreak, state or federal regulations restrict movement of animals and quarantines are placed on facilities with positive animals. Animals with clinical signs are isolated from the rest of the herd. Animals cannot be moved from an infected property for at least 21 days after all lesions have healed unless they are going to slaughter.
Management and Control in Humans
People can avoid infection with VSV by practicing good hygiene including the use of gloves when handling animals and animal samples. Insect control is important for both humans and animals. Both formalin-inactivated and attenuated live virus vaccines are available for human use, but are rarely administered.
Vesicular stomatitis (VS) is a highly contagious, sporadic, viral disease of livestock characterized by vesicular lesion on the tongue, mouth, teats, or coronary bands. Vesicular stomatitis virus (VSV) is a member of the Rhabdoviridae family in the genus Vesiculovirus and is a large, bullet-shaped, helical, single-stranded, negative sense RNA virus. There are more than twenty serotypes in this viral genus, but only two strains of VSV are important in North America: the Indiana (VSV-I, which has subtypes 1 (Alagoas), 2 (cocal or Argentina), and 3) and the New Jersey strains (VSV-NJ). VS is found in the warmer regions of North, Central, and South America. In the southwestern United States, VS is more common during the warmer months. The transmission of VSV remains unclear, but is believed to be transmitted by insect vectors because of its typical occurrence during the warm months along rivers and in valleys. Once in a herd or group of animals, VSV is transmitted between animals by direct contact, fomites contaminated with saliva, indirect transmission from the hands of contaminated workers, or from the fluid of ruptured vesicles. Humans become infected by contact with vesicular fluid or saliva from infected animals. In laboratories aerosol transmission is possible. Arthropod transmission is also possible in people. VS can occur in a variety of animals with the first clinical sign in most animals is excessive salivation, followed by development of vesicles. The characteristic vesicular lesions are raised blisters that may be seen on the lips, nares, hooves, teats, or in the mouth.
The incidence of VS in people is low and is most frequently contracted in the laboratory than from animal sources. Most people with VS are asymptomatic or may have influenza-like symptoms. VS cannot be distinguished visually from other vesicular diseases such as foot-and-mouth disease and swine vesicular disease; therefore, laboratory diagnosis is needed to confirm cases of VS. Virus detection from vesicle material is diagnostic through propagation of the virus in cell culture. Viral antigen is detected by serologic tests such as ELISA, complement fixation, and virus neutralization; antibody levels are detected by paired serum serologic tests using ELISA, complement fixation, and virus neutralization. Human VS infections can be diagnosed with virus isolation from throat swabs or from blood using RT-PCR techniques or serologic tests. There is no anti-viral treatment for VS. The spread of VSV can be limited by proper disinfection, proper animal management including isolation of animals and strict rules when adding animals to a herd, arthropod control, avoiding the use of rough, coarse feed during outbreaks to prevent pain, avoiding livestock contact with other animals, and keeping people and vehicles entering the premises to a minimum. People can avoid infection with VSV by practicing good hygiene including the use of gloves when handling animals and animal samples. Both formalin-inactivated and attenuated live virus vaccines are available for human use, but are rarely administered.
Togaviruses, derived from the Greek toga meaning gown or cloak, are named in reference to the loose cloak appearance of the envelope surrounding the virus (the envelope has been shown to be quite tightly bound with the use of electron microscopy). Togaviruses used to be classified into four genera; however, in 1984 it was divided into three families (Flaviviridae, Pestiviridae, and Togaviridae). The Togaviridae family currently consists of two genera: Alphavirus (containing 27 genera of which 11 are recognized to be pathogenic for man) and Rubivirus (containing one genus Rubella the causative agent of Rubella or German Measles that is transmitted by direct human contact, inhalation of viral infected aerosol, or congenitally). Alphaviruses will be the only Togaviruses covered in this section. All alphaviruses of clinical significance infect invertebrate hosts (mosquitoes) and vertebrate hosts (many bird and mammal species) and are geographically distributed mainly in the new world. Viruses normally replicate in animal reservoirs and only occasionally spread to humans by insect vectors. Vector transmission from person to person has not been documented as a result of the low viral concentration in the human host making transmission ineffective. The alphavirus' natural cycle usually involves birds and mammals and rarely humans.
All clinically relevant alphaviruses are transmitted by mosquitoes with bird migration playing a critical role in the import of virus into northern hemisphere countries. Alphaviruses predominate in the southern hemisphere; however, different variants of Eastern and Western equine encephalitis are found in South and North America suggesting that the virus may be able to survive during winter in cooler climates. The survival of alphavirus in certain regions depends on the ability of the vector and the vertebrate to develop viremic infections with low pathogenicity. Amplification hosts include birds, rodents, and monkeys. The diseases caused by alphaviruses include those caused by the agents of American encephalitides (EEE, WEE, and VEE) that produce a noncharacteristic febrile disease and those caused by a group that produce mild to severe arthropathies and rashes (Chikungunya virus, Sindbis virus, and Barmah Forest virus). Subclinical infections are possible with all alphavirus infections.
Alphavirus is the zoonotic genus in this group with the major diseases being Eastern, Western, and Venezuelan equine encephalitis. All of these encephalitides occur following the bite of an infected mosquito resulting in an asymptomatic viremia unless the virus invades neural tissue resulting in encephalitis. Venezuelan equine encephalitis (VEE), in contrast to Eastern equine (EEE) and Western equine encephalitis (WEE), has more systemic manifestations with less neural involvement. WEE was first isolated in the United States in 1930 and is typically seen in the western plain states. WEE is spread by the Culex tarsalis, a mosquito that breeds in ditches. This virus can multiply at cool temperatures and may be seen in northern areas. EEE was first isolated in the United States in 1933 and is transmitted by Culiseta melanura, a mosquito that lives in fresh water swamps and rarely bites animals. EEE is rare, but fatal in up to 90% of cases. VEE virus was isolated in 1938 and is found in rodents in the forests and marshes of the more tropical parts of America. It is transmitted by Cu. melanoconion. VEE does not cause significant disease in humans and the last epidemic of VEE in horses was in 1971 in southern Texas.
There are 27 species of Alphavirus that are spread mainly by mosquitoes and ticks. Alphaviruses are small, enveloped, polyhedral, single-stranded, positive sense RNA viruses that multiply in the cytoplasm of host cells. The RNA is enclosed in an icosahedral capsid and a surrounding envelope containing two viral glycoproteins: E1 (the protein associated with hemagglutination) and E2 (the receptor binding protein). Members of this genus contain a nucleoprotein capsid surrounded by a lipid bilayer envelope that is derived from the host cell membrane. Alphaviruses enter host cells by pinocytosis and they replicate in the cytoplasm. Translation of RNA produces a large protein that is cleaved to yield an RNA polymerase and the structural proteins. Once assembled, the virions bud from the host cell from which they acquire their envelope. Within their hosts they replicate in a wide variety of cells including neurons and glial cells, skeletal and smooth muscle cells, cells of lymphoid origin, and synovial cells.
Alphaviruses of the family Togaviridae are viruses that utilize insect vectors.
Encephalitis is an acute inflammatory process primarily involving the brain and meninges. Bacteria, fungi, and autoimmune disorders can cause encephalitis, but most cases are viral in origin. The equine encephalitides are a group of diseases cause by four viruses in the Alphavirus genus (Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), Venezulan Equine Encephalitis (VEE), and Everglades). Clinical disease caused by these four viruses varies from an asymptomatic infection to clinical illness similar to mild influenza to advanced neurologic disease. The probability of contracting these viruses and developing encephalitis vary widely among the different viruses with the incidence highest for the EEE virus and lowest for the VEE virus. The mortality rates for each of the encephalitides vary from 5% for WEE, 35% for VEE, to 50% for EEE. Everglades encephalitis virus causes very mild, influenza-like illness with no known fatalities.
Alphaviruses only infect humans incidently.
WEE virus was first isolated from the brains of dead horses in the San Joaquin Valley of California in the 1930s. Karl Meyer and his associates investigated this outbreak and were able to isolate a virus from the brain of an infected horse. This initial outbreak affected over 6,000 horses with mortality exceeding 50%. In 1938, WEE virus was isolated from a child's brain that had died from encephalitis making a link between the disease in animals and people. In 1941, the virus was isolated from Cu. tarsalis mosquitoes in the Yakima Valley of Washington and in the San Joaquin Valley of California. A large epidemic/epizootic of WEE spread over the western portion of the United States and Canadian prairies in that same year, infecting an estimated 300,000 horses and mules (50,000 developed the disease with 15,000 of them dying) and causing infection in over 3,000 people. WEE is still a threat to horses, but cases have declined as a result of proper vaccination.
EEE was the cause of epizootics in North American horses since 1831. EEE was first recognized by Dr. Alfred Large at the New York City Veterinary College who described a cerebrospinal meningitis occurring in horses on Long Island over a 20-year period. EEE was commonly referred to as staggers or putrid fever prior to a series of outbreaks that occurred on the eastern coastal area in 1933 (Delaware, Maryland, New Jersey and Virginia). EEE virus was first isolated from a dead horse's brain during that epizootic. In 1934 and 1935 outbreaks of EEE occurred in Virginia and North Carolina. The disease was discovered to occur annually in horses along the eastern seaboard of the United States (occasionally making its way as far inland as the Midwest and as far north as southeastern Canada). The virus continues to affect horses in North America, but the incidence of disease has decreased significantly as a result of effective vaccination protocols.
In 1936, VEE was first recognized as a disease in horses in Venezuela following a major outbreak. From 1936 to 1968, outbreaks of VEE continued to occur in equines in several South American countries. In 1969, the disease spread north throughout Central America and spread to Mexico and Texas in 1971. Since then major outbreaks of VEE occurred in 1993 (southern Mexico) and in 1995 (Colombia). Prolonged and heavy rainy seasons that cause increases in mosquito populations are largely responsible for outbreaks of VEE. The VEE virus strain that is pathogenic for humans is amplified in horses with equine disease occurring prior to human disease. This is in contrast to the EEE and WEE viruses, where horses appear to be dead-end hosts.
The Everglades encephalitis virus (also known as VEE sylvatic subtype II virus) is an alphavirus in the VEE serocomplex and its geographic location is restricted to the state of Florida. Everglades encephalitis virus was first recognized in South Florida in the 1960s, when Seminole Indians living north of Everglades National Park were shown to have as high as a 58% seropositive rate. Everglades encephalitis virus circulates among rodents and mosquitoes and infects humans, causing a febrile disease occasionally accompanied by mild neurologic signs. In most people clinical signs include very mild, influenza-like illness that begins with a gradual onset of respiratory problems and gradual recovery. No new cases of Everglades encephalitis virus causing human disease have been reported since 1971. In horses it is considered nonpathogenic. Many people consider Everglades encephalitis virus to be an enzootic subtype of VEE.
EEE and WEE are maintained in nature between mosquitoes and birds; VEE is maintained in nature between mosquitoes and rodents.
All equine encephalitis viruses (EEE, WEE, VEE, and Everglades) are members of the genus Alphavirus and the family Togaviridae. Alphaviruses are single-stranded, positive sense RNA viruses in which replication takes place in the cytoplasm of the infected host cell (Figure 7-44). EEE virus typically cycles among passerine birds and the bird-feeding mosquito Culiseta melanura. A less harmful variant of EEE virus exists in Central and parts of South America. EEE causes disease in humans, horses, and some species of birds. WEE virus typically cycles among birds and the mosquito Culex tarsalis (the same mosquito that transmits SLE virus). Five subtypes (WEE, Buggy Creek, Fort Morgan, Highland J (all in North America), and Aura in South America) are found in the WEE complex. WEE causes disease in humans, horses, and some species of birds. VEE virus typically cycles among rodents and the mosquito Culex melanoconion (birds may also be involved in some cycles). There are at least 8 subtypes that are divided into epizootic and enzootic groups. Epizootic subtypes are responsible for most epidemics and are highly pathogenic for horses (can cause mild illness in people). Enzootic (sylvatic) subtypes (Everglades encephalitis virus) are found in limited geographic areas occurring naturally between rodents and mosquitoes. Enzootic types can cause human disease and are usually nonpathogenic in horses.
[FIGURE 7-44 OMITTED]
Epizootiology and Public Health Significance All of the equine encephalitis viruses are found in North, Central, and South America. Geographic differences between the viruses include:
* EEE virus is found in eastern Canada, all states east of the Mississippi River, Arkansas, Minnesota, South Dakota, Texas, the Caribbean, and regions of Central and South America (particularly along the Gulf coast). EEE occurs in the United States in approximately 12 to 17 people annually with an infection rate of about 33% and morbidity rate of 90%. Most cases of EEE are seen in people older than 55 years and children younger than 15 years. Case fatality rates vary from 33% to 70% with permanent neurologic deficits occurring in survivors.
* WEE virus is found in western Canada, Mexico, parts of South America, and west of the Mississippi River. WEE occurs in the United States at a variable rate. In 1941 there was an epidemic in which 3,000 cases occurred. Most infections in adults are asymptomatic or mild; therefore, accurate case numbers are difficult to attain. Overall mortality rates are 3% to 4%.
* VEE virus is endemic in South and Central America and Trinidad. VEE in humans typically follows an epizootic in horses. Ninety percent to 100% of exposed people will contract the disease with almost 100% of infections being symptomatic. Less than 1% develops encephalitis and approximately 10% of these cases are fatal. Very young or very old people tend to develop severe infections.
* Everglades encephalitis virus (enzootic subtypes of VEE) is found in Florida. A few isolated cases have been seen in the Rocky Mountains and northern plains of the United States.
The equine encephalitis viruses are transmitted by mosquitoes. The differences between modes of transmission revolve around the types of mosquito and the animals in which the virus cycles. EEE and WEE viruses cycle between birds and mosquitoes with humans and horses being incidental, dead-end hosts. EEE virus can be isolated from 27 species of mosquito in the United States with the most important vector being Culiseta melanura (a mosquito that feeds primarily on birds). WEE cycles between passerine birds and culicine mosquitoes with the most important vector being Cu. tarsalis (Figure 7-16). In birds, EEE and WEE can be spread by feather picking and cannibalism. VEE virus cycles between rodents and mosquitoes with the most important vectors coming from the Culex spp. (Culex melanoconion). Humans and horses are incidental hosts of VEE virus. Enzootic subtypes (Everglades) can also have birds involved in their cycle. Epizootic subtypes can be found in other mammals such as cattle, pigs, and dogs, but they do not become ill nor spread the virus. Horses are the main amplifiers of epizootic subtypes during epidemics. In some cases, humans have developed VEE from being exposed to laboratory rodent debris.
Certain environmental conditions such as increased rainfall and warm temperatures allow mosquito populations to flourish.
After being bitten by an infected mosquito vector, muscle tissue is the primary site of initial viral replication. From the muscle, the virus travels to the regional lymph nodes and multiplies in neutrophils and macrophages. If the immune system cannot rid the body of the virus, the viral particles can be found in several tissues including the liver and spleen, where they continue to replicate. As viral quantities increase, a fever typically develops. Approximately 3 to 5 days postinfection the virus reaches the brain causing a wide variety of lesions and pathologic processes such as cerebral edema, petechial hemorrhage, focal brain necrosis, and edema of the meninges. In contrast to EEE and WEE, VEE virus causes a systemic infection with viremia rather than a localized brain infection. Viremia as a result of VEE virus typically leads to respiratory and gastrointestinal signs.
Clinical Signs in Animals
Eastern Equine Encephalitis
EEE virus can infect horses, pigs, birds, bats, reptiles, amphibians, and rodents. The incubation period for EEE is about 1 to 3 days with signs of clinical illness lasting from 2 to 9 days. EEE in horses typically presents with fever and anorexia (prodromal (initial) stage). In severe cases, this initial stage is followed by neurologic signs such as impaired vision, aimless wandering, head pressing, circling, ataxia, paralysis, and seizures. Other signs that can be seen include periods of excitement, pruritus, and lateral recumbency with paddling. Death can occur with EEE viral infections (average mortality rate of about 90% in clinically affected horses) (Figure 7-45). Most EEE virus infections in birds are asymptomatic; however, disease can be seen in partridges, pheasants, psittacine birds, ratites, and whooping cranes. Disease in these birds can be fatal.
WEE virus is not as invasive in the nervous system as EEE virus; therefore, encephalitis caused by WEE is not as severe as that caused by EEE.
Western Equine Encephalitis
WEE virus can infect birds, horses, and a variety of mammals. The incubation period for WEE is 2 to 9 days and the clinical signs of disease will last between 2 and 9 days. WEE in horses is clinically similar to EEE. Both EEE and WEE can be asymptomatic, cause mild disease, or cause severe neurologic signs (Figure 7-46). WEE typically does not progress beyond the general, milder signs. Death as a result of WEE virus ranges from 5% to 20%. Most WEE infections in birds are asymptomatic.
[FIGURE 7-45 OMITTED]
[FIGURE 7-46 OMITTED]
Venezuelan Equine Encephalitis
VEE virus can infect rodents, horses, mules, burros, and donkeys. Birds, cattle, pigs, and dogs can be infected with the virus without producing clinical signs. The incubation period for VEE is 1 to 5 days and the clinical signs of disease will last between 2 and 9 days. In horses, the epizootic subtypes can cause either asymptomatic signs; a febrile, prodromal disease followed by neurologic disease (and occasionally diarrhea and colic with death occurring within hours after the onset of neurologic signs); or a generalized acute febrile disease without neurologic signs (Figure 7-47).
Everglades Equine Encephalitis
Enzootic VEE (Everglades) virus can infect rodents, equine, and a variety of laboratory animals. The enzootic subtypes of VEE are usually asymptomatic in horses.
[FIGURE 7-47 OMITTED]
Clinical Signs in Humans
EEE and WEE present similarly in people with an incubation period of 4 to 15 days. EEE usually starts acutely with clinical signs of fever, muscle pain, headache, and occasionally nausea and vomiting. These initial signs may be followed by neurologic signs such as confusion, neck stiffness, depression, coma, seizures, and paralysis. Mortality rates for EEE in people are high. WEE can present like EEE, but is usually asymptomatic in adults (nonspecific signs of illness that present acutely such as fever, headache, vomiting, and lethargy with few fatalities). WEE can be severe in children resembling the more severe signs of EEE.
The equine encephalidites cause illness only in horses and humans; although these viruses can infect a variety of other animals, they are often asymptomatic.
VEE in people typically presents with an acute, mild illness with clinical signs such as fever, lethargy, severe headache, and muscle pain (especially in the legs and lumbosacral region). These initial symptoms can last 24 to 72 hours and may be followed by a cough, nausea, vomiting, and diarrhea. The disease course is typically 1 to 2 weeks. In pregnant women, VEE virus can cause fetal damage including encephalitis, abortion, or congenital neurologic abnormalities. Encephalitis from VEE virus is about 4% in children and approximately 0.4% in adults. Encephalitis typically occurs with the second peak of the biphasic fever. Enzootic VEE (Everglades) does not typically cause clinical disease in people.
Diagnosis in Animals
In horses, EEE and WEE are diagnosed by serologic methods such as hemagglutination inhibition, ELISA, and complement fixation. Cross-reaction between EEE and WEE antibodies may occur with some tests. Clinical infections in birds are typically diagnosed by virus isolation. Virus isolation in horses (in brain, hepatic, or splenic tissue) is used for cases of EEE, but is not accurate for cases of WEE. EEE and WEE viruses can be isolated from animal culture such as mice or chicks.
VEE is diagnosed in horses via virus isolation or serologic methods. The virus can be isolated from blood collected during the febrile state and occasionally from the brains of animals with encephalitis. Serologic methods used for VEE virus identification include complement fixation, hemagglutination inhibition, ELISA, and immunofluorescent assays. Everglades encephalitis virus is identified by the same methods as VEE virus.
[FIGURE 7-48 OMITTED]
Postmortem gross lesions in horses are nonspecific; EEE cases may demonstrate brain and meningeal congestion; VEE cases may show no nervous system lesions while some show necrosis with hemorrhages. Microscopic brain tissue examination of all the equine encephalitides viruses can demonstrate inflammation of the gray matter and perivascular cuffing (Figure 7-48).
Diagnosis in Humans
EEE, WEE, and VEE viruses can be diagnosed in people using virus isolation and serologic methods such as ELISA, complement fixation, immunofluorescent antibodies, and hemagglutination inhibition. PCR testing is also available.
Treatment in Animals
Treatment of EEE, WEE, and VEE is supportive in animals. Fever reduction is important with EEE and WEE.
Treatment in Humans
Treatment of EEE, WEE, and VEE is supportive. Physical therapy is important during the recovery phase of EEE. Fever reduction is important with EEE and WEE. VEE and Everglades is usually mild and does not require treatment.
Management and Control in Animals
Equine vaccines are available for EEE, WEE, and VEE (have been available for about 30 years). EEE vaccines are also available for birds. Mosquito control is also important to control the spread of disease.
Management and Control in Humans
There is no human vaccine available against these viruses. Prevention of these diseases in people depends on the surveillance of these viruses in mosquitoes, birds, rodents, and horses. Mosquito control is indicated in areas with a high mosquito population including the use of insect repellants and environmental spraying.
Encephalitis is an acute inflammatory process primarily involving the brain and meninges. The equine encephalitides are a group of diseases cause by four viruses in the Alphavirus genus, Togaviridae family (Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), Venezulan Equine Encephalitis (VEE), and Everglades). (For less common zoonotic Alphaviruses, see Table 7-19.) Clinical disease caused by these four viruses varies from an asymptomatic infection to clinical illness similar to mild influenza to advanced neurologic disease. All of the equine encephalitis viruses are found in North, Central, and South America. The equine encephalitis viruses are transmitted by mosquitoes. EEE and WEE viruses cycle between birds and mosquitoes with humans and horses being incidental, dead-end hosts. VEE virus cycles between rodents and mosquitoes with humans and horses being incidental hosts of VEE virus. In animals, EEE virus can infect horses, pigs, birds, bats, reptiles, amphibians, and rodents. EEE in horses typically present with fever and anorexia that may progress to neurologic signs such as impaired vision, aimless wandering, head pressing, circling, ataxia, paralysis, and seizures. Death can occur in about 90% of EEE viral infections in horses. WEE virus can infect birds, horses, and a variety of mammals. WEE in horses is clinically similar to EEE with death being rarer in cases of WEE. VEE virus can infect rodents, horses, mules, burros, and donkeys. In horses, the epizootic subtypes of VEE can cause asymptomatic signs; a fever followed by neurologic disease; or a generalized acute febrile disease. Enzootic VEE (Everglades) virus can infect rodents, equine, and a variety of laboratory animals. The enzootic subtypes of VEE are usually asymptomatic in horses. In people, EEE and WEE have similar clinical signs. EEE usually starts acutely with clinical signs of fever, muscle pain, headache, and occasionally nausea and vomiting that may be followed by neurologic signs such as confusion, neck stiffness, depression, coma, seizures, and paralysis. WEE is usually asymptomatic in adults, but can resemble the more severe signs of EEE in children. VEE in people typically presents with an acute, mild illness with clinical signs such as fever, lethargy, severe headache, and muscle pain (especially in the legs and lumbosacral region). In horses, EEE and WEE are diagnosed by serologic methods such as hemagglutination inhibition, ELISA, and complement fixation. VEE is diagnosed in horses via virus isolation or serologic methods. Microscopic brain tissue examination of all the equine encephalitides viruses can demonstrate inflammation of the gray matter and perivascular cuffing. EEE, WEE, and VEE viruses can be diagnosed in people using virus isolation and serologic methods such as ELISA, complement fixation, immunofluorescent antibodies, and hemagglutination inhibition. PCR testing is also available. Treatment of EEE, WEE, and VEE is supportive in animals and people. Equine vaccines are available for EEE, WEE, and VEE. EEE vaccines are also available for birds. Prevention of these diseases in people depends on the surveillance of these viruses in mosquitoes, birds, rodents, and horses. Mosquito control is indicated in areas with a high mosquito population including the use of insect repellants and environmental spraying. There is no human vaccine for these viruses.
1. Viruses are
a. prokaryotic cells.
b. eukaryotic cells.
c. animal cells.
2. In general, DNA viruses mature in the --, whereas RNA viruses replicate in the --.
a. nucleus, nucleoplasm
b. cytoplasm, ribosomes
c. nucleus, ribosomes
d. nucleus, cytoplasm
3. Persistent viral infections that exhibit a long noninfectious stage between the original disease and the subsequent disease are called
4. Common ways to identify viruses are
a. culture on agar and staining methods.
b. staining methods and biochemical tests.
c. antigen/antibody testing and gene amplification.
d. cell culture and staining methods.
5. Emerging viral infections occur because of
a. a relaxation of public health standards.
b. changes in weather patterns.
c. airline travel and its effect on travel to disease endemic areas.
d. all of the above.
6. Hantavirus pulmonary syndrome
a. can result in death as a result of kidney failure much as in HFRS.
b. is an emerging disease resulting from mutations of hantavirus the causative agent of HFRS.
c. occurs in the desert southwest of the United States especially during years of heavy rainfall.
d. has flying foxes as its reservoir hosts.
7. Negri bodies are associated with
a. dengue fever.
b. hantavirus pulmonary syndrome.
8. One characteristic of influenza viruses is the tendency to cause pandemics. New epidemics arise because of the organism's ability to undergo major structural changes and genetic reassortment. This phenomenon is called
a. antigenic shift.
b. continental drift.
c. Reye's syndrome.
9. Dengue hemorrhagic fever is as a result of
a. preformed antibodies to the infecting serotypes of dengue virus.
b. acute respiratory distress/shock syndrome.
c. development of autoantibodies.
d. preformed antibodies to a different serotype of dengue virus.
10. What is the most common pediatric arboviral encephalitis in the United States?
a. West Nile encephalitis
b. St. Louis encephalitis
c. La Crosse encephalitis
d. Everglades encephalitis
11. What played a major role in the emergence of SARS?
a. SARS is caused by a coronavirus, which are viruses with a high frequency of mutation and a high frequency of recombination so that new strains can form to adapt to changing conditions.
b. Civet cats are asymptomatic when they first acquire the virus and spread the virus to people prior to the development of clinical signs (respiratory and neurologic signs are common).
c. People can carry the SARS virus for years and not show clinical signs while they are transmitting the virus to other people. d. The disease is contracted most commonly on airplanes (95%) and with the increase in air travel the virus spread quickly through travelers.
12. What mosquito-borne flavivirus causes sows to abort and piglets to die; has spread over the past 50 years across Southeast Asia, India, southern China, and the Pacific reaching Australia in 1998; and is of great concern of spreading worldwide?
a. Powassan virus
b. Louping ill virus
c. Tick-borne encephalitis virus
d. Japanese encephalitis virus
13. What arbovirus is transmitted from wild birds and domestic fowl to people via mosquitoes?
b. St. Louis encephalitis virus
d. Fowlpox virus
14. What viral encephalitis was introduced into the United States in 1999 and can cause severe neurologic disease in horses?
a. Eastern equine encephalitis
b. Western equine encephalitis
c. Everglades encephalitis
d. West Nile fever
15. What is the appropriate treatment of monkeys following a nonhuman primate bite?
a. Wound cleaning and debridement with chlorhexidine solution.
b. Wound cleaning and flushing with saline.
c. Delayed wound cleaning that could force viruses like Herpes B deeper into the wound.
d. Wound cleaning with chlorhexidine solution, flushing the wound with saline, and suturing of the wound with nonabsorbable suture.
16. What is true regarding avian influenza?
a. Most avian influenza strains are highly pathogenic strains that cause fowl plaque, a severe, often fatal disease in domestic poultry.
b. Most avian influenza strains are low pathogenic strains that produce subclinical or mild respiratory infections in infected birds.
c. Most avian influenza strains are the same strain as swine influenza and can mutate causing disease in birds, pigs, and humans.
d. Most avian influenza strains are severely pathogenic in ducks and geese who develop viremia producing death in 24_48 hours.
17. For what disease are birds quarantined for upon entry into the United States?
b. fowl plaque
d. exotic Newcastle disease
18. What is the reservoir host of Nipah virus?
c. fruit bats
19. Federal authorities need to be contacted whenever a vesicular disease is seen in animal because of the fear of
a. swine vesicular disease.
b. foot-and-mouth disease.
c. equine herpes virus.
d. feline herpes virus.
20. What type of sample is submitted for rabies virus determination in animals?
c. whole blood
21. What form of equine encephalitis is most deadly in horses?
22. What form of equine encephalitis is most deadly in people?
23. The vector for Colorado tick fever is
a. Aedes mosquitoes.
b. Phlebotomus sandflies.
c. Ixodes scapularis ticks.
d. Dermacentor andersonii ticks.
24. What viral disease causes 80% morbidity in unvaccinated flocks of sheep, malnutrition in lambs because ewes with sore teats will not let them nurse, and typically presents with papules/pustules/vesicles on the lips, nares, ears, and eyelids?
a. foot-and-mouth disease
b. vesicular stomatitis
c. herpes virus
d. contagious ecthyma
25. What viral diseases are transmitted by mosquitoes and have monkeys as reservoir hosts?
a. Dengue fever and yellow fever
b. Rift Valley fever and herpes B virus
c. Ebola virus and Marburg virus
d. Lassa fever and hantavirus
26. What virus was isolated in monkeys in Reston, Virginia, in 1989?
a. Marburg virus
b. Ebola virus
27. An example of a robovirus is
a. St. Louis encephalitis virus.
c. Herpes B virus.
d. Colorado tick fever virus.
28. What virus was seen for the first time in the United States in 2003 in prairie dogs?
a. Rift Valley fever virus
b. monkeypox virus
c. Epstein-Barr virus
29. Chickens that have clinical signs of diarrhea, head and wattle edema, neurologic signs, and decreased egg production should be tested for
b. vesicular disease.
d. Newcastle disease.
30. The first pandemic of the 21st century was
d. dengue shock syndrome.
Matching 31. -- Meurto Canyon virus A. Bunyavirus that typically causes severe encephalitis and neurologic sequelae in children younger than 16 years of age 32. -- Ebola virus B. soremouth in sheep 33. -- SARS C. Flavivirus that is spreading from Asia to other parts of the world and is found in swine (abortion may occur in infected animals) 34. -- Newcastle disease D. virus that causes small, depressed virus scars upon healing 35. -- Nipah virus E. Hantavirus more commonly known as the Sin Nombre strain 36. -- lymphocytic F. Filoviridae virus that causes hemorchoriomeningitis virus rhagic fever in humans, chimpanzees, and gorillas 37. -- foot-and-mouth G. most widespread flavivirus disease virus 38. -- swine vesicular H. disease caused by a coronavirus that disease mutated from civet cats 39. -- dengue fever I. reovirus that may cause a biphasic fever 40. --contagious ecthyma J. Arenavirus whose natural host is the house mouse (Mastomys musculus) 41. -- La Crosse K. bullet-shaped virus that produces encephalitis virus neurologic signs 42. -- Colorado tick fever L. disease that causes excessive virus salivation, followed by the development of oral blisters in animals 43. -- herpes B virus M. most frequently seen mosquito-borne viral infection worldwide 44. -- St. Loius N. orthomyxovirus that has three encephalitis virus serotypes: A (zoonotic), B, and C 45. -- poxvirus O. picornavirus spreads rapidly through cattle herds having great economic impact on a country 46. -- rabies virus P. paramyxovirus that causes unilateral conjunctivitis and influenza-like symptoms in people 47. -- Japanese Q. paramyxovirus that is asymptomatic encephalitis virus in pigs and has a reservoir host of fruit bats 48. -- vesicular R. disease that presents clinically stomatitis identical to foot-and-mouth disease except it is only in pigs 49. -- influenza virus S. virus of concern for laboratory workers and zoo workers who work with nonhuman primates 50. -- West Nile virus T. Flavivirus that is mosquito-borne, uses birds as amplifying hosts, and is seen in North America
51. Three weeks after returning from a camping trip to Arizona, a 25-year-old female developed a fever and severe muscle aches. She also had a dry cough, headaches, nausea, and vomiting. Four days later the symptoms became progressively worse as fluid began to accumulate in her lungs and she went to the emergency room. She developed dyspnea and her blood pressure dropped. She was intubated and put on a ventilator. Microbiological tests on various bacterial pathogens were negative. The patient's symptoms worsened and she had cardiopulmonary arrest and died. An epidemiologist was called in to investigate this person's cause of death.
a. Based on this person's travel history and clinical signs, what disease may she have?
b. What type of sample should be run from this patient?
c. What would the epidemiologist be looking for at and near the campsite?
d. What other investigation should be done?
52. A 7-year-old boy had recently started taking horseback riding lessons during his summer vacation. During a particularly rainy period he did not take lessons for 2 weeks, but started taking lessons again the following month. At the end of the summer he started developing neck stiffness, fever, and mental confusion. He was taken to the hospital where a spinal tap was done on the boy (results were negative for bacterial meningitis). He got progressively worse and developed seizures over the next few days. He was put on anticonvulsant medication and antipyretics to reduce his fever. Over the next few days he started to improve with symptomatic care.
a. What may have been a cause of this boy's neurologic problems?
b. What in the history leads you to this conclusion?
c. What should be asked of the owners of the horseback riding establishment?
d. What samples could be tested on this boy for confirmation of this disease?
e. What should this boy do next time he goes horseback riding?
53. On September 1, a 10-year-old boy from rural Mississippi developed a fever and headache. He was evaluated by a pediatrician three days later and had a temperature of 102.6[degrees]F and was noted to have sensations he described as an "itchy" scalp. The pediatrician diagnosed viral illness and the patient was advised to return if symptoms worsened. Two days later the boy's condition worsened and he was taken to the emergency room. All laboratory tests and chest radiography were within normal limits and he was sent home. The boy's clinical signs worsened throughout the day, and he returned to the emergency room that evening with symptoms of fever, insomnia, urinary urgency, paresthesia of the right side of the scalp and right arm, dysphagia, disorientation, and ataxia. He was admitted to the hospital for suspected encephalitis. Shortly after admission, the patient's neurologic status deteriorated rapidly with his speech becoming slurred and he began to hallucinate. He became increasingly agitated and combative and required sedation. In his agitated state, the patient bit a family member. The next morning the patient was transferred to a tertiary care facility. Within hours after transfer, he became lethargic and was intubated. During the next 10 days, the boy continued to worsen and experienced wide fluctuations in blood pressure and temperature. On the eleventh day of his symptoms he had onset of cerebral edema and subsequent brain herniation. His life support was withdrawn, and the patient died the next day.
a. What should the medical staff check for on this patient's body?
b. What samples should be tested in this patient?
c. Assuming the boy may have contracted rabies, what should be investigated?
d. Pending test results, what should happen to the family member who the boy had bitten?
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Table 7-17 Lyssaviruses Geographic Virus Type Host Location Rabies virus (lyssavirus type 1) Mammals (especially Worldwide canine species) Lagos bat virus Bats Africa (lyssavirus type 2) Mokola virus (lyssavirus type 3) Bats Africa Duvenhage virus Bats South Africa (lyssavirus type 4) European bat virus type 1 Bats Europe (lyssavirus type 5) European bat virus type 2 Bats Europe (lyssavirus type 6) Australian bat virus Flying foxes Australia (lyssavirus type 7) Table adapted from Krauss. Table 7-18 Vesiculoviruses Geographic Virus Type Location Vesicular Stomatitis Virus type 1 (Indiana) U.S. Vesicular Stomatitis Virus type 2 (New Jersey) U.S. Vesicular Stomatitis Virus type 3 (Cocal) U.S. Vesicular Stomatitis Virus type 4 (Alagoas) U.S. Chandipura virus India Isfahan virus Iran Piry virus Brazil Table 7-19 Less Common Zoonotic Alphaviruses Alphavirus Disease Semliki Semliki forest fever Forest virus First isolated from mosquitoes in the Semliki Forest, Uganda in 1944 Sindbis Sinbis fever virus First isolated in 1955 from Culex mosquitoes in Sinbis, Eygpt O'Nyong- O'Nyong-Nyong fever Nyong virus First time disease was a major epidemic in Uganda in 1959 O'Nyong-Nyong means very painful and weak in Acholi language Mayaro virus Mayaro fever Disease information based on three epidemics with fewer than 100 cases per epidemic; each outbreak was associated with close human contact with forests. Ross River Epidemic polyarthritis, Ross virus River fever Named after the river in northern Queensland where it was first identified Barmah Barmah Forest fever Forest virus First isolated in 1974 in Barmah Forest area of Murray River in northern Victoria, Australia Chikungunya Chikungunya fever virus Chikungunya is Swahili for what bends (joints) Predominant Alphavirus Signs in People Semliki Fever, headaches, joint and Forest virus muscle pain. Occasional diarrhea, abdominal pain, and conjunctivitis. Sindbis Disease begins with low-grade virus fever, headaches, and joint pain of hands and feet. A rash develops on the body. Acute disease last for about 10 days. High percentage of seropositive people in the Nile Valley and other parts of Africa. O'Nyong- Acute onset of fever, chills, Nyong virus and epistaxis. Occasionally have back and joint pain, headache, and ocular pain. A pruritic rash on face and body occurs later in the disease. Disease usually resolved in 5 days. Morbidity during epidemics can be as high as 70%. Mayaro virus Fever, headaches, abdominal pain, joint pain, chills, and a rash. Ross River Initially mild fever and virus polyarthritis (especially small joints of hands and feet), generalized rash, and enlarged lymph nodes. Encephalitis in rare cases. Cases resolve in 4 to 7 months. Barmah Similar to Ross River fever Forest virus except milder Chikungunya Sudden fever, joint pain, and virus rash. Fever lasts 3 to 10 days and is typically biphasic Clinical Signs Alphavirus in Animals Transmission Semliki * Horses develop Infection is acquired Forest virus encephalitis via a mosquito bite; aerosol contamination possible Sindbis * Wild birds are Infection is acquired virus asymptomatic via a variety of mosquito species (Anopheles, Mansonia, Aedes, and Culex). O'Nyong- * Proof of animal Infection is acquired Nyong virus disease is via a variety of unsubstantiated mosquito species (Anopheles gambiae and Anopheles funestus). Mayaro virus * New World Infection is acquired monkeys are via a variety of asymptomatic mosquito species (Haemagogus spp., Culex spp., etc). Ross River * Animals and Infection is acquired virus birds are via a variety of asymptomatic mosquito species (Aedes vigilax and Culex annulirostris) Barmah * Animals and Infection is acquired Forest virus birds are via a variety of asymptomatic mosquito species Chikungunya * Monkeys Infection is acquired virus develop via a variety of Dengue-like mosquito species signs (fever, (Aedes aegypti is headaches, main vector in Asia; joint and Aedes aegypti and muscle pain, Culex spp. and other rash) Aedes spp. are main * Birds are vectors in Africa) asymptomatic Geographic Alphavirus Animal Source Distribution Semliki Horses, birds, wild n African Forest virus rodents, and a countries variety of domestic and parts of animals Asia Sindbis Wild birds n Nile Valley virus Latent infection and parts of seen in cloven- Africa, Asia, hoofed animals Europe, and Australia O'Nyong- Natural reservoir * East Africa Nyong virus unknown Mayaro virus South American * Brazil, monkey species, Trinidad, marmosets are Bolivia, amplification hosts Suriname, in tropical rain Guyana, forests, wild birds. Columbia, Peru, Panama Ross River Wild and domestic Australia virus animals (cattle, (widespread) pigs, sheep, horses, and Oceania kangaroos, wallabies rodents, dogs); wild birds Barmah Wild and domestic Western Forest virus animals (cattle, Australia pigs, sheep, horses, (widespread) kangaroos, wallabies rodents, dogs); wild birds Chikungunya Non-human Africa (all virus primates countries south of the Sahara), Southern and Southeastern Asia Found in areas near the jungle Alphavirus Diagnosis Control Semliki Cell culture, Mosquito Forest virus PCR, and control; vaccines ELISA tests have not been developed. Sindbis RT-PCR and Mosquito virus ELISA tests control; vaccines available have not been Rarely by developed. virus isolation O'Nyong- Cell culture Mosquito Nyong virus from blood control; vaccines during have not been febrile stage, developed. RT-PCR, neutralization test based on 80% plaque reduction Mayaro virus Cell culture, Mosquito RT-PCR, ELISA control; vaccines have not been developed. Ross River Cell culture, Mosquito virus RT-PCR, ELISA control; vaccines have not been developed. Barmah Cell culture, Mosquito Forest virus RT-PCR, ELISA control; vaccines have not been developed. Chikungunya Cell culture, Mosquito virus RT-PCR control; vaccines have not been developed.
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|Title Annotation:||Part 4: RHABDOVIRUSES-References|
|Author:||Romich, Janet Amundson|
|Publication:||Understanding Zoonotic Diseases|
|Article Type:||Disease/Disorder overview|
|Date:||Jan 1, 2008|
|Previous Article:||Chapter 7 Viral zoonoses.|
|Next Article:||Chapter 8 Prion zoonoses.|