Tick-Borne Encephalitis
Epidemiology and etiology Tick-borne encephalitis (TBE) is caused by two closely related viruses of the family Flaviviri-dae, genus Flavivirus.44 The eastern subtype of the TBE virus is transmitted by Ixodes persulcatus and causes Russian spring-summer encephalitis, which occurs from Eastern Europe to China. The western subtype is transmitted by I. ricinus and causes Central European encephalitis, which occurs from Scandinavia in the north to Greece and Serbia and Montenegro in the south. Of the two subtypes, Russian spring-summer encephalitis is the more severe infection, having a mortality of 5% to 20%, compared with less than 2% for the western subtype. Both viruses are maintained in natural cycles involving a variety of mammals and ticks. Human exposure occurs through work or recreational activities in the spring and summer months in temperate zones and in fall and winter in the Mediterranean, when the ticks are most active. Infection may also occur through the ingestion of raw milk or cheese from cows, sheep, or goats.
Diagnosis The incubation period of TBE is usually 7 to 14 days. The western subtype typically produces a biphasic illness. Infection usually presents as a mild, influenzalike illness lasting 2 to 7 days, followed by an afebrile or relatively asymptomatic period lasting 2 to 10 days. Approximately one third of patients then develop higher fevers with aseptic meningitis or meningoencephalitis. The eastern subtype usually progresses without an asymptomatic phase. Permanent paresis develops in 2% to 10% of patients with the western subtype and in 10% to 25% of patients with the eastern subtype. Rarely, cases occur in United States citizens who visit enzootic areas. Infections can be confirmed serologically by the CDC on request of state and local health departments.
Treatment and prevention Treatment of TBE is supportive. Inactivated vaccines against both eastern and western subtypes of TBE viruses are available in Europe, but they are not commercially available in the United States44; candidate vaccines are in development in the United States.45 Prevention strategies include avoiding tick bites and pasteurizing milk.
West Nile Virus
Epidemiology and etiology West Nile virus (family Flaviviri-dae, genus Flavivirus), first isolated in 1937 in the West Nile district of Uganda, has historically had a wide geographic distribution in Africa, Asia, the Middle East, and Europe.46 The virus was first recognized in the Western Hemisphere during an epizootic among birds and horses and a human encephalitis outbreak in the New York City area in 1999.47 From the 1950s to the 1970s, human outbreaks were reported infrequently, mostly in the Middle East. However, since the mid-1990s, outbreaks of neurologic disease in humans and horses, with an increase in death rates, may have marked the evolution of a new West Nile virus variant.46,48 By 2002, the virus’s known geographic distribution extended to southeastern Canada, the Grand Cayman Islands, and throughout the eastern United States.48,49 Up-to-date maps of the virus’s spread in the United States are available at www.cdc.gov/ ncidod/dvbid/westnile/surv&control.htm. The virus has a natural maintenance cycle involving wild birds and Culex mosquitoes and is thought to spread via migrating birds.46,48 In temperate climates, the incidence of infection peaks during late summer and early fall; however, year-round transmission is possible in more tropical areas. Human infections result primarily from infectious mosquito bites; however, in 2002, five new modes of transmission were recognized: blood product transfusion, organ transplantation, transplacental transmission, breast-feeding, and occupational exposure in laboratory workers.
Diagnosis The incubation period of West Nile virus ranges from 3 to 14 days. Serologic surveys during recent outbreaks suggest that approximately 20% of persons who are infected develop a systemic febrile illness.50 Common symptoms are fever; headache; myalgia; GI complaints; and an erythematous macu-lar, papular, or morbilliform skin rash.46,47 Lymphadenopathy may be present, but it has been reported less frequently in recent outbreaks. Overall, fewer than 1% of infected persons develop encephalitis.50 Older persons are at increased risk for meningitis or encephalitis; once these complications develop, such individuals have a higher case-fatality rate and a higher incidence of residual neurologic deficits.47 Of note, muscle weakness and flaccid paralysis, when present, may provide a clue to a West Nile virus etiology. Overall, case-fatality rates in severe cases are about 10%. The diagnosis is most efficiently confirmed serolog-ically; testing can be obtained through state and local health departments.
Treatment and prevention Treatment of West Nile virus infection is supportive. Prevention relies on mosquito control and protection from mosquito bites. There is no human vaccine for West Nile virus infection. An equine vaccine is available.
Powassan Virus
Powassan virus (family Flaviviridae, genus Flavivirus) is related to the Eastern Hemisphere’s tick-borne encephalitis viruses. It was thought to be a rare cause of encephalitis in eastern Canada and the northern United States; however, West Nile virus surveillance has increased the recognition of this pathogen.51 The case-fatality rate is 5% to 10%, with a high incidence of residual neurologic dysfunction in survivors. Serologic surveys indicate an antibody prevalence of 1% to 4%. The virus is transmitted between Ixodes ticks and rodents; humans become infected via tick bites. The clinical features are those of viral encephalitis, with localizing neurologic signs and convulsions.44 There is no specific treatment or vaccine.
Viruses of the family togaviridae
Eastern Equine Encephalitis
Epidemiology Eastern equine encephalitis (EEE) virus (family Togaviridae, genus Alphavirus) is widely distributed throughout North, Central, and South America and the Caribbean; however, little is known about the epidemiology of EEE outside North America. In the United States, human infections are usually sporadic, and small outbreaks occur each summer, mostly in the upper Midwest and along the Atlantic and Gulf coasts. In North America, wild birds and Culiseta melanura (a mosquito found in swamp areas that support cedar, red maple, and loblolly bay trees) maintain the virus. In central Alabama, high rates of EEE virus infection were found in Uranotaenia sap-phirina, a mosquito that commonly feeds on amphibians and reptiles, which suggests that species other than birds may serve as a reservoir for EEE in hardwood swamps in the southeastern United States and elsewhere.52
Diagnosis The incubation period of EEE exceeds 1 week; onset is abrupt, with high fever. About 2% of infected adults and 6% of infected children develop encephalitis. EEE causes the most severe of the arboviral encephalitides, with a mortality of 50% to 75%. Symptoms and signs include dizziness, decreasing level of consciousness, tremors, seizures, and focal neurologic signs. Death can occur within 3 to 5 days after onset. Sequelae, which are common in nonfatal encephalitis, include convulsions, paralysis, and mental retardation. Illness from EEE in South America is less severe. Infection can be confirmed serologically by the CDC on request of state and local health departments.
Treatment and prevention No specific treatment is available. Prevention focuses on avoidance of mosquito bites and mosquito control in suburban areas. Inactivated vaccines have been used successfully in horses, and an inactivated vaccine has been used in laboratory workers or others at high risk of exposure, but it is not commercially available.
EEE is a potential agent of bioterrorism through the aerosol route.
Venezuelan Equine Encephalitis
In the Venezuelan equine encephalitis (VEE) virus (family To-gaviridae, genus Alphavirus) complex, six subtypes (I to VI) have been identified. Five antigenic variants exist in subtype I (IAB, IC, ID, IE, and IF). These subtypes and variants are classified asepizootic or enzootic on the basis of their apparent virulence and epidemiology. Epizootic variants of subtype I (IAB and IC) cause equine epizootics and are associated with more severe human disease. Enzootic strains (ID to IF, II [Everglades], III [Macambo, Tonate, Paramana], IV [Pixuna], V [Cabassou], VI [unnamed]) do not cause epizootics in horses, but they may produce sporadic disease in man. Epizootic strains are transmitted by many different types of mosquitoes; enzootic strains are transmitted by culicine mosquitoes. VEE has a widespread geographic distribution, from Florida to South America, where it is an important veterinary and public health problem. Focal outbreaks occur periodically, but occasionally, large regional epizootics occur, with thousands of equine and human infections.
VEE is infectious via aerosols, making it an occupational risk to certain laboratory workers and a potential agent of bioterrorism.
Diagnosis After an incubation period of 1 to 6 days, there is a brief febrile illness of sudden onset, characterized by malaise, nausea or vomiting, headache, and myalgia.53 Fewer than 0.5% of adults and fewer than 4% of children develop encephalitis. Long-term sequelae and fatalities are uncommon.
Treatment and prevention Treatment is supportive. Effective prevention of both human and equine disease can be accomplished by immunizing horses and other equine animals, which serve as the primary amplification host for the epizootic VEE viruses and without which there would be little human disease. During epidemics, mosquito vectors can be controlled by insecticides. Live attenuated and inactivated vaccines have been used for laboratory workers; however, human vaccines are not commercially available.
Western Equine Encephalitis
Western equine encephalitis (WEE) virus (family Togaviridae, genus Alphavirus) is a complex of closely related viruses found in North and South America. Flooding, which increases breeding of culicine mosquitoes, may precipitate summer outbreaks of WEE. Large outbreaks in humans and horses occurred in the western United States in the 1950s and 1960s; however, a declining horse population, equine vaccination, and improved vector control have reduced disease incidence. The younger the patient, the greater the likelihood of symptomatic infection: the ratio of asymptomatic to symptomatic infection is less than 1:1,000 in adults but increases to 1:1 in infants.
Diagnosis After an incubation period of about 7 days, headache, vomiting, stiff neck, and backache are typical in WEE. In children, restlessness and irritability are seen, and convulsions are common. Neurologic sequelae are relatively common in infants, but they are rare in older children and adults. The case-fatality rate is 3% to 7%. The diagnosis can be confirmed serologically by the CDC on request of state and local health departments.
Treatment and prevention No specific treatment is available for WEE. Prevention focuses on mosquito control and personal measures to avoid mosquito bites. Inactivated vaccine is available for horses. Although inactivated vaccine has been used for laboratory staff and others at high risk for exposure, it is not commercially available for use in humans. WEE is a potential agent of bioterrorism through the aerosol route.
Viruses of the family rhabdoviridae
Rabies
Epidemiology The rabies virus (family Rhabdoviridae, genus Lyssavirus) occurs worldwide. Dogs remain the major source of human rabies worldwide. In the United States, however, vaccination has sharply limited canine rabies, and consequently, wildlife rabies has increased in importance. About 90% of all reported cases of animal rabies in the United States now occur in wildlife, particularly wild carnivores (e.g., raccoons, skunks, foxes, coyotes, and bobcats) and bats.
The major wildlife reservoir for rabies in the United States is the raccoon, which accounts for 37% of all reported cases of rabies in animals; skunks (29%), bats (17%), and foxes (6%) represent the other major reservoirs for animal rabies.54 Raccoon rabies is the most prevalent in the eastern states; skunk rabies is predominant in the central and western states.54 Rodents (e.g., squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, and mice) and lagomorphs (rabbits and hares) are rarely infected and have not been identified as sources of human rabies in the United States.55 In the United States since 1990, indigenous rabies virus variants associated with insectivorous bats and foreign canine rabies virus variants have accounted for 30 of the 32 human cases. Although 74% of the 32 cases since 1990 have been attributed to bat-associated variants of the virus, a history of a bite was established in only three cases.56
Etiology and pathogenesis In most cases of rabies, an infected animal inoculates saliva containing rabies virus into the patient, and the virus may replicate in muscle cells near the bite. After replication, the virus spreads via retrograde axoplasmic flow in unmyelinated motor or sensory nerves to the CNS. It then replicates in the brain before moving via the nerves into other tissues, including the salivary glands, from which it can be shed.
Clinical manifestations The infectivity of rabies virus varies with the site and mode of transmission. A bite on the face presents a 60% chance of disease; a bite on the hand or arm reduces the chance of disease to between 15% and 40%, and a bite on the leg presents only a 3% to 10% chance of disease. The risk of disease from a bite is almost 50 times greater than the risk from scratches by a rabid animal. Although a less common mode of transmission, the virus also can be inhaled, which accounts for rabies in laboratory workers exposed to viral aerosols and in a few explorers of bat-infested caves.
The incubation period of rabies ranges from 12 days to many years and probably averages 30 to 90 days or less. The clinical course is quite variable. The initial clinical presentation is a prodromal phase typically lasting a day or two. It is marked by pain and paresthesias in the area of the bite, GI and upper respiratory symptoms, irritability, apprehension, and a sense of impending death. Hydrophobia and aerophobia occur in some patients and, like the history of a bite, call attention to this disease. Thereafter, the patient enters an excitation state, marked by hyperventila-tion, hyperactivity, disorientation, and even seizures. During the next few days, the patient becomes lethargic and begins to show paralysis, particularly in areas innervated by the cranial nerves and in the somatic muscles, bladder, and bowels. Gradual involvement of cardiac muscles and paralysis of respiratory muscles lead to death. Rabies virus infection in humans is uniformly fatal once symptoms occur.
Diagnosis Rabies should be considered if classic signs of hydrophobia, aerophobia, and excited behavior are present or in any case of encephalitis or myelitis of unknown etiology, even in the absence of an exposure history. The CSF shows nonspecific elevation in levels of leukocytes and protein, as occurs in other viral encephalitides. Fluorescent antibody staining, virus isolation, and reverse transcriptase/PCR constitute the most accurate means of diagnosing rabies infection.57 Circulating antibodies may be detected in unvaccinated persons as early as the sixth day of illness and usually appear within the first 2 weeks after infection. Rabies virus can be isolated from the second day through the second week of illness from a throat swab or saliva sample, as well as from tears, urine sediment, and CSF.
Treatment and prevention Three rabies vaccines are currently available in the United States: human diploid cell rabies vaccine (HDCV), rabies vaccine absorbed (RVA), and purified chick embryo cell vaccine (PCEC).58 Each is licensed for preexpo-sure or postexposure vaccination. Clinical trials with RVA and PCEC have demonstrated immunogenicity equivalent to that of HDCV.58 Corticosteroids, other immunosuppressing agents and conditions, and antimalarials may interfere with the development of active immunity after vaccination. Preexposure prophylaxis is indicated for persons in high-risk groups such as certain laboratory workers, persons whose occupation puts them in frequent contact with animal species at risk for having rabies, and certain international travelers.
Disease onset can be prevented by prompt postexposure prophylaxis. Postexposure prophylaxis begins with immediate and thorough washing of all bite wounds with soap and water and irrigation with a virucidal agent such as a povidone-iodine solution. Previously unimmunized persons should receive human rabies immunoglobulin and rabies vaccine. Guidelines for the indications and dosing schedules for postexposure prophylaxis are available from the CDC at www.cdc.gov/ncidod/dvrd/ rabies/.55 Local or state public health officials should be consulted if questions arise about the need for rabies prophylaxis.
At present, therapy for clinical rabies is supportive. In unvac-cinated patients, the disease is invariably fatal. A patient with rabies or suspected rabies should be kept in isolation, and standard infection control precautions should be followed, although laboratory-confirmed person-to-person transmission has not been documented.
Viruses of the family paramyxoviridae
Nipah virus
Nipah virus (family Paramyxoviridae) is closely related to the Hendra virus, which has rarely caused fever, pneumonia, and encephalitis in persons exposed to ill horses in Australia. Nipah virus was newly discovered in Malaysia during an outbreak involving 265 persons, with 105 deaths in 1998 and 1999; in 2004, outbreaks involving 25 persons occurred in Bangladesh.59 Most affected persons had contact with live pigs and were pig farmers. The reservoir for Nipah virus is believed to be fruit bats, and it is thought that humans are infected by contact with an infected bat or by contact with an intermediate animal host such as pigs.
Diagnosis The incubation period is unknown, but more than 90% of the hospitalized Malaysian patients had had contact with pigs in the previous 2 weeks. Among hospitalized patients, fever was almost invariably present, with headache, dizziness,and vomiting common presenting symptoms. Predominant neurologic symptoms were decreased level of consciousness, segmental myoclonus, meningismus, and seizures. Pneumonia was noted in 25% of the patients in Singapore, but it was not prominent in the Malaysian patients. The diagnosis can be confirmed serologically by viral culture or by detection of viral nucleic acid.
Treatment Treatment is supportive. An open-label trial suggested that ribavirin reduced mortality.60 Prevention is avoidance of pig farms.
Viruses of the family reoviridae
Colorado Tick Fever
The Colorado tick fever virus (family Reoviridae, genus Coltivirus) is transmitted to humans in the western United States and Canada mainly by the wood tick, Dermacentor andersoni. Human incidence corresponds to the wood tick’s geographic distribution in mountainous areas at elevations of 4,000 to 10,000 ft. Transmission occurs from March to September, but it peaks from April to June.
Diagnosis The mean incubation period for Colorado tick fever virus is 3 to 4 days. In 90% of cases, the patient reports a tick bite or tick exposure. Fever, chills, myalgias, and prostration are common presenting symptoms. A petechial or maculopapu-lar rash occurs in 15% of patients.61 Although acute symptoms last about a week, fever may recur several days later. Fatigue is often prolonged. Meningitis or encephalitis develops in 5% to 10% of children; fatal cases with hemorrhage and shock have been rarely reported. Leukopenia is very common. The virus infects marrow erythrocytic precursors, which accounts for the ability to recover the virus from peripheral blood up to 6 weeks after illness onset. Transmission via blood transfusion has been reported. The diagnosis can also be confirmed serologically by the CDC on request through state and local health departments.
Treatment Treatment is supportive. Prevention rests on avoiding tick bites in endemic areas.
Rash Arthralgia
viruses of the family togaviridae
Several alphaviruses belonging to the family Togaviridae can cause a viral syndrome associated with rash and arthralgias or arthritis. Diagnosis requires serologic testing of paired acute-phase and convalescent-phase serum. Virus can also be isolated from or detected in acute-phase serum samples.
There are no vaccines available for general use against al-phaviruses. Prevention depends on mosquito control and decreasing exposure to mosquitoes.
Barmah Forest Virus
Barmah Forest virus (family Togaviridae, genus Alphavirus) causes sporadic disease and epidemics in Australia.42 Clinically, Barmah Forest virus causes a Ross River virus-like illness, but the rash tends to be more florid, and true arthritis is less common. Outbreaks have coincided with Ross River virus outbreaks, and Barmah Forest virus has been identified in the same mosquito species as Ross River virus.42,62
Chikungunya
Chikungunya (CHIK) virus (family Togaviridae, genus Al-phavirus) is found in Africa and Asia and is transmitted by Aedes mosquitoes. After a 20-year hiatus, outbreaks of CHIK virus infection occurred in Indonesia from September 2001 to March 2003, suggesting a reemergence of the virus.63 In urban settings, the virus is transmitted from human to human via A. aegypti mosquitoes. Explosive urban epidemics occur during the rainy season. The native name for the disease means "doubled up," because of the excruciating joint pains.
Diagnosis In patients with CHIK, after an incubation period of 2 to 4 days, there is a sudden onset of fever and crippling joint pains, accompanied by chills, flushed face, headache, myalgias, backache, and photophobia. Arthralgias are polyarticular, are migratory, and mostly involve the small joints. Papular or macu-lopapular skin rashes, typically on the trunk and limbs, usually occur during the second to fifth day of illness. The clinical picture resembles that of dengue fever, with which chikungunya is often confused.64 Most infections are probably asymptomatic. Arthralgias may last several months. In Asia, but not Africa, mild hemorrhagic manifestations have been reported; CHIK virus is not a cause of severe hemorrhagic disease. The diagnosis can be confirmed serologically by the CDC on request through state and local health departments. Confirmation by culture or detection of viral nucleic acid is possible early in illness.
Treatment There is no specific treatment for CHIK. Anti-inflammatory drugs may relieve arthralgia. Chloroquine phosphate has been used for refractory arthralgias. Prevention depends on mosquito control and decreasing mosquito exposure.
Mayaro Virus
Mayaro (MAY) virus (family Togaviridae, genus Alphavirus) is closely related to CHIK virus and causes a similar illness. The virus has been isolated from mosquitoes (mostly Haemagogus) in various countries in the Caribbean and South America. Little is known about the natural history of the disease. MAY virus causes febrile illness with headache, backache, myalgias, epigastric pain, chills, nausea, photophobia, arthralgias, and maculopapu-lar rash. Polyarthritis occurs and may persist for several weeks. Arthralgia may recur, as indicated in a report of a patient with a previous case of MAY virus infection.65 Cases of MAY disease have been imported into the United States.66 MAY virus infection should be considered in the differential diagnosis in patients with a recent travel history to South America. Diagnosis can be confirmed serologically by the CDC on request through state and local health departments.
O’nyong-nyong
O’nyong-nyong (ONN) virus (family Togaviridae, genus Al-phavirus) was first isolated during an epidemic in Uganda in 1959 and spread to an estimated two million people in neighboring countries by 1962. Another ONN epidemic began in south-central Uganda in 1996.67 ONN virus is transmitted to humans by Anopheles and other mosquitoes. Clinically, ONN fever is similar to CHIK, although fever is less pronounced and lym-phadenopathy is more common in ONN.
Ross River Fever
Ross River virus (family Togaviridae, genus Alphavirus) has caused so-called epidemic polyarthritis in Australia, southwestern Pacific Islands, and Fiji.42 Several species of Aedes and Culex mosquitoes are important vectors.42 The natural maintenance cycle of Ross River virus is not fully known. Although the magnitude, regularity, seasonality, and locality of outbreaks are wide ranging, rainfall seems to be the single most important risk fac-tor.68 Humans have significant viremia, and the virus may follow a human-mosquito-human transmission cycle.69
After an incubation period of 2 to 21 days, the illness begins suddenly with myalgia and marked arthralgias in the small joints of the hands and feet. True arthritis occurs in over 40% of patients. A maculopapular rash occurs in 50% of patients within 2 days after onset. Myalgia, headache, anorexia, nausea, and tenosynovitis are common, but temperature is only slightly elevated. Arthralgia frequently persists for several weeks or longer— sometimes for longer than a year.
Viruses of the family flaviviridae
Dengue
In addition to their role in hemorrhagic fever (see above), dengue viruses are a common cause of rash and arthralgia.
Other viruses causing rash and arthralgia
There are a number of other viral zoonoses that cause similar nonspecific febrile illness in humans, but they occur infrequently or are rare. These include Igbo-Ora (family Togaviridae, genus Al-phavirus) in Africa; Sindbis and Sindbis-like viruses (family To-gaviridae, genus Alphavirus) in Africa, Asia, Australia, and Europe; Group C arboviruses (family Bunyaviridae, genus Bunyavirus) in South America; Oropouche (family Bunyaviridae, genus Bun-yavirus) in South and Central America; Sandfly fever (family Bun-yaviridae, genus Phlebovirus) in the Mediterranean, Middle East, West Asia, and South America; Zika virus (family Flaviviridae, genus Flavivirus) in Africa and Asia; and vesicular stomatitis virus (family Rhabdoviridae, genus Vesiculovirus) in the Americas.
Miscellaneous Viral Zoonoses
Monkey b virus disease
Monkey B virus (Herpesvirus simiae or B virus) causes persistent latent infections in at least 70% of captive adult macaques. Monkey B virus disease in humans usually results from macaque bites or scratches; most documented infections have occurred in laboratory personnel working with apparently healthy rhesus, cynomolgus, or African green monkeys or their tissues, including kidney cell cultures.71 Human infection from a muco-cutaneous exposure to the eye and one human-to-human transmission have been reported. In humans, monkey B virus causes acute ascending myelitis and fulminant meningoencephalitis, which leads to death within days.
Infection can be diagnosed in humans by demonstrating a rise in antibody titer and by isolating the virus from the CNS. Car-diopulmonary support is the most important aspect of management. Human infection carries a high mortality; however, patients treated early with intravenous acyclovir or ganciclovir have survived. Significant neurologic residua are common in survivors. Monkey handlers should wear protective clothing and a face mask.72 Bites, scratches, or mucosal surfaces exposed to macaque biologic materials should be cleansed thoroughly.69 Postexposure management should include referral to a medical consultant knowledgeable about monkey B virus.
Ruminant and primate poxvirus diseases
Several ruminant and primate poxviruses rarely cause human illness. Cowpox (vaccinia virus) is an orthopoxvirus related to variola. In humans, it produces vesicular lesions on the hands. Generalized infections are rare. Monkeypox, the only other or-thopoxvirus of significance to humans, is enzootic in monkeys and squirrels in western and central Africa; infection in humans is sporadic and produces a vesicular rash similar to variola. Secondary infections occur. The case-fatality rate is 1.5%.73 Tanapox virus is a yatapoxvirus that causes vesicular lesions in monkeys along the Tana River in Kenya and Zaire. It produces a monkey-poxlike illness in humans. The parapoxviruses produce disease in humans through direct contact with infected animals. These include bovine papular stomatitis virus, milkers’ nodule (pseudocowpox) in cattle, and orf in sheep and goats. Infection results in vesicles that progress to pustules and scabbing at the site of contact with the original infected species or contaminated objects.
Newcastle disease virus infection
Newcastle disease is an often fatal systemic infection of poultry that is caused by a paramyxovirus. The virus is occasionally transmitted to humans from infected birds or in the laboratory, presumably by direct inoculation. In humans, the illness appears as acute, sometimes hemorrhagic conjunctivitis without corneal involvement. It can be accompanied by lymphangitis, headache, malaise, and chills but is usually self-limited. Patients recover within 2 weeks.
Vesicular stomatitis virus infection
Vesicular stomatitis virus is a rhabdovirus whose structure resembles that of rabies virus. The agent is responsible for oral ulcers in cattle. Occasionally, laboratory workers become infected and experience fever, vesicular enanthemas, headache, and myalgias.
Foot-and-mouth disease
Foot-and-mouth disease is a highly infectious viral infection of cloven-hoofed animals. The causative agent of the disease is aphthovirus, a member of the family Picornaviridae that is indistinguishable morphologically from rhinovirus. Persons contacting infected animals occasionally have fever, vesicular lesions on the hands, and an increase in neutralizing and complement-fixing titers. The infection is mild and transient, but relapses occur.
