Other Arbovirus Infections

Mayaro virus is an alphavirus in the Togavirus family and is transmitted by Haemagogus species mosquitoes.

Mayaro virus has been found in Central America, the Caribbean, and parts of South America. It is endemic in the tropical areas of South America (Trinidad, Suriname, French Guyana, Brazil, Peru, Bolivia, and Venezuela), with the greatest number of cases reported in Brazil.

Mayaro disease is a dengue-like disease with predominantly mild symptoms of fever, headache, myalgias, arthralgias, and rash. The disease is most often self-limited. Severe manifestations are rare, but chronic polyarthritis, hemorrhage, myocarditis, and neurologic complications have been reported (1,2).

Serologic tests cross-react with related arboviruses, complicating the diagnosis. Confirmation of positive serology by reverse transcriptase–polymerase chain reaction (RT-PCR) is needed.

There are no specific antiviral medications available for Mayaro, and treatment is supportive care for symptoms when needed (3).

Prevention of Mayaro disease involves avoiding mosquito bites and mosquito control. No vaccine is available.

Oropouche virus is a Simbu group bunyavirus.

The Oropouche virus is transmitted to humans by Culicoides paraensis, a species of biting midges (small flying insects) present in South and Central America and the Caribbean. Vertical transmission during pregnancy can occur. A case report of detection of Oropouche virus in the semen of a patient who had Oropouche infection raises concerns for possible risk of sexual transmission (1).

Transmission of the Oropouche virus occurs in 2 cycles:

• Wild

• Urban-epidemic

In the wild cycle, the reservoir for the Oropouche virus is wildlife (eg, primates, sloths, certain arthropods). In the urban-epidemic cycle, humans are the principal reservoir, and the infection cycle is human to human via the midge vector.

The Oropouche virus has major epidemic potential throughout the area in which it occurs. Several outbreaks of Oropouche fever have been reported in countries in South America and the Caribbean, closer to urban centers outside of Amazon basin (2). The World Health Organization recommends that Oropouche fever be included in the clinical differential diagnosis for other common febrile arboviral infections (eg, chikungunya disease, dengue, yellow fever, Zika) (3).

In humans, Oropouche fever resembles dengue, causing acute fever and infection. Rarely, patients with severe cases present with meningitis and meningoencephalitis.

Infection with Oropouche virus during pregnancy is associated with poor pregnancy outcomes (eg, fetal deaths, stillbirths, birth defects).

Diagnosis is by viral detection through culture or RT-PCR when available (4). Treatment is supportive.

Prevention of Oropouche fever involves avoiding midge bites. No vaccine is available.

Tick-borne encephalitis is caused by a flavivirus that has 3 major subtypes (European, Siberian, and Far Eastern) and 2 additional subtypes (Baikalian and Himalayan).

Tick-borne encephalitis is transmitted to humans primarily through the bite of infected hard–bodied ticks, Ixodes ricinus in Europe and Ixodes persulcatus in Siberia and the Far East. Ticks are both the vector and virus reservoir, and small rodents are the primary amplifying host. Tick-borne encephalitis can also be acquired by ingesting unpasteurized dairy products (eg, milk, cheese) from infected goats, sheep, or cows or by blood transfusion, organ transplantation, breastfeeding, and exposure through laboratory handling of specimens.

Cases have been reported in areas extending from eastern France to northern Japan and parts of northern Africa. The highest incidence in Europe is in the Czech Republic, Baltic countries, and Slovenia. Cases in the United States are rare, occurring among persons who traveled to Europe or China (1).

Cases occur from early spring to late summer when ticks are most active.

Initially, a mild flu-like illness occurs that usually subsides within a few days (2). Some patients develop more severe symptoms (eg, meningitis, meningoencephalitis). Incidence is highest and severity of disease is greatest in people ≥ 50 years. The case fatality rate and frequency of neurologic sequelae vary by viral subtype with the Far Eastern subtype having the highest mortality (3).

Tick-borne encephalitis should be suspected in travelers who have both of the following:

• A nonspecific febrile illness that progresses to neuroinvasive disease within 4 weeks after arriving from an endemic area

• Risk of tick exposure

The diagnosis of tick-borne encephalitis is usually made serologically by detection of specific IgM antibodies in blood or cerebrospinal fluid, which typically appear only after onset of neurologic manifestations. The virus that causes tick-borne encephalitis can sometimes be detected in serum by virus isolation or reverse transcriptase polymerase chain reaction (RT-PCR) earlier in disease before antibody titers have risen.

As with other viral meningoencephalitides, treatment is supportive.

Prevention of tick-borne encephalitis involves avoiding tick bites. A vaccine is available in some areas where tick-borne encephalitis is endemic (4). A vaccine is available in the United States for U. S. travelers visiting endemic areas who are at risk of tick exposure (5).

In the United States, tick-borne encephalitis is caused mainly by Powassan virus, a flavivirus that is antigenically related to West Nile, St. Louis encephalitis, and tick-borne encephalitis viruses. Powassan virus infections have been reported primarily in the northeastern states and the Great Lakes region but have also been reported in southeastern Canada and Russia (southeastern Siberia, northeast of Vladivostok).

In the United States, there are 2 types of Powassan virus, both linked to human disease:

• Lineage 1 Powassan virus: Associated with Ixodes cookei or Ixodes marxi ticks

• Lineage 2 Powassan virus (sometimes called deer tick virus): Associated with Ixodes scapularis ticks, the same tick that spreads Lyme disease, anaplasmosis, and babesiosis

Most infections are caused by lineage 2 Powassan virus because I. cookei ticks rarely bite people.

The time an infected tick must be attached to transmit Powassan virus is probably much shorter (15 minutes) than that needed for Lyme disease transmission (24 to 48 hours) (1).

Powassan virus encephalitis is rare (fewer than 50 cases per year in the United States reported in 2019), but risk of infection is likely increasing, given a high prevalence of Powassan virus in ticks and wild mammals in the United States (2). Cases occur in the late spring to mid-fall, when ticks are most active (3).

A flu-like prodrome can be followed by neurologic manifestations. Neurologic sequelae (eg, psychosis, drowsiness, dysarthria, spasticity, headache) are common. The reported case-fatality rate is high (up to 10 to 15%) (1) but may reflect reporting bias because seropositivity in endemic regions is higher than reported case rates, suggesting asymptomatic infection.

Powassan virus infection should be considered in patients with encephalitis, especially in patients with a history of tick bite, significant outdoor exposure, or recent travel to or residence in an endemic area. Diagnosis is similar to that of tick-borne encephalitis, with serologic tests to detect Powassan virus–specific IgM antibody in serum or cerebrospinal fluid and confirmed by neutralizing antibody testing of acute- and convalescent-phase serum specimens at a state public health laboratory or the CDC.

Treatment is largely supportive as there are no specific antiviral therapies. The effectiveness of corticosteroids is uncertain, in case reports (2). There is no vaccine for Powassan virus infection; the vaccine for tick-borne encephalitis is not protective against Powassan virus.

People at risk should use personal protective measures to prevent tick bites.

Other tick-borne viruses in the United States include:

• Bourbon virus: This virus was isolated from a single patient who died with multiorgan failure in Bourbon County, Kansas. A limited number of cases have been reported in the southern and midwestern United States (1). Infection presents as a flu-like illness with a rash.

• Heartland virus: As of 2022, there have been more than 60 cases of Heartland virus disease reported from states in the midwestern, northeastern, and southern United States (2). Heartland virus has been detected in deer, raccoons, coyotes, and moose in 13 states, from Texas to North Carolina and Florida to Maine. Infection with this virus usually causes a self-limited, nonspecific febrile illness, which may be accompanied by leukopenia, thrombocytopenia, and elevated liver transferases. One patient died. Consider Heartland virus infection in patients receiving treatment for ehrlichiosis who are not responding to doxycycline therapy. Heartland virus does not have a specific treatment and managed with supportive care. who are not responding to doxycycline therapy. Heartland virus does not have a specific treatment and managed with supportive care.

• Colorado tick fever virus: A coltivirus causes Colorado tick fever. Colorado tick fever has been diagnosed in areas of the western United States and Canada that are 4000 to 10,000 feet (1200 to 3000 meters) above sea level where the vector tick Dermacentor andersoni is located. The disease is rare, with a median of 7 reported cases per year in the United States (3). It causes a nonspecific febrile illness that is rarely complicated by meningitis or encephalitis. Rarely, it is transmitted by blood transfusion.

The California encephalitis serogroup viruses, including California encephalitis virus, snowshoe hare virus, La Crosse virus, and Jamestown Canyon virus, are arboviruses and belong to the Bunyaviridae family. These viruses are transmitted and maintained by Aedes mosquitoes and occur in the Rocky Mountains, eastern United States, southeast Canada, and western Europe.

California encephalitis serogroup viruses cause a febrile illness with central nervous system symptoms (eg, fever, somnolence, obtundation, focal neurologic findings, seizures) and can lead to encephalitis or meningoencephalitis (1). Symptoms primarily occur in children except for Jamestown Canyon virus, which may also affect adults. Temporal lobe involvement may mimic herpes encephalitis; 20% of patients develop behavioral problems or recurrent seizures (2).

No treatment is available. Prevention involves avoiding mosquito bites and mosquito control.

Omsk hemorrhagic fever and Kyasanur Forest disease are arboviruses and transmitted by hard ticks or by direct contact with an infected animal (eg, rodent, monkey). Omsk hemorrhagic fever is caused by a flavivirus; it occurs in Russia, including Siberia. Kyasanur Forest disease, also caused by a flavivirus, occurs in India.

Omsk hemorrhagic fever and Kyasanur Forest disease are acute febrile illnesses accompanied by bleeding diathesis, abdominal pain, low blood pressure, leukopenia, and thrombocytopenia; some patients develop encephalitis in the third week (1). The case fatality rate is < 3% for Omsk hemorrhagic fever and 3 to 5% for Kyasanur Forest disease (2, 3).

Prevention involves avoiding tick bites and infected animals. A vaccine for Kyasanur fever virus is produced in India.

Rift Valley fever, caused by a phlebovirus, is an arbovirus and spread by mosquitoes and can be transmitted by the following:

• Direct or indirect contact with the blood or organs of infected animals (eg, during slaughtering, butchering, or veterinary procedures)

• Inhalation of infected aerosols

• Ingestion of raw milk from infected animals

Eggs from virus-infected Aedes mosquitoes can contain the virus. Those infected eggs can persist for months to years and, when flooded, can hatch and produce infected adult female mosquitoes capable of transmission.

Rift Valley fever occurs in South Africa, East and West Africa, the Arabian Peninsula, and Egypt (1).

Rift Valley fever presents as a febrile illness with gastrointestinal disturbances. Approximately 5 to 20% of patients with symptoms develop severe complications, including ocular disorders, meningoencephalitis (1 to 5% of cases), or a hemorrhagic form (which has a 50% case fatality rate). Extensive clusters of abortions may develop in livestock before human cases appear (2).

A vaccine for livestock is available, and a human vaccine is in clinical trial as of 2024 (3).