They’re transmitted by insect vectors, which is why they’re called arboviruses (arthropod-borne viruses). More than 100 arboviruses are known to cause human infections, and they belong to several different virus families. Rodent-borne viruses are also called roboviruses.

Arboviruses can cause rash, arthralgias, encephalitis, and hemorrhagic fevers.

Major arboviruses

Family	Important Viruses
Togavirus	Eastern and Western Equine Encephalitis Viruses
Flavivirus	St. Louis Encephalitis, Yellow Fever, Dengue and West Nile Viruses
Bunyavirus	California Encephalitis Virus
Reovirus	Colorado Tick Fever Virus

Eastern Equine Encephalitis Virus

*Insect vector is mosquito. Animal reservoirs are wild birds from where humans and horses get infected. Seen during the summer months in Atlantic and Gulf coast states. It presents as a severe encephalitis with fever, nuchal rigidity, headache, seizures, stupor and coma. Long term sequelae are seen even after the patient survives the primary encephalitis. Diagnosis is by detection of rising antibody titres.

Western Equine Encephalitis Virus

The vector is the Culex mosquito, and the reservoir is wild birds. It’s seen in the western USA. It causes a milder encephalitis than EEE. Diagnosis is by isolation of the virus in culture or detection of antibody in serum.

St. Louis Encephalitis Virus

The vector is the Culex mosquito. Animal reservoirs are small wild birds such as English sparrows. It’s seen in southern, central, and western states, especially in urban areas. It causes a moderately severe encephalitis. Detection is by serology.

California Encephalitis Virus

The vector is the Aedes mosquito, and the reservoir is rodents. Disease occurs in the north and central states. La Crosse Virus is a type of CE Virus and is the most common cause of arboviral encephalitis in the USA. Disease severity ranges from mild to severe. Diagnosis is by serology.

Colorado Tick Fever Virus

The vector is the Dermacentor tick. Reservoirs include small rodents, chipmunks, and squirrels. It’s seen in the Rocky Mountain area, especially among hikers. Disease presents with fever, headache, retro orbital pain, and myalgia. Diagnosis is by viral isolation or detection of rising antibody titres.

West Nile Virus

Cases appeared for the first time in 1999 in the USA. The vector is a Culex mosquito, and reservoirs are wild birds. Cases are seen throughout the USA, but more commonly along the east coast. It presents as a severe encephalitis with muscle weakness that can mimic GBS. Diagnosis is made by isolation of the virus in tissue culture or antibody detection in blood or CSF. Viral RNA can be detected by PCR. Nucleic acid probes are used for rapid screening of the virus in blood to prevent blood borne infections.

Yellow Fever Virus

It’s not endemic in the USA, but it can be seen in travellers to tropical Africa and South America. Urban yellow fever is transmitted by Aedes mosquito, while the jungle form is transmitted by Haemagogus mosquitoes and primarily affects monkeys. Disease presents with sudden onset of fever, headache, myalgia, and photophobia, followed by jaundice, gastrointestinal hemorrhages, hematemesis, renal failure, and shock. It has a high mortality rate. Diagnosis is by viral isolation and antibody detection.

Dengue Virus

It is not endemic in the USA, but it can be seen in travellers to tropical countries, Southeast Asia, and the Caribbean. The vector is the Aedes aegypti mosquito. It is a Flavivirus. Dengue Virus has 4 serotypes (1 to 4). It typically presents with sudden onset of fever, headache, malaise, and cough, followed by debilitating pain in muscles and joints (breakbone fever). Maculopapular rash, thrombocytopenia, and leukopenia can occur.

Re-infection with a different serotype can cause an exaggerated immune response, resulting in life threatening dengue hemorrhagic fever. This is characterised by hemorrhages into the skin, gastrointestinal tract, and internal organs, and DIC. It has been postulated that virus-antibody immune complexes activate complement, causing the typical clinical features, and that antibodies actually increase the entry of virus into monocytes and macrophages, resulting in massive release of cytokines. Diagnosis is made by virus isolation in cell culture or by the demonstration of rising antibody titres by ELISA.