Colorado Tick Fever And Other Arthropod-borne Reoviruses

Article about Colorado tick fever and other arthropod-borne reoviruses.

Topics covered:

  • Essentials
  • Coltiviruses
  • Orbiviruses
  • Seadornaviruses
  • Prevention
  • Further reading


Human pathogens are found in six genera of Reoviridae: Reovirus, Rotavirus, Orthoreovirus, and three arthropod-borne genera—Coltivirus (Colorado tick fever, Salmon River virus, and Eyach viruses), Orbivirus (Kemerovo, Changuinola, Orungo, and Lebombo) and Seadornavirus (Banna virus).

Colorado tick fever—common in parts of north-western North America; acquired from tick (ixodid) bites, most often by hikers and campers, presenting 3 to 6 days later with sudden fever, rigors, generalized aches, myalgia, headache and backache, rashes (12%) and gastrointestinal symptoms (20%). Diagnosis confirmed by detection of viral antigen in erythrocytes or serum, or by serodiagnosis. Management is symptomatic. Illness usually resolves in 10 to 14 days, but convalescence may be prolonged. Prevention is by avoiding, repelling, and rapidly removing ticks; no vaccines are available.


Colorado tick fever

The virus responsible for Colorado tick fever or ‘mountain fever’ is an 80-nm double-shelled particle covered with capsomeres. The icosahedral core contains 12 segments of double-stranded negative-sense RNA. The virus can infect human erythrocytes and this may also occur with the other coltiviruses and orbiviruses.

Colorado tick fever is a zoonosis involving hard (ixodid) ticks (principally Dermacentor andersoni, but also D. occidentalis, D. parumapertus, D. albipictus, etc.) and wild mammals, including porcupines, deer, coyotes, squirrels, chipmunks, deer mice, and other rodents. Ticks pass Colorado tick fever virus trans-stadially and transovarially.


Colorado tick fever is acquired from tick bites in western and north-western parts of the United States of America (including California) and Canada (British Columbia and Alberta). Very rarely, it has been caused by an infected blood transfusion. Several hundred cases are reported each year in the United States of America, but the true incidence is thought to be at least 10 times higher than that. It is the second most commonly diagnosed arboviral infection in the United States of America, after West Nile virus. Hikers and campers are at special risk in rodent- and tick-infested terrain. The prevalence of antibody to Colorado tick fever among shepherds is 32%. The highest incidence is from May to July when ticks are most active. Infection usually confers lasting immunity.

Clinical features

In adults, the infection is nearly always mild, but in children it is occasionally severe but rarely fatal. Three to 6 days after the tick bite (extreme range 1–19 days) there is a sudden fever for about 3 days, with rigors, generalized aches, myalgia, headache, and backache. In one-half of the patients there is a biphasic fever. Rashes then appear in up to 12% of patients, usually a transient peripheral maculopapular rash or petechiae on flexor surfaces of arms or perhaps widespread and it may be hyperaesthetic. Gastrointestinal symptoms occur in 20% of patients. Laboratory findings include leukopenia with relative lymphocytosis, occasional thrombocytopenia, and mild lymphocyte pleocytosis.

The illness usually resolves in about 10 to 14 days, but convalescence may be prolonged. Severe manifestations include meningism and drowsiness, sometimes associated with gastrointestinal symptoms, spontaneous bleeding, thrombocytopenia, and disseminated intravascular coagulation. Late, possibly immunological effects, include myocarditis, pericarditis, pleurisy, arthritis, and epididymitis. Colorado tick fever infection may precipitate abortion, or transplacental infection but the teratogenic effects reported in mice have not been observed in humans.


Viral antigen may be detected in erythrocytes by immunofluorescence 1 to 120 days after the start of symptoms. Erythrocyte precursors are infected in the marrow, but their survival is apparently not affected. Virus can be isolated from the blood and, if there is central nervous system involvement, the cerebrospinal fluid. Colorado tick fever virus produces a cytopathic effect on several cell lines, but intracerebral injection of ground blood clot or preferably washed erythrocytes into suckling mice is more sensitive for diagnostic isolation. Antigen can be detected in serum during acute infections by polymerase chain reaction (PCR) or Western blot, but enzyme-linked immunosorbent assay (ELISA) techniques have been less sensitive. An indirect fluorescent antibody test can provide early serodiagnosis. Neutralizing antibody and specific IgM enzyme immunoassays become positive after 14 to 21 days and the IgM disappears after 45 days.

Differential diagnosis

Many other tick-borne acute febrile illnesses, some with rashes and nervous system involvement, can be acquired in the area endemic for Colorado tick fever. These include Rocky Mountain spotted fever, tularaemia, Lyme disease, and relapsing fever. Tick paralysis caused by D. andersoni and other ixodid ticks presents as a poliomyelitis-like, ascending, flaccid paralysis that is unlikely to be mistaken for the meningitic or encephalitic syndromes of Colorado tick fever.


The symptomatic treatment of fever and pain should exclude salicylates in case of thrombocytopenia. Tribavirin (ribavirin) inhibits the replication of Colorado tick fever virus experimentally, but its use in humans has not been reported. Immunity is long lasting.

Salmon River virus

This virus is closely related to Colorado tick fever virus. It was isolated from a patient with similar symptoms in Idaho.


This European coltivirus has been found in Germany and France. There is serological evidence of human infection in Czechoslovakia causing meningoencephalitis or neuropathies.


Although antibody to the tick-borne Great Island virus and insect-borne Corripata orbiviruses have been found in humans, there is no evidence of their pathogenicity.


Three serotypes of Kemerovo virus have been isolated from ixodid and hyalomma ticks in Russia and Central Europe. They cause benign febrile illnesses and, occasionally, meningitis or encephalitis in spring and early summer when ticks are active. Rodents and birds are involved in the zoonotic cycle.

Oklahoma tick fever is another Kemerovo virus rarely causing febrile illness in the United States of America.


There is a single report of human febrile illness with the orbivirus Changuinola in Panama. The virus has been isolated from phlebotomine flies and mammals in that area.


Orungo virus is found mainly in West Africa but also in Uganda and the Central African Republic. Up to 75% of some human populations are seropositive. The clinical effects are unknown, but fever and diarrhoea occur in some people, perhaps with encephalitis as in experimental mice. There is no rash or jaundice. It is transmitted by anopheles, aedes, and other mosquitoes. Monkeys, sheep, and cattle may be infected.


This orbivirus was isolated from one febrile child in Nigeria. Lebombo is also found in mosquitoes and rodents.


These viruses from south-east Asia and Indonesia include Banna virus from China, which has been isolated from patients with encephalitis. It is likely to be misdiagnosed as Japanese encephalitis.


Tick-borne infections are prevented by avoiding, repelling, and rapidly removing ticks. No vaccines are available.

Further reading


Attoui H, et al. (2005). Coltiviruses and seadornaviruses in North America, Europe, and Asia. Emerg Infect Dis, 11, 1673–9. 

Brown SE, Knudson DL (1995). Coltivirus infections. In: Porterfield JS (ed.) Exotic viral infections, pp. 329–42. Chapman & Hall, London.

Labuda M, Nuttall PA (2008). Viruses transmitted by ticks. In: Bowman AS, Nuttall PA (eds) Ticks: biology, disease and control, pp. 989–92. Cambridge University Press, Cambridge.

Libikova H, et al. (1978). Orbiviruses of the Kemerovo complex and neurological diseases. Med Microbiol Immunol, 166, 255–63.

McGinley-Smith DE, Tsao SS (2003). Dermatoses from ticks. J Am Acad Dermatol, 49, 363–92.

Romero JR, Simonsen KA (2008). Powassan encephalitis and Colorado tick fever. Infect Dis Clin North Am, 22, 545–59.