HistoryThis section has been translated automatically.
Tanapoxcken was first described in 1957 and 1962 in endemics temporally associated with floods in the lower Tana River in Kenya (eponymous).
DefinitionThis section has been translated automatically.
Tanapoxvirus infections are infections caused by Poxviridae of the genus Yatapoxvirus (TANV), a large double-stranded DNA virus. TANV encodes a putative apoptosis inhibitory protein 16L. Approximately 10% of the population along the Tana River possess antibodies to tanapoxvirus (Suraweera CD et al. 2020). Very occasionally, tana pox is also detected in return travellers (travel sickness) in Europe (Stich A et al. 2002).
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Occurrence/EpidemiologyThis section has been translated automatically.
Epidemiological studies suggest that the virus is transmitted from monkeys to humans by a mosquito or arthropod as an intermediate host. Tanapox infections show seasonal courses consistent with local arthropod activity. Rare cases of transmission to humans following direct contact with a primate have been described. However, there is no evidence of direct human-to-human transmission.
Serological studies have shown that transmission to humans was initially restricted to the areas of the Tana River. Later, human infections were detected in the forest area of Zaire (Democratic Republic of Congo). Tanapox is restricted to East and Central Africa, although some infections have been reported in travelers returning to Europe and the United States from this area. The primary maintenance hosts are not known; many monkeys, particularly the velvet monkey (Cercopithecus aethiops), are susceptible and are common in endemic areas (Lang W et al. 2000).
Clinical featuresThis section has been translated automatically.
General: Incubation period: 2-24 days. Followed by fever for 2-4 days, headache, muscle aches, sweats, chills, cough, lymphadenopathy.
Integument: Usually 2-10 acute skin lesions localized mainly to the extremities, papular and/or vesiculopustular. Initially, a small red macule is visible, which becomes progressively more elevated centrally and changes to a plaque. The center of the papule/plaque becomes necrotic. Approximately 1 week after the initial macule becomes visible, the plaque is about 10-15 mm in size. There is surrounding erythema and surrounding edema. With increasing duration, the plaques disintegrate and begin to ulcerate (usually stimulated by scratch artifacts) or increase in firmness and consistency until red nodules approximately 20 mm in diameter have formed. Scarring spontaneous healing of the nodules over 6-8 weeks with formation of typical "pockmarks". Secondary impetiginisation is common with ulceration.
Note(s)This section has been translated automatically.
Since there is no immunological relationship between Orthpox viruses and Tanapox viruses, immunity to vaccinia viruses does not protect against this infection.
LiteratureThis section has been translated automatically.
- Lang W et al.(2000) Tropical medicine in clinic and practice. Georg Thiem Verlag p.346
- Monroe BP et al. (2014) Estimating the geographic distribution of human Tanapox and potential reservoirs using ecological niche modeling. Int J Health Geogr 25;13:34.
- Najarro P et al (2006) Yaba-like disease virus chemokine receptor 7L, a CCR8 orthologue. J Gen Virol 87(Pt 4):809-816.
- Stich A et al. (2002) Tanapox: first report in a European traveller and identification by PCR. Trans R Soc Trop Med Hyg 96:178-179.
- Suraweera CD et al (2020) Structural insight into tanapoxvirus-mediated inhibition of apoptosis. FEBS J 287:3733-3750.
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