The malaria incubation period is defined as the time elapsed between exposure to the infectious agent (through the bite of the Anopheles mosquito) and the manifestation of the first clinical sign or symptom. Usually, these periods vary depending on the species of Plasmodium causing malaria. The average incubation period is 9-14 days for Plasmodium falciparum, 12-17 days for infections by Plasmodium vivax and 18-40 days for infections caused by Plasmodium malariae .
The relapse patterns and variations in the length of the incubation period, including a delay of four months or longer, was first described by Korteweg in Holland between 1901 and 1902 (cited by Swellengrebel and De Buck ). Later, in 1935, Nikolaev proposed that there were two strains of P. vivax (cited by Tiburskaya ) with different incubation periods and gave the sub-specific taxonomic name of P. vivax hibernans to the variety with the longest incubation period. It was suggested that this sub-species had adapted to more northern latitudes where the anopheles vector was absent for much of the year. Shute (1946)  proposed that the sporozoite infective inoculum would be inversely related to the prepatent and incubation period. However, in Moscow, Tiburskaya  demonstrated situations in which the length of the incubation period did not depend on the number of inoculated sporozoites, but instead was determined by the inherent properties of the strains. It was also believed that strains with prolonged latency could be attributed either to the "senility" of the sporozoite towards the end of the season or to the low number of sporozoites in the infective bite .
According to Shute , the differences between the P. vivax strains could be explained by the assumption that, in varying proportions, all strains of P. vivax produce two types of sporozoites: one eliciting short prepatent periods (Type I) and the other lying dormant or developing slowly to give rise to long prepatent periods (Type II). In this model, the latter type would greatly predominate in "temperate strains", but not in tropical ones. It was thought that relapses of P. vivax could in reality correspond to a delayed parasitaemia arising from Type II sporozoites. In the same year, Garnham stated that the length of the incubation period was considered the major biological difference between Dutch, Madagascar, and USSR strains, and although there was no evidence of specifically dormant forms, it was believed that if certain sporozoites failed to develop in the normal time, they could be reactivated by an unknown factor one year or more after inoculation .
In 1980, Warwick  proposed that the ambient winter temperatures could extend the incubation period of P. vivax in humans, based on the concept that temperatures persistently above a minimum of 23.9°C were required for sporozoite maturation , thereby limiting vector transmission in cold areas. Finally, in 2007, Nishiura et al in Korea  suggested that the incubation periods would likely reflect adaptation to the behaviour of the principal vector of the region, which hibernates during the winter season. Currently, several reports associate the extension of the incubation period to malaria prophylaxis among travellers [10, 11].
The opportunity to study some cases of P. vivax malaria in Rio de Janeiro, where there is no vector transmission, has made it possible to detect and to evaluate certain peculiar aspects of the natural evolution of the disease in human beings. One main aspect was the extension of time required for the parasites to progress through liver schizogony and produce symptoms by their propagation in the bloodstream.
Plasmodium vivax infections with prolonged periods of incubation and no association with malaria prophylaxis in patients from the Amazon region in Brazil and in one patient from Indonesia are presented.
In addition to demonstrating an interesting clinical situation and the need for clinicians to consider the diagnosis of malaria in a patient presenting symptoms a long time after exposure, even in the absence of chemoprophylaxis, our cases raise questions regarding the understanding of the biology of the host/P. vivax interactions.