The ICT failed to detect P ovale in the first

blood sample as well, but the test is known for its low sensitivity for this parasite (approximately 60%).6 The PCR has a 50% higher sensitivity for detecting submicroscopic P falciparum infection,7 and higher detection rates for mixed-species infections.8 With higher parasitemia and concentration of antigen in the second sample, signaling pathway P falciparum was easily detectable by microscopy and ICT. In the second sample, one additional P falciparum clone was suggested by PCR to be present, probably due to the release of new parasites from the liver to the blood. Another explanation for the late manifestation of P falciparum is the suppression of P falciparum by P ovale after simultaneous infection. In some reports, non-falciparum strains were described as dominating P falciparum in number and clinical manifestation in mixed-species infections in non-immune travelers,9 although most reports describe the opposite.10

Alternatively, preexisting P falciparum-specific immune responses could have led to a delayed onset of falciparum malaria, and click here antibodies to P falciparum were present at low titers determined by indirect immunofluorescence test (1 : 80; cutoff, 1 : 20) on the first day of presentation. However, it seems more likely that an initially low-level P 5FU falciparum infection during 12 days grew to the threshold of microscopic detection and clinical manifestation. Thereby, chloroquine treatment may have temporarily suppressed multiplication without eliminating the parasite, in line with its chloroquine-resistance genotype.

Primaquine treatment started simultaneously with the (presumed) onset of falciparum malaria and thus could not exert its preerythrocytic activity. On the blood stages of P falciparum, primaquine has hardly any effect.11 Diagnosing malaria is and will remain a challenge despite technical progress. Microscopy and ICT need a certain parasite density and antigen concentration, respectively. PCR can detect cryptic mixed infections including P falciparum earlier but is inapplicable for the first-line routine diagnostic procedure. From the clinical perspective, infections with P falciparum are much more frequent than those with P ovale.1 Therefore, a single infection with P ovale is rather unlikely in a traveler and needs to attract the clinician’s attention when there are signs of a possible recrudescence. The individual presenting with malaria was obviously at risk of infection with all Plasmodium species prevalent at the travel destination. Thus, recrudescent malaria in travelers may be falciparum malaria despite initial diagnosis of malaria by a Plasmodium species with a normally longer incubation period.