Detection of new infections from relapses in vivax malaria elimination programme is a big challenge, as a routine diagnostic method that can distinguish these cases from there. Please help us out if you have experience in this field.
I don't think we can diagnose\differentiate the relapse with reinfection by looking in to blood smear in case of P. vivax, though to some extent it is possible in case of P. falciparum because of the synchronicity of the parasite in case of P. falciparum. In case of P. vivax the decision on whether it is a case of relapse or reinfection can only be taken on epidemiological ground only.
Differentiation of reifection and relapse P. vivax is possible through molecular study only. It can be done through genomic study of adequate numbers of samples in a community.
In facility limited center, a thin and thick smear;(thin film to show its P vivax, thick to check parasite density which may be low in relapse). Molecular diagnosis confirms the same strain for a relapse, a different strain for a reinfection.
Differentiation requires genotyping of strains circulating at initial infection and compare with strains collected during the relapsed or new infection (re-infection). Our lab has the capacity to perform Plasmodium genotyping
It is currently still not possible to distinguish reinfection from relapse by genetic or any other means. Parasites in the bloodstream in a recurrent Plasmodium vivax infection can be either homologous or heterologous as compared with those that caused the initial clinical manifestations, but that information does not tell us anything definitive about reinfection versus relapse. Inter alia, the implications of homologous recurrences in terms of their origin in an infected person are discussed in three recent publications: Markus MB. 2015. Do hypnozoites cause relapse in malaria? Trends in Parasitology 31: 239-245; Markus MB. 2016. Mouse-based research on quiescent primate malaria parasites. Trends in Parasitology 32: 271-273; Markus MB. 2016. Malaria relapse. In Encyclopedia of Parasitology (ed. H. Mehlhorn), online version and 4th edition. Springer-Verlag: Berlin & Heidelberg.
Further to my previous posting, the presence of heterologous Plasmodium vivax parasites in the bloodstream will often be indicative of a reinfection rather than a hypnozoite-mediated relapse following upon the previous clinical malarial (or asymptomatic parasitaemic) episode. However, sporozoites in even a single inoculum injected by the mosquito are not all of the same genotype. Hypnozoites (four decades have elapsed since I coined this term) are basically dormant sporozoites, as far as is known. Therefore, it is assumed that a heterologous recurrence can (alternatively to being evidence of reinfection) reflect that hypnozoite activation has taken place. As a third possibility (leaving aside the matters of mutation and haplotype variation), a recurrence that is heterologous might have as its source a hypnozoite(s) derived from sporozoite inoculation further back in time. In other words, this would be a relapse indirectly ascribed to past infection of the patient earlier than when he or she experienced the last clinical attack.
As for homologous P. vivax recurrences, an explanation could be quiescent merozoite reactivation (as opposed to hypnozoite activation or reinfection of the patient), the habitat(s) in the body of the latent merozoite(s) concerned being something yet to be confirmed. This is a new concept based on logical extrapolation (see Markus, 2015, Trends in Parasitology 31: 239-245). On the other hand, a homologous recurrence could, at least in theory, originate from a hypnozoite that is a meiotic sibling organism from the mosquito or, more likely, a meiosis-associated parasite descendant (see the abovementioned 2015 paper). Whether or not homologous bloodstream parasites in recurrences can also be the result of reinfection with any degree of regularity is not yet clear; although it has been suggested that they can, this being a guess (which might or might not be correct) based on genotypes circulating in some human populations.
CONCLUSION: At present, it is not possible to distinguish relapse from reinfection by molecular techniques.
The most recent publication to comment on this subject appeared online a week ago (Q. Bassat et al., 2016):
http://dx.doi.org/10.4269/ajtmh.16-0180
The article mentions the need to develop strategies to distinguish between relapses, recrudescences and re-infections. In other words, there aren’t any ways of doing so at present.
Epidemiologists have attempted to determine the proportion of relapses on a population basis by including the use of drugs in their research (leaving aside the details and rationale). This does not give definitive answers for individual cases, however.
Differentiation of reifection and relapse P. vivax is possible through molecular study only. It can be done through genomic study of adequate numbers of samples in a community.
Well...molecular study is the ultimate answer to a scientific query. However, a malaria worker with limited facilities in the field can also try to answer this question on clinical and epidemiological ground to some extent. I have experienced in the field that in case of a relapse of P. vivax infection the bout of fever will come daily where as in case of fresh infection the 48 hrs periodicity is clearly maintained.
Please see our publication in this regard ( Genotyping of P vivax by minisatellite markers--(https://malariajournal.biomedcentral.com/articles/10.1186/s12936-016-1139-3) published in Malaria Journal (2016), the conclusion of which is: The CH1T1M13779 can be potential minisatellite marker which can be used to differentiate between relapse and new infection of P. vivax strain.
The TPP PvB2 is designed to answer the needs for high quality tests for epidemiological surveillance activities . This TPP is similar to PvB1 in the sense that it aims to detect all infections, including asymptomatic and low parasitaemia typically not seen by RDTs or microscopy, but it differs from PvB1 in that the diagnostic outcome is not directly linked with treatment interventions at the individual level.