Table 1.

Variation in life-history traits associated with growth and reproduction exhibited by malaria (Plasmodium) parasites. We highlight traits for which variation is observed across species (species), within species (genotype), and during infections (infection). This list is by no means exhaustive, but is indicative of the empirical literature to date

Function	Trait	Examples of variation	Refs
Growth	Cell cycle duration and synchronicity	Species. The species of parasite infecting humans can be diagnosed from the regularity of fevers resulting from each synchronous replication cycle (P. vivax and P. falciparum for fevers every 48 h and P. malariae every 72 h). In the rodent malarias, P. berghei is asynchronous with cell cycle duration of 22–23 h, whereas mature P. chabaudi parasites rupture synchronously every 24 h	Mons et al. (1985), Carter and Walliker (1975), Mackinnon et al. (2002a,b), Reilly et al. (2007) and Garnham (1966)
		Genotype. In-vitro evidence that two clones of P. falciparum have an average difference of ∼5 h in their cell cycle duration
		Infection. Observations suggest that P. chabaudi synchronicity decreases as infections progress
	Number of merozoites per schizont	Species. Species-specific data are normally presented as ranges (e.g. P.falciparum 8–32 merozoites per schizont), but it is not known if this represents genetic or within-infection variation. Species-specific estimates for the number of merozoites produced per schizont range from 4 to 5 in P. juxtanucleare (an avian malaria) to over 90 for P. giganteum (a lizard malaria)	Reilly et al. (2007), Garnham (1966), Kissinger et al. (2002) and Schall (1990)
		Genotype. Different clones of P. falciparum produce different modal numbers of merozoites per schizont, and this may also vary with the type of tissue in which parasites sequester
		Infection. P. berghei produces more merozoites per schizont in reticulocytes than in mature RBC
	Red blood cell preference	Species. In human malarias, P. ovale and P. vivax prefer reticulocytes, P. malariae prefers mature RBCs and P. falciparum is able to infect both age classes. Similar patterns occur in the rodent malarias; preference spans the continuum from strict preference for reticulocytes (e.g. P. berghei) to specialists for mature RBCs (e.g. P. vinckei) with generalists (e.g. P. chabaudi) in between. Similar examples can be found in bird malarias	Antia et al. (2008), Simpson et al. (1999), Paul and Brey (2003),Killick-Kendrick and Peters (1978) and Taylor-Robinson and Phillips (1994)
		Genotype. Some evidence that P. chabaudi genotypes may vary in the age range of cells they can infect
		Infection. P. falciparum may become less selective as infections progress. A clone of P. chabaudi changes from strict preference for mature RBCs to reticulocytes around peak parasitaemia, changing again to strict preference for mature RBCs during the chronic stage of the infection
	Cytoadherence	Species. Sequestration* occurs in most (e.g. P. falciparum and P. berghei) but not all (e.g. P. malariae and P. knowlesii) species investigated. Rosetting† rates vary across species, but has been observed in all species analysed	Mackinnon et al. (2002a,b), Garnham (1966), Sherman et al. (2003)
		Genotype. Genetic variation for rosetting rates observed in P. chabaudi (from 10% to 40%)
		Infection. Highest rosetting rates observed before peak parasitaemia in P. chabaudi. Some lines of P. falciparum lose the ability to sequester with serial culture
Reproduction	Conversion	Species. Rarely calculated, potentially because data on cell cycle duration, gametocyte development time and longevity are required	Graves et al. (1984), Reece et al. (2005), Buckling et al. (1997, 1999)
		Genotype. In vitro data suggest genetic variation for conversion in P. falciparum
		Infection. P. chabaudi increases conversion in response to EPO and antimalarial drugs. P. falciparum also increases conversion in response to antimalarial drugs
	Sex ratio	Species, genotype and infection. See Fig. 2 and text (Explaining sex ratio variation in malaria parasites)	West et al. (2001), Reece et al. (2008) and Paul et al. (2000)

^*Sequestration: withdrawal of infected RBCs from the peripheral circulation to the microvasculature where they adhere to endothelial cells.

^†Rosetting: adherence of uninfected RBCs to infected cells leading to the formation of small clusters of cells.