Timing of host feeding drives rhythms in parasite replication

Circadian rhythms enable organisms to synchronise the processes underpinning survival and reproduction to anticipate daily changes in the external environment. Recent work shows that daily (circadian) rhythms also enable parasites to maximise fitness in the context of ecological interactions with their hosts. Because parasite rhythms matter for their fitness, understanding how they are regulated could lead to innovative ways to reduce the severity and spread of diseases. Here, we examine how host circadian rhythms influence rhythms in the asexual replication of malaria parasites. Asexual replication is responsible for the severity of malaria and fuels transmission of the disease, yet, how parasite rhythms are driven remains a mystery. We perturbed feeding rhythms of hosts by 12 hours (i.e. diurnal feeding in nocturnal mice) to desynchronise the hosts' peripheral oscillators from the central, light-entrained oscillator in the brain and their rhythmic outputs. We demonstrate that the rhythms of rodent malaria parasites in day-fed hosts become inverted relative to the rhythms of parasites in night-fed hosts. Our results reveal that the hosts' peripheral rhythms (associated with the timing of feeding and metabolism), but not rhythms driven by the central, light-entrained circadian oscillator in the brain, determine the timing (phase) of parasite rhythms. Further investigation reveals that parasite rhythms correlate closely with blood glucose rhythms. In addition, we show that parasite rhythms resynchronise to the altered host feeding rhythms when food availability is shifted, which is not mediated through rhythms in the host immune system. Our observations suggest that parasites actively control their developmental rhythms. Finally, counter to expectation, the severity of disease symptoms expressed by hosts was not affected by desynchronisation of their central and peripheral rhythms. Our study at the intersection of disease ecology and chronobiology opens up a new arena for studying host-parasite-vector coevolution and has broad implications for applied bioscience

Isospora plectrophenaxia n. sp (Apicomplexa: Eimeriidae), a new coccidian parasite found in Snow Bunting (Plectrophenax nivalis) nestlings on Spitsbergen

Faecal samples were collected from four 8 days old snow bunting nestlings from one nest in Ny-Aalesund, Spitsbergen, in summer 2006. After sporulation, samples were examined for coccidian parasites using flotation centrifuging. We found isosporan oocysts in three birds, intensity of infection varied between individuals from 35 to 6,000 oocysts per defecation. All oocysts belonged to one species, which is described here as a new species. The spherical or subspherical oocysts (Fig. 1) have a brownish, smooth, relatively thin (about 1.1 mu m) bilayered wall. Average size of sporulated oocysts was 26.2+/-0.13x23.6+/-0.16 mu m (24.1-28.4x21.5-26.9; n=10) with a shape index (length/width) of 1.11+/-0.01 (1.01-1.29). The sporulated oocysts have no micropyle or residuum but enclose one large (3.3x2.8 mu m) ring-formed polar granule. The sporocysts are ovoidal, slightly pointed at the end opposite the Stieda body, 18.2+/-0.06x9.9+/-0.03 mu m (17.1-19.0x9.0-10.8; n=14), shape index 1.85+/-0.008 (1.70-1.99). The Stieda body has a prominent knob-like cap and a well-visible round substieda body. Sporocysts contain compact sporocyst residuum composed of small, uniform granules and sporozoits with usually three large refractile bodies and a smaller nucleus. The prepatent period is less than 8 days. This is the first description of an avian isosporan parasite that succeeds transmission while in the High Arctic