Water striders Gerridae are insects of characteristic length 1 cm and weight 10 dynes that reside on the surface of ponds, rivers, and the open ocean. Their weight is supported by the surface tension force generated by curvature of the free surface, and they propel themselves by driving their central pair of hydrophobic legs in a sculling motion. Previous investigators have assumed that the hydrodynamic propulsion of the water strider relies on momentum transfer by surface waves. This assumption leads to Denny's paradox: infant water striders, whose legs are too slow to generate waves, should be incapable of propelling themselves along the surface. We here resolve this paradox through reporting the results of high-speed video and particle-tracking studies. Experiments reveal that the strider transfers momentum to the underlying fluid not primarily through capillary waves, but rather through hemispherical vortices shed by its driving legs. This insight guided us in constructing a self-contained mechanical water strider whose means of propulsion is analogous to that of its natural counterpart.
Explaining parasite virulence is a great challenge for evolutionary biology. Intuitively, parasites that depend on their hosts for their survival should be benign to their hosts, yet many parasites cause harm. One explanation for this is that within-host competition favors virulence, with more virulent strains having a competitive advantage in genetically diverse infections. This idea, which is well supported in theory, remains untested empirically. Here we provide evidence that within-host competition does indeed select for high parasite virulence. We examine the rodent malaria Plasmodium chabaudi in laboratory mice, a parasite-host system in which virulence can be easily monitored and competing strains quantified by using strain-specific real-time PCR. As predicted, we found a strong relationship between parasite virulence and competitive ability, so that more virulent strains have a competitive advantage in mixed-strain infections. In transmission experiments, we found that the strain composition of the parasite populations in mosquitoes was directly correlated with the composition of the bloodstage parasite population. Thus, the outcome of within-host competition determined relative transmission success. Our results imply that within-host competition is a major factor driving the evolution of virulence and can explain why many parasites harm their hosts.competition ͉ evolution ͉ parasite ͉ Plasmodium ͉ mixed infection E xplaining virulence is fundamental to understanding the life history of parasites, arguably the most abundant group of creatures on the planet (1). The problem is to explain why parasites, which rely on their hosts for survival and fitness, should cause disease or indeed kill their hosts (2-6). Many explanations of parasite virulence have been put forward (3, 4), but the idea that has received the most attention is that virulence is a consequence of a parasite's efforts to maximize its fitness: parasites require extensive within-host replication to achieve transmission to the next host, but at the same time such replication damages host tissues, increasing the chances of killing the host (2, 3, 7-9). Higher levels of virulence than predicted by this model, however, could arise due to within-host competition between parasite strains (9-14). Many, if not most, parasite infections consist of genetically distinct strains of the same parasite species or contain virulent mutants that have arisen de novo (15). It is generally assumed that parasites that exploit their hosts prudently suffer great fitness losses in hosts simultaneously infected with more aggressive parasites. This is because virulent parasites could kill the host or competitively exclude prudent parasites before the latter have realized transmission. Even though host death also reduces the fitness of virulent parasites, prudent parasites suffer disproportionately and are eliminated by natural selection, a process commonly known as ''the tragedy of the commons'' (16).Several authors (17, 18) have gone so far as to claim that reducing t...
Using a rodent malaria model, we found that exposure to surfaces treated with fungal entomopathogens following an infectious blood meal reduced the number of mosquitoes able to transmit malaria by a factor of about 80. Fungal infection, achieved through contact with both solid surfaces and netting for durations well within the typical post-feed resting periods, was sufficient to cause >90% mortality. Daily mortality rates escalated dramatically around the time of sporozoite maturation, and infected mosquitoes showed reduced propensity to blood feed. Residual sprays of fungal biopesticides might replace or supplement chemical insecticides for malaria control, particularly in areas of high insecticide resistance.
This article reports on the quality of care delivered by private and public providers of primary health care services in rural and urban India. To measure quality, the study used standardized patients recruited from the local community and trained to present consistent cases of illness to providers. We found low overall levels of medical training among health care providers; in rural Madhya Pradesh, for example, 67 percent of health care providers who were sampled reported no medical qualifications at all. What’s more, we found only small differences between trained and untrained doctors in such areas as adherence to clinical checklists. Correct diagnoses were rare, incorrect treatments were widely prescribed, and adherence to clinical checklists was higher in private than in public clinics. Our results suggest an urgent need to measure the quality of health care services systematically and to improve the quality of medical education and continuing education programs, among other policy changes.
Background The SARS-CoV-2 Omicron variant, designated as a Variant of Concern(VOC) by the World Health Organization, carries numerous spike mutations which have are known to evade neutralizing antibodies elicited by COVID-19 vaccines. A deeper understanding of the susceptibility of Omicron variant to vaccine-induced neutralizing antibodies is urgently needed for risk assessment. Methods Omicron variant strains HKU691 and HKU344-R346K were isolated from patients using TMPRSS2-overexpressing VeroE6 cells. Whole genome sequence was determined using nanopore sequencing. Neutralization susceptibility of ancestral lineage A virus and the Omicron, Delta and Beta variants to sera from 25 BNT162b2 and 25 Coronavac vaccine recipients was determined using a live virus microneutralization assay. Results The Omicron variant strain HKU344-R346K has an additional spike R346K mutation, which is present in 8.5% of strains deposited in GISAID database. Only 20% and 24% of BNT162b2 recipients had detectable neutralizing antibody against the Omicron variant HKU691 and HKU344-R346K, respectively, while none of the Coronavac recipients had detectable neutralizing antibody titer against either Omicron isolate. For BNT162b2 recipients, the geometric mean neutralization antibody titers(GMT) of the Omicron variant isolates(5.43 and 6.42) were 35.7-39.9-fold lower than that of the ancestral virus(229.4), and the GMT of both Omicron variant isolates were significantly lower than those of the Beta and Delta variants. There was no significant difference in the GMT between HKU691 and HKU344-R346K. Conclusions Omicron variant escapes neutralizing antibodies elicited by BNT162b2 or Coronavac. The additional R346K mutation did not affect the neutralization susceptibility. Our data suggest that the Omicron variant may be associated with lower COVID-19 vaccine effectiveness.
The development rate of parasites and pathogens within vectors typically increases with temperature. Accordingly, transmission intensity is generally assumed to be higher under warmer conditions. However, development is only one component of parasite/pathogen life history and there has been little research exploring the temperature sensitivity of other traits that contribute to transmission intensity. Here, using a rodent malaria, we show that vector competence (the maximum proportion of infectious mosquitoes, which implicitly includes parasite survival across the incubation period) tails off at higher temperatures, even though parasite development rate increases. We also show that the standard measure of the parasite incubation period (i.e. time until the first mosquitoes within a cohort become infectious following an infected blood-meal) is incomplete because parasite development follows a cumulative distribution, which itself varies with temperature. Including these effects in a simple model dramatically alters estimates of transmission intensity and reduces the optimum temperature for transmission. These results highlight the need to understand the interactive effects of environmental temperature on multiple host-disease life-history traits and challenge the assumptions of many current disease models that ignore this complexity.
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