Minimum evolution tree of several specimens of <i>Schistosoma mansoni</i> and <i>S. rodhaini</i> based on 512 bp of mitochondrial DNA including part of the 16S ribosomal RNA gene, all of thetRNA-Cys gene, and part of the 12S ribosomal RNA gene.

<p>Uncorrected p-distance is given for scale.</p

Percentage of snails infected with 1–9 genotypes of schistosome parasites from this study and previous studies (n indicates snail sample size).

<p>Kenya SM refers to <i>S. mansoni</i> and Kenya SR to <i>S. rodhaini</i> from this study.</p

Total adults recovered of 3 genotypes of <i>S. rodhaini</i> (R1-R3) and 1 genotype of <i>S. mansoni</i> (M1) that emerged from the same snail during 4 time intervals.

<p>Total adults recovered of 3 genotypes of <i>S. rodhaini</i> (R1-R3) and 1 genotype of <i>S. mansoni</i> (M1) that emerged from the same snail during 4 time intervals.</p

The number of snails infected with <i>Schistosoma mansoni</i> (SM), <i>Schistosoma rodhaini</i> (SR), unidentified mammalian schistosomes (US), and total schistosomes (TS) at various sites in the Lake Victoria Basin of Kenya.

<p>The total number of snails collected, prevalence of schistosome infection (P), and prevalence of confirmed <i>S. mansoni</i> (SM P) and <i>S. rodhaini</i> (SR P) infections are given for each site. Prevalence for each species was also adjusted as denoted by an asterisk to accommodate unidentified schistosomes by multiplying the prevalence of schistosomes by the percentage of identified schistosomes for each species.</p

Collection sites for snails of the genus <i>Biomphalaria</i> and their schistosome parasites in Western Kenya.

<p>Global Positioning System coordinates are projected in North American Datum 1983 decimal degrees.</p

Population assignment graph of <i>S. mansoni</i> and <i>S. rodhaini</i> based on 7 microsatellite markers.

<p>The dot plot indicates the log-likelihood (absolute value) that each individual belongs to either species. The lower the log likelihood value, the more likely the individual belongs to that species.</p

Results of the Fisher's Exact tests to determine if the proportions of genotypes of <i>S. mansoni</i> released from snails are consistent over timed replicates.

<p>P indicates the probability of significance, n indicates the number of worms sampled, R is the number of replicates tested, and G is the number of genotypes present in a snail. Mode indicates whether the proportions remained constant over replicates, followed a replacement pattern, or was variable.</p

Four replicates of circadian emergence of cercariae from a snail infected with 3 genotypes of <i>S. rodhaini</i> and 1 genotype of <i>S. mansoni</i>.

<p>Time units are hourly units beginning with 0:00–1:00 hours.</p

No Apparent Reduction in Schistosome Burden or Genetic Diversity Following Four Years of School-Based Mass Drug Administration in Mwea, Central Kenya, a Heavy Transmission Area

<div><p>Background</p><p>Schistosomiasis is a debilitating neglected tropical disease that infects over 200 million people worldwide. To combat this disease, in 2012, the World Health Organization announced a goal of reducing and eliminating transmission of schistosomes. Current control focuses primarily on mass drug administration (MDA). Therefore, we monitored transmission of <i>Schistosoma mansoni</i> via fecal egg counts and genetic markers in a typical school based MDA setting to ascertain the actual impacts of MDA on the targeted schistosome population.</p><p>Methods</p><p>For 4 years, we followed 67 children enrolled in a MDA program in Kenya. Infection status and egg counts were measured each year prior to treatment. For 15 of these children, for which there was no evidence of acquired resistance, meaning they became re-infected following each treatment, we collected microsatellite genotype data from schistosomes passed in fecal samples as a representation of the force of transmission between drug treatments. We genotyped a total of 4938 parasites from these children, with an average of 329.2 parasites per child for the entire study, and an average of 82.3 parasites per child per annual examination. We compared prevalence, egg counts, and genetic measures including allelic richness, gene diversity (expected heterozygosity), adult worm burdens and effective number of breeders among time points to search for evidence for a change in transmission or schistosome populations during the MDA program.</p><p>Findings</p><p>We found no evidence of reduced transmission or schistosome population decline over the course of the program. Although prevalence declined in the 67 children as it did in the overall program, reinfection rates were high, and for the 15 children studied in detail, schistosome egg counts and estimated adult worm burdens did not decline between years 1 and 4, and genetic diversity increased over the course of drug treatment.</p><p>Interpretation</p><p>School based control programs undoubtedly improve the health of individuals; however, our data show that in an endemic area, such a program has had no obvious effect on reducing transmission or of significantly impacting the schistosome population as sampled by the children we studied in depth. Results like these, in combination with other sources of information, suggest more integrated approaches for interrupting transmission and significantly diminishing schistosome populations will be required to achieve sustainable control.</p></div

Prevalence (percent of snails infected) of <i>S. rodhaini</i> (top) and <i>S. mansoni</i> (bottom) at various sites in the Lake Victoria basin of Kenya over a 2 year period.

<p>Blank spaces indicate that either snails were not present or no collections were made.</p