Main vectors and rodent reservoirs in Madagascar.

<p>Fleas involved in plague transmission in Madagascar: <i>Synopsyllus fonquerniei</i> female <i>(1)</i> and <i>Synopsyllus fonquerniei</i> male <i>(3)</i> are found on outdoor rats, whereas <i>Xenopsylla cheopis</i> female <i>(2)</i> and <i>Xenopsylla cheopis</i> male <i>(4)</i> live on indoor rats. Rat species involved in plague transmission in Madagascar: <i>Rattus rattus (5)</i> and <i>Rattus norvegicus (6)</i>.</p

Factors related to human plague.

<p>According to <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002382#pntd.0002382-Duplantier1" target="_blank">[3]</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002382#pntd.0002382-Rahelinirina1" target="_blank">[14]</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002382#pntd.0002382-Migliani1" target="_blank">[20]</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002382#pntd.0002382-Boisier1" target="_blank">[27]</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002382#pntd.0002382-Rahalison1" target="_blank">[28]</a>.</p

Plague transmission cycle.

<p>A) <i>Plague cycle in the rural area of Madagascar</i>. Rural plague foci of the highlands are organized into three habitats: houses (arrow), sisal hedges (arrowhead), and rice fields (star). The black rat, <i>R. rattus (3)</i>, is the main rodent involved in transmission associated with <i>X. cheopis (1)</i> and the endemic flea <i>S. fonquerniei (2)</i>. (Photo of plague foci: S. Rahelinirina). B) <i>Plague cycle in the urban areas of Madagascar</i>. Urban plague occurs mainly in the cities of Antananarivo (Isotry Market, left) <i>(7)</i> and Mahajanga (Abattoir suburb, right) <i>(6)</i>. <i>R. norvegicus (4)</i> and <i>X. cheopis (1)</i> are involved in each focus. The Asian shrew (<i>S. murinus</i>) <i>(5)</i> has long been suspected to play a major role in the epidemiological cycle of plague in Mahajanga. C) <i>Plague cycle in the forest area</i>. A sylvatic transmission occurs in Madagascar with <i>R. rattus (3)</i> and endemic micromammals (such as <i>Setifer setosus</i>) <i>(8)</i> as reservoirs. <i>S. fonquerniei (2)</i> is the major vector of the disease in this area. The role of other endemic fleas <i>(9)</i> is not yet determined. (Photo of forest of Ampahitra: S. Telfer; <i>Setifer setosus</i>: V. Soarimalala).</p

Short term kinetic of anti-F1 IgM in <i>R. rattus</i> after inoculation with <i>Y. pestis</i>.

<p>Wild healthy rats (<i>Rattus rattus</i>) were inoculated with different doses of living <i>Y. pestis</i> (0 to 30,000 cfu) and blood sampled over one month. Anti-F1 IgM was detected by a sandwich ELISA. Results were expressed as the ratio of the mean optical density (OD) of the sample on the mean OD obtained for negative control rats +3 SD. Rats are from two villages Ambohimasina and Maromanana. (median; bar: 10% and 90% percentiles) A/Time course of the median OD ratio of each group: OD ratio peaked at Day 13 and decreased rapidly after B/Median of OD ratio obtained at Day13 and Day 25 for the two villages according to the dose inoculated. Rats from Ambohimasina produced a stronger IgM response against <i>Y. pestis</i> than Maromanana rats C/Median fraction of maximal anti-F1 IgM titer (OD ratio, mostly at Day 13) remaining at Day 18 and Day 25 according to the dose inoculated. For each rat the maximal OD ratio is noted as well as the OD ratio at Day 18 and Day 25, the fractions are calculated and the median of each group is plotted according to the dose inoculated. The speed of decay of IgM increases with the dose inoculated. D/Percent of rats remaining seronegative after inoculation. For each dose the fraction of rats remaining negative for anti-F1 IgM at Day 13 and IgG at Day 25 is plotted. It decreases from 15 to 30,000 cfu.</p

Short term kinetic of anti-F1 IgG in <i>R. rattus</i> after inoculation with <i>Y. pestis.</i>

<p>Wild healthy rats (<i>Rattus rattus</i>) were inoculated with different doses of living <i>Y. pestis</i> and blood sampled over one month. Anti-F1 IgG was detected by ELISA. Results were expressed as the ratio of the mean optical density (OD) of the sample on the mean OD obtained for negative control rats +3SD. (bar: 10% and 90% percentiles) A/Time course of the median anti-F1 IgG OD ratio of each group: OD ratio peaked between Day 13 and Day 25 and remained stable. Rats are from the two villages Ambohimasina and Maromanana B/Median anti-F1 IgG OD ratio at Day 13 and Day 25 according to the dose of <i>Y. pestis</i> inoculated. OD reaches a plateau for 500 cfu. Rats are from the two villages Ambohimasina and Maromanana C/Scatter plot of the OD ratio (IgM at Day 13/IgG at Day25) of rats from Ambohimasina and Maromanana. Logarithmic regression highlighted positive correlations between IgM and IgG responses to <i>Y. pestis</i>, (for Maromanana (solid line) Day 25-IgG  = 0,5322+8,7431*log10(Day 13-IgM); for Ambohimasina (dashed line) Day 25-IgG  = 0,4428+6,4026*log10(Day 13-IgM) ). D/Comparison of the dose/anti-F1 IgG titer relation for four different villages. For each group of dose, median OD ratio at Day 13 and Day 25 are plotted. Different sensitivity of the rats according to the village can be shown.</p

Long term kinetic of anti-F1 IgG in <i>R. rattus</i> after inoculation with 125 cfu of <i>Y. pestis.</i>

<p>Rats captured in three villages were inoculated with 125 cfu of living <i>Y. pestis</i> and blood sampled over 12.5 months using seropads. Anti-F1 IgG measured by ELISA delta OD are plotted. A/Mean of delta OD of survival rats were plotted according to time. Columns represent the number of deaths registered at each time point. Data are separated in two groups, i.e. rats with long-lasting IgG response and those with short-lasting response. Almost no death was registered in the long-lasting group. (n: number of remaining rat in the group at time point) B/Same plot but with data separated according to the villages. No difference between villages was found C/Same plot according to the capture site of the rats showing no difference.</p

Multiple regression analysis of the anti-F1 IgM and IgG titers.

<p>four separate logistic regressions (1) to (4) were conducted on the set of 118 rats from Ambohimasina and Maromanana studied for short term follow up of IgM and IgG, to check effect of parameters (beta coefficient are reported when parameters are used in the regression and plotted in bold when significant at less than p = 0.05).</p

World Antimalarial Resistance Network (WARN) II: In vitro antimalarial drug susceptibility-0

<p><b>Copyright information:</b></p><p>Taken from "World Antimalarial Resistance Network (WARN) II: In vitro antimalarial drug susceptibility"</p><p>http://www.biomedcentral.com/1475-2875/6/120</p><p>Malaria Journal 2007;6():120-120.</p><p>Published online 6 Sep 2007</p><p>PMCID:PMC2008206.</p><p></p>e of the web site

The importance of public health, poverty reduction programs and women’s empowerment in the reduction of child stunting in rural areas of Moramanga and Morondava, Madagascar

<div><p>Background</p><p>Malnutrition accounts for 45% of mortality in children under five years old, despite a global mobilization against chronic malnutrition. In Madagascar, the most recent data show that the prevalence of stunting in children under five years old is still around 47.4%. This study aimed to identify the determinants of stunting in children in rural areas of Moramanga and Morondava districts to target the main areas for intervention.</p><p>Methods</p><p>A case-control study was conducted in children aged from 6 to 59.9 months, in 2014–2015. We measured the height and weight of mothers and children and collected data on child, mother and household characteristics. One stool specimen was collected from each child for intestinal parasite identification. We used a multivariate logistic regression model to identify the determinants of stunting using backwards stepwise methods.</p><p>Results</p><p>We included 894 and 932 children in Moramanga and in Morondava respectively. Stunting was highly prevalent in both areas, being 52.8% and 40.0% for Moramanga and Morondava, respectively. Stunting was most associated with a specific age period (12mo to 35mo) in the two study sites. Infection with <i>Trichuris trichiura</i> (aOR: 2.4, 95% CI: 1.1–5.3) and those belonging to poorer households (aOR: 2.3, 95% CI: 1.6–3.4) were the major risk factors in Moramanga. In Morondava, children whose mother had activities outside the household (aOR: 1.7, 95% CI: 1.2–2.5) and those perceived to be small at birth (aOR: 1.6, 95% CI: 1.1–2.1) were more likely to be stunted, whereas adequate birth spacing (≥24months) appeared protective (aOR: 0.4, 95% CI: 0.3–0.7).</p><p>Conclusion</p><p>Interventions that could improve children’s growth in these two areas include poverty reduction, women’s empowerment, public health programmes focusing on WASH and increasing acceptability, and increased coverage and quality of child/maternal health services.</p></div

Characteristics of children included in the case-control study in Moramanga and Morondava.

<p>Characteristics of children included in the case-control study in Moramanga and Morondava.</p