The “vicious cycle" of enteropathogens, malnutrition, and impaired childhood development, and multifaceted opportunities for intervention.

<p>Figure adapted from Nutr Rev. 2008 September; 66(9): 487–505 <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002125#pntd.0002125-Guerrant1" target="_blank">[15]</a>.</p

Floors and Toilets: Association of Floors and Sanitation Practices with Fecal Contamination in Peruvian Amazon Peri-Urban Households

Over two billion people worldwide lack access to an improved sanitation facility that adequately retains or treats feces. This results in the potential for fecal material containing enteric pathogens to contaminate the environment, including household floors. This study aimed to assess how floor type and sanitation practices impacted the concentration of fecal contamination on household floors. We sampled 189 floor surfaces within 63 households in a peri-urban community in Iquitos, Peru. All samples were analyzed for colony forming units (CFUs) of <i>E. coli</i>, and households were evaluated for their water, sanitation, and hygiene characteristics. Results of multivariate linear regression indicated that households with improved sanitation and cement floors in the kitchen area had reduced fecal contamination to those with unimproved sanitation and dirt floors (Beta: −1.18 log₁₀ <i>E. coli</i> CFU/900 cm²; 95% confidence interval [CI]: −1.77, −0.60). Households that did not versus did share their sanitation facility also had less contaminated kitchen floors (Beta: −0.65 log₁₀ <i>E. coli</i> CFU/900 cm²; 95% CI: −1.15, −0.16). These findings suggest that the sanitation facilities of a home may impact the microbial load found on floors, contributing to the potential for household floors to serve as an indirect route of fecal pathogen transmission to children

Semi-formal care work: the case of private foster care

Differences between labelled and unlabelled primers of Microsatellite 9

Poisson model of risk factors for <i>Campylobacter.</i>

*<p>significant at <0.100 level,</p>**<p>significant and <0.050 level,</p>***<p>significant at <0.010 level.</p><p>Sex, seasonal terms, maternal age, breastfeeding status, birth weight, private household latrine, and the presence of household poultry, were not significant in any model and are not shown.</p><p>The association between prior nutritional status and prior diarrhea, and prior <i>Campylobacter</i>, were examined via correlations and kappa statistics and found to be low (rho<0.05).</p

Association between <i>Campylobacter</i> and weight gain.

<p>*significant at the p< = 0.10 level.</p>**<p>significant at the p< = 0.05 level.</p>***<p>significant at the p< = 0.01 level.</p><p>Weight models adjusted for stunting at onset of interval, WHZ category at onset of interval, season, age, birth weight and per capita income.</p><p>Fractional polynomial age term 1: ; age term 2: where <i>age</i> is the child's age, in days, divided by 1000.</p><p>In model 1, <i>Campylobacter</i>-related variables were asymptomatic <i>Campylobacter</i>, and symptomatic (diarrhea-associated) <i>Campylobacter</i> (2 variables).</p><p>In model 2, <i>Campylobacter-</i>related variables were asymptomatic <i>campylobacter</i>, symptomatic treated <i>campylobacter</i>, and symptomatic untreated <i>campylobacter</i> (three variables).</p

Association between <i>Campylobacter</i> and linear growth.

*<p>significant at the p = 0.10 level.</p>**<p>significant at the p = 0.05 level.</p>***<p>significant at the p = 0.01 level.</p><p>Height models adjusted for stunting at onset of interval, WHZ category at onset of interval, season, age, birth weight and per capita income.</p><p>Fractional polynomial age term 1: ; age term 2: where <i>age</i> is the child's age, in days, divided by 1000.</p><p>In model 1, <i>Campylobacter</i>-related variables were asymptomatic <i>Campylobacter</i>, and symptomatic (diarrhea-associated) <i>Campylobacter</i> (2 variables).</p><p>In model 2, <i>Campylobacter-</i>related variables were asymptomatic <i>campylobacter</i>, symptomatic treated <i>campylobacter</i>, and symptomatic untreated <i>campylobacter</i> (three variables).</p

Diarrhea episodes and asymptomatic stools, by <i>Campylobacter</i> species.

*<p>Diarrheal episodes were considered associated with <i>Campylobacter</i> when at least one stool sample from the episode was culture-positive for Campylobacter. A stool sample was considered associated with the episode when it was collected during, or up to one day after, the episode. Only stool samples that could be associated with anthropometry are reported here.</p><p>Asymptomatic stools were collected quarterly.</p

Smoothed plots of incidence versus age, and the percentage of stools positive by etiology.

<p>The peak incidence of <i>Campylobacter</i>-associated diarrhea occurs at approximately 18 months of age, and declines rapidly thereafter. However, its isolation rate in diarrheal and asymptomatic stool samples remains roughly constant from 18–72 months of age.</p

Development of <i>Taenia solium</i> postoncospheral forms at two week of incubation using different cells lines.

<p>Development of <i>Taenia solium</i> postoncospheral forms at two week of incubation using different cells lines.</p

Western blot of <i>T</i>. <i>solium</i> antigens at different forms.

<p>(a) Using rabbit anti-oncosphere sera. (b) Using rabbit anti-cysticerci sera.</p