25 research outputs found
The āvicious cycle" of enteropathogens, malnutrition, and impaired childhood development, and multifaceted opportunities for intervention.
<p>Figure adapted from Nutr Rev. 2008 September; 66(9): 487ā505 <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.Ā 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: ā1.18 log<sub>10</sub> <i>E.Ā coli</i> CFU/900 cm<sup>2</sup>; 95%
confidence interval [CI]: ā1.77, ā0.60). Households
that did not versus did share their sanitation facility also had less
contaminated kitchen floors (Beta: ā0.65 log<sub>10</sub> <i>E.Ā coli</i> CFU/900 cm<sup>2</sup>; 95% CI: ā1.15,
ā0.16). 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<ā=ā0.10 level.</p>**<p>significant at the p<ā=ā0.05 level.</p>***<p>significant at the p<ā=ā0.01 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 pā=ā0.10 level.</p>**<p>significant at the pā=ā0.05 level.</p>***<p>significant at the pā=ā0.01 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 18ā72 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