Effects of Animations on Students’ Achievement in Kiswahili Reading Comprehension in Public Secondary Schools in Njoro Sub -County, Kenya

The study aimed at investigating the effects of using animations in teaching Kiswahili reading comprehension on students achievement among secondary school students’ in Njoro Sub- County Kenya. Solomon Four Non-Equivalent control group design was used in the study. Target Population comprised all 14,292 students in the public co-educational secondary schools in Njoro Sub County. The accessible population included the 4,745 Form Two students from public co-educational secondary schools in the Sub-county. Purposive sampling technique was used to select one form two class from each of the four co-educational secondary schools which provided the sample size for the study 160 students. The four schools were randomly assigned to experimental and control groups. For the experimental group, animations were used during the lessons while conventional methods were used for the control groups. Data was collected using Kiswahili Reading comprehension achievement test, whose reliability coefficient of 0.76 was attained using Kuder -Richardson 20 (KR-20). The null hypothesis was tested at 0.05 level of significance. Data was analysed using t-test, ANOVA and ANCOVA. Before the treatment, a pre-test was administered then after four weeks a post-test. The findings proved that after the treatment, the students in the experimental groups attained higher scores compared to the ones in the control groups. This signifies that the use of animations in teaching had an effect on students’ achievement in Kiswahili reading comprehension. Therefore, teachers are encouraged to incorporate the use of animations in teaching Kiswahili reading comprehension in attempt to improve achievement in Kiswahili subject. Key words: Animation, Achievement, Kiswahili DOI: 10.7176/JEP/14-23-03 Publication date:August 31st 202

Determinants of vaccination coverage among children aged 12-23 months in rural KwaZulu-Natal

To evaluate the impact of maternal HIV-infection on routine childhood immunization coverage, comparison was made on the immunization status of children born to HIV-infected and HIV-uninfected women in rural KwaZulu Natal. The study population was all children enrolled in the routine demographic surveillance system as at 31st December 2005 (n=18,171) in Africa Centre Demographic Surveillance Area. Sampling of subjects was done based on the dates of birth that were between the period 1st Jan 2004 and 31st December 2005 (n=2,020). This was further divided based on maternal HIV status namely; 236 HIV (+), 777 HIV (-) and 1,007 HIV (unknown). The main outcome measure was the percent of complete routine childhood immunizations recommended by the WHO as assessed from the Road-to- Health cards or maternal recall during household interviews. For all vaccines, children born to HIV-infected mothers had lower immunization coverage than children born to HIV-negative mothers (78.21% vs. 86.52%). The children of mothers who were HIV-infected were 31-55% (P-value <0.020) less likely to be immunized compared to children of mothers who were HIVuninfected. We conclude that maternal HIV-infection is associated with childhood under immunisation. VCT health workers should encourage HIV-infected mothers to complete childhood immunization. Improving access to immunization services could benefit vulnerable populations such as children born to HIV-infected mothers

Maternal HIV infection associated with small-for-gestational age infants but not preterm births: evidence from rural South Africa

BACKGROUND: Human immunodeficiency virus (HIV) is prevalent in many countries where small-for-gestational age (SGA) and premature delivery are also common. However, the associations between maternal HIV, preterm delivery and SGA infants remain unclear. We estimate the prevalence of SGA and preterm (&lt;37 weeks) births, their associations with antenatal maternal HIV infection and their contribution to infant mortality, in a high HIV prevalent, rural area in South Africa.METHODS: Data were collected, in a non-randomized intervention cohort study, on all women attending antenatal clinics (2001-2004), before the availability of antiretroviral treatment. Newborns were weighed and gestational age was determined (based on last menstrual period plus midwife assessment antenatally). Poisson regression with robust variance assessed risk factors for preterm and SGA birth, while Cox regression assessed infant mortality and associated factors.RESULTS: Of 2368 live born singletons, 16.6% were SGA and 21.4% were preterm. HIV-infected women (n= 1189) more commonly had SGA infants than uninfected women (18.1 versus 15.1%; P = 0.051), but percentages preterm were similar (21.8 versus 20.9%; P = 0.621). After adjustment for water source, delivery place, parity and maternal height, the SGA risk in HIV-infected women was higher [adjusted relative risk (aRR) 1.28, 95% confidence interval (CI): 1.06-1.53], but the association between maternal HIV infection and preterm delivery remained weak and not significant (aRR: 1.07, 95% CI: 0.91-1.26). In multivariable analyses, mortality under 1 year of age was significantly higher in SGA and severely SGA than in appropriate-for-gestational-age infants [adjusted hazard ratio (aHR): 2.12, 95% CI: 1.18-3.81 and 2.77, 95% CI: 1.56-4.91], but no difference in infant mortality was observed between the preterm and term infants (aHR: 1.18 95% CI: 0.79-1.79 for 34-36 weeks and 1.31, 95% CI: 0.58-2.94 for &lt;34 weeks).CONCLUSIONS: Maternal HIV infection increases the risk of SGA, but not preterm births, in this cohort

Levels of childhood vaccination coverage and the impact of maternal HIV status on child vaccination status in rural KwaZulu-Natal, South Africa*

Objectives To analyse coverage of childhood vaccinations in a rural South African population and investigate whether maternal HIV status is associated with children’s vaccination status. Methods 2 431 children with complete information, 12–23 months of age at some point during the period January 2005 through December 2006 and resident in the Africa Centre Demographic Surveillance Area at the time of their birth were investigated. We examined the relationship between maternal HIV status and child vaccination status for five vaccinations [Bacillus Calmette‐Guérin (BCG), diphtheria‐tetanus‐pertussis (DTP3), poliomyelitis (polio3), hepatitis B (HepB3), and measles] in multiple logistic regressions, controlling for household wealth, maternal age, maternal education and distances to roads, fixed and mobile clinics. Results Coverage of the five vaccinations ranged from 89.3% (95% CI 81.7–93.9) for BCG to 77.3% (67.1–83.6) for measles. Multivariably, maternal HIV‐positive status was significantly associated with lower adjusted odds ratios (AOR) of child vaccination for all vaccines [(AOR) 0.60–0.74, all P ≤ 0.036] except measles (0.75, P = 0.073), distance to mobile clinic was negatively associated with vaccination status (all P ≤ 0.029), household wealth was positively (all P ≤ 0.013) and distance to nearest road negatively (all P ≤ 0.004) associated with vaccination status. Conclusion Positive maternal HIV status independently reduces children’s probability to receive child vaccinations, which likely contributes to the morbidity and mortality differential between children of HIV‐positive and HIV‐negative mothers. As a means of increasing vaccination coverage, policy makers should consider increasing the number of mobile clinics in this and similar communities in rural Africa

Validating child vaccination status in a demographic surveillance system using data from a clinical cohort study: evidence from rural South Africa

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; Childhood vaccination coverage can be estimated from a range of sources. This study aims to validate vaccination data from a longitudinal population-based demographic surveillance system (DSS) against data from a clinical cohort study.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods:&lt;/b&gt; The sample includes 821 children in the Vertical Transmission cohort Study (VTS), who were born between December 2001 and April 2005, and were matched to the Africa Centre DSS, in northern KwaZulu-Natal. Vaccination information in the surveillance was collected retrospectively, using standardized questionnaires during bi-annual household visits, when the child was 12 to 23 months of age. DSS vaccination information was based on extraction from a vaccination card or, if the card was not available, on maternal recall. In the VTS, vaccination data was collected at scheduled maternal and child clinic visits when a study nurse administered child vaccinations. We estimated the sensitivity of the surveillance in detecting vaccinations conducted as part of the VTS during these clinic visits.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; Vaccination data in matched children in the DSS was based on the vaccination card in about two-thirds of the cases and on maternal recall in about one-third. The sensitivity of the vaccination variables in the surveillance was high for all vaccines based on either information from a South African Road-to-Health (RTH) card (0.94-0.97) or maternal recall (0.94-0.98). Addition of maternal recall to the RTH card information had little effect on the sensitivity of the surveillance variable (0.95-0.97). The estimates of sensitivity did not vary significantly, when we stratified the analyses by maternal antenatal HIV status. Addition of maternal recall of vaccination status of the child to the RTH card information significantly increased the proportion of children known to be vaccinated across all vaccines in the DSS.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; Maternal recall performs well in identifying vaccinated children aged 12-23 months (both in HIV-infected and HIV-uninfected mothers), with sensitivity similar to information extracted from vaccination cards. Information based on both maternal recall and vaccination cards should be used if the aim is to use surveillance data to identify children who received a vaccination.&lt;/p&gt

The Impact of Human Immunodeficiency Virus and Human Papillomavirus Co-Infection on HPV Genotype Distribution and Cervical Lesion Grade in a Semi-Urban Population in Tigoni, Kenya

1. IntroductionCervical cancer is an important global public healthproblem and a common cause of death among women,and it is attributable to human papillomavirus (HPV)(Walboomers et al, 1999; Parkin et al, 2008). In a largeseries of invasive cervical cancer from around theworld, HPV-DNA was detected in 99.7% of the tumors,leading to the conclusion that HPV was a necessarycause of cervical cancer (Bosch et al, 1995; Walboomerset al, 1999; Bosch et al, 2007). The identification ofHPV’s role in cervical cancer has led to importantadvances in primary prevention through vaccinationand diagnosis through HPV detection (Stanley et al,2008; Bosch et al, 2008). However, tangible reductionin the incidence of cervical cancer and the impact onglobal public health will probably take decades. As HPVtypes are divergent, efficacy of current vaccines is typerestricted,and therefore development of the nextgeneration of HPV vaccines will require inclusion ofrelevant antigens from several HPV types (Lowy, 2008).Geographical profiling of HPV type distribution will beimportant in making vaccines more relevant for targetpopulations.Most women will be infected with HPV sometime intheir lifetime. Results from large meta-analyses studiesindicate that at any given point in time, 10.4% (95%confidence interval (CI) 10.2-10.7) of womenworldwide are positive for cervical HPV DNA (Bosch etal, 2008). The prevalence of HPV is higher in lessdeveloped regions (13.4%; 95% CI: 13.1-13.7) than inthe more developed regions (8.4%; 95% CI: 8.3-8.6)(Bosch et al, 2008). The same studies indicate thatAfrican women at 22.1% (95% CI: 20.9-23.4) and EastAfrican women in particular, have the highest HPVprevalence rates (31.6%; 95% CI: 29.5-33.8) (Bosch etal, 2008). HPV type 16 is the most common in allcontinents, with an estimated point prevalence of 2.6%(95% CI: 2.5-2.8) worldwide, and HPV type 18 thesecond most frequently detected type (Clifford et al,2005). Regional differences are thought to be related togeographical and immunogenetic factors, such asdefects in cellular immunity through chronic cervicalinflammation, malnutrition and more recently, HIVinfection; Type 16 though appears to be less influencedby immune impairment than other types (Clifford et al,2005).Although many women get infected with HPV, most donot develop cervical cancer. Several co-factors arepostulated to influence the disease process. Thepotential co-factors include exogenous factors such astobacco smoking, hormonal contraceptives, and coinfectionswith other sexually transmitted infections(Munoz et al, 2006). In addition, viral co-factors, suchspecific HPV types, viral load, and viral integration, aswell as host co-factors such as endogenous hormones,genetic factors, and factors related to the immuneresponse may variably influence the course of HPVinfection (Munoz et al, 2006).Women with HIV infection have been shown to be morelikely not only to have a concurrent HPV infection butalso to have an increased risk for a high grade cervicalsquamous intraepithelial lesion (La Ruche et al, 1998;Temmerman et al, 1999; Womack et al, 2000; Baay et al,2004; Hawes et al, 2006; Didelot-Rousseau et al, 2006;Ngándwe et al, 2007). HPV is the commonest sexuallytransmitted infection, with more than 75% of sexuallyactive adults acquiring one or more genotypes in theirlifetime (Bosch et al, 2008). However, by age 30 years,most women clear the infection due to an effective cellmediatedimmune response, and only a small numberthereafter are diagnosed with a HPV-associated lesion(Schiffman, 1992). It is thought that it is through itseffect on CD4+ cells and regulation of immuneresponses to a variety of antigens that HIV attenuatesthe systemic response to HPV (Palefsky, 2006).The prevalence of HIV among adult Kenyan women was13% in 2003 with trends reported to have decreased to5.1% by 2006 (KDHS, 2003). The high prevalence ofHIV may increase the incidence of cervical pre-cancerand potentially, of cervical cancer. Gichangi et al (2002),however, demonstrated that a two to three-foldincrease in HIV prevalence did not translate to aproportionate increment in incidence of cervical cancer.They hypothesized that HIV-infected women die fromHIV-related opportunistic infections before theydevelop invasive cervical cancer. The mean survivaltime for women with HIV in 2008 was reported to be 5years (Yamada et al, 2008) while typically more than 10years elapse before the development of cervical cancerafter HPV infection. Yamada et al (2008) also advancedthe possibility that sub-clinical cervical cancer may bemissed in many women dying prematurely from AIDSrelatedopportunistic infections.This study was carried out to establish whether the coinfectionof HIV and HPV has an influence on HPVgenotype distribution and on the prevalence and gradeof cervical neoplasia

The Impact of Human Immunodeficiency Virus and Human Papillomavirus Co-Infection on HPV Genotype Distribution and Cervical Lesion Grade in a Semi-Urban Population in Tigoni, Kenya

1. IntroductionCervical cancer is an important global public healthproblem and a common cause of death among women,and it is attributable to human papillomavirus (HPV)(Walboomers et al, 1999; Parkin et al, 2008). In a largeseries of invasive cervical cancer from around theworld, HPV-DNA was detected in 99.7% of the tumors,leading to the conclusion that HPV was a necessarycause of cervical cancer (Bosch et al, 1995; Walboomerset al, 1999; Bosch et al, 2007). The identification ofHPV’s role in cervical cancer has led to importantadvances in primary prevention through vaccinationand diagnosis through HPV detection (Stanley et al,2008; Bosch et al, 2008). However, tangible reductionin the incidence of cervical cancer and the impact onglobal public health will probably take decades. As HPVtypes are divergent, efficacy of current vaccines is typerestricted,and therefore development of the nextgeneration of HPV vaccines will require inclusion ofrelevant antigens from several HPV types (Lowy, 2008).Geographical profiling of HPV type distribution will beimportant in making vaccines more relevant for targetpopulations.Most women will be infected with HPV sometime intheir lifetime. Results from large meta-analyses studiesindicate that at any given point in time, 10.4% (95%confidence interval (CI) 10.2-10.7) of womenworldwide are positive for cervical HPV DNA (Bosch etal, 2008). The prevalence of HPV is higher in lessdeveloped regions (13.4%; 95% CI: 13.1-13.7) than inthe more developed regions (8.4%; 95% CI: 8.3-8.6)(Bosch et al, 2008). The same studies indicate thatAfrican women at 22.1% (95% CI: 20.9-23.4) and EastAfrican women in particular, have the highest HPVprevalence rates (31.6%; 95% CI: 29.5-33.8) (Bosch etal, 2008). HPV type 16 is the most common in allcontinents, with an estimated point prevalence of 2.6%(95% CI: 2.5-2.8) worldwide, and HPV type 18 thesecond most frequently detected type (Clifford et al,2005). Regional differences are thought to be related togeographical and immunogenetic factors, such asdefects in cellular immunity through chronic cervicalinflammation, malnutrition and more recently, HIVinfection; Type 16 though appears to be less influencedby immune impairment than other types (Clifford et al,2005).Although many women get infected with HPV, most donot develop cervical cancer. Several co-factors arepostulated to influence the disease process. Thepotential co-factors include exogenous factors such astobacco smoking, hormonal contraceptives, and coinfectionswith other sexually transmitted infections(Munoz et al, 2006). In addition, viral co-factors, suchspecific HPV types, viral load, and viral integration, aswell as host co-factors such as endogenous hormones,genetic factors, and factors related to the immuneresponse may variably influence the course of HPVinfection (Munoz et al, 2006).Women with HIV infection have been shown to be morelikely not only to have a concurrent HPV infection butalso to have an increased risk for a high grade cervicalsquamous intraepithelial lesion (La Ruche et al, 1998;Temmerman et al, 1999; Womack et al, 2000; Baay et al,2004; Hawes et al, 2006; Didelot-Rousseau et al, 2006;Ngándwe et al, 2007). HPV is the commonest sexuallytransmitted infection, with more than 75% of sexuallyactive adults acquiring one or more genotypes in theirlifetime (Bosch et al, 2008). However, by age 30 years,most women clear the infection due to an effective cellmediatedimmune response, and only a small numberthereafter are diagnosed with a HPV-associated lesion(Schiffman, 1992). It is thought that it is through itseffect on CD4+ cells and regulation of immuneresponses to a variety of antigens that HIV attenuatesthe systemic response to HPV (Palefsky, 2006).The prevalence of HIV among adult Kenyan women was13% in 2003 with trends reported to have decreased to5.1% by 2006 (KDHS, 2003). The high prevalence ofHIV may increase the incidence of cervical pre-cancerand potentially, of cervical cancer. Gichangi et al (2002),however, demonstrated that a two to three-foldincrease in HIV prevalence did not translate to aproportionate increment in incidence of cervical cancer.They hypothesized that HIV-infected women die fromHIV-related opportunistic infections before theydevelop invasive cervical cancer. The mean survivaltime for women with HIV in 2008 was reported to be 5years (Yamada et al, 2008) while typically more than 10years elapse before the development of cervical cancerafter HPV infection. Yamada et al (2008) also advancedthe possibility that sub-clinical cervical cancer may bemissed in many women dying prematurely from AIDSrelatedopportunistic infections.This study was carried out to establish whether the coinfectionof HIV and HPV has an influence on HPVgenotype distribution and on the prevalence and gradeof cervical neoplasia

Mortality in patients with HIV-1 infection starting antiretroviral therapy in South Africa, Europe, or North America: a collaborative analysis of prospective studies

Analyzing survival in HIV treatment cohorts, Andrew Boulle and colleagues find mortality rates in South Africa comparable to or better than those in North America by 4 years after starting antiretroviral therapy. Please see later in the article for the Editors' Summar

Cell-free (RNA) and cell-associated (DNA) HIV-1 and postnatal transmission through breastfeeding

&lt;p&gt;Introduction - Transmission through breastfeeding remains important for mother-to-child transmission (MTCT) in resource-limited settings. We quantify the relationship between cell-free (RNA) and cell-associated (DNA) shedding of HIV-1 virus in breastmilk and the risk of postnatal HIV-1 transmission in the first 6 months postpartum.&lt;/p&gt; &lt;p&gt;Materials and Methods - Thirty-six HIV-positive mothers who transmitted HIV-1 by breastfeeding were matched to 36 non-transmitting HIV-1 infected mothers in a case-control study nested in a cohort of HIV-infected women. RNA and DNA were quantified in the same breastmilk sample taken at 6 weeks and 6 months. Cox regression analysis assessed the association between cell-free and cell-associated virus levels and risk of postnatal HIV-1 transmission.&lt;/p&gt; &lt;p&gt;Results - There were higher median levels of cell-free than cell-associated HIV-1 virus (per ml) in breastmilk at 6 weeks and 6 months. Multivariably, adjusting for antenatal CD4 count and maternal plasma viral load, at 6 weeks, each 10-fold increase in cell-free or cell-associated levels (per ml) was significantly associated with HIV-1 transmission but stronger for cell-associated than cell-free levels [2.47 (95% CI 1.33–4.59) vs. aHR 1.52 (95% CI, 1.17–1.96), respectively]. At 6 months, cell-free and cell-associated levels (per ml) in breastmilk remained significantly associated with HIV-1 transmission but was stronger for cell-free than cell-associated levels [aHR 2.53 (95% CI 1.64–3.92) vs. 1.73 (95% CI 0.94–3.19), respectively].&lt;/p&gt; &lt;p&gt;Conclusions - The findings suggest that cell-associated virus level (per ml) is more important for early postpartum HIV-1 transmission (at 6 weeks) than cell-free virus. As cell-associated virus levels have been consistently detected in breastmilk despite antiretroviral therapy, this highlights a potential challenge for resource-limited settings to achieve the UNAIDS goal for 2015 of eliminating vertical transmission. More studies would further knowledge on mechanisms of HIV-1 transmission and help develop more effective drugs during lactation.&lt;/p&gt

National and regional estimates of term and preterm babies born small for gestational age in 138 low-income and middle-income countries in 2010.

BACKGROUND: National estimates for the numbers of babies born small for gestational age and the comorbidity with preterm birth are unavailable. We aimed to estimate the prevalence of term and preterm babies born small for gestational age (term-SGA and preterm-SGA), and the relation to low birthweight (<2500 g), in 138 countries of low and middle income in 2010. METHODS: Small for gestational age was defined as lower than the 10th centile for fetal growth from the 1991 US national reference population. Data from 22 birth cohort studies (14 low-income and middle-income countries) and from the WHO Global Survey on Maternal and Perinatal Health (23 countries) were used to model the prevalence of term-SGA births. Prevalence of preterm-SGA infants was calculated from meta-analyses. FINDINGS: In 2010, an estimated 32·4 million infants were born small for gestational age in low-income and middle-income countries (27% of livebirths), of whom 10·6 million infants were born at term and low birthweight. The prevalence of term-SGA babies ranged from 5·3% of livebirths in east Asia to 41·5% in south Asia, and the prevalence of preterm-SGA infants ranged from 1·2% in north Africa to 3·0% in southeast Asia. Of 18 million low-birthweight babies, 59% were term-SGA and 41% were preterm-SGA. Two-thirds of small-for-gestational-age infants were born in Asia (17·4 million in south Asia). Preterm-SGA babies totalled 2·8 million births in low-income and middle-income countries. Most small-for-gestational-age infants were born in India, Pakistan, Nigeria, and Bangladesh. INTERPRETATION: The burden of small-for-gestational-age births is very high in countries of low and middle income and is concentrated in south Asia. Implementation of effective interventions for babies born too small or too soon is an urgent priority to increase survival and reduce disability, stunting, and non-communicable diseases. FUNDING: Bill & Melinda Gates Foundation by a grant to the US Fund for UNICEF to support the activities of the Child Health Epidemiology Reference Group (CHERG)