Schistosoma haematobium and soil-transmitted Helminths in Tana Delta District of Kenya:infection and morbidity patterns in primary schoolchildren from two isolated villages

BACKGROUND: Schistosomes and soil-transmitted helminths (STH) (hookworm, Trichuris trichiura and Ascaris lumbricoides) are widely distributed in developing countries where they infect over 230 million and 1.5 billion people, respectively. The parasites are frequently co-endemic and many individuals are co-infected with two or more of the species, but information on how the parasites interact in co-infected individuals is scarce. The present study assessed Schistosoma haematobium and STH infection and morbidity patterns among school children in a hyper-endemic focus in the Tana River delta of coastal Kenya. METHODS: Two hundred and sixty-two children aged 5–12 years from two primary schools were enrolled in the study. For each child, urine was examined for S. haematobium eggs and haematuria, stool was examined for STH eggs, peripheral blood was examined for eosinophilia and haemoglobin level, the urinary tract was ultrasound-examined for S. haematobium-related pathology, and the height and weight was measured and used to calculate the body mass index (BMI). RESULTS: Prevalences of S. haematobium, hookworm, T. trichiura and A. lumbricoides infection were 94, 81, 88 and 46 %, respectively. There was no significant association between S. haematobium and STH infection but intensity of hookworm infection significantly increased with that of T. trichiura. Lower BMI scores were associated with high intensity of S. haematobium (difference =−0.48, p > 0.05) and A. lumbricoides (difference =−0.67, p < 0.05). Haematuria (both macro and micro) was common and associated with S. haematobium infection, while anaemia was associated with high intensity of S. haematobium (OR = 2.08, p < 0.05) and high hookworm infections OR = 4.75; p < 0.001). The majority of children had eosinophilia, which was significantly associated with high intensity of hookworm infection (OR = 5.34, p < 0.05). Overall 38 % of the children had ultrasound-detectable urinary tract morbidity, which was associated with high intensity of S. haematobium infection (OR = 3.13, p < 0.05). CONCLUSION: Prevalences of S. haematobium and STH infections among the primary school children were high and the parasites were responsible for significant morbidity. A clear synergistic interaction was observed between hookworm and T. trichiura infections. Increased coverage in administration of praziquantel and albendazole in the area is recommended to control morbidity due to these infections

Urinary cytokines in <i>Schistosoma haematobium</i>-infected schoolchildren from Tana Delta District of Kenya

BACKGROUND: Pathological changes due to infection with Schistosoma haematobium include cytokine-mediated urinary tract inflammation. The involved cytokines may be excreted in urine and their presence in urine may therefore reflect S. haematobium-related urinary tract pathology. The present study, for the first time, reports on the relationship between selected cytokines in urine and infection with S. haematobium in children from an area highly affected by this parasite. METHODS: Children aged 5–12 years from two primary schools in Tana Delta District of Kenya were examined for S. haematobium eggs using urine filtration technique, for haematuria using dipstix and for eosinophil cationic protein (ECP), IL-6, IFN- γ, TNF-α and IL-10 levels using ELISA, and for S. haematobium-related urinary tract pathology using ultrasonography. In addition, venous blood was examined for serum IL-6, IFN- γ, TNF-α and IL-10 levels using ELISA. RESULTS: There was no significant correlation between urinary and serum levels of IL-6, IFN- γ, TNF-α or IL-10. There was no significant difference in geometric mean intensity (GMI) in any of the serum cytokines, or in urinary TNF-α or IFN-γ, between children with light and heavy S. haematobium infections. However, children with heavy S. haematobium infections had significantly higher GMI of urinary IL-6 (p < 0.001) and lower GMI of urinary IL-10 (p = 0.002) than children with light infections. There was also a significant positive correlation between urinary IL-6 and urinary ECP (p < 0.001) and a significant negative correlation between urinary IL-10 and urinary ECP (p = 0.012). CONCLUSION: Urinary IL-6 was positively correlated to and IL-10 was negatively correlated to infection intensity and urinary tract inflammation in S. haematobium-infected children. Urinary IL-6 and IL-10 ELISA may be a useful non-invasive tool to complement the already available tools for studying S. haematobium-related urinary tract pathology in children. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2334-14-501) contains supplementary material, which is available to authorized users

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

Effect of locally produced complementary foods on fat-free mass, linear growth, and iron status among Kenyan infants: A randomized controlled trial.

The impact of quality complementary food products on infant growth and body composition has not been adequately investigated. This study evaluated the effect on fat-free mass (FFM) accrual, linear growth, and iron status of locally produced complementary food products comparing to a standard product. In a randomized, double-blind trial, 499 infants at 6 months received nine monthly rations of (a) WinFood Classic (WFC) comprising germinated amaranth (71%), maize (10.4%), small fish (3%), and edible termites (10%); (b) WinFood Lite (WFL) comprising germinated amaranth (82.5%), maize (10.2%), and multimicronutrient premix; or (c) fortified corn-soy blend plus (CSB+). Primary outcomes were changes in FFM, length, and plasma ferritin and transferrin receptors (TfR). FFM was determined using deuterium dilution. Analysis was by intention to treat, based on available cases. Compared with CSB+, there were no differences in change from 6 to 15 months in FFM for WFC 0.0 kg (95% CI [-0.30, 0.29]) and WFL 0.03 kg (95% CI [-0.25, 0.32]) and length change for WFC -0.3 cm (95% CI [-0.9, 0.4]) and WFL -0.3 cm (95% CI [-0.9, 0.3]). TfR increased in WFC group 3.3 mg L-1 (95% CI [1.7, 4.9]) and WFL group 1.7 mg L-1 (95% CI [0.1, 3.4]) compared with CSB+. Compared with the increase in Hb in CSB+ group, there was a reduction in Hb in WFC of -0.9 g dl-1 (95% CI [-1.3, -0.5]) and a lower increase in WFL -0.4 g dl-1 (95% CI [-0.8, 0.0]). In conclusion, the tested WinFoods had the same effect on FFM and length as CSB+, whereas Hb and iron status decreased, suggesting inhibited iron bioavailability from the amaranth-based WinFoods

Impact of HIV infection on invasive cervical cancer in Kenyan women

Objectives: To determine the association between invasive cervical cancer (ICC) and HIV infection in Kenyan women. Study design: Case-control, with ICC patients as cases, and women with uterine fibroids as controls. Methods: Medical and socio-demographic data were collected from 367 ICC patients, and 226 women with fibroids. After informed consent, HIV testing was done. Results: ICC patients were older than fibroid patients (48 versus 41 years; P \u3c 0.001), with an HIV seroprevalence of 15% and 12% respectively (P \u3e 0.05). However, cases younger than 35 years were 2.6-times more likely to be HIV positive than controls of similar age [35% versus 17%; odds ratio (OR), 2.6; P = 0.043]. ICC HIV-seropositive patients were, on average, 10 years younger than HIV-seronegative patients (40 versus 50 years; P \u3c 0.001). Eighty per cent of HIV-seropositive and 77% of HIV-seronegative ICC patients were in FIGO stage IIb or above. However, the odds of having poorly differentiated tumours was three times higher for HIV-seropositive than for HIV-seronegative ICC patients (77% versus 52%; OR, 3.1; P = 0.038) after adjusting for histological cell type and clinical stage. Mean CD4 cell count was 833 × 106 cells/l in ICC and 1025 × 106 cells/l in fibroid patients (P = 0.001). Conclusion: Young women with ICC were more often HIV infected than women with fibroids of the same age groups. HIV infection was associated with poor histological differentiation of the tumours. These findings suggest an accelerated clinical progression of premalignant cervical lesions to ICC in HIV-infected women

Malaria vector abundance is associated with house structures in Baringo County, Kenya.

Malaria, a major cause of morbidity and mortality, is the most prevalent vector borne disease in Baringo County; a region which has varied house designs in arid and semi-arid areas. This study investigated the association between house structures and indoor-malaria vector abundance in Baringo County. The density of malaria vectors in houses with open eaves was higher than that for houses with closed eaves. Grass thatched roof houses had higher density of malaria vectors than corrugated iron sheet roofs. Similarly, mud walled houses had higher vector density than other wall types. Houses in the riverine zone were significantly associated with malaria vector abundance (p<0.000) possibly due to more varied house structures. In Kamnarok village within riverine zone, a house made of grass thatched roof and mud wall but raised on stilts with domestic animals (sheep/goats) kept at the lower level had lower mosquito density (5.8 per collection) than ordinary houses made of same materials but at ground level (30.5 mosquitoes per collection), suggestive of a change in behavior of mosquito feeding and resting. House modifications such as screening of eaves, improvement of construction material and building stilted houses can be incorporated in the integrated vector management (IVM) strategy to complement insecticide treated bed nets and indoor residual spray to reduce indoor malaria vector density

“We don’t want our clothes to smell smoke”: changing malaria control practices and opportunities for integrated community-based management in Baringo, Kenya

Abstract Background The decline in global malaria cases is attributed to intensified utilization of primary vector control interventions and artemisinin-based combination therapies (ACTs). These strategies are inadequate in many rural areas, thus adopting locally appropriate integrated malaria control strategies is imperative in these heterogeneous settings. This study aimed at investigating trends and local knowledge on malaria and to develop a framework for malaria control for communities in Baringo, Kenya. Methods Clinical malaria cases obtained from four health facilities in the riverine and lowland zones were used to analyse malaria trends for the 2005–2014 period. A mixed method approach integrating eight focus group discussions, 12 key informant interviews, 300 survey questionnaires and two stakeholders’ consultative forums were used to assess local knowledge on malaria risk and develop a framework for malaria reduction. Results Malaria cases increased significantly during the 2005–2014 period (tau = 0.352; p < 0.001) in the riverine zone. March, April, May, June and October showed significant increases compared to other months. Misconceptions about the cause and mode of malaria transmission existed. Gender-segregated outdoor occupation such as social drinking, farm activities, herding, and circumcision events increased the risk of mosquito bites. A positive relationship occurred between education level and opinion on exposure to malaria risk after dusk (χ2 = 2.70, p < 0.05). There was over-reliance on bed nets, yet only 68% (204/300) of respondents owned at least one net. Complementary malaria control measures were under-utilized, with 90% of respondents denying having used either sprays, repellents or burnt cow dung or plant leaves over the last one year before the study was conducted. Baraza, radios, and mobile phone messages were identified as effective media for malaria information exchange. Supplementary strategies identified included unblocking canals, clearing Prosopis bushes, and use of community volunteers and school clubs to promote social behaviour change. Conclusions The knowledge gap on malaria transmission should be addressed to minimize the impacts and enhance uptake of appropriate malaria management mechanisms. Implementing community-based framework can support significant reductions in malaria prevalence by minimizing both indoor and outdoor malaria transmissions