Knowledge and Perceptions on Malaria and Its Association with Aquatic Habitats

Background: Malaria remains the major cause of morbidity and mortality among children in Kenya. About 70 percent of the population is at risk of infection, and roughly 34,000 young children die of malaria-related causes annually.Objective: To investigate the knowledge and perceptions of the local people for malaria in relation to aquatic habitats along the Kenyan Lake Victoria basin.Design: Community-based cross-sectional study.Setting: The Kenyan Lake Victoria basin Region.Subjects: Two hundred and fourty three individuals (both women and men residing in the beaches and surrounding areas) were interviewed about their knowledge and perceptions regarding malaria.Results: Mosquitoes were perceived to be the main cause of malaria. Most respondents were familiar with the main signs and symptoms of mild malaria. Majority of the respondents had poor knowledge of mosquito breeding habitats with 45% mentioning the lake and only 18.6 and 8.9% mentioning ponds and dams, respectively. Most female respondents did not know the difference between mosquitoes and lake flies, P=0.03, Fishers exact test. The majority (97.5%) of the respondents reported seeking conventional malaria treatment from health institutions.Conclusion: Mosquitoes are perceived to be the main cause of malaria by both males and females. A significant proportion of the respondents were familiar with the main signs and symptoms of malaria and sought conventional medicine for treatment of the disease. Most of the respondents, however, had poor knowledge on the breeding habitats of mosquitoes. Concerted effort is needed to scale-up health education and improve the knowledge of the community about mosquitoes and their breeding habitats, particularly malaria vectors which do not breed in deep lake waters. Effective anti-malarial drugs should also be available at the grassroots level where the problem of malaria is rampant

Community perceptions of schistosomiasis transmission, prevalence and control in relation to aquatic habitats in the Lake Victoria basin of Kenya

Background: Intestinal schistosomiasis caused by Schistosoma mansoni and urinary schistosomiasis caused by Schistosoma haematobium are widely distributed parasites in several localities of the Lake Victoria basin of Kenya, the former being more prevalent. In Kenya, transmission of the intestinal form of bilharzia (S. mansoni) tends to be closely confined to narrow zones along the shores of large bodies of water such as Lake Victoria where it is endemic and the intermediate host is found. The prevalence of S. mansoni along the Kenyan Lake Victoria basin ranges between 40% and 80%.Objective: To assess the community’s knowledge and perceptions of schistosomiasis prevalence, transmission and control in relation to aquatic habitats in the Lake Victoria basin of Kenya.Design: Community-based cross-sectional study.Setting: The Kenyan Lake Victoria basin.Subjects: Two hundred and forty three individuals (both women and men residing in the beaches and surrounding areas) were interviewed about their knowledge and perceptions regarding schistosomiasis.Results: The community regarded schistosomiasis as a naturalistic disease not caused by supernatural forces but by an agent of contamination in water. Knowledge on schistosomiasis transmission and control was low, with 42% of the respondents having no idea on how schistosomiasis is contracted, while 22% and 18% of the respondents mentioned contact with contaminated water and drinking / eating dirty water / food, respectively. Most respondents were familiar with the snails’ habitats, but had poor knowledge on aquatic plants harbouring snails, as 57% of the respondents did not know about aquatic plants being associated with schistosomiasis snails. Only 3% of the respondents associated snails with schistosomiasis transmission. Sixty percent (60%) of the respondents mentioned use of tablets and injections as means of treating schistosomiasis, while 38% had no idea how it is treated and 2% mentioned use of local herbs and services of medicine men.Conclusion: Majority of Kenyan Lake Victoria basin inhabitants had little awareness about schistosomiasis despite high prevalence of the disease in the region. There is need to adapt prevention and control strategies to the people’s livelihoods. There is also need to target the less advantaged members of the community such as women, uneducated and subsistence farmers for intense health education strategies aimed at increasing participation in the control of schistosomiasis. Study to elicit divergence between biomedical and local understandings of schistosomiasis/bilharzia is suggested.

Some results on blow up for semilinear parabolic problems

The authors describe the asymptotic behavior of blow-up for the semilinear heat equation ut=uxx+f(u) in R×(0,T), with initial data u0(x)>0 in R, where f(u)=up, p>1, or f(u)=eu. A complete description of the types of blow-up patterns and of the corresponding blow-up final-time profiles is given. In the rescaled variables, both are governed by the structure of the Hermite polynomials H2m(y). The H2-behavior is shown to be stable and generic. The existence of H4-behavior is proved. A nontrivial blow-up pattern with a blow-up set of nonzero measure is constructed. Similar results for the absorption equation ut=uxx−up, 0<p<1, are discussed

Virus Replication Strategies and the Critical CTL Numbers Required for the Control of Infection

Vaccines that elicit protective cytotoxic T lymphocytes (CTL) may improve on or augment those designed primarily to elicit antibody responses. However, we have little basis for estimating the numbers of CTL required for sterilising immunity at an infection site. To address this we begin with a theoretical estimate obtained from measurements of CTL surveillance rates and the growth rate of a virus. We show how this estimate needs to be modified to account for (i) the dynamics of CTL-infected cell conjugates, and (ii) features of the virus lifecycle in infected cells. We show that provided the inoculum size of the virus is low, the dynamics of CTL-infected cell conjugates can be ignored, but knowledge of virus life-histories is required for estimating critical thresholds of CTL densities. We show that accounting for virus replication strategies increases estimates of the minimum density of CTL required for immunity over those obtained with the canonical model of virus dynamics, and demonstrate that this modeling framework allows us to predict and compare the ability of CTL to control viruses with different life history strategies. As an example we predict that lytic viruses are more difficult to control than budding viruses when net reproduction rates and infected cell lifetimes are controlled for. Further, we use data from acute SIV infection in rhesus macaques to calculate a lower bound on the density of CTL that a vaccine must generate to control infection at the entry site. We propose that critical CTL densities can be better estimated either using quantitative models incorporating virus life histories or with in vivo assays using virus-infected cells rather than peptide-pulsed targets

CD8+ Lymphocytes Control Viral Replication in SIVmac239-Infected Rhesus Macaques without Decreasing the Lifespan of Productively Infected Cells

While CD8+ T cells are clearly important in controlling virus replication during HIV and SIV infections, the mechanisms underlying this antiviral effect remain poorly understood. In this study, we assessed the in vivo effect of CD8+ lymphocyte depletion on the lifespan of productively infected cells during chronic SIVmac239 infection of rhesus macaques. We treated two groups of animals that were either CD8+ lymphocyte-depleted or controls with antiretroviral therapy, and used mathematical modeling to assess the lifespan of infected cells either in the presence or absence of CD8+ lymphocytes. We found that, in both early (day 57 post-SIV) and late (day 177 post-SIV) chronic SIV infection, depletion of CD8+ lymphocytes did not result in a measurable increase in the lifespan of either short- or long-lived productively infected cells in vivo. This result indicates that the presence of CD8+ lymphocytes does not result in a noticeably shorter lifespan of productively SIV-infected cells, and thus that direct cell killing is unlikely to be the main mechanism underlying the antiviral effect of CD8+ T cells in SIV-infected macaques with high virus replication

In Vivo CD8+ T-Cell Suppression of SIV Viremia Is Not Mediated by CTL Clearance of Productively Infected Cells

The CD8+ T-cell is a key mediator of antiviral immunity, potentially contributing to control of pathogenic lentiviral infection through both innate and adaptive mechanisms. We studied viral dynamics during antiretroviral treatment of simian immunodeficiency virus (SIV) infected rhesus macaques following CD8+ T-cell depletion to test the importance of adaptive cytotoxic effects in clearance of cells productively infected with SIV. As previously described, plasma viral load (VL) increased following CD8+ T-cell depletion and was proportional to the magnitude of CD8+ T-cell depletion in the GALT, confirming a direct relationship between CD8+ T-cell loss and viral replication. Surprisingly, first phase plasma virus decay following administration of antiretroviral drugs was not slower in CD8+ T-cell depleted animals compared with controls indicating that the short lifespan of the average productively infected cell is not a reflection of cytotoxic T-lymphocyte (CTL) killing. Our findings support a dominant role for non-cytotoxic effects of CD8+ T-cells on control of pathogenic lentiviral infection and suggest that cytotoxic effects, if present, are limited to early, pre-productive stages of the viral life cycle. These observations have important implications for future strategies to augment immune control of HIV

Inhibition of Adaptive Immune Responses Leads to a Fatal Clinical Outcome in SIV-Infected Pigtailed Macaques but Not Vervet African Green Monkeys

African green monkeys (AGM) and other natural hosts for simian immunodeficiency virus (SIV) do not develop an AIDS-like disease following SIV infection. To evaluate differences in the role of SIV-specific adaptive immune responses between natural and nonnatural hosts, we used SIVagmVer90 to infect vervet AGM and pigtailed macaques (PTM). This infection results in robust viral replication in both vervet AGM and pigtailed macaques (PTM) but only induces AIDS in the latter species. We delayed the development of adaptive immune responses through combined administration of anti-CD8 and anti-CD20 lymphocyte-depleting antibodies during primary infection of PTM (n = 4) and AGM (n = 4), and compared these animals to historical controls infected with the same virus. Lymphocyte depletion resulted in a 1-log increase in primary viremia and a 4-log increase in post-acute viremia in PTM. Three of the four PTM had to be euthanized within 6 weeks of inoculation due to massive CMV reactivation and disease. In contrast, all four lymphocyte-depleted AGM remained healthy. The lymphocyte-depleted AGM showed only a trend toward a prolongation in peak viremia but the groups were indistinguishable during chronic infection. These data show that adaptive immune responses are critical for controlling disease progression in pathogenic SIV infection in PTM. However, the maintenance of a disease-free course of SIV infection in AGM likely depends on a number of mechanisms including non-adaptive immune mechanisms

Immunization with Single-Cycle SIV Significantly Reduces Viral Loads After an Intravenous Challenge with SIVmac239

Strains of simian immunodeficiency virus (SIV) that are limited to a single cycle of infection were evaluated for the ability to elicit protective immunity against wild-type SIVmac239 infection of rhesus macaques by two different vaccine regimens. Six animals were inoculated at 8-week intervals with 6 identical doses consisting of a mixture of three different envelope variants of single-cycle SIV (scSIV). Six additional animals were primed with a mixture of cytoplasmic domain-truncated envelope variants of scSIV and boosted with two doses of vesicular stomatitis virus glycoprotein (VSV G) trans-complemented scSIV. While both regimens elicited detectable virus-specific T cell responses, SIV-specific T cell frequencies were more than 10-fold higher after boosting with VSV G trans-complemented scSIV (VSV G scSIV). Broad T cell recognition of multiple viral antigens and Gag-specific CD4+ T cell responses were also observed after boosting with VSV G scSIV. With the exception of a single animal in the repeated immunization group, all of the animals became infected following an intravenous challenge with SIVmac239. However, significantly lower viral loads and higher memory CD4+ T cell counts were observed in both immunized groups relative to an unvaccinated control group. Indeed, both scSIV immunization regimens resulted in containment of SIVmac239 replication after challenge that was as good as, if not better than, what has been achieved by other non-persisting vaccine vectors that have been evaluated in this challenge model. Nevertheless, the extent of protection afforded by scSIV was not as good as typically conferred by persistent infection with live, attenuated SIV. These observations have potentially important implications to the design of an effective AIDS vaccine, since they suggest that ongoing stimulation of virus-specific immune responses may be essential to achieving the degree of protection afforded by live, attenuated SIV