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Age-dependent mortality changes in haematophagous insects are difficult to measure but are important determinants of population dynamics and vectorial capacity. A Markov process was used to model age-dependent changes in wing fray in tsetse (Glossina spp), calibrated using published mark-recapture data for male G. m. morsitans in Tanzania. The model was applied to female G. m. morsitans, captured in Zimbabwe using a vehicle-mounted electric net and subjected to ovarian dissection and wing fray analysis. Rates of fray increased significantly with age in males but not females, where the rate was constant for ovarian categories 0-3. A jump in mean fray between ovarian categories 3 and 4 + 4n is consistent with the latter category including flies that have ovulated 4, 8, 12, 16 times and so on. The magnitude of the jump could, theoretically, facilitate improved mortality estimates. In practice, although knowledge of fly mortality was required for modelling wing fray, mortality estimates derived from ovarian dissection data are independent of patterns and rates of change in wing fray. Significantly better fits to ovarian age data resulted when age-specific mortality was modelled as the sum of two exponentials, with high mortality in young and old flies, than when mortality was constant at 2.3% per day.

A population model for tsetse species was used to assess the optimal number and spacing of airborne sprays to reduce or eradicate a tsetse population. It was found that the optimal spray spacing was determined by the time (days) from adult emergence to the first larviposition and, for safety, spacing was assigned to that duration minus 2 days. If sprays killed all adults, then the number of sprays required for eradication is determined by a simple formula. If spray efficiency is less than 100% kill per spray, then a simulation was used to determine the optimal number, which was strongly affected by spray efficiency, mean daily temperature, pupal duration, age to first larviposition and the acceptance threshold for control, rather than eradication. For eradication, it is necessary to have a spray efficiency of greater than 99.9% to avoid requiring an excessive number of sprays. Output from the simulation was compared with the results of two aerial spraying campaigns against tsetse and a least squares analysis estimated that, in both cases, the kill efficiency of the sprays was not significantly less than 100%.

Environmental temperature is an important driver of the population dynamics of tsetse (Glossinaspp) because the fly's immature stages are particularly vulnerable to temperatures (T) outside the rangeT= 16–32°C. Laboratory experiments carried out 50 years ago provide extensive measures of temperature-dependent rates of development, fat consumption and mortality in tsetse pupae. We improve on the models originally fitted to these data, providing better parameter estimates for use in population modelling. A composite function accurately models rates of pupal development forT= 8–32°C. Pupal duration can be estimated by summing the temperature-dependent daily percentage of development completed. Fat consumption is modelled as a logistic function of temperature; the total fat consumed during pupal development takes a minimum forT≈ 25°C. Pupae experiencing constant temperatures T≤ 30°C, the fat consumption during this period. The new results will be particularly useful in the construction of various models for tsetse population dynamics, and will have particular relevance for agent-based models where the lives of individual tsetse are simulated using a daily time step.

Background It has been suggested that attempts to eradicate populations of tsetse (Glossina spp.) using stationary targets might fail because smaller, less mobile individuals are unlikely to be killed by the targets. If true, tsetse caught in stationary traps should be larger than those from mobile baits, which require less mobility on the part of the flies. Results Sampling tsetse in the Zambezi Valley of Zimbabwe, we found that the number of tsetse caught from stationary traps, as a percent of total numbers from traps plus a mobile vehicle, was ~5% for male G. morsitans morsitans (mean wing length 5.830 mm; 95% CI: 5.800–5.859 mm) and ~10% for females (6.334 mm; 95% CI: 6.329–6.338 mm); for G. pallidipes the figures were ~50% for males (6.830 mm; 95% CI: 6.821–6.838 mm) and ~75% for females (7.303 mm, 95% CI: 7.302–7.305 mm). As expected, flies of the smaller species (and the smaller sex) were less likely to be captured using stationary, rather than mobile sampling devices. For flies of a given sex and species the situation was more complex. Multivariable analysis showed that, for females of both species, wing lengths changed with ovarian age and the month, year and method of capture. For G. pallidipes, there were statistically significant interactions between ovarian age and capture month, year and method. For G. m. morsitans, there was only a significant interaction between ovarian age and capture month. The effect of capture method was, however, small in absolute terms: for G. pallidipes and G. m. morsitans flies caught on the mobile vehicle had wings only 0.24 and 0.48% shorter, respectively, than flies caught in stationary traps. In summary, wing length in field samples of tsetse varies with ovarian age, capture month and year and, weakly, with capture method. Suggestions that a target-based operation against G. f. fuscipes in Kenya caused a shift towards a smaller, less mobile population of tsetse, unavailable to the targets, failed to account for factors other than capture method. Conclusions The results are consistent with the successful use of targets to eradicate populations of tsetse in Zimbabwe. Until further, more nuanced, studies are conducted, it is premature to conclude that targets alone could not, similarly, be used to eradicate G. f. fuscipes populations in Kenya. Electronic supplementary material The online version of this article (10.1186/s13071-018-3274-x) contains supplementary material, which is available to authorized users.

As insect populations decline, due to climate change and other environmental disruptions, there has been an increased interest in understanding extinction probabilities. Generally, the life cycle of insects occurs in well-defined stages: when counting insects, questions naturally arise about which life stage to count. Using tsetse flies (vectors of trypanosomiasis) as a case study, we develop a model that works when different life stages are counted. Previous branching process models for tsetse populations only explicitly represent newly emerged adult female tsetse and use that subpopulation to keep track of population growth/decline. Here, we directly model other life stages. We analyse reproduction numbers and extinction probabilities and show that several previous models used for estimating extinction probabilities for tsetse populations are special cases of the current model. We confirm that the reproduction number is the same regardless of which life stage is counted, and show how the extinction probability depends on which life stage we start from. We demonstrate, and provide a biological explanation for, a simple relationship between extinction probabilities for the different life stages, based on the probability of recruitment between stages. These results offer insights into insect population dynamics and provide tools that will help with more detailed models of tsetse populations. Population dynamics studies of insects should be clear about life stages and counting points.

BackgroundA relatively simple life history allows us to derive an expression for the extinction probability of populations of tsetse, vectors of African sleeping sickness. We present the uncertainty and sensitivity analysis of extinction probability for tsetse population, to offer key insights into parameters in the control/eradication of tsetse populations.MethodsWe represent tsetse population growth as a branching process, and derive closed form estimates of population extinction from that model. Statistical and mathematical techniques are used to analyse the uncertainties in estimating extinction probability, and the sensitivity of the extinction probability to changes in input parameters representing the natural life history and vital dynamics of tsetse populations.ResultsFor fixed values of input parameters, the sensitivity of extinction probability depends on the baseline parameter values. For example, extinction probability is more sensitive to the probability that a female is inseminated by a fertile male when daily pupal mortality is low, whereas the extinction probability is more sensitive to daily mortality rate for adult females when daily pupal mortality, and extinction probabilities, are high. Global uncertainty and sensitivity analysis showed that daily mortality rate for adult females has the highest impact on the extinction probability.ConclusionsThe strong correlation between extinction probability and daily female adult mortality gives a strong argument that control techniques to increase daily female adult mortality may be the single most effective means of ensuring eradication of tsetse population.Author summaryTsetse flies (Glossina spp) are vectors of Trypanosomiasis, a deadly disease commonly called sleeping sickness in humans and nagana in livestock. The relatively simple life history of tsetse enabled us to model its population growth as a stochastic branching process. We derived a closed-form expression for the probability that a population of tsetse goes extinct, as a function of death, birth, development and insemination rates in female tsetse. We analyzed the sensitivity of the extinction probability to the different input parameters, in a bid to identify parameters with the highest impact on extinction probability. This information can, potentially, inform policy direction for tsetse control/elimination. In all the scenarios we considered, the daily mortality rate for adult females has the greatest impact on the magnitude of extinction probability. Our findings suggest that the mortality rate in the adult females is the weakest link in tsetse life history, and this fact should be exploited in achieving tsetse population control, or even elimination.

Background A relatively simple life history allows us to derive an expression for the extinction probability of populations of tsetse, vectors of African sleeping sickness. We present the uncertainty and sensitivity analysis of the extinction probability, to offer key insights into factors affecting the control or eradication of tsetse populations. Methods We represent tsetse population growth as a branching process, and derive closed form estimates of population extinction from that model. Statistical and mathematical techniques are used to analyse the uncertainties in estimating extinction probability, and the sensitivity of the extinction probability to changes in input parameters representing the natural life history and vital dynamics of tsetse populations. Results For fixed values of input parameters, the sensitivity of extinction probability depends on the baseline parameter values. Extinction probability is most sensitive to the probability that a female is inseminated by a fertile male when daily pupal mortality is low, whereas the extinction probability is most sensitive to daily mortality rate for adult females when daily pupal mortality, and extinction probabilities, are high. Global uncertainty and sensitivity analysis show that daily mortality rate for adult females has the highest impact on the extinction probability. Conclusions The high correlation between extinction probability and daily female adult mortality gives a strong argument that control techniques which increase daily female adult mortality may be the single most effective means of ensuring eradication of tsetse population., Author summary Tsetse flies (Glossina spp.) are vectors of African trypanosomiasis, a deadly disease commonly called sleeping sickness in humans and nagana in livestock. The relatively simple life history of tsetse enabled us to model its population growth as a stochastic branching process. We derived a closed-form expression for the probability that a population of tsetse goes extinct, as a function of death, birth, development and insemination rates in female tsetse. We analyzed the sensitivity of the extinction probability to the different input parameters, in a bid to identify parameters with the highest impact on extinction probability. This information can, potentially, inform policy direction for tsetse control/elimination. In all the scenarios we considered for the global sensitivity analysis, the daily mortality rate for adult females had the greatest impact on the magnitude of extinction probability. Our findings suggest that the mortality rate in the adult females is the weakest link in tsetse life history, and this fact should be exploited in achieving tsetse population control, or even eradication.

Increases in temperature over recent decades have led to a significant reduction in the populations of tsetse flies (Glossinaspp) in parts of the Zambezi Valley of Zimbabwe. If this is true for other parts of Africa, populations of tsetse may actually be going extinct in some parts of the continent. Extinction probabilities for tsetse populations have not so far been estimated as a function of temperature. We develop a time-homogeneous branching process model for situations where tsetse flies live at different levels of fixed temperatures. We derive a probability distributionpk(T) for the number of female offspring an adult female tsetse is expected to produce in her lifetime, as a function of the fixed temperature at which she is living. We show thatpk(T) can be expressed as a geometric series: its generating function is therefore a fractional linear type. We obtain expressions for the extinction probability, expected number of female offspring per female tsetse, and time to extinction. No tsetse population can escape extinction if subjected, for extended periods, to temperatures outside the range 16 °C - 32°C. Extinction probability increases more rapidly as temperatures approach and exceed the upper and lower limits. If the number of females is large enough, the population can still survive even at high temperatures (28°C - 31°C). Small decreases or increases in constant temperature in the neighbourhoods of 16°C and 31°C, respectively, can drive tsetse populations to extinction. Further study is needed to estimate extinction probabilities for tsetse populations in field situations where temperatures vary continuously.Author summaryTsetse flies (Glossinaspp) are the vectors of the African sleeping sickness. We derived an expression for the extinction probability, and mean time to extinction, of closed populations of the flies experiencing different levels of fixed temperatures. Temperatures play a key role in tsetse population dynamics: no tsetse populations can escape extinction at constant temperatures < 16°C > 32°C. The effect of temperature is more severe if tsetse populations are already depleted. Increasingly high temperatures due to climate change may alter the distribution of tsetse populations in Africa. The continent may witness local extinctions of tsetse populations in some places, and appearances in places hitherto too cold for them.

Laboratory assays that identify recent HIV infections are important for assessing impacts of interventions aimed at reducing HIV incidence. Kinetics of HIV humoral responses can vary with inherent assay properties, and between HIV subtypes, populations, and physiological states. They are important in determining mean duration of recent infection (MDRI) for antibody-based assays for detecting recent HIV infections. We determined MDRIs for multi-subtype peptide representing subtypes B, E and D (BED)-capture enzyme immunoassay, limiting antigen (LAg), and Bio-Rad Avidity Incidence (BRAI) assays for 101 seroconverting postpartum women, recruited in Harare from 1997 to 2000 during the Zimbabwe Vitamin A for Mothers and Babies trial, comparing them against published MDRIs estimated from seroconverting cases in the general population. We also compared MDRIs for women who seroconverted either during the first 9 months, or at later stages, postpartum. At cutoffs (C) of 0.8 for BED, 1.5 for LAg, and 40% for BRAI, estimated MDRIs for postpartum mothers were 192, 104, and 144 days, 33%, 32%, and 52% lower than published estimates of 287, 152 and 298 days, respectively, for clade C samples from general populations. Point estimates of MDRI values were 7%–19% shorter for women who seroconverted in the first 9 months postpartum than for those seroconverting later. MDRI values for three HIV incidence biomarkers are longer in the general population than among postpartum women, particularly those who recently gave birth, consistent with heightened immunological activation soon after birth. Our results provide a caution that MDRI may vary significantly between subjects in different physiological states.

Theory suggests females should optimize resource allocation across reproductive bouts to maximize lifetime reproduction, balancing current and future reproductive efforts according to physiological state and projected survival and reproduction. Tests of these ideas focus on long-lived vertebrates: few measure age-related reproductive output in iteroparous invertebrates, or partition reserves between those allocated to offspring versus mothers. We investigated how maternal age, and environmental and physiological factors influence reproductive investment in wild tsetse, Glossina pallidipes Austen and G. morsitans morsitans Westwood. Tsetse provide a tractable system to measure reproductive allocation. Females exhibit high maternal investment, producing single, large offspring that rely exclusively on maternal reserves. We find that mothers in better physiological condition and experiencing cooler temperatures produce larger offspring. Pupal size increases significantly but weakly with age. In both species, females with less fat invest proportionately more in offspring. Post-partum fat decreases in flies with badly frayed wings: poor flight capability may limit their feeding efficiency, or they may sacrifice more reserves as a terminal investment. Our results support evidence that offspring size increases with maternal size, investment depends on the environment, and females with lower chances of future reproduction invest more into current offspring. We discuss the implications of maternal effects for predicting vector population responses to environmental change.

We present a mathematical model for the transmission of Trypanosoma brucei rhodesiense by tsetse vectors to a multi-host population. To control tsetse and T. b. rhodesiense, a proportion, ψ, of cattle (one of the hosts considered in the model) is taken to be kept on treatment with insecticides. Analytical expressions are obtained for the basic reproduction number, R 0n in the absence, and $R_{0n}^{T}$ in the presence of insecticide-treated cattle (ITC). Stability analysis of the disease-free equilibrium was carried out for the case when there is one vertebrate host untreated with insecticide. By considering three vertebrate hosts (cattle, humans and wildlife) the sensitivity analysis was carried out on the basic reproduction number ( $R_{03}^{T}$ ) in the absence and presence of ITC. The results show that $R_{03}^{T}$ is more sensitive to changes in the tsetse mortality. The model is then used to study the control of tsetse and T. b. rhodesiense in humans through application insecticides to cattle either over the whole-body or to restricted areas of the body known to be favoured tsetse feeding sites. Numerical results show that while both ITC strategies result in decreases in tsetse density and in the incidence of T. b. rhodesiense in humans, the restricted application technique results in improved cost-effectiveness, providing a cheap, safe, environmentally friendly and farmer based strategy for the control of vectors and T. b. rhodesiense in humans.

A published study used a stochastic branching process to derive equations for the mean and variance of the probability of, and time to, extinction in population of tsetse flies (Glossina spp) as a function of adult and pupal mortality, and the probabilities that a female is inseminated by a fertile male. The original derivation was partially heuristic and provided no proofs for inductive results. We provide these proofs, together with a more compact way of reaching the same results. We also show that, while the published equations hold good for the case where tsetse produce male and female offspring in equal proportion, a different solution is required for the more general case where the probability (β) that an offspring is female lies anywhere in the interval (0, 1). We confirm previous results obtained for the special case where β = 0.5 and show that extinction probability is at a minimum for β > 0.5 by an amount that increases with increasing adult female mortality. Sensitivity analysis showed that the extinction probability was affected most by changes in adult female mortality, followed by the rate of production of pupae. Because females only produce a single offspring approximately every 10 days, imposing a death rate of greater then about 3.5% per day will ensure the eradication of any tsetse population. These mortality levels can be achieved for some species using insecticide-treated targets or cattle – providing thereby a simple, effective and cost-effective method of controlling and eradicating tsetse, and also human and animal trypanosomiasis. Our results are of further interest in the modern situation where increases in temperature are seeing the real possibility that tsetse will go extinct in some areas, without the need for intervention, but have an increased chance of surviving in other areas where they were previously unsustainable due to low temperatures.Author summaryWe derive equations for the mean and variance of the probability of, and time to, extinction in population of tsetse flies (Glossina spp), the vectors of trypanosomiasis in sub-Saharan Africa. In so doing we provide the complete proofs for all results, which were not provided in a previously published study. We also generalise the derivation to allow the probability that an offspring is female to lie anywhere in the interval (0, 1). The probability of extinction was most sensitive to changes in adult female mortality. The unusual tsetse life cycle, with very low reproductive rates means that populations can be eradicated as long as adult female mortality is raised to levels greater than about 3.5% per day. Simple bait methods of tsetse control, such as insecticide-treated targets and cattle, can therefore provide simple, affordable and effective means of eradicating tsetse populations. The results are of further interest in the modern situation where increases in temperature are seeing the real possibility that tsetse will go extinct in some areas, but have an increased chance of surviving in others where they were previously unsustainable due to low temperatures.

Tsetse exhibit a U-shaped age-mortality curve, with high losses after eclosion and a well-marked ageing process, which is particularly dramatic in males. A three-parameter (k(1) -k(3) ) model for age-dependent adult instantaneous mortality rates was constructed using mark-recapture data for the tsetse fly Glossina morsitans morsitans Westwood (Diptera: Glossinidae). Mortality changed linearly with k(1) over all ages; k(2) affected only losses in roughly the first week of adult life, and k(3) controlled the ageing rate. Mortality pooled over age was twice as sensitive to changes in k(3) as in k(1) . Population growth rate was, however, similarly affected by these two parameters, reflecting the disproportionate effect of k(3) on mortality in the oldest flies that contribute least to the growth rate. Pooled-age mortality and growth rate were insensitive to changes in k(2) . The same model also provided good fits to data for laboratory colonies of female G. m. morsitans and Glossina austeni Newstead and should be applicable to all tsetse of both sexes. The new model for tsetse mortality should be incorporated into models of tsetse and trypanosome population dynamics; it will also inform the estimation of adult female mortality from ovarian dissection data.

Background Prevention of mother-to-child transmission of HIV (PMTCT) programs collect socio-demographic and HIV testing information similar to that collected by unlinked anonymous testing sero-surveillance (UAT) in antenatal settings. Zimbabwe evaluated the utility of PMTCT data in replacing UAT. Methods A UAT dataset was created by capturing socio-demographic, testing practices from the woman’s booking-card and testing remnant blood at a laboratory from 1 June to 30 September 2012. PMTCT data were collected retrospectively from ANC registers. UAT and PMTCT data were linked by bar-code labels that were temporarily affixed to the ANC register. A questionnaire was used to obtain facility-level data at 53 sites. Results Pooled HIV prevalence was 15.8 % (95 % CI 15.3–16.4) among 17,349 women sampled by UAT, and 16.3 % (95 % CI 15.8 %–16.9 %) among 17,150 women in PMTCT datasets for 53 sites. Pooled national percent-positive agreement (PPA) was 91.2 %, and percent-negative agreement (PNA) was 98.7 % for 16,782 women with matched UAT and PMTCT data. Based on UAT methods, overall median prevalence was 12.9 % (Range 4.0 %–19.4 %) among acceptors and refusers of HIV test in PMTCT compared to 12.5 % ((Range 3.4 %–19.5 %) among acceptors in ANC registers. There were variations in prevalence by site. Conclusion Although, there is no statistical difference between pooled HIV prevalence in UAT compared to PMTCT program, the overall PPA of 91.2 % and PNA of 98.7 % fall below World Health Organisation (WHO) benchmarks of 97.6 % and 99.6 % respectively. Zimbabwe will need to strengthen quality assurance (QA) of rapid HIV testing and data collection practices. Sites with good performance should be prioritised for transitioning. Electronic supplementary material The online version of this article (doi:10.1186/s12879-016-1425-2) contains supplementary material, which is available to authorized users.

Introduction: Herpes simplex virus type 2 (HSV-2) facilitates sexual acquisition of HIV-1 but data on transmission are less clear. In this study the interaction between genital shedding of HIV-1 and HSV-2 was explored among Zimbabwean sex workers. Methods: Women (n = 214) were interviewed about genital symptoms. Blood samples were analysed for HIV-1 and HSV-2 antibodies, HIV-1 plasma viral load (PVL) and CD4 lymphocyte count and genital swabs for detection of HIV-1 and HSV-2 genital shedding, Chlamydia trachomatis, Neisseria gonorroheae and Trichomonas vaginalis, and a cervico-vaginal lavage (CVL) for quantitative measurement of HIV-1 shedding. Shedding analyses were undertaken on women co-infected with HSV-2 and HIV-1. Results: A total of 124 women were co-infected with HIV-1 and HSV-2; 58 were infected with HSV-2 alone. Most HIV-1-infected women were co-infected with HSV-2 (95.4%). Genital HIV-1 shedding was detected in 84.3% of co-infected women and was associated with low CD4 cell count and high PVL but not with reported symptoms of genital herpes or genital shedding of HSV-2. There was no difference in HIV-1 shedding among women shedding HSV-2 (79.3%) and women not shedding HSV-2 (83.2%) (P = 0.64). The adjusted odds ratio for HIV-1 shedding between HSV-2 shedders and non-shedders was 0.8 [95% confidence interval (CI), 0.2-3.3]. HIV-1 PVL(log(10)) and CVL viral load(log(10)) were correlated (r = 0.38; 95% Cl, 0.2-0.5). After adjusting for PVL, genital symptoms and age, HSV-2 shedding had no effect on CVL viral load (P = 0.13). Conclusion: Rate and quantity of HIV-1 genital shedding do not appear to be altered by presence of HSV-2 genital shedding. (C) 2006 Lippincott Williams & Wilkins.

The distributions of insecticide-treated cattle from sites in Tanzania and Zimbabwe were assessed from interviews with livestock owners, analysis of secondary livestock data and mapping technologies. The time-course of tsetse control operations at these sites were then simulated using a mathematical model that assumed diffusive movement and logistic growth in fly populations. A simulation of a tsetse control operation in Mudzi district, north-east Zimbabwe, was in accord with observations that the use of insecticide-treated cattle was unable to prevent substantial re-invasion of tsetse from Mozambique, consequent on the patchy distribution of cattle. The simulation was also consistent with the observed efficacy of a 10-km wide barrier of insecticide-treated targets deployed evenly at 4 km−2. Simulation of a control operation on Mkwaja Ranch in Tanzania was in accord with the observation that the use of insecticide-treated cattle reduced the tsetse population on the ranch by c. 90%. Insecticide-treated cattle were used to better effect in the Kagera Region of Tanzania. Simulation of this operation predicts that the deployment of 35,000 treated cattle in the area would result in > 99% control of the tsetse population, consistent with the observed decline, by 1–2 orders of magnitude, in cases of trypanosomiasis in the region. The greater success of the Kagera operation was due to the size and shape of the treated area and, particularly, to the restriction of re-invasion to 20% of the perimeter, compared with > 80% on Mkwaja. Simulation was used to assess how tsetse control could have been improved at Mkwaja. The results suggest that splitting herds into smaller, more numerous, units could have achieved some improvement but, in general, the disease problem would not have been solved by the use of insecticide-treated cattle alone. Only by deploying odour-baited targets in ungrazed areas, or in a 1–3-km barrier around the ranch, could substantially better control (99–99.9%) have been achieved. Sensitivity analyses of the Mkwaja simulation showed that the general conclusions were robust to assumptions regarding cattle distribution and the rates of fly movement and growth. Properly managed and appropriately applied insecticide-treated baits are powerful weapons for tsetse control but should not be used without regard to potential levels of re-invasion, consequent largely on considerations of the size and shape of the treatment area and the density and distribution of the baits.

Objective: To determine the feasibility and acceptability of conducting a community randomized trial (CRT) of an adolescent reproductive health intervention (ARHI) using biological measures of effectiveness.Setting: Four secondary schools and surrounding communities in rural Zimbabwe.Methods: Discussions were held with pupils, parents, teachers and community leaders to determine acceptability. A questionnaire and urine sampling survey was undertaken among Form 1 and 2 pupils. Studies were undertaken to inform likely participation and follow up in a future CRT A community survey of 16-19-year-olds was conducted to determine levels of secondary school attendance and likely HIV prevalence at final follow up in the event of a trial.Results: Form 1 and 2 pupils aged 12-18 years (n = 723; median age, 15 years) participated in the research. Prevalences of HIV, Chlamydia and gonorrhoea were 3.6% [95% confidence interval (CI), 2.3-5.3%], 0.4% (95% CI, 0.1-1.3%) and 1.9% (95% CI, 1.0-3.3%) respectively. There was poor correlation between biological evidence of sexual experience and questionnaire responses, due to concerns about confidentiality. Only 13% (95% CI, 4-27%) of those infected with HIV and/or a sexually transmitted disease admitted to having had sex. in the community survey of 573 adolescents aged 16-19 years, 6.6% (95% CI, 3.9-10.3%) of females and 5.1% (95% CI, 2.9-8.2%) of males were HIV positive. High participation and retention rates are achievable within a trial in this setting.Conclusions: It is acceptable and feasible to conduct rand omized trials to establish the effectiveness of ARHIs. However, self-reported behavioural outcomes will probably be biased, emphasizing the importance of using externally validated biological outcome measures to determine effectiveness. (C) 2002 Lippincott Williams Wilkins.

Human and animal trypanosomiasis, spread by tsetse flies (Glossina spp), is a major public health concern in much of sub-Saharan Africa. The basic reproduction number of vector-borne diseases, such as trypanosomiasis, is a function of vector mortality rate. Robust methods for estimating tsetse mortality are thus of interest for understanding population and disease dynamics and for optimal control. Existing methods for estimating mortality in adult tsetse, from ovarian dissection data, often use invalid assumptions of the existence of a stable age distribution, and age-invariant mortality and capture probability. We develop a dynamic model to estimate tsetse mortality from ovarian dissection data in populations where the age distribution is not necessarily stable. The models correspond to several hypotheses about how temperature affects mortality: no temperature dependence (model 1), identical temperature dependence for mature adults and immature stages, i.e., pupae and newly emerged adults (model 2), and differential temperature dependence for mature adults and immature stages (model 3). We fit our models to ovarian dissection data for G. pallidipes collected at Rekomitjie Research Station in the Zambezi Valley in Zimbabwe. We compare model fits to determine the most probable model, given the data, by calculating the Akaike Information Criterion (AIC) for each model. The model that allows for a differential dependence of temperature on mortality for immature stages and mature adults (model 3) performs significantly better than models 1 and 2. All models produce mortality estimates, for mature adults, of approximately 3% per day for mean daily temperatures below 25°C, consistent with those of mark-recapture studies performed in other settings. For temperatures greater than 25°C, mortality among immature classes of tsetse increases substantially, whereas mortality remains roughly constant for mature adults. As a sensitivity analysis, model 3 was simultaneously fit to both the ovarian dissection and trap data; while this fit also produces comparable mortality at temperatures below 25°C, it is not possible to obtain good fits to both data sources simultaneously, highlighting the uncertain correspondence between trap catches and population levels and/or the need for further improvements to our model. The modelling approach employed here could be applied to any substantial time series of age distribution data., Author summary Trypanosomiasis, spread by tsetse flies (Glossina spp.), is a disease that is fatal for both humans and livestock if left untreated, and is a serious threat to public health in many regions of sub-Saharan Africa. In order to understand the dynamics of the disease it is important also to understand tsetse population dynamics. Tsetse fly mortality estimates are central to this understanding, but are difficult to acquire from wild populations. Previous methods for estimating mortality from age-distribution data assume a stable age structure and age-invariant mortality and capture probability. Based on prior fieldwork, none of these assumptions appears justified. Building on previous mortality estimation techniques, and incorporating what is known about tsetse population dynamics, we develop simulation techniques to estimate mortality for tsetse populations where the age distribution is not necessarily stable. We fit our models to age-distribution data produced in 1991 and 1992 at Rekomitjie Research Station in the Zambezi Valley in Zimbabwe. Our final model produces mortality estimates consistent with those of mark-recapture studies performed in other settings. We find that mortality increases with temperature, a result consistent with field and laboratory findings, and that the temperature effects are much more severe for pupae and newly emerged adults than for mature adults. Our dynamical modelling approach could be used for mortality estimation for any population where substantial age distribution data are available: specifically, it could be used to answer substantive questions about tsetse flies in other settings.

Objective The BED assay was developed to estimate the proportion of recent HIV infections in a population. We used the BED assay as a proxy for acute infection to quantify the associated risk of mother-to-child-transmission (MTCT) during pregnancy and delivery. Design A total of 3773 HIV-1 sero-positive women were tested within 96 h of delivery using the BED assay, and CD4 cell count measurements were taken. Mothers were classified according to their likelihood of having recently seroconverted. Methods The risk of MTCT in utero and intra-partum was assessed comparing different groups defined by BED and CD4 cell count, adjusting for background factors using multinomial logistic models. Results Compared with women with BED ≥ 0.8/CD4 ≥ 350 (typical of HIV-1 chronic patients) there was insufficient evidence to conclude that women presenting with BED

Background: Several approaches have been used for measuring HIV incidence in large areas, yet each presents specific challenges in incidence estimation. Methodology/Principal Findings: We present a comparison of incidence estimates for Kenya and Uganda using multiple methods: 1) Epidemic Projections Package (EPP) and Spectrum models fitted to HIV prevalence from antenatal clinics (ANC) and national population-based surveys (NPS) in Kenya (2003, 2007) and Uganda (2004/2005); 2) a survey-derived model to infer age-specific incidence between two sequential NPS; 3) an assay-derived measurement in NPS using the BED IgG capture enzyme immunoassay, adjusted for misclassification using a locally derived false-recent rate (FRR) for the assay; (4) community cohorts in Uganda; (5) prevalence trends in young ANC attendees. EPP/Spectrum-derived and survey-derived modeled estimates were similar: 0.67 [uncertainty range: 0.60, 0.74] and 0.6 [confidence interval: (CI) 0.4, 0.9], respectively, for Uganda (2005) and 0.72 [uncertainty range: 0.70, 0.74] and 0.7 [CI 0.3, 1.1], respectively, for Kenya (2007). Using a local FRR, assay-derived incidence estimates were 0.3 [CI 0.0, 0.9] for Uganda (2004/2005) and 0.6 [CI 0, 1.3] for Kenya (2007). Incidence trends were similar for all methods for both Uganda and Kenya. Conclusions/Significance: Triangulation of methods is recommended to determine best-supported estimates of incidence to guide programs. Assay-derived incidence estimates are sensitive to the level of the assay’s FRR, and uncertainty around high FRRs can significantly impact the validity of the estimate. Systematic evaluations of new and existing incidence assays are needed to the study the level, distribution, and determinants of the FRR to guide whether incidence assays can produce reliable estimates of national HIV incidence.

BACKGROUND: Whereas HAART initiated at CD4 cell counts 351-450 cells/ml reduces mortality compared with starting at lower CD4 levels there is currently no evidence for the advantages of initiating treatment at CD4 cell counts greater than 450 cells/ml. METHODS: Mortality hazard as a function of CD4 cell count was estimated among postpartum HIV-positive women in Zimbabwe using HIV-negative women as the reference group. RESULTS: Mortality within 24 months postpartum was 54 times higher among women with CD4 cell counts less than 200 cells/ml fell to 5.4 times higher for those with CD4 cell counts 400-600 cells/ml but fell little thereafter. For CD4 cell counts greater than 600 cells/ml the hazard was 6.2 (95% confidence interval 3.2-11.9). CONCLUSION: Early HAART initiation for all HIV-positive pregnant women may benefit individual mothers and infants and simultaneously reduce population HIV incidence.

Vitamin A deficiency is common among women in resource-poor countries and is associated with greater mortality during HIV.Fourteen thousand one hundred ten mothers were tested for HIV and randomly administered 400,000 IU vitamin A or placebo at less than 96 hours postpartum. The effects of vitamin A and HIV status on mortality, health care utilization, and serum retinol were evaluated.Four thousand four hundred ninety-five (31.9%) mothers tested HIV positive. Mortality at 24 months was 2.3 per 1000 person-years and 38.3 per 1000 person-years in HIV-negative and HIV-positive women, respectively. Vitamin A had no effect on mortality. Tuberculosis was the most common cause of death, and nearly all tuberculosis-associated deaths were among HIV-positive women. Among HIV-positive women, vitamin A had no effect on rates of hospitalization or overall sick clinic visits, but did reduce clinic visits for malaria, cracked and bleeding nipples, pelvic inflammatory disease, and vaginal infection. Among HIV-negative women, serum retinol was responsive to vitamin A, but low serum retinol was rare. Among HIV-positive women, serum retinol was largely unresponsive to vitamin A, and regardless of treatment group, the entire serum retinol distribution was shifted 25% less than that of HIV-negative women 6 weeks after dosing.Single-dose postpartum vitamin A supplementation had no effect on maternal mortality, perhaps because vitamin A status was adequate in HIV-negative women and apparently unresponsive to supplementation in HIV-positive women.

Human leukocyte antigen (HLA)-E and HLA-G molecules act as powerful modulators of the innate immune response. The present study shows that the HLA-E G genetic variant (the HLA-E*0103 allele) alone is significantly (P = .001) associated with a 4.0-fold decreased risk of human immunodeficiency virus 1 (HIV-1) infection in Zimbabwean women. Furthermore, women carrying the combination of the protective HLA-E G homozygote and HLA-G*0105N heterozygote genotypes had a 12.5-fold decreased risk of HIV-1 infection (P = .03), compared with women carrying neither genotype. These associations remained significant after adjustment was made for other significant sociodemographic risk factors for HIV prevalence in this population. In conclusion, HLA-E and HLA-G polymorphisms can independently and synergistically influence susceptibility to heterosexual acquisition of HIV-1.

To map the characteristics of rural based sex workers in Zimbabwe with regard to demographics, mobility, behavior, HIV and sexually transmitted infection (STI) prevalence, to explore the appropriateness and feasibility of presumptive periodic treatment (PPT) for bacterial STIs as an HIV prevention intervention among these women, and to compare tolerability of 2 PPT regimens (1 g of azithromycin and 2 g of metronidazole+/-500 mg of ciprofloxacin). Five commercial farms and 2 mines in Mashonaland West, Zimbabwe. Three hundred sixty-three sex workers were recruited and completed a structured interviewer-administered questionnaire. Each participant had blood tested for antibody to HIV, herpes simplex virus 2 (HSV-2), and syphilis; urine tested for Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG); and a vaginal swab tested for Trichomonas vaginalis (TV). Women were randomly assigned to receive a single dose of 1 of 2 PPT regimens and then followed to assess rates of side effects and reinfection. The overall prevalence of antibody to HIV was 55.7% (95% confidence interval [CI]: 50.6-60.9) and that of HSV-2 was 80.8% (95% CI: 76.7-84.9). The prevalence of CT and NG was low (CT=1.7%, 95% CI: 0.3-3.0); (NG=1.9%, 95% CI: 0.5-3.4), with a much higher prevalence of TV (TV=19.3%, 95% CI: 15.2-23.4). Prevalence of CT, NG, and TV was appreciably reduced 1 month after PPT but rose to pretreatment levels at the 2- and 3-month visits. The rate of moderate or severe side effects after PPT was low, but it was higher in the women who received ciprofloxacin in addition to azithromycin and metronidazole (P=0.007). It was feasible to access women who reported exchanging money or gifts for sex in rural communities, although many of these women engaged in sex work only infrequently. The prevalence of bacterial STIs was low, suggesting that PPT may not be an appropriate intervention in this setting. Rapid reinfection after PPT suggests that this needs to be given at monthly intervals to reduce prevalence of STIs.

In the Zambezi Valley of Zimbabwe, ULV applications of non-residual insecticide (endo-sulphan and NRDC 161) were made to a 1.8 × 1.8 km block of woodland infested with Glossina morsitans morsitans Westw. and G. pallidipes Austen. The recapture rates of marked flies released in the centre of the block, and recaptured in odour-baited traps in and around the block, indicated that the insecticides killed about 97% of flies that had been released 1–4 hr before spraying. Catches of unmarked male G. m. morsitans in the centre of the block declined after the insecticide applications, but there was no clear effect on catches of female G. m. morsitans and both sexes of G. pallidipes. Data for the movement of marked flies suggested that the minimum daily rates of movement were about 700 m for male G. m. morsitans and about 800 m for the other tsetse. An increase in dawn temperatures, from 17.5 to 27.5°C, was associated with an increase in the rate movement of G. pallidipes in the early morning. The failure to detect changes in the unmarked populations of female G. m. morsitans and both sexes of G. pallidipes was attributed to the high mobilities of these flies and demonstrated that unmarked populations could not be studied satisfactorily in small plots; studies based on marked populations are recommended for such plots.