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Poultry production is an important way of enhancing the livelihoods of rural populations, especially in low- and middle-income countries (LMICs). As poultry production in LMICs remains dominated by backyard systems with low inputs and low outputs, considerable yield gaps exist. Intensification can increase poultry productivity, production and income. This process is relatively recent in LMICs compared to high-income countries. The management practices and the constraints faced by smallholders trying to scale-up their production, in the early stages of intensification, are poorly understood and described. We thus investigated the features of the small-scale commercial chicken sector in a rural area distant from major production centres. We surveyed 111 commercial chicken farms in Kenya in 2016. We targeted farms that sell the majority of their production, owning at least 50 chickens, partly or wholly confined and provided with feeds. We developed a typology of semi-intensive farms. Farms were found mainly to raise dual-purpose chickens of local and improved breeds, in association with crops and were not specialized in any single product or market. We identified four types of semi-intensive farms that were characterized based on two groups of variables related to intensification and accessibility: (i) remote, small-scale old farms, with small flocks, growing a lot of their own feed; (ii) medium-scale, old farms with a larger flock and well located in relation to markets and (iii) large-scale recently established farms, with large flocks, (iii-a) well located and buying chicks from third-party providers and (iii-b) remotely located and hatching their own chicks. The semi-intensive farms we surveyed were highly heterogeneous in terms of size, age, accessibility, management, opportunities and challenges. Farm location affects market access and influences the opportunities available to farmers, resulting in further diversity in farm profiles. The future of these semi-intensive farms could be compromised by several factors, including the competition with large-scale intensive farmers and with importations. Our study suggests that intensification trajectories in rural areas of LMICs are potentially complex, diverse and non-linear. A better understanding of intensification trajectories should, however, be based on longitudinal data. This could, in turn, help designing interventions to support small-scale farmers. [ABSTRACT FROM AUTHOR]

During the latter months of 1998, cases of sleeping sickness caused by Trypanosoma brucei rhodesiense presented in Soroti district, eastern Uganda, a region which had not previously experienced cases of the disease. Cattle are the main reservoir for T b rhodesiense, by contrast with sleeping sickness caused by Trypanosoma brucei gambiense in west Africa where there appears to be no epidemiologically significant animal reservoir. Several factors have been identified that interacted to produce ideal conditions for the establishment of a new disease focus. After a period of civil unrest, Soroti, which is within the tsetse belt, was repopulated by people and later, cattle. Both the cattle restocking and the subsequent trade in these cattle at a local cattle market had a role in the appearance of the disease. Recently, molecular biology techniques have become available for the detection and genotype identification of T b rhodesiense and thus it is now possible to distinguish human infective and non-infective trypanosomes in cattle. In light of these advances in identification and in both field and epidemiological techniques, successful disease control management has become an achievable goal and will require the collaboration and expertise of clinicians, veterinarians, epidemiologists and laboratory scientists. [Copyright &y& Elsevier]

The article discusses the epidemiology and control of human African trypanosomiasis (HAT), which is also known as sleeping sickness. The disease is classified into two types, one is caused by Trypanosoma brucei rhodesience while the other is caused by T. b. gambiense. The choice of treatment depends on the parasite species involved and on the stage of the disease.

Background: Sleeping sickness, caused by two trypanosome subspecies, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, is a parasitic disease transmitted by the tsetse fly in sub-Saharan Africa. We report on a recent outbreak of T b rhodesiense sleeping sickness outside the established south-east Ugandan focus, in Soroti District where the disease had previously been absent. Soroti District has been the subject of large-scale livestock restocking activities and, because domestic cattle are important reservoirs of T b rhodesiense, we investigated the role of cattle in the origins of the outbreak.Methods: We identified the origins of cattle entering the outbreak area in the 4 years preceding the outbreak. A matched case-control study was conducted to assess whether the distance of villages from the main market involved with restocking was a risk factor for sleeping sickness. We investigated the spatial clustering of sleeping sickness cases at the start of the outbreak.Findings: Over 50% (1510 of 2796) of cattle traded at the market were reported to have originated from endemic sleeping sickness areas. The case-control study revealed that distance to the cattle market was a highly significant risk factor for sleeping sickness (p<0.001) and that there was a significant clustering of cases (27 of 28) close to the market at the start of the outbreak (p<0.001). As the outbreak progressed, the average distance of cases moved away from the cattle market (0.014 km per day, 95% CI 0.008-0.020 km per day, p<0.001).Interpretations: The results are consistent with the disease being introduced by cattle infected with T b rhodesiense imported to the market from the endemic sleeping sickness focus. The subsequent spread of the disease away from the market suggests that sleeping sickness is becoming established in this new focus. Public health measures directed at controlling the infection in the animal reservoir should be considered to prevent the spread of sleeping sickness. [ABSTRACT FROM AUTHOR]

Background: The expansion of sleeping sickness caused by Trypanosoma brucei rhodesiense beyond its traditional focus in southeast Uganda has been linked with large-scale livestock restocking. To assess the risk presented to the human population by domestic livestock, human-infective T b rhodesiense must be distinguished from non-human-infective T brucei brucei, since both parasites can be present in cattle. We investigated the use of a simple genetic marker to characterise parasites collected from cattle in villages within the new sleeping sickness focus in Soroti District, Uganda.Methods: 70 T brucei sl samples of known human infectivity status collected from human beings and cattle in Tororo District, Uganda, from 1989 to 1991 were screened for the presence of the human-serum-resistance-associated (SRA) gene by conventional PCR. In 2000-01, blood samples from 200 randomly selected cattle in six villages and two markets in Soroti District were screened for T brucei sl parasites by PCR; positive samples were screened for the presence of the SRA gene.Findings: The SRA gene was present in all 29 samples from patients with sleeping sickness in Tororo District. Of the 41 samples collected from cattle at the same time, the SRA gene was present in the eight samples that tested resistant to human serum in vitro, whereas it was absent from all 33 isolates that were sensitive to human serum in vitro. Of the 200 cattle sampled in Soroti District, we estimated that up to 18% (95% CI 12-23) were infected with T b rhodesiense.Interpretation: Detection of the SRA gene could provide the basis for a simple diagnostic test to enable targeted control of T b rhodesiense in the domestic livestock reservoir, thereby reducing the public-health burden of sleeping sickness in east Africa. [ABSTRACT FROM AUTHOR]

In many livestock production systems in sub-Saharan Africa, cattle are owned by individual keepers but regularly mix with animals from other herds while grazing communal land, at watering points or through the use of shared bulls for breeding and ploughing. Such contacts may have important implications for disease transmission and control but are not well documented. We describe between-farm contacts in Kimilili sub-county of Bungoma County, a mixed farming area of predominately smallholder farmers. Between-farm contacts occurring during grazing or at shared water points over the past four weeks were captured in seven randomly selected villages using a photo-elicitation tool. The use of shared bulls for breeding and ploughing and cattle introductions from farms within the same village in the past 12 months were also captured. Contact networks were constructed for each contact type in each village. In total 329 farms were included in the study. Networks resembled undirected scale-free graphs with a network density ranging between 9.6 and 14.0. Between 45.6 and 100% of the farms in each study village had been in contact over the past four weeks through grazing and watering contacts. Between 88.9 and 100% were considered to have been in contact over the past 12 months. The topology of the networks was heterogeneous, with some farms exhibiting a high degree of contact. The degree of farm contact and distances between farms were negatively correlated (Pearson correlation coefficient range -0.2 to -0.4). Effective disease control and surveillance must take into consideration the frequency and range of contacts that occur between farms within a single village. Cattle keepers are highly interconnected and pathogens that are transmitted through direct or indirect animal contact would be expected to spread rapidly in the study system. However, the observed heterogeneity in between-farm contact may present opportunities for interventions to be targeted to particular herds to limit infectious disease spread., (Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.)

Tularaemia is a highly contagious infectious zoonosis caused by the bacterial agent Francisella tularensis . The aim of this study was to investigate the presence of antibodies to F. tularensis in febrile patients in northeastern Kenya. During 2014-2015, 730 patients were screened for anti- F. tularensis antibodies using a combination of ELISA and Western blot. Twenty-seven (3.7%) individuals were positive for F. tularensis . Tularaemia was not suspected by the treating clinicians in any of them. Our results suggest that tularaemia may be present in Kenya but remain unreported, and emphasizes the need for local clinicians to broaden their diagnostic repertoire when evaluating patients with undifferentiated febrile illness.

In developing countries, cities are rapidly expanding and urban and peri-urban agriculture (UPA) has an important role in feeding these growing urban populations; however such agriculture also carries public health risks such as zoonotic disease transmission. It is important to assess the role of UPA in food security and public health risks to make evidence-based decisions on policies. Describing and mapping the peri-urban interface (PUI) are the essential first steps for such an assessment. Kampala, the capital city of Uganda is a rapidly expanding city where the PUI has not previously been mapped or properly described. In this paper we provide a spatial representation of the entire PUI of Kampala economic zone and determine the socio-economic factors related with peri-urbanicity using a population-dynamics focussed rapid rural mapping. This fills a technical gap of rapid rural mapping and offers a simple and rapid methodology for describing the PUI which can be applied in any city in developing countries for wide range of studies.

We present the results of a study to determine the value of central point sampling in cattle markets as a means of estimating the trypanosomiasis (T. brucei s.l.) prevalence in the surrounding landscape in Uganda. We find that in the epidemic area studied, central point sampling is a good predictor of prevalence in surrounding villages, but not in endemic areas. We also find that animals infected with trypanosomiasis are more likely to be brought for sale in livestock markets in endemic areas; we discuss these results in relation to the prevention of the spread of sleeping sickness.

The epidemic of Trypanosoma brucei rhodesiense sleeping sickness in eastern Uganda, which began in 1998 as a result of movements of the livestock reservoir of the parasite, has continued to spread. An additional 133 000 people have been put at risk of infection in Kaberamaido, another newly affected district. The few resources committed to control interventions in Soroti district have failed to contain the epidemic. The high prevalence of the parasite in cattle presents a significant risk for transmission to human beings and further spread of this neglected zoonotic disease. Targeted interventions are urgently needed to control epidemics and reduce the high mortality resulting from sleeping sickness.

We have carried out a study of risk factors for early detection of Trypanosoma brucei rhodesiense sleeping sickness. Records of sleeping sickness patients from 1987 to 2001 from Tororo and Busia districts in Uganda were reviewed for their village of origin and clinical stage (early or late). All villages that reported sleeping sickness and fixed post-diagnostic sleeping sickness health units in Tororo and Busia districts were geo-referenced. The spatial distribution of early and late stage patient detection by health units was analysed using Geographical Information Systems (GIS). Of 1316 sleeping sickness patients admitted at the Livestock Health Research Institute and Busolwe hospitals and Lumino health centre from Tororo and Busia districts, 471 (35.8%) were early stage, 825 (62.7%) were late stage, while 20 (1.5%) were not staged. Five hundred and eighty-five (44.5%) came from within a 10 km radius of the reporting health units. After multivariate analysis, the proportion of early stage patients detected was found to be significantly associated with patients originating from within a 10 km radius of the health unit (P < 0.01), with adults (>19 years) (P < 0.01), and with annual parish incidence (P < 0.01). Application of GIS and the early to late stages ratio are an informative and powerful means of determining efficiency of surveillance of sleeping sickness.

For those with sleeping sickness, the consequences of delayed diagnosis include poor prognosis at treatment and an increased risk of tsetse infection. Data on their socio-demographic and clinical characteristics, health-seeking behaviour and delays in presentation and diagnosis were collected from 119 diagnosed cases of rhodesiense sleeping sickness in eastern Uganda. The median total delay, from onset of the illness to diagnosis, was 60 days. The median service-provider delay (30 days) was markedly longer than the median patient delay (17 days). Each of these delays was, however, considerable and independently associated with patients presenting with late-stage sleepiness, giving odds ratios and (95% confidence intervals) of 7.29 (3.10-17.14) and 2.98 (1.38-6.43), respectively. A blood examination at the first visit was also associated with the service-provider delay (odds ratio = 0.45; 95% confidence interval = 0.22-0.95). Most of the patients (77.4%) had either been referred to the local sleeping-sickness hospital by other members of their community or presented at the hospital on their own initiative; few had been referred by other components of the local health system. The results are disappointing, not only in showing long delays in diagnosis (and therefore in treatment) but also in indicating that much of the delay is attributable to the service provider failing to diagnose sleeping sickness among symptomatic individuals.

Sleeping sickness has long been a major public health problem in Uganda. From 1900 to 1920, more than 250,000 people died in an epidemic that affected the southern part of the country, particularly the Busoga region. The epidemic has traditionally been ascribed to Trypanosoma brucei gambiense, a parasite now confined to central and western Africa. The Busoga region still reports sleeping sickness, although it is caused by T.b. rhodesiense, commonly believed to have spread to Uganda from Zambia in the 1940s. Our analysis of clinical data recorded in the early 1900s shows that the clinical course of sleeping sickness cases during the 1900-1920 epidemic in Uganda was markedly different from T.b. gambiense cases, but similar to T.b. rhodesiense. These findings suggest that T.b. rhodesiense was present in Uganda and contributed to the epidemic. The historic context is reassessed in the light of these data.

We describe the development of a single-primer amplification system, which uses the trypanosomal mobile genetic element RIME as a molecular marker for the differentiation of Trypanosoma brucei stocks. Using a well-characterised set of T. brucei stocks from southeast Uganda, Kenya and Zambia, we have evaluated the application of this technique, termed MGE-PCR (mobile genetic element PCR) for the typing of trypanosome strains. The technique revealed considerable variation between stocks and was sufficiently specific to amplify trypanosomal DNA in the presence of host DNA. The results showed a clear distinction between human-infective and non-human-infective stocks. Comparative studies on these stocks using markers for the human serum resistance associated (SRA) gene, which identifies human-infective stocks, demonstrated complete agreement between MGE-PCR derived groups and human-infectivity status. Furthermore, MGE-PCR detects high levels of variability within the T. b. brucei and T. b. rhodesiense groups and is therefore a powerful discriminatory tool for tracking individual T. brucei genotypes and strains.

Sleeping sickness presents clinically as two distinct diseases, reflecting the fact that two very different trypanosomes are responsible. The African Rift separating East and West Africa defines the distribution of the two diseases. In this review, Susan Welburn, Eric Fèvre, Paul Coleman, Martin Odiit and Ian Maudlin discuss the biology and distribution of these two diseases in relation to the evolution of hominids in Africa.

Drug resistance is a major problem affecting progress on malaria control, while many current programmes are seeking to introduce impregnated bednets to reduce transmission and hence child mortality and morbidity. David Molyneux, Katherine Floyd, Guy Barnish and Eric Fèvre propose that more consideration should be given to the interaction between transmission control and the development of drug resistance, and that vector control as a means of reducing disease transmission is involved in reducing the rate of development, and the level, of resistance. Therefore, investment in vector control can have important benefits in reducing the future expenditure on drugs (as well as other costs, such as hospitalization, management of resistant cases and severe disease, drug development and household expenditure on malaria chemotherapy). Modelling the many parameters that impact on this complex relationship will better inform policy makers.

The sensitivity in vitro of Plasmodium falciparum to mefloquine, quinine and artemisinin was assessed in an area of multi-drug resistance on the Thai-Myanmar border, using the World Health Organization's microtest, based on schizont maturation inhibition. Participating individuals were exclusively those who had contracted their infections within Myanmar. A total of 34 successful tests were carried out for mefloquine and quinine, showing a marked decrease in sensitivity compared to previously published results. Ten artemisinin tests were successful, with many failures due to the poor storage stability of the test plates. The implications of the shelf-life of the artemisinin plates is discussed. These results contribute to setting a base line of sensitivity to artemisinin in vitro.