Evaluating the potential for the environmentally sustainable control of foot and mouth disease in Sub-Saharan Africa

Strategies to control transboundary diseases have in the past generated unintended negative consequences for both the environment and local human populations. Integrating perspectives from across disciplines, including livestock, veterinary and conservation sectors, is necessary for identifying disease control strategies that optimise environmental goods and services at the wildlife-livestock interface. Prompted by the recent development of a global strategy for the control and elimination of foot-and-mouth disease (FMD), this paper seeks insight into the consequences of, and rational options for potential FMD control measures in relation to environmental, conservation and human poverty considerations in Africa. We suggest a more environmentally nuanced process of FMD control that safe-guards the integrity of wild populations and the ecosystem dynamics on which human livelihoods depend while simultaneously improving socio-economic conditions of rural people. In particular, we outline five major issues that need to be considered: 1) improved understanding of the different FMD viral strains and how they circulate between domestic and wildlife populations; 2) an appreciation for the economic value of wildlife for many African countries whose presence might preclude the country from ever achieving an FMD-free status; 3) exploring ways in which livestock production can be improved without compromising wildlife such as implementing commodity-based trading schemes; 4) introducing a participatory approach involving local farmers and the national veterinary services in the control of FMD; and 5) finally the possibility that transfrontier conservation might offer new hope of integrating decision-making at the wildlife-livestock interface

Carnivore parvovirus ecology in the Serengeti ecosystem: vaccine strains circulating and new host species identified

Carnivore parvoviruses infect wild and domestic carnivores and cross- species transmission is believed to occur. However, viral dynamics are not well understood nor the consequences to wild carnivore populations of the introduction of new strains into wild ecosystems. To clarify the ecology of these viruses in a multi-host system such as the Serengeti ecosystem and identify potential threats for wildlife conservation we analyzed, through real-time PCR, 152 samples belonging to 14 wild carnivore species and 62 samples from healthy domestic dogs. We detected parvovirus DNA in several wildlife tissues. Of the wild carnivore and domestic dog samples tested, 13% and 43%, respectively, were positive for carnivore parvovirus infection, but little evidence of transmission between the wild and domestic carnivores was detected. Instead, we describe two different epidemiological scenarios with separated routes of transmission: first, an endemic feline parvovirus (FPV) route of transmission maintained by wild carnivores inside the Serengeti National Park (SNP); and second, a canine parvovirus (CPV) route of transmission among domestic dogs living around the periphery of the SNP. Twelve FPV sequences were characterized, new host-virus associations involving wild dogs, jackals and hyaenas were discovered and our results suggest mutations in the fragment of the gene were not required to infect different carnivore species. In domestic dogs, six sequences belonged to the CPV-2a strain, whilst 11 belonged to the CPV-2 vaccine-derived strain. This is the first description of a vaccine-derived parvovirus strain being transmitted naturally. IMPORTANCE: Carnivore parvoviruses are widespread among wild and domestic carnivores, which are vulnerable to severe disease under certain circumstances. The findings from this study, which further the understanding of carnivore parvovirus epidemiology, suggest that feline parvoviruses are endemic in wild carnivores in the Serengeti National Park (SNP); further, that canine parvoviruses are present in the dog population living around the SNP, with little evidence of transmission into wild carnivore species; and finally, that the detection of vaccine-derived virus (described here for the first time circulating naturally in domestic dogs) highlights the importance of performing epidemiological research in the region

Mapping of Mycobacterium tuberculosis Complex Genetic Diversity Profiles in Tanzania and Other African Countries

The aim of this study was to assess and characterize Mycobacterium tuberculosis complex (MTBC) genotypic diversity in Tanzania, as well as in neighbouring East and other several African countries. We used spoligotyping to identify a total of 293 M. tuberculosis clinical isolates (one isolate per patient) collected in the Bunda, Dar es Salaam, Ngorongoro and Serengeti areas in Tanzania. The results were compared with results in the SITVIT2 international database of the Pasteur Institute of Guadeloupe. Genotyping and phylogeographical analyses highlighted the predominance of the CAS, T, EAI, and LAM MTBC lineages in Tanzania. The three most frequent Spoligotype International Types (SITs) were: SIT21/CAS1-Kili (n = 76; 25.94%), SIT59/LAM11-ZWE (n = 22; 7.51%), and SIT126/EAI5 tentatively reclassified as EAI3-TZA (n = 18; 6.14%). Furthermore, three SITs were newly created in this study (SIT4056/EAI5 n = 2, SIT4057/T1 n = 1, and SIT4058/EAI5 n = 1). We noted that the East-African-Indian (EAI) lineage was more predominant in Bunda, the Manu lineage was more common among strains isolated in Ngorongoro, and the Central-Asian (CAS) lineage was more predominant in Dar es Salaam (p-value<0.0001). No statistically significant differences were noted when comparing HIV status of patients vs. major lineages (p-value = 0.103). However, when grouping lineages as Principal Genetic Groups (PGG), we noticed that PGG2/3 group (Haarlem, LAM, S, T, and X) was more associated with HIV-positive patients as compared to PGG1 group (Beijing, CAS, EAI, and Manu) (p-value = 0.03). This study provided mapping of MTBC genetic diversity in Tanzania (containing information on isolates from different cities) and neighbouring East African and other several African countries highlighting differences as regards to MTBC genotypic distribution between Tanzania and other African countries. This work also allowed underlining of spoligotyping patterns tentatively grouped within the newly designated EAI3-TZA lineage (remarkable by absence of spacers 2 and 3, and represented by SIT126) which seems to be specific to Tanzania. However, further genotyping information would be needed to confirm this specificity

Response to Rift Valley Fever in Tanzania: Challenges and Opportunities

Rift Valley Fever (RVF) is an arthropod borne viral disease affecting livestock (cattle, sheep, goats and camels), wildlife and humans caused by Phlebovirus. The disease occurs in periodic cycles of 4-15 years associated with flooding from unusually high precipitations in many flood-prone habitats. Aedes and Culex spp and other mosquito species are important epidemic vectors. Because of poor living conditions and lack of knowledge on the pathogenesis of RVF, nomadic pastoralists and agro-pastoralists are at high risk of contracting the disease during epidemics. RVF is a professional hazard for health and livestock workers because of poor biosafety measures in routine activities including lack of proper Personal Protective Equipment (PPE). Direct exposure to infected animals can occur during handling and slaughter or through veterinary and obstetric procedures or handling of specimens in laboratory. The episodic nature of the disease creates special challenges for its mitigation and control and many of the epidemics happen when the governments are not prepared and have limited resource to contain the disease at source. Since its first description in 1930s Tanzania has recorded six epidemics, three of which were after independence in 1961. However, the 2007 epidemic was the most notable and wide spread with fatal human cases among pastoralists and agro-pastoralists concurrent with high livestock mortality. Given all the knowledge that exist on the epidemiology of the disease, still the 2006/2007 epidemic occurred when the government of Tanzania was not prepared to contain the disease at source. This paper reviews the epidemiology, reporting and outbreak investigation, public awareness, preparedness plans and policy as well as challenges for its control in Tanzania

Whole-genome sequencing reveals evidence for inter-species transmission of the yaws bacterium among nonhuman primates in Tanzania

Background Treponema pallidum subspecies pertenue (TPE) is the causative agent of human and nonhuman primate (NHP) yaws infection. The discovery of yaws bacterium in wild populations of NHPs opened the question of transmission mechanisms within NHPs, and this work aims to take a closer look at the transmission of the disease. Methodology/Principal Findings Our study determined eleven whole TPE genomes from NHP isolates collected from three national parks in Tanzania: Lake Manyara National Park (NP), Serengeti NP, and Ruaha NP. The bacteria were isolated from four species of NHPs: Chlorocebus pygerythrus (vervet monkey), Cercopithecus mitis (blue monkey), Papio anubis (olive baboon), and Papio cynocephalus (yellow baboon). Combined with previously generated genomes of TPE originating from NHPs in Tanzania (n = 11), 22 whole-genome TPE sequences have now been analyzed. Out of 231 possible combinations of genome-to-genome comparisons, five revealed an unexpectedly high degree of genetic similarity in samples collected from different NHP species, consistent with inter-species transmission of TPE among NHPs. We estimated a substitution rate of TPE of NHP origin, ranging between 1.77 × 10-7 and 3.43 × 10-7 per genomic site per year. Conclusions/Significance The model estimations predicted that the inter-species transmission happened recently, within decades, roughly in an order of magnitude shorter time compared to time needed for the natural diversification of all tested TPE of Tanzanian NHP origin. Moreover, the geographical separation of the sampling sites (NPs) does not preclude TPE transmission between and within NHP species

Nonhuman primates across sub-Saharan Africa are infected with the yaws bacterium Treponema pallidum subsp. pertenue

Dear Editor, The bacterium Treponema pallidum (TP) causes human syphilis (subsp. pallidum; TPA), bejel (subsp. endemicum; TEN), and yaws (subsp. pertenue; TPE) (1). Although syphilis has reached a worldwide distribution (2), bejel and yaws have remained endemic diseases. Bejel affects individuals in dry areas of Sahelian Africa and Saudi Arabia, whereas yaws affects those living in the humid tropics (1). Yaws is currently reported as endemic in 14 countries, and an additional 84 countries have a known history of yaws but lack recent epidemiological data (3,4). Although this disease was subject to global eradication efforts in the mid-20th century, it later reemerged in West Africa, Southern Asia, and the Pacific region (5). New large-scale treatment options triggered the ongoing second eradication campaign, the goal of which is to eradicate yaws globally by 2020 (5). References: (1) Giacani, L. & Lukehart, S.A. The endemic treponematoses. Clin. Microbiol. Rev. 27, 89–115 (2014). (2) Arora, N. et al. Origin of modern syphilis and emergence of a pandemic Treponema pallidum cluster. Nat. Microbiol. 2, 16245 (2016). (3) Marks, M. Yaws: towards the WHO eradication target. Trans. R Soc. Trop. Med. Hyg. 110, 319–320 (2016). (4) World Health Organization. Eradication of yaws: procedures for verification and certification of interruption of transmission (World Health Organization, Geneva, 2018). (5) Asiedu, K., Fitzpatrick, C. & Jannin, J. Eradication of yaws: historical efforts and achieving WHO’s 2020 target. PLoS Negl. Trop. Dis. 8, e3016 (2014)

Alcelaphine Herpesvirus-1 (Malignant Catarrhal Fever Virus) in Wildebeest Placenta: Genetic Variation of ORF50 and A9.5 Alleles

<div><p>Alcelaphine herpesvirus–1 (AlHV-1), a causative agent of malignant catarrhal fever in cattle, was detected in wildebeest (<i>Connochaetes taurinus</i>) placenta tissue for the first time. Although viral load was low, the finding of viral DNA in over 50% of 94 samples tested lends support to the possibility that placental tissue could play a role in disease transmission and that wildebeest calves are infected <i>in utero</i>. Two viral loci were sequenced to examine variation among virus samples obtained from wildebeest and cattle: the ORF50 gene, encoding the lytic cycle transactivator protein, and the A9.5 gene, encoding a novel polymorphic viral glycoprotein. ORF50 was well conserved with six newly discovered alleles differing at only one or two base positions. In contrast, while only three new A9.5 alleles were discovered, these differed by up to 13% at the nucleotide level and up to 20% at the amino acid level. Structural homology searching performed with the additional A9.5 sequences determined in this study adds power to recent analysis identifying the four-helix bundle cytokine interleukin-4 (IL4) as the major homologue. The majority of MCF virus samples obtained from Tanzanian cattle and wildebeest encoded A9.5 polypeptides identical to the previously characterized A9.5 allele present in the laboratory maintained AlHV-1 C500 strain. This supports the view that AlHV-1 C500 is suitable for the development of a vaccine for wildebeest-associated MCF.</p></div

Widespread Treponema pallidum Infection in Nonhuman Primates, Tanzania

We investigated Treponema pallidum infection in 8 nonhuman primate species (289 animals) in Tanzania during 2015–2017. We used a serologic treponemal test to detect antibodies against the bacterium. Infection was further confirmed from tissue samples of skin-ulcerated animals by 3 independent PCRs (polA, tp47, and TP_0619). Our findings indicate that T. pallidum infection is geographically widespread in Tanzania and occurs in several species (olive baboons, yellow baboons, vervet monkeys, and blue monkeys). We found the bacterium at 11 of 14 investigated geographic locations. Anogenital ulceration was the most common clinical manifestation; orofacial lesions also were observed. Molecular data show that nonhuman primates in Tanzania are most likely infected with T. pallidum subsp. pertenue–like strains, which could have implications for human yaws eradication

Predicting uptake of a malignant catarrhal fever vaccine by pastoralists in northern Tanzania: opportunities for improving livelihoods and ecosystem health

Malignant Catarhal Fever (MCF), caused by a virus transmitted from asymptomatic wildebeest, is a lethal disease in cattle that threatens livestock-based livelihoods and food security in many areas of Africa. Many herd owners reduce transmission risks by moving cattle away from infection hot-spots, but this imposes considerable economic burdens on their households. The advent of a partially-protective vaccine for cattle opens up new options for disease prevention. In a study of pastoral households in northern Tanzania, we use stated preference choice modelling to investigate how pastoralists would likely respond to the availability of such a vaccine. We show a high probability of likely vaccine uptake by herd owners, declining at higher vaccine costs. Acceptance increases with more efficaceous vaccines, in situations where vaccinated cattle are ear-tagged, and where vaccine is delivered through private vets. Through analysis of Normalized Density Vegetation Index (NDVI) data, we show that the reported MCF incidence over 5 years is highest in areas where the mean and interannual varibility in vegetative greeness is relatively low and where herds sizes are smaller. Trends towards lower rainfall and greater landscape-level constraints on cattle movement suggest that MCF avoidance through traditional movement away from wildebeest will become more challenging and that demand for an MCF vaccine will likely increase

Assessment of animal hosts of pathogenic Leptospira in northern Tanzania

Funding: This work was supported by the Wellcome Trust (grant number 096400/Z/11/Z; https://wellcome.ac.uk/). JEBH, VPM, JAC, and SC received support from the Research Councils UK, UK Department for International Development, and UK Biotechnology and Biological Sciences Research Council (BBSRC) (grant numbers BB/J010367/1, BB/L018926, BB/L017679, BB/L018845; http://www.bbsrc.ac.uk/). JAC and VPM also received support from the US National Institutes of Health (NIH)-National Science Foundation (NSF) Ecology and Evolution of Infectious Disease program (R01TW009237; https://www.fic.nih.gov/programs/pages/ecology-infectious-diseases.aspx). MM received support from the BBSRC East of Scotland Bioscience Doctoral Training Partnership (http://www.eastscotbiodtp.ac.uk/). MJM received support from a University of Otago Frances G. Cotter Scholarship and a University of Otago MacGibbon PhD Travel Fellowship (http://www.otago.ac.nz/). VPM and JAC received support from the US National Institutes of Health National Institute for Allergy and Infectious (grant number R01 AI121378; https://www.niaid.nih.gov/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Data Availability: Datasets supporting this manuscript are available through: http://dx.doi.org/10.5525/gla.researchdata.582. Unique sequences generated through this study are available through GenBank (accession numbers MF955862 to MF955882).Peer reviewedPublisher PD