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Jamonneau, V.

Publications and source records attributed to Jamonneau, V..

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A SHERLOCK toolbox for the eco-epidemiological surveillance of animal African trypanosomosis reveals a similar parasite diversity in domestic pigs in two ancient sleeping sickness foci in Western Africa.

Animal African trypanosomosis (AAT), caused by protist parasites of the genus Trypanosoma, puts upward of a million head of livestock at risk across 37 countries in Africa. The economic impact of AAT and the presence of human-infectious trypanosomes in animals place a clear importance on improving diagnostics for animal trypanosomes to map the distribution of the veterinary parasites and identify reservoirs of human-infectious trypanosomes. We have adapted the CRISPR-based detection toolkit SHERLOCK (Specific High-sensitivity Enzymatic Reporter unLOCKing) for trypanosomatid parasites responsible for AAT (SHERLOCK4AAT) including Pan- trypanosomatid, Trypanozoon, T. vivax, T. congolense, T. theileri, T. simiae and T. suis assays. To test the applicability of this technique in the field, we analysed dried blood spots collected from 200 farm and 224 free-ranging pigs in endemic and historical human African trypanosomiasis foci in Guinea and Cote dIvoire, respectively. The results revealed that SHERLOCK4AAT can detect and discriminate between trypanosome species involved in multiple infections with a high sensitivity. 62.7 % [58.1, 67.3] of pigs were found infected with at least one trypanosome species. T. brucei gambiense, a human-infectious trypanosome, was found in one animal at both sites, highlighting the risk that these animals may act as persistent reservoirs. These data suggest that, due to their proximity to humans and their attractiveness to tsetse flies, pigs could act as sentinels to monitor T. b. gambiense circulation using the SHERLOCK4AAT toolbox.

microbiology↗

Trypanosoma brucei gambiense group 2 experimental in vivo life cycle: from procyclic to bloodstream form.

Trypanosoma brucei gambiense (Tbg) group 2 is a subgroup of trypanosomes able to infect humans in West and Central Africa. Unlike other agents causing sleeping sickness such as Tbg group 1 and Trypanosoma brucei rhodesiense, Tbg2 lacks the typical molecular markers associated with resistance to human serum. Only thirty-six strains of Tbg2 have been documented, and therefore, very limited research has been conducted despite its zoonotic nature. Some of these strains are only available in their procyclic form which hinders human serum resistance assays and mechanistic studies. Furthermore, the understanding of Tbg2s potential to infect tsetse flies and mammalian hosts is limited. In this study, 165 Glossina palpalis gambiensis flies were experimentally infected with procyclic Tbg2 parasites. 35 days post-infection, 43 flies out of the 80 still alive flies were found Tbg2 PCR-positive in the saliva. These flies were able to infect 3 out of the 4 mice used for blood-feeding. Dissection revealed that only six flies really carried mature infections in their midguts and salivary glands. Importantly, a single fly with a mature infection was sufficient to infect a mammalian host. This Tbg2 transmission success confirms that Tbg2 strains can establish in tsetse flies and infect mammalian hosts. The study describes an effective in vivo protocol for transforming Tbg2 from procyclic to bloodstream form, reproducing the complete Tbg2 cycle from G. p. gambiensis to mice. These findings provide valuable insights into Tbg2s host infectivity, and will facilitate further research on mechanisms of human serum resistance.

microbiology↗

Molecular epidemiology of Animal African Trypanosomosis in southwest Burkina Faso

BackgroundAnimal African Trypanosomosis (AAT) is a parasitic disease of livestock that has a major socio-economic impact in the affected areas. It is caused by several species of uniflagellate extracellular protists of the genus Trypanosoma mainly transmitted by tsetse flies: T. congolense, T. vivax and T. brucei brucei. In Burkina Faso, AAT hampers the proper economic development of the southwestern part of the country, which is yet the best watered area particularly conducive to agriculture and animal production. It was therefore important to investigate the extend of the infection in order to better control the disease. The objective of the present study was to assess the prevalence of trypanosome infections and collect data on the presence of tsetse flies. MethodsBuffy coat, Trypanosoma species-specific PCR, Indirect ELISA Trypanosoma sp and trypanolysis techniques were used on 1898 samples collected. An entomological survey was also carried out. ResultsThe parasitological prevalence of AAT was 1.1%, and all observed parasites were T. vivax. In contrast, the molecular prevalence was 23%, of which T. vivax was predominant (89%) followed by T. congolense (12%) and T. brucei s.l. (7.3%) with a sizable proportion as mixed infections (9.1%). T. brucei gambiense, responsible of sleeping sickness in humans, was not detected. The serological prevalence reached 49%. Once again T. vivax predominated (86.2%), but followed by T. brucei (9.6%) and T. congolense (4.2%), while 34.6% of positive samples tested positive for at least two trypanosome species. Seven samples, from six cattle and one pig, were found positive by trypanolysis. The density per trap of Glossina tachinoides and G. palpalis gambiensis was about three flies. Conclusions/SignificanceOverall, our study showed a high prevalence of trypanosome infection in the area, pointing out an ongoing inadequacy of control measures. Authors summaryIn Burkina Faso, like in most countries of sub-Saharan Africa, Animal African Trypanosomosis (AAT) is hampering economic development. It was therefore important to investigate the extent of trypanosome infections after years of control. This study examined circulating trypanosomes in domestic animals using parasitological, molecular and serological tools in southwest Burkina Faso. The prevalence levels observed show that the known epidemiological situation in the region has not really changed. The trypanosome species usually found in the area such as T. congolense, T. vivax and T. brucei s.l. have remained the same, with a stronger presence of T. vivax. The low occurrence of tsetse fly and the predominance of T. vivax attests to the role of the mechanical vectors in maintaining the disease. Although no cases of T. brucei gambiense infection was encountered in the animals examined, trypanolysis tests suggest that there are contact cases in this historical focus of sleeping sickness. Efforts are therefore necessary to reduce or even eliminate the trypanosome burden, and the data provided by this study can assist the decision making.

microbiology↗

Ebola outbreak brings to light an unforeseen impact of tsetse control on sleeping sickness transmission in Guinea.

In addition to the thousands of deaths due the unprecedented ebola outbreak that stroke West Africa (2014-2016), national health systems in affected countries were deeply challenged impacting a number of diseases control programs. Here we describe the case of Human African Trypanosomiasis (HAT), a deadly neglected tropical disease due to a trypanosome transmitted by tsetse flies for which no vaccine nor chemoprophylaxis exists. Data are presented for the disease focus of Boffa in Guinea where a pilot elimination project combining medical screening and vector control was launched in 2012. During ebola, HAT active screening activities were postponed and passive surveillance also was progressively impaired. However, tsetse control using small insecticide impregnated targets could be maintained. The over two years disruption of screening activities led to a dramatic increase of HAT prevalence, from 0.7% in 2013 (21/2885) to 2% (69/3448) in 2016, reaching epidemic levels (>5%) in some villages. In deep contrast, control levels reached in 2013 (0.1%; 7/6564) were maintained in areas covered with impregnated targets as no cases were found in 2016 (0/799). In Boffa, ebola has thus incidentally provided a unique framework to assess the impact of current HAT control strategies. A first lesson is that the \"screen and treat\" strategy is fragile as rapid bursts of the disease may occur in case of disruption. A second lesson is that vector control reducing human-tsetse contacts, even implemented alone, is effective in providing a good level of protection against infection. This advocates for a greater attention being paid to the combination of tsetse control together with medical activities in aiming to reach the HAT elimination objective in Africa.

epidemiology↗

T cell activation and the HLA locus associate with latent infections of human African trypanosomiasis

Infections by many pathogens can result in a wide range of phenotypes, from severe to mild, or even asymptomatic. Understanding the genetic basis of these phenotypes can lead to better tools to treat patients or detect reservoirs. To identify human genetic factors that contribute to symptoms diversity, we examined the range of disease severities caused by the parasite T. b. gambiense, the primary cause of human African trypanosomiasis (HAT). We analyzed the transcriptomes of immune cells from both symptomatic HAT cases and individuals with latent infections. Our analysis identified several genes and pathways that associated with the latent phenotype, primarily suggesting increased T and B cell activation in HAT patients relative to latent infections. We also used these transcriptome data to conduct an exome-wide single nucleotide polymorphism (SNP) association study. This suggested that SNPs in the human major histocompatibility locus (HLA) associate with severity, supporting the transcription data and suggesting that T cell activation is a determining factor in outcome. Finally, to establish if T cell activation controls disease severity, we blocked co-stimulatory dependent T cell activation in an animal model for HAT. This showed that reducing T cell activation during trypanosome infection improves symptoms and reduces parasitemia. Our data has used a combination of transcriptome-wide analysis and an in vivo model to reveal that T cell activation and the HLA locus associate with the development of symptoms during HAT. This may open new avenues for the development of new therapeutics and prognostics.

genetics↗