Assessment of α-cypermethrin Pour-on Application and Diminazene Aceturate for the Treatment of Trypanosome-related Diseases Caused by Tsetse Flies in Cattle in Mô (Togo)

BackgroundThe effects of tsetse-transmitted trypanosomosis control in high tsetse challenge and trypanocidal drug resistance settings remain poorly understood in Togo, owing to the poor data underlying the current disease impact. This study was implemented in the framework of the PDRI-Mô project which is an African animal trypanosomosis control project using trypanocides and insecticides on cattle. This project, planned by the agricultural ministry, focused on all the sedentary cattle breeds in the 1000 km² area of the prefecture of Mô. Until 2013, the locality remained unconnected to outside areas, with long-term limited access to quality medicines, veterinary services, animal husbandry and new AAT control technologies. Methods From March 2014 to November 2017, a database of zoo-sanitary surveys integrating the evolution of the incidence of the disease and the coverage of interventions made it possible to quantify the apparent effect attributable to control effort in herds. The strategy involved an initial phase with cross-sectional entomological and parasitological surveys, including a rapid trypanocidal drug sensitivity testing. Treatment efficacy was assessed using parasitological status post-treatment of trypanosome-positive animals in each village, randomly assigned to three groups, one treated with 0.5 mg/kg b.w. Isometamidium chloride, the second with 3.5 mg/kg b.w. Diminazene diaceturate and the third with distillated water as control. Using parasitological status of blood sample collected on day 0, day 14 and day 28 post-treatment as the outcome result, trypanosome phenotype resistance of drugs treatment was determined if relapse occur. Then, three times a year, 20% of the herd received α-cypermethrin pour-on, and parasitaemic cattle with poor health were individually given diminazene aceturate at 7 mg/kg of body weight (b.w.).ResultsThe tsetse density in the area decreased significantly (P-value ˂ 0.001) from 1.78 ± 0.37 in March 2014 prior to the α-cypermethrin application to 0.48 ± 0.07 in February 2017. Prior to the trypanocidal treatment, relapse of trypanosome infections in the cattle was approximately 12.5% for diminazene at 3.5 mg/kg of b.w., 35% for isometamidium at 0.5 mg/kg of b.w. and null for diminazeen at 7 mg/kg of b.w. Target deployment led to the largest reduction in disease incidence from 28.1% in 2014 to 7.8% in 2017, an improvement in haematocrit from 24.27±4.9% to 27.5±4.6% and a reduction in calf mortality from 15.9±11% to 5.9%.ConclusionsImproving the access to these interventions for different types of livestock and maintaining their effectiveness in the face of high tsetse challenges should be the primary focus of control strategies in areas of Togo.

African Trypanosomosis Obliterates DTPa Vaccine-Induced Functional Memory So That Post-Treatment Bordetella pertussis Challenge Fails to Trigger a Protective Recall Response

Salivarian trypanosomes are extracellular parasites causing anthroponotic and zoonotic infections. Anti-parasite vaccination is considered the only sustainable method for global trypanosomosis control. Unfortunately, no single field applicable vaccine solution has been successful so far. The active destruction of the host’s adaptive immune system by trypanosomes is believed to contribute to this problem. Here, we show that Trypanosome brucei brucei infection results in the lasting obliteration of immunological memory, including vaccine-induced memory against non-related pathogens. Using the well-established DTPa vaccine model in combination with a T. b. brucei infection and a diminazene diaceturate anti-parasite treatment scheme, our results demonstrate that while the latter ensured full recovery from the T. b. brucei infection, it failed to restore an efficacious anti-B. pertussis vaccine recall response. The DTPa vaccine failure coincided with a shift in the IgG1/IgG2a anti-B. pertussis antibody ratio in favor of IgG2a, and a striking impact on all of the spleen immune cell populations. Interestingly, an increased plasma IFNγ level in DTPa-vaccinated trypanosome-infected mice coincided with a temporary antibody-independent improvement in early-stage trypanosomosis control. In conclusion, our results are the first to show that trypanosome-inflicted immune damage is not restored by successful anti-parasite treatment.

Aggravation of pathogenesis mediated by ochratoxin A in mice infected with Trypanosoma brucei rhodesiense

SUMMARYMice fed 1·5 mg ochratoxin A (OTA) per kg body weight and infected with Trypanosoma brucei rhodesiense were compared with trypanosome-infected placebo-fed and uninfected OTA-fed controls. Uninfected OTA-fed mice showed fever, lethargy, facial and eyelid oedemas, mild hepatitis and nephritis, and high survival. Infected placebo-fed controls had mean pre-patent period (PPP) of 3·26 days, lethargy, dyspnoea, fever, facial and scrotal oedema, survival of 33–65 days, reduced red cell counts (RCC: 10·96–6·87×106 cells/μl of blood), packed cell volume (PCV: 43·19–26·36%), haemoglobin levels (Hb: 13·37–7·92 g/dL) and mean corpuscular volume (MCV) of 37·96–41·31 fL, hepatosplenomegaly, generalized oedemas, heart congestion, hepatitis and nephritis. Compared to infected placebo-fed controls, infected OTA-fed mice had significantly (P<0·05) shorter mean PPP (2·58 days), reduced survival (6–47 days), more pronounced fever and dyspnoea. The latter had significantly (P<0·05) reduced RCC (10·74–4·56×106 cells/μl of blood), PCV (43·90–20·78%), Hb (13·06–5·74 g/dL), increased MCV (39·10–43·97 fL), severe generalized oedemas, haemorrhages, congestion, hepatic haemosiderosis, hepatitis, nephritis, endocarditis, pericarditis and exclusively, splenic macrophage and giant cell hyperplasia, expanded red pulp and splenic erythrophagocytosis. It was concluded that OTA aggravated the pathogenesis of T. b. rhodesiense infection in mice, and should therefore be taken into consideration during trypanosomosis control programmes.

Half a Century of Tsetse and Animal Trypanosomosis Control on the Adamawa Plateau in Cameroon

L’invasion des glossines sur le plateau de l’Adamaoua se situe dans les années 1950 et a entrainé une mortalité élevée des bovins à cause de la trypanosomose et des émigrations massives des éleveurs de la zone infestée. Trois espèces de mouches tsé-tsé ont été relevées : Glossina morsitans submorsitans, G. fuscipes fuscipes et G. tachinoides. Entre 1960 et 1975, le Gouvernement camerounais a organisé des campagnes de traitement aux trypanocides de masse du bétail. Des activités de lutte contre les glossines ont ensuite été initiées. Entre 1976 et 1994, plusieurs campagnes régulières de pulvérisation aérienne ont été réalisées aboutissant à l’assainissement de 3 200 000 hectares de pâturage. Malheureusement des réinvasions ponctuelles de la mouche tsé-tsé dans la zone assainie n’ont pas pu être évitées. Afin de prévenir la réinvasion des glossines à partir de la plaine de Koutine (au niveau du plateau de l’Adamaoua), des barrières constituées de pièges et d’écrans ont été créées. Cependant des feux de brousse ont détruit la plupart des piètes et de écrans peu après leur mise en place en 1994. Ils ont alors été remplacés par un programme de traitements insecticides du bétail. Des enquêtes transversales et longitudinales parasitologiques et entomologiques en 2004 et 2005 ont montré que la barrière constituée de bétail traité aux insecticides avait réussi à maintenir le plateau relativement indemne de glossines. L’incidence de la trypanosomose enregistrée chez le bétail du plateau variait entre 0 et 2,1 p. 100. Cependant une prévalence élevée inquiétante de résistance aux produits trypanocides a été rapportée récemment dans le département du Faro et Déo. Dans le cadre de la campagne panafricaine d’éradication des mouches tsétsé et des trypanosomoses (Pattec), le Cameroun est actuellement en train de préparer un projet commun avec le Tchad, la République d’Afrique centrale et le Nigeria pour éradiquer les mouches tsé-tsé et les trypanosomoses.