We previously reported, significantly higher levels of Chymase and Tryptase in early stage plasma of DSS patients prior to the occurrence of shock suggesting a possible role of mast cells in dengue pathogenesis. To further investigate, we analyzed CMA1 promoter SNP (rs1800875) and TPSAB1 gene alleles, which encode the Human Chymase and α- and β- tryptase 1 enzymes respectively, for susceptibility to Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) in patients from hospitals in Vietnam (Ho Chi Minh City and Vinh Long) and the Philippines. While the CMA1 promoter SNP (rs1800875) was not associated with DHF/DSS, the homozygous form of α-tryptase allele was associated with DSS patients in Vinh Long and the Philippines (OR=3.52, p<0.0001; OR=3.37, p<0.0001, respectively) and with DHF in Ho Chi Minh City (OR=2.54, p=0.0084). Also, a statistically significant association was observed when DHF and DSS were combined in Vinh Long (OR=1.5, p=0.034) and the Philippines (OR=2.36, p=0.0004); in Ho Chi Minh City when DHF and DSS were combine an association was observed, but it was not statistically significant (OR=1.5, p=0.0505). Therefore, the α-tryptase might have a possible effect on the susceptibility to severe form of Dengue infection.

Tick-borne pathogens such as species of Borrelia, Babesia, Anaplasma, Rickettsia, and Ehrlichia are widespread in the United States and Europe among wildlife, in passerines as well as in domestic and farm animals. Transmission of these pathogens occurs by infected ticks during their blood meal, carnivorism, and through animal bites in wildlife, whereas humans can become infected either by an infected tick bite, through blood transfusion and in some cases, congenitally. The reservoir hosts play an important role in maintaining pathogens in nature and facilitate transmission of individual pathogens or of multiple pathogens simultaneously to humans through ticks. Tick-borne co-infections were first reported in the 1980s in white-footed mice, the most prominent reservoir host for causative organisms in the United States, and they are becoming a major concern for public health now. Various animal infection models have been used extensively to better understand pathogenesis of tick-borne pathogens and to reveal the interaction among pathogens co-existing in the same host. In this review, we focus on the prevalence of these pathogens in different reservoir hosts, animal models used to investigate their pathogenesis and host responses they trigger to understand diseases in humans. We also documented the prevalence of these pathogens as correlating with the infected ticks’ surveillance studies. The association of tick-borne co-infections with other topics such as pathogens virulence factors, host immune responses as they relate to diseases severity, identification of vaccine candidates, and disease economic impact are also briefly addressed here.

BackgroundThe National Program for Chagas disease was implemented in Bolivia in 2006, and it greatly decreased the number of infections through vector control. Subsequently, a treatment regimen of benznidazole (BNZ) was started in seropositive school-age children living in certified vector control areas.Methods and findingsWe conducted a 12-month follow-up study and seven blood samples were taken during and after the treatment. Serology, conventional diagnostic PCR (cPCR) and quantitative Real-time PCR (qPCR) were performed. Plasma Th1/Th2/Th17 cytokines levels were also determined. Approximately 73 of 103 seropositive children complied with BNZ, with three interruptions due to side effects.To evaluate each individual’s treatment efficacy, the cPCR and qPCR values during the final 6 months of the follow-up period were observed. Among 57 children who completed follow-up, 6 individuals (11%) showed both cPCR(+) and qPCR(+) (non reactive), 24 (42%) cPCR(-) but qPCR(+) (ambiguous) and 27 (47%) cPCR(-) and qPCR(-) (reactive).Within 14 Th1/Th2/Th17 cytokines, IL-17A showed significantly higher levels in seropositive children before the treatment compared to age-matched seronegative children and significantly decreased to the normal level one-year after. Moreover, throughout the follow-up study, IL-17A levels were positively co-related to parasite counts detected by qPCR. At the 12 months’ time point, IL-17A levels of non-reactive subjects were significantly higher than either those of reactive or ambiguous subjects suggesting that IL-17A might be useful to determine the reactivity to BNZ treatment.ConclusionsPlasma levels of IL-17A might be a bio-marker for detecting persistent infection of T. cruzi and its chronic inflammation.

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